Mechanical Ventilation [1st ed.] 9781284125931

Table of contents :
Title Page......Page 2
Copyright Page......Page 3
Dedication......Page 5
Brief Contents......Page 6
Contents......Page 7
Foreword......Page 24
Preface......Page 25
How to Use This Text......Page 27
Note from the Authors......Page 35
Acknowledgements......Page 37
Contributing Authors......Page 38
Reviewers......Page 41
Chapter 1 Introduction to Critical Respiratory Care......Page 43
Overview......Page 46
Critical Respiratory Care......Page 47
Types of Intensive Care Units......Page 50
Patients......Page 53
Personnel......Page 56
Intensive Care Unit Design......Page 61
Other Units......Page 64
Review of the Medical Record......Page 67
Patient History......Page 77
Physical Examination......Page 79
Laboratory Studies......Page 81
Imaging in the ICU......Page 83
Bronchoscopy and Thoracentesis......Page 84
Cardiac Monitoring in the ICU......Page 85
Types of Respiratory Care Provided in the ICU......Page 88
Summary......Page 91
Key Points......Page 92
References......Page 94
Chapter 2 Respiratory Failure......Page 95
Overview......Page 99
Respiratory Failure......Page 100
Types of Respiratory Failure......Page 101
Indications for Mechanical Ventilatory Support......Page 107
Clinical Manifestations of Respiratory Failure......Page 108
Oxygenation......Page 113
Assessment of Ventilation......Page 155
Alveolar Ventilation and Dead Space......Page 157
Alveolar Ventilation and PaCO2......Page 164
Assessment of Acid-Base Balance......Page 167
Assessment of Cardiac and Circulatory Status......Page 182
Assessment of Cognitive and Neurologic Status......Page 186
Nutritional Status......Page 193
Prediction of ICU Outcomes......Page 195
Acute Asthma Exacerbation......Page 197
Acute Exacerbation of COPD......Page 201
Acute Respiratory Distress Syndrome......Page 210
Heart Failure......Page 214
Acute Myocardial Infarction......Page 217
Shock......Page 218
Sepsis......Page 220
Trauma......Page 221
Pulmonary Embolus and Deep Vein Thrombosis......Page 224
Neurologic and Neuromuscular Disease......Page 226
Summary......Page 234
Key Points......Page 235
References......Page 240
Chapter 3 Principles of Mechanical Ventilation......Page 244
Introduction to Mechanical Ventilation......Page 248
Ventilation......Page 253
Spontaneous Breathing......Page 256
Negative Pressure Breathing......Page 259
Positive Pressure Breathing......Page 261
Invasive vs. Noninvasive Ventilation......Page 273
Input Power and Control Systems......Page 282
Ventilator Variables: Breath Trigger......Page 289
Ventilator Variables: Breath Cycle......Page 291
Operator Interface......Page 298
Ventilator Classification or Taxonomy......Page 300
Continuous Mandatory Ventilation......Page 306
Intermittent Mandatory Ventilation......Page 310
Positive End-Expiratory Pressure......Page 314
Continuous Positive Airway Pressure......Page 316
Pressure-Support Ventilation......Page 320
Airway Pressure-Release Ventilation......Page 321
Automatic Tube Compensation......Page 325
Proportional Assist Ventilation......Page 328
Dual Modes and Adaptive Control......Page 330
High-Frequency Ventilation......Page 335
Neurally Adjusted Ventilatory Assist......Page 339
Flow Waveforms......Page 345
Inspiratory Pause......Page 347
FIO2......Page 349
PEEP/CPAP......Page 350
Alarms......Page 351
Humidification......Page 354
Sigh Breaths......Page 355
Pulmonary System......Page 358
Cardiovascular System......Page 368
Renal System......Page 370
Gastrointestinal System......Page 371
Central Nervous System......Page 372
Pulmonary......Page 375
Extrapulmonary Organ Systems......Page 378
Key Points......Page 382
References......Page 386
Chapter 4 Mechanical Ventilators......Page 389
Introduction......Page 392
HAMILTON-G5......Page 394
HAMILTON-C3......Page 411
HAMILTON–C1......Page 426
Getinge Servo-i......Page 438
Getinge Servo-u......Page 453
Covidien Puritan Bennett 840 Ventilator......Page 467
Covidien Puritan Bennett 980 Ventilator......Page 479
Newport e360 Ventilator......Page 491
Vyaire AVEA......Page 503
Vyaire VELA......Page 519
Dräger Evita Infinity V500......Page 532
Dräger Evita XL......Page 546
GE Healthcare CARESCAPE R860......Page 558
Philips Respironics V60 Ventilator......Page 572
Vyaire 3100B High-Frequency Oscillator......Page 581
Percussionaire VDR-4......Page 585
Bunnell Life Pulse......Page 589
HAMILTON-T1......Page 594
HAMILTON–MR1......Page 606
Airon pNeuton......Page 620
pNeuton mini......Page 622
pNeuton Models A and S......Page 623
Bio-Med Devices Crossvent 4+......Page 625
Vyaire ReVel......Page 630
Vyaire LTV 1200......Page 643
Dräger Carina......Page 652
Dräger Oxylog 3000 Plus......Page 659
Medtronic Newport HT70 Plus......Page 669
ZOLL Eagle II......Page 678
Philips Respironics Trilogy Ventilator......Page 686
DeVilbiss IntelliPAP Bilevel S......Page 696
DeVilbiss IntelliPAP AutoBilevel......Page 699
ResMed Lumis Tx......Page 702
ResMed Astral 100/150......Page 709
Dräger Babylog VN500......Page 717
Smiths Medical Pneupac babyPAC 100......Page 728
Vyaire Infant Flow SiPAP......Page 733
Key Points......Page 739
References......Page 741
Chapter 5 Indications for Mechanical Ventilation......Page 743
Introduction......Page 746
Ventilation......Page 748
Ventilatory Capacity......Page 751
Ventilatory Requirements......Page 759
Assessment of Ventilation......Page 762
Clinical Manifestations of Respiratory Failure......Page 767
Goals of Mechanical Ventilatory Support......Page 771
Apnea......Page 772
Acute Ventilatory Failure......Page 775
Impending Ventilatory Failure......Page 780
Severe Oxygenation Problems......Page 784
Contraindications to Mechanical Ventilation......Page 790
Patient Assessment for Ventilator Initiation......Page 794
Initial Ventilator Settings......Page 798
Key Points......Page 803
References......Page 806
Chapter 6 Ventilator Initiation......Page 808
Introduction......Page 811
Goals of Mechanical Ventilation......Page 813
Negative-Pressure Ventilation......Page 815
Positive-Pressure Ventilation......Page 816
Endotracheal Intubation......Page 830
Tracheostomy......Page 836
Choice of a Ventilator......Page 840
Choice of Mode......Page 842
More on Nomenclature......Page 845
Full and Partial Ventilatory Support......Page 846
Major Modes of Ventilation......Page 849
Pressure Control-Continuous Spontaneous Ventilation......Page 868
Other Modes of Ventilation......Page 874
Mode......Page 893
Tidal Volume and Rate......Page 895
Inspiratory Phase, Expiratory Phase, and I:E Ratio......Page 900
Alarms and Limits......Page 914
Patient Assessment......Page 915
Acute Exacerbation of COPD......Page 916
Acute Respiratory Distress Syndrome......Page 917
Neuromuscular Disease......Page 918
Summary......Page 920
Key Points......Page 921
References......Page 925
Chapter 7 Patient Stabilization: Adjusting Ventilatory Support......Page 927
Introduction......Page 930
Initiation of Mechanical Ventilation......Page 931
Patient–Ventilator Interaction......Page 934
Trigger Asynchrony......Page 936
Flow Asynchrony......Page 941
Cycle Asynchrony......Page 943
Mode Asynchrony......Page 947
Oxygenation......Page 949
FIO2......Page 950
PEEP/CPAP......Page 955
Recruitment Maneuvers......Page 971
Prone Positioning......Page 972
Bronchial Hygiene......Page 973
Tidal Volume, Rate, and Minute Ventilation......Page 975
Alveolar Ventilation......Page 976
Alveolar Ventilation and Paco2......Page 977
PaCO2 during Mechanical Ventilation......Page 979
Acid-Base Balance......Page 989
Respiratory Alkalosis......Page 992
Metabolic Alkalosis......Page 993
Cardiac and Cardiovascular Support......Page 995
Use of Sedation and Neuromuscular Blockade......Page 999
Summary......Page 1000
Key Points......Page 1001
References......Page 1005
Chapter 8 Critical Care Patient Assessment and Monitoring: Part I: Assessment......Page 1006
Introduction......Page 1010
Medical Record Review......Page 1011
History......Page 1014
Patient and/or Family Interview......Page 1016
Physical Assessment......Page 1023
Assessment of Mental Status......Page 1042
Neurologic Examination......Page 1046
Pain Monitoring......Page 1047
Ancillary Use of Equipment......Page 1049
Chest Tubes, Drainage, and Management......Page 1050
Urine Output Monitoring......Page 1052
Bedside Assessment in the ICU......Page 1053
Arterial Sampling......Page 1055
Arterial Line Insertion and Sampling......Page 1059
Venous Blood Gases......Page 1062
Sample Analysis......Page 1063
Arterial Blood Gas Interpretation......Page 1064
Hemoglobin and Hematocrit......Page 1066
Complete Blood Count......Page 1067
Clinical Chemistry......Page 1070
Portable Chest Radiographs......Page 1077
Ultrasound Imaging......Page 1078
Bedside Tests of Spontaneous Breathing......Page 1079
Electrocardiogram......Page 1089
Key Points......Page 1105
References......Page 1109
Chapter 9 Critical Care Patient Assessment and Monitoring Part II: Monitoring and Care......Page 1111
Overview......Page 1115
Introduction......Page 1116
ICU Patient Assessment......Page 1117
Monitoring Ventilation......Page 1118
Respiratory Rate......Page 1120
Tidal Volume and Minute Ventilation Measurement and Evaluation......Page 1121
Alveolar Ventilation and Dead Space......Page 1128
I:E Ratio......Page 1130
Tests of Spontaneous Breathing......Page 1133
Airway Pressures......Page 1135
Compliance, Resistance, and Work of Breathing......Page 1140
Pressure, Flow, and Volume Curves......Page 1151
Optimal PEEP and Recruitment Maneuvers......Page 1171
Types of Recruitment Maneuvers......Page 1173
Pulse Oximetry......Page 1178
Capnometry, Capnography, and VD/VT......Page 1185
Transcutaneous O2/CO2......Page 1197
Exhaled Nitric Oxide......Page 1202
Electrocardiogram Monitoring......Page 1203
Hemodynamic Monitoring......Page 1204
Cardiopulmonary Calculations......Page 1215
Mechanical Circulatory Assistance......Page 1218
Pain Monitoring......Page 1220
Renal Function and Urine Output Monitoring......Page 1221
Temperature Monitoring and Regulation in the ICU......Page 1222
Nutritional Support......Page 1223
Managing and Monitoring the Patient Airway......Page 1225
Endotracheal Tube Characteristics......Page 1231
Cuff Pressure and Volume......Page 1235
Managing the Artificial Airway......Page 1236
Tracheostomy Tubes......Page 1247
Patient Care......Page 1252
Bronchial Hygiene and Airway Care......Page 1253
Patient–Ventilator System Monitoring......Page 1256
Recognition and Treatment of Common Complications......Page 1260
Key Points......Page 1280
References......Page 1285
Chapter 10 Noninvasive Ventilation......Page 1289
Introduction......Page 1291
Chronic Obstructive Pulmonary Disease......Page 1292
Asthma......Page 1293
Cardiogenic Pulmonary Edema......Page 1294
Preintubation......Page 1295
Acute Respiratory Distress Syndrome......Page 1296
Bronchoscopy......Page 1298
Sleep Apnea and Obesity Hypoventilation Syndrome......Page 1299
Trauma......Page 1300
Neuromuscular Disease......Page 1301
Interface......Page 1304
Types of Ventilators......Page 1307
Settings......Page 1310
Ongoing Management......Page 1313
Monitoring......Page 1315
Discontinuing NIV......Page 1316
Facial Pressure Ulcers......Page 1317
High-Flow Nasal Cannula......Page 1320
Specialty Modes of NIV Support......Page 1321
Key Points......Page 1322
References......Page 1323
Chapter 11 High-Frequency Oscillatory Ventilation for Acute Respiratory Distress Syndrome in Adults......Page 1327
Introduction......Page 1329
Oxygenation......Page 1332
Lung Recruitment Maneuvers during HFOV......Page 1338
Ventilation......Page 1339
Prone Positioning......Page 1342
Inhaled Nitric Oxide......Page 1343
Tracheostomy......Page 1344
Transition to Extracorporeal Membrane Oxygenation......Page 1345
Fluctuation of mPaw and ∆P......Page 1347
Transition from HFOV to Lung-Protective Conventional Ventilation......Page 1348
Transport of Patients on HFOV......Page 1349
Bronchoscopy During HFOV......Page 1350
Pneumothorax......Page 1353
Endotracheal Tube Misplacement or Obstruction......Page 1354
Infection Control......Page 1355
Key Points......Page 1357
References......Page 1358
Chapter 12 Diagnostic and Supportive Procedures in the ICU......Page 1364
Introduction......Page 1367
Diagnostic Bronchoscopy......Page 1368
Thoracentesis......Page 1373
Temperature Regulation in the ICU......Page 1377
Overview and Definitions......Page 1383
Nutrition in the ICU......Page 1386
Indications......Page 1393
Methods......Page 1394
Discontinuance......Page 1396
Indications......Page 1400
Methods......Page 1401
Monitoring......Page 1406
Discontinuance of Mechanical Circulatory Support......Page 1407
Key Points......Page 1409
References......Page 1411
Chapter 13 Point-of-care Ultrasound in Critical Care......Page 1413
The History and Evolution of Point-of-care Ultrasound......Page 1415
Types of Transducers......Page 1416
Holding and Moving the Transducer......Page 1417
General Concepts......Page 1419
Parasternal Long-axis View......Page 1420
Parasternal Short-axis View......Page 1422
Apical Four-chamber View......Page 1423
Subcostal View......Page 1426
Assessment of Volume Responsiveness......Page 1428
General Concepts......Page 1431
Detection of Pneumothorax......Page 1432
Evaluation of Pleural Effusion......Page 1433
Characteristics of Pleural Effusion......Page 1434
Pleural Drainage Procedures......Page 1435
Determining the Etiology of Respiratory Failure......Page 1436
Anatomic Landmarks......Page 1438
Assessment for Ascites and Paracentesis......Page 1439
Vascular Access......Page 1441
Detection of Deep Vein Thrombosis......Page 1442
Ultrasound-Guided Lumbar Puncture......Page 1443
Key Points......Page 1445
References......Page 1447
Chapter 14 Mechanical Ventilation During Extracorporeal Membrane Oxygenation......Page 1448
Introduction......Page 1450
Decision to Transition to ECMO......Page 1451
Approach to ECMO......Page 1452
Transitioning Off ECMO......Page 1459
Emergent Transition from ECMO to Mechanical Ventilation......Page 1462
Special Respiratory Care Issues During ECMO......Page 1463
Key Points......Page 1465
References......Page 1466
Chapter 15 Neonatal and Pediatric Critical Care......Page 1468
Introduction......Page 1471
Fetal Lung Development......Page 1472
Fetal Circulation......Page 1473
Transition to Extrauterine Life......Page 1476
Recognizing Respiratory Distress......Page 1477
Other Causes of Respiratory Distress......Page 1478
Assess the Gestational Age of the Patient......Page 1479
Respiratory Distress Syndrome......Page 1481
Persistent Pulmonary Hypertension of the Newborn......Page 1485
Meconium Aspiration Syndrome......Page 1486
Chronic Lung Disease......Page 1487
Other Conditions Seen in Premature Infants......Page 1488
Pediatric ARDS......Page 1491
Asthma......Page 1495
Neurologic Conditions......Page 1497
Neuromuscular Diseases......Page 1499
Bronchiolitis......Page 1500
Cystic Fibrosis......Page 1501
Monitored Parameters......Page 1504
Expected Values for Important Respiratory Parameters......Page 1506
Endotracheal Tube Selection and Management......Page 1507
Securing the Endotracheal Tube......Page 1508
Noninvasive Support......Page 1509
Conventional Mechanical Ventilation......Page 1511
Helium–Oxygen Mixtures......Page 1519
Nitric Oxide......Page 1520
Subambient Oxygen and Inhaled Carbon Dioxide......Page 1526
Anesthetic Gas Mixtures......Page 1528
Extracorporeal Membrane Oxygenation......Page 1532
Indications......Page 1537
Cardiac Applications......Page 1539
Complications......Page 1540
Patient Transport......Page 1541
Mechanical Ventilation during Transport......Page 1542
Safety Implications......Page 1543
Key Points......Page 1544
References......Page 1546
Chapter 16 Ventilator Discontinuance......Page 1554
Introduction......Page 1556
Ventilator Discontinuation......Page 1558
Factors That Contribute to Ventilator Dependence......Page 1560
Ventilatory Capacity Versus Ventilatory Requirements......Page 1562
Reversal or Improvement of Disease or Condition......Page 1566
Assessment of Ventilation and Acid-Base Balance......Page 1567
Assessment of Cardiovascular and Hemodynamic Status......Page 1572
Assessment of Medical Condition......Page 1575
Assessment of the Airway......Page 1581
Weaning Indices......Page 1587
Methods......Page 1594
IMV/SIMV......Page 1595
Pressure-Support Ventilation......Page 1596
Spontaneous Breathing Trials......Page 1597
Newer Methods......Page 1600
Selection and Approach......Page 1601
Monitoring......Page 1602
Monitoring Following Extubation......Page 1603
Management of Postextubation Upper Airway Obstruction......Page 1606
Extubation Failure......Page 1607
Long-Term Ventilator Dependence......Page 1610
Terminal Weaning......Page 1615
Key Points......Page 1616
References......Page 1619
Appendix A Patient Assessment and the National Board for Respiratory Care (NBRC) Examinations......Page 1621
Appendix B Abbreviations......Page 1634
Appendix C Equations......Page 1640
Glossary......Page 1643
Index......Page 1664

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Brief Contents © Anna RubaK/ShutterStock, Inc.

Chapter 1

Introduction to Critical Respiratory Care

Chapter 2

Respiratory Failure

Chapter 3

Principles of Mechanical Ventilation

Chapter 4

Mechanical Ventilators

Chapter 5

Indications for Mechanical Ventilation

Chapter 6

Ventilator Initiation

Chapter 7

Patient Stabilization: Adjusting Ventilatory Support

Chapter 8

Critical Care Patient Assessment and Monitoring: Part I: Assessment

Chapter 9

Critical Care Patient Assessment and Monitoring Part II: Monitoring and Care

Chapter 10

Noninvasive Ventilation

Chapter 11

High-Frequency Oscillatory Ventilation for Acute Respiratory Distress Syndrome in Adults

Chapter 12

Diagnostic and Supportive Procedures in the ICU

Chapter 13

Point-of-care Ultrasound in Critical Care

Chapter 14

Mechanical Ventilation During Extracorporeal Membrane Oxygenation

Chapter 15

Neonatal and Pediatric Critical Care

Chapter 16

Ventilator Discontinuance

Contents © Anna RubaK/ShutterStock, Inc.

Foreword Preface How to Use This Text Note from the Authors Acknowledgements Contributing Authors Reviewers Chapter 1

Introduction to Critical Respiratory Care David C. Shelledy and Jay I. Peters Overview Critical Respiratory Care Types of Intensive Care Units Patients Personnel Intensive Care Unit Design Other Units Assessment of the Patient in the ICU Review of the Medical Record Patient History Physical Examination Laboratory Studies Imaging in the ICU Bronchoscopy and Thoracentesis Cardiac Monitoring in the ICU

Types of Respiratory Care Provided in the ICU Summary Key Points References Chapter 2

Respiratory Failure Jay I. Peters and David C. Shelledy Overview Respiratory Failure Types of Respiratory Failure Indications for Mechanical Ventilatory Support Clinical Manifestations of Respiratory Failure Assessment for Respiratory Failure Oxygenation Assessment of Ventilation Alveolar Ventilation and Dead Space Alveolar Ventilation and PaCO2 Assessment of Acid-Base Balance Assessment of Cardiac and Circulatory Status Assessment of Cognitive and Neurologic Status Nutritional Status Prediction of ICU Outcomes Management Principles for Patients in Respiratory Failure Acute Asthma Exacerbation Acute Exacerbation of COPD Acute Respiratory Distress Syndrome Heart Failure Acute Myocardial Infarction Shock Sepsis Trauma Pulmonary Embolus and Deep Vein Thrombosis Neurologic and Neuromuscular Disease Summary

Key Points References Chapter 3

Principles of Mechanical Ventilation Gregory A. Holt, Sheila A Habib, and David C. Shelledy Introduction to Mechanical Ventilation Ventilation Spontaneous Breathing Negative Pressure Breathing Positive Pressure Breathing Invasive vs. Noninvasive Ventilation Ventilator Principles Input Power and Control Systems Ventilator Variables: Breath Trigger Ventilator Variables: Breath Cycle Operator Interface Ventilator Classification or Taxonomy Ventilator Modes Continuous Mandatory Ventilation Intermittent Mandatory Ventilation Positive End-Expiratory Pressure Continuous Positive Airway Pressure Pressure-Support Ventilation Airway Pressure-Release Ventilation Automatic Tube Compensation Proportional Assist Ventilation Dual Modes and Adaptive Control High-Frequency Ventilation Neurally Adjusted Ventilatory Assist Ventilator Parameters Flow Waveforms Inspiratory Pause FIO2 PEEP/CPAP

Alarms Humidification Sigh Breaths Effects of Mechanical Ventilation on Organ Systems Pulmonary System Cardiovascular System Renal System Gastrointestinal System Central Nervous System Complications of Mechanical Ventilation Pulmonary Extrapulmonary Organ Systems Key Points References Chapter 4

Mechanical Ventilators John Davies Introduction Critical Care Ventilators HAMILTON-G5 HAMILTON-C3 HAMILTON–C1 Getinge Servo-i Getinge Servo-u Covidien Puritan Bennett 840 Ventilator Covidien Puritan Bennett 980 Ventilator Newport e360 Ventilator Vyaire AVEA Vyaire VELA Dräger Evita Infinity V500 Dräger Evita XL GE Healthcare CARESCAPE R860 Philips Respironics V60 Ventilator High-Frequency Ventilators

Vyaire 3100B High-Frequency Oscillator Percussionaire VDR-4 Bunnell Life Pulse Portable Ventilators HAMILTON-T1 HAMILTON–MR1 Airon pNeuton pNeuton mini pNeuton Models A and S Bio-Med Devices Crossvent 4+ Vyaire ReVel Vyaire LTV 1200 Dräger Carina Dräger Oxylog 3000 Plus Medtronic Newport HT70 Plus ZOLL Eagle II Philips Respironics Trilogy Ventilator DeVilbiss IntelliPAP Bilevel S DeVilbiss IntelliPAP AutoBilevel ResMed Lumis Tx ResMed Astral 100/150 Neonatal Ventilators Flow SiPAP Dräger Babylog VN500 Smiths Medical Pneupac babyPAC 100 Vyaire Infant Flow SiPAP Key Points References Chapter 5

Indications for Mechanical Ventilation David C. Shelledy and Jay I. Peters Introduction Ventilation Ventilatory Capacity

Ventilatory Requirements Assessment of Ventilation Clinical Manifestations of Respiratory Failure Goals of Mechanical Ventilatory Support Indications for Mechanical Ventilation Apnea Acute Ventilatory Failure Impending Ventilatory Failure Severe Oxygenation Problems Complications, Hazards, and Contraindications Contraindications to Mechanical Ventilation Patient Assessment for Ventilator Initiation Initial Ventilator Settings Key Points References Chapter 6

Ventilator Initiation David C. Shelledy and Jay I. Peters Introduction Goals of Mechanical Ventilation Methods of Ventilation Negative-Pressure Ventilation Positive-Pressure Ventilation Establishment of the Airway Endotracheal Intubation Tracheostomy Choice of a Ventilator Choice of Mode More on Nomenclature Full and Partial Ventilatory Support Major Modes of Ventilation Pressure Control-Continuous Spontaneous Ventilation Other Modes of Ventilation Initial Ventilator Settings

Mode Tidal Volume and Rate Breath Trigger Inspiratory Phase, Expiratory Phase, and I:E Ratio PEEP and CPAP Alarms and Limits Humidification Patient Assessment Management of Specific Disease States and Conditions Asthma Acute Exacerbation of COPD Severe Pneumonia Acute Respiratory Distress Syndrome Neuromuscular Disease Summary Key Points References Chapter 7

Patient Stabilization: Adjusting Ventilatory Support David C. Shelledy and Jay I. Peters Introduction Initiation of Mechanical Ventilation Patient–Ventilator Interaction Trigger Asynchrony Flow Asynchrony Cycle Asynchrony Mode Asynchrony Oxygenation FIO2 PEEP/CPAP Recruitment Maneuvers Prone Positioning Bronchial Hygiene Ventilation

Tidal Volume, Rate, and Minute Ventilation Alveolar Ventilation Alveolar Ventilation and Paco2 PaCO2 during Mechanical Ventilation Acid-Base Balance Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis Cardiac and Cardiovascular Support Use of Sedation and Neuromuscular Blockade Summary Key Points References Chapter 8

Critical Care Patient Assessment and Monitoring: Part I: Assessment J. Brady Scott, Joe Hylton, Jon C. Inkrott, and David C. Shelledy Introduction History and Physical Assessment Medical Record Review History Patient and/or Family Interview Physical Assessment Assessment of Mental Status Neurologic Examination Pain Monitoring Ancillary Use of Equipment Chest Tubes, Drainage, and Management Urine Output Monitoring Bedside Assessment in the ICU Blood Gases Arterial Sampling Arterial Line Insertion and Sampling

Venous Blood Gases Sample Analysis Arterial Blood Gas Interpretation Laboratory Studies Hemoglobin and Hematocrit Complete Blood Count Clinical Chemistry Imaging in the ICU Portable Chest Radiographs Ultrasound Imaging Pulmonary Function Testing Bedside Tests of Spontaneous Breathing Electrocardiogram Key Points References Chapter 9

Critical Care Patient Assessment and Monitoring Part II: Monitoring and Care J. Brady Scott, Joe Hylton, Jon C. Inkrott, and David C. Shelledy Overview Introduction ICU Patient Assessment Monitoring Oxygenation Monitoring Ventilation Ventilatory Parameters and Mechanical Ventilation Respiratory Rate Tidal Volume and Minute Ventilation Measurement and Evaluation Alveolar Ventilation and Dead Space I:E Ratio Tests of Spontaneous Breathing Monitoring During Mechanical Ventilation Airway Pressures Compliance, Resistance, and Work of Breathing Ventilator Graphics

Pressure, Flow, and Volume Curves Optimal PEEP and Recruitment Maneuvers Types of Recruitment Maneuvers Noninvasive Monitoring Pulse Oximetry Capnometry, Capnography, and VD/VT Transcutaneous O2/CO2 Exhaled Nitric Oxide Cardiac and Hemodynamic Monitoring Electrocardiogram Monitoring Hemodynamic Monitoring Cardiopulmonary Calculations Mechanical Circulatory Assistance Other Assessment Parameters Assessment of the Mental Status and Neurologic Function Pain Monitoring Intracranial Pressure Monitoring Renal Function and Urine Output Monitoring Chest Tubes, Drainage, and Management Temperature Monitoring and Regulation in the ICU Nutritional Support Managing and Monitoring the Patient Airway Endotracheal Tube Characteristics Cuff Pressure and Volume Managing the Artificial Airway Tracheostomy Tubes Patient Care Bronchial Hygiene and Airway Care Patient–Ventilator System Monitoring Recognition and Treatment of Common Complications Key Points References

Chapter 10

Noninvasive Ventilation Keith D. Lamb, J. Brady Scott, and Carl R. Hinkson Introduction Indications Chronic Obstructive Pulmonary Disease Asthma Cardiogenic Pulmonary Edema Immunocompromised Patients Postextubation Preintubation Acute Respiratory Distress Syndrome Palliative Care Bronchoscopy Community-Acquired Pneumonia Sleep Apnea and Obesity Hypoventilation Syndrome Trauma Long-Term Applications Neuromuscular Disease Equipment Interface Types of Ventilators Initiation Settings Ongoing Management Monitoring Recognizing Failure of NIV Where NIV Should Be Started and Managed Discontinuing NIV Complications and Hazards Facial Pressure Ulcers Special Considerations High-Flow Nasal Cannula Specialty Modes of NIV Support

Key Points References Chapter 11

High-Frequency Oscillatory Ventilation for Acute Respiratory Distress Syndrome in Adults Stephen Derdak Introduction Oxygenation Lung Recruitment Maneuvers during HFOV Ventilation Adjuncts to HFOV Prone Positioning Aerosol Medication Delivery Inhaled Nitric Oxide Tracheostomy Transition to Extracorporeal Membrane Oxygenation Fluctuation of mPaw and ∆P Transition from HFOV to Lung-Protective Conventional Ventilation Transport of Patients on HFOV Bronchoscopy During HFOV Troubleshooting During HFOV Pneumothorax Endotracheal Tube Misplacement or Obstruction Infection Control Key Points References

Chapter 12

Diagnostic and Supportive Procedures in the ICU Adriel Malave and Kevin Proud Introduction Bronchoscopy Diagnostic Bronchoscopy Thoracentesis Supportive Procedures

Temperature Regulation in the ICU Dialysis in the ICU Overview and Definitions Nutrition in the ICU Extracorporeal Membrane Oxygenation Indications Methods Monitoring During ECMO Discontinuance Mechanical Circulatory Assistance Indications Methods Monitoring Discontinuance of Mechanical Circulatory Support Key Points References Chapter 13

Point-of-care Ultrasound in Critical Care Kevin Proud, Sheila Habib, Patricio De Hoyos, and Nilam Soni Introduction The History and Evolution of Point-of-care Ultrasound Types of Transducers Holding and Moving the Transducer Cardiac Ultrasound General Concepts Parasternal Long-axis View Parasternal Short-axis View Apical Four-chamber View Subcostal View Assessment of Volume Responsiveness Lung Ultrasound General Concepts Detection of Pneumothorax Evaluation of Pleural Effusion

Characteristics of Pleural Effusion Pleural Drainage Procedures Determining the Etiology of Respiratory Failure Abdominal Ultrasound General Concepts Anatomic Landmarks Assessment for Ascites and Paracentesis Vascular Ultrasound Vascular Access Detection of Deep Vein Thrombosis Ultrasound-Guided Lumbar Puncture Key Points References Chapter 14

Mechanical Ventilation During Extracorporeal Membrane Oxygenation Stephen Derdak Introduction Goals of ECMO Decision to Transition to ECMO Approach to ECMO Transitioning Off ECMO Emergent Transition from ECMO to Mechanical Ventilation Special Respiratory Care Issues During ECMO Key Points References

Chapter 15

Neonatal and Pediatric Critical Care Craig Wheeler and Craig D. Smallwood Introduction Fetal Lung Development Fetal Circulation Transition to Extrauterine Life Recognizing Respiratory Distress

Is the Process of Primary Cardiac or Respiratory Origin? Other Causes of Respiratory Distress Assess the Gestational Age of the Patient Common Neonatal Respiratory Conditions Respiratory Distress Syndrome Transient Tachypnea of the Newborn Persistent Pulmonary Hypertension of the Newborn Meconium Aspiration Syndrome Chronic Lung Disease Other Conditions Seen in Premature Infants Common Pediatric Respiratory Conditions Pediatric ARDS Asthma Neurologic Conditions Neuromuscular Diseases Bronchiolitis Cystic Fibrosis Monitored Parameters Expected Values for Important Respiratory Parameters Endotracheal Tube Selection and Management Securing the Endotracheal Tube Noninvasive Support Conventional Mechanical Ventilation Inhaled Gas Mixtures Helium–Oxygen Mixtures Nitric Oxide Subambient Oxygen and Inhaled Carbon Dioxide Anesthetic Gas Mixtures Extracorporeal Membrane Oxygenation Indications Cardiac Applications Complications Patient Transport

Adverse Events Mechanical Ventilation during Transport Safety Implications Key Points References Chapter 16

Ventilator Discontinuance Kevin Proud, David Shelledy, and Jay Peters Introduction Ventilator Discontinuation Factors That Contribute to Ventilator Dependence Ventilatory Capacity Versus Ventilatory Requirements Patient Evaluation Reversal or Improvement of Disease or Condition Assessment of Oxygenation Assessment of Ventilation and Acid-Base Balance Assessment of Cardiovascular and Hemodynamic Status Assessment of Medical Condition Assessment of the Airway Weaning Indices Methods IMV/SIMV Pressure-Support Ventilation Spontaneous Breathing Trials Newer Methods Selection and Approach Monitoring Extubation Monitoring Following Extubation Management of Postextubation Upper Airway Obstruction Extubation Failure Long-Term Ventilator Dependence Terminal Weaning Key Points

References Appendix A Patient Assessment and the National Board for Respiratory Care (NBRC) Examinations Appendix B Abbreviations Appendix C Equations Glossary Index

Foreword © Anna RubaK/ShutterStock, Inc.

s a practicing pulmonary and critical care physician for over 25 years, and as a professor, researcher, and mentor actively involved in the education of physicians, nurses, and respiratory therapists, I am delighted to see a new textbook aimed at developing advanced practice, critical care respiratory therapists. Respiratory therapists, advanced nurse practitioners, physicians, and physician assistants caring for patients receiving mechanical ventilation in the intensive care unit (ICU) need a textbook and reference to help them provide the respiratory care needed for their critically ill patients. The complexity of modern critical care medicine, as well as the dizzying array of options available to provide ventilatory support, make it essential that all members of the interprofessional team be able to learn and understand the important concepts, assessment skills, tasks, and procedures needed to provide safe and effective mechanical ventilation. I believe this text will help fill the gap for respiratory care clinicians as they strive to provide the very best care for their patients.

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Antonio R. Anzueto, MD Professor Division of Pulmonary and Critical Care Medicine University of Texas Health San Antonio

Preface © Anna RubaK/ShutterStock, Inc.

his text was created for students and clinicians concerned with the care of patients requiring mechanical ventilatory support. It is our intent to provide a comprehensive guide to the assessment and evaluation of the critically ill patient, initiation of mechanical ventilatory support, patient stabilization, monitoring, and ventilator discontinuance.

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Chapter Overview The text begins with Chapter 1 An Introduction to Critical Respiratory Care followed by Chapter 2 Respiratory Failure, which includes: Assessment of oxygenation Ventilation Acid-base status Chapters 3 and 4 review principles of mechanical ventilation followed by a detailed description of the commonly used ventilators seen in the ICU. Chapter 5 Indications for mechanical ventilation are next discussed to include invasive and noninvasive ventilation. Ventilator commitment (Chapter 6) is then described to include: Establishment of the airway Choice of ventilator Mode of ventilation Initial ventilator settings Patient stabilization is then described in Chapter 7 with a focus on: Patient–ventilator synchrony

The use of ventilator graphics Maintenance of oxygenation Ventilation Acid-base balance Hemodynamic status This is followed by a thorough review of the care and monitoring of the patient (Chapters 8 and 9), to include use of sedation and nutritional status. The text continues with Chapters 10 through 14 on noninvasive ventilation, highfrequency ventilation, and special procedures in the ICU, to include diagnostic procedures (e.g., ultrasound in the ICU) and supportive procedures to include mechanical circulatory assistance and ECMO. Chapter 15 covers neonatal and pediatric critical respiratory care. The text concludes with Chapter 16, which is devoted to the evaluation of the patient for ventilator discontinuance and methods and techniques used in the care and monitoring of the patient following extubation. It is important to note that integration of the content that will be needed to successfully pass the National Board for Respiratory Care examinations is provided throughout.

How to Use This Text © Anna RubaK/ShutterStock, Inc.

his text allows the reader to bridge the gap between theory and practice in the care of critically ill patients requiring mechanical ventilatory support. The reader will apply assessment skills to the evaluation of patients in impending or actual respiratory failure, and learn the techniques needed for the management of patients requiring mechanical ventilation. Clinical Focus Exercises. Each chapter includes “Clinical Focus” exercises designed to help the reader refine his or her critical-thinking and problem-solving skills. The “Clinical Focus” exercises serve as mini-case studies with problems for the reader to solve. They can be used for individual study, as course assignments, or as part of a robust class discussion.

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CLINICAL FOCUS 3-1 Negative Pressure Ventilation Your patient is a 4-year-old boy diagnosed with spinal muscle atrophy (SMA) since birth. He is chronically hypercarbic and a decision must be made concerning tracheostomy and mechanical ventilation. The parents are adamantly opposed to tracheostomy. The patient’s respiratory rate (f) is 28 breaths/min, blood pressure (BP) is 135/68, and heart rate (HR) is 105. He is diaphoretic and appears to be in distress. The most recent arterial blood gas (ABG) on room air (RA) is: pH PaCO2

7.31 65 mmHg

PaO2

55 mmHg

HCO3−

32 mEq/L

SaO2

89%

A decision to institute negative pressure ventilation was agreed upon. The Hayek chest cuirass was used and set to –18 cm H2O to maintain a VT between

100 to 130 mL/breath (patient weight is 14 kg and the estimated VT desired was 8 mL/kg). The ventilator was set in a respiratory synchronization mode with a backup rate of 18 breaths/min. Supplemental O2 was bled into the system at 4 L/min. Within the next 2 hours, the patient seemed more comfortable. An ABG drawn at 15 minutes post negative pressure ventilation initiation is shown in (A) and at 2 hours in (B):

The plan was to reduce the backup rate as the patient’s spontaneous rate increased. Urine output and renal function would be monitored. PETCO2 and O2 by pulse oximetry would be monitored continuously and ABGs would be drawn in the morning and as needed (PRN). The parents seemed happy. Questions: 1. How would you classify each of the three ABGs? 2. Was the chest cuirass successful in reversing the ventilatory failure? 3. Do you anticipate a continued decrease in the bicarbonate level? Answers: 1. Blood gas classification Initial: Partially compensated respiratory acidosis with moderate hypoxemia. A. Compensated respiratory acidosis with normoxemia. B. Within normal limits (WNL). 2. Yes. 3. Possibly. If the PaCO2 rises, the HCO3− may increase. If the PaCO2 does not change, the HCO3− may decrease a bit as the pH moves closer to 7.40.

RC Insights are interspersed throughout the text to provide the clinician with useful tips on patient assessment and management.

RC Insights Respiratory rate ≥ 35 breaths/min, severe respiratory distress with air hunger, diaphoresis, and accessory muscle use may signal impending respiratory arrest and the need to institute mechanical ventilatory support.

Key Points are listed at the end of each chapter and summarize the important facts and concepts that students should learn.

Key Points The primary function of a mechanical ventilator is to augment or replace normal ventilation. The four major indications for mechanical ventilation are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. The major goals of mechanical ventilation are to provide adequate alveolar ventilation, ensure adequate tissue oxygenation, restore and maintain acid-base balance, and reduce the work of breathing. The most common trigger variables are time and patient effort (i.e., patient triggered). Cycle variables include volume, pressure, flow and time. With volume control ventilation a constant tidal volume is delivered; inspiratory pressure varies with changes in the patient’s compliance and resistance. With pressure control ventilation a constant inspiratory pressure is delivered; tidal volume varies with changes in the patient’s compliance, resistance, and inspiratory effort. With continuous mandatory ventilation (CMV), every breath is a mandatory breath. With intermittent mandatory ventilation (IMV) mandatory breaths are interspersed with spontaneous breaths. Each chapter contains Tables that highlight important information. TABLE 2-5 Mixed Venous Oxygen Levels

A mixed venous blood sample is obtained from a pulmonary artery (Swan-Ganz) catheter and contains venous blood that has been returned to the right side of the heart via the superior and inferior vena cava. A blood sample may be drawn from the distal port of the pulmonary artery catheter and analyzed to determine oxygen levels. Normal values, as well as clinically acceptable values, are listed.

In addition, this text is highly illustrated with diagrams and photos demonstrating a variety of concepts such as Figure 3-19.

FIGURE 3-19 Graphic Representation of Anticipated Aeration of Lung Units in ARDS Patients in the Supine (A, C) and Prone (B, D) Positions. From Henderson WR Griesdale DE Dominelli P, Ronco R Does prone positioning improve oxygenation and reduce mortality in patients with acute respiratory distress syndrome? Can Respir J. 2014;21(4):213–215.

Throughout the text, key points are illustrated and important information is highlighted in Boxes to ensure comprehension and to aid the study of critical

materials.

BOX 2-3 Ventilatory Failure Ventilatory failure may be defined as an elevated PaCO2 greater than 45–50 mmHg. Other terms sometimes used to describe an elevated PaCO2 (i.e., ventilatory failure) include hypoventilation, hypercapnea, and respiratory acidosis. Types of ventilatory failure include: ∎ Acute ventilatory failure: a sudden increase in arterial PaCO with a 2 corresponding decrease in pH. ∎ Chronic ventilatory failure: a chronically elevated PaCO with a normal or 2 near-normal pH due to metabolic compensation (although complete compensation generally does not occur—see expected compensation). ∎ Acute ventilatory failure superimposed on chronic ventilatory failure: a chronically elevated PaCO2 followed by an acute increase in PaCO2 and a corresponding decrease in pH. Patients with ventilatory failure are generally hypoxemic if supplemental oxygen is not provided. Apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems requiring PEEP or CPAP are indications for mechanical ventilation.

The text should be of great value to individuals preparing for the examinations administered by the National Board for Respiratory Care (NBRC). Integration of the content that will be needed to successfully pass the NBRC Therapist Multiple-Choice Examination, clinical simulation examination, and adult critical-care specialist examination is included throughout. A brief note on the use of abbreviations: aka is used in place of “also known as”; e.g. is the abbreviation for the Latin phrase, exempli gratia, which means “for example”; and i.e. (which comes from the Latin phrase id est) means “that is” or “in other words.”

Instructor Resources Qualified instructors will receive a full suite of instructor resources, including the following: A comprehensive chapter-by-chapter PowerPoint deck

A test bank containing questions on a chapter-by-chapter basis as well as a midterm and a final A sample syllabus to organize the structure of the class. A comprehensive PowerPoint deck dedicated to all current Mechanical Ventilators broken into four sections: Section I Representative Critical Care Ventilators HAMILTON-G5 Getinge Servo-u Covidien Puritan Bennett 980 Ventilator Vyaire AVEA Dräger Evita Infinity V500 Philips Respironics V60 Ventilator Section II Additional Critical Care Ventilators HAMILTON-C3 HAMILTON-C1 Getinge Servo-i Covidien Puritan Bennett 840 Ventilator Newport e360 Ventilator Vyaire AVEA Dräger Evita XL GE Healthcare CARESCAPE R860 Section III High-Frequency Ventilators Vyaire 3100B High-Frequency Oscillator Percussionaire VDR-4 Bunnell Life Pulse Section IV Portable, Transport and Non-invasive Ventilators HAMILTON-T1 HAMILTON-MR1 Airon pNeuton pNeuton mini pNeuton A and S Bio-Med Devices Crossvent 4+ Vyaire ReVel Vyaire LTV 1200

Dräger Carina Dräger Oxylog 3000 Plus Medtronic Newport HT 70 Plus ZOLL Eagle II Philips Respironics Trilogy Ventilator DeVilbiss IntelliPAP Bilevel S DeVilbiss IntelliPAP AutoBilevel ResMed Lumis Tx ResMed Astral 100/150 Section IV Neonatal Ventilators Dräger Babylog VN500 Smiths Medical Pneupac babyPAC 100 Vyaire Infant Flow SiPAP

Note from the Authors © Anna RubaK/ShutterStock, Inc.

espiratory therapists spend much of their time in the acute care setting taking care of critically ill patients receiving mechanical ventilatory support. Types of respiratory care provided in the ICU include mechanical ventilation, patient monitoring, and development and administration of respiratory care plans and protocols and performance of special procedures. Critically ill patients are at high risk for actual or potential life-threatening problems, and the management of these patients is a core competency for the advanced practice respiratory therapist. The advanced practice respiratory therapist provides diagnostic, therapeutic, and critical care services. Advanced practice respiratory therapists should be able to take medical histories and record progress notes, examine and treat patients, interpret diagnostic tests, assist with diagnostic studies, and provide acute and critical care to patients. The respiratory therapist serving in the critical care unit should able to initiate, adjust, monitor, and manage mechanical ventilatory support. This includes recognition of acute respiratory failure, establishment and maintenance of the airway, initial ventilator setup, application of advanced modes of ventilation, patient stabilization, and monitoring and application of rescue techniques such as recruitment maneuvers, high-frequency ventilation, prone positioning, and extracorporeal life-support (ECMO). The application of techniques and procedures for successful ventilator discontinuance and positive patient outcomes is essential. Although this text is primarily aimed at providing the advanced practice respiratory therapist with the knowledge and skills needed to provide respiratory care and ventilatory support to critically ill patients, we believe that the information contained will be of great value to those who prescribe respiratory care, and for all healthcare practitioners interested in optimizing outcomes for patients in the ICU. Throughout

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the text we use the term respiratory care clinician to refer to healthcare practitioners who, as a part of the interprofessional team, provide respiratory assessment, treatment, and care of patients in the ICU. It’s our hope that this text will allow the reader to bridge the gap between theory and practice. Evidence-based recommendations are included throughout. This text should also be of great value to individuals preparing for the examinations administered by the National Board for Respiratory Care.

Acknowledgments © Anna RubaK/ShutterStock, Inc.

here are number of people to thank for their contributions to the success of this project. We would especially like to thank our chapter authors whose hard work is demonstrated within these pages. We would also like to thank everyone at Jones & Bartlett Learning who patiently assisted us in the process of developing an outstanding text. We would also offer our sincere thanks to the faculty and staff at the University of Texas Health Science Center at San Antonio (UT Health San Antonio). Without their support, this text would not have been possible.

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Contributing Authors © Anna RubaK/ShutterStock, Inc.

John Davies, MA, RRT, FAARC, FCCP Clinical Research Coordinator Duke Health System Durham, North Carolina Patricio De Hoyos, MD Senior Research Fellow Division of Pulmonary & Critical Care Medicine UT Health San Antonio San Antonio, Texas Stephen Derdak, DO Clinical Professor Pulmonary/Critical Care Medicine San Antonio Military Medical Center Ft Sam Houston, Texas Sheila A. Habib, MD Assistant Professor of Medicine Division of Pulmonary & Critical Care Medicine UT Health San Antonio South Texas Veterans Health Care System San Antonio, Texas Carl R. Hinkson, MSc, RRT-ACCS, RRT-NPS, FAARC Director, Pulmonary Service Line Providence Regional Medical Center Everett Everett, Washington Gregory A. Holt, PhD RRT FAASM Diplomate, American Board of Sleep Medicine Respiratory Quality Services Director of Operations–Houston, Texas

Joe Hylton, MA, BSRT, RRT-ACCS/NPS, NRP, FAARC, FCCM Clinical Application Specialist Hamilton Medical, AG Reno, Nevada Transport Respiratory Therapist/Paramedic Atrium Health Air Charlotte, North Carolina Jon C. Inkrott, RRT, RRT-ACCS Flight Respiratory Therapist, Florida Flight 1 Department of Flight Medicine and EMS Florida Hospital Orlando Orlando, Florida Keith D Lamb, RRT, RRT-ACCS, FAARC, FCCM Director, ECMO INOVA Heart and Vascular Institute INOVA Fairfax Medical Campus Falls Church, Virginia Adriel Malavé, MD, FCCP Associate Professor of Medicine Division of Pulmonary & Critical Care Medicine UT Health San Antonio South Texas Veterans Health Care System San Antonio, Texas J Brady Scott, MSc, RRT, RRT-ACCS, AE-C, FAARC, FCCP Associate Professor and Director of Clinical Education Department of Cardiopulmonary Sciences College of Health Sciences Rush University Rush University Medical Center Chicago, Illinois Nilam J. Soni, MD, MSc Associate Professor of Medicine Divisions of General & Hospital Medicine and Pulmonary & Critical Care Medicine South Texas Veterans Health Care System UT Health San Antonio San Antonio, Texas Craig D Smallwood, PhD, RRT Research Associate

Department of Anesthesia, Critical Care and Pain Medicine Boston Children’s Hospital Boston, Massachusetts Harvard Medical School Boston, Massachusetts Craig Wheeler MS, RRT-NPS Supervisor Department of Respiratory Care Boston Children’s Hospital Boston, Massachusetts

Reviewers © Anna RubaK/ShutterStock, Inc.

We would like to acknowledge the following reviewers: Stacia E Biddle, Med, RRT Associate Professor, Program Director The University of Akron Akron, Ohio Misty Carlson, M.S., RRT Director of Clinical Education, Assistant Professor Daytona State College Daytona Beach, Florida Stephanie U Cross, MS, RRT, RPFT Program Director, Assistant Professor Shenandoah University Winchester, Virginia Christopher D Henderson, MSSL, RRT Assistant Professor Marshall University Huntington, West Virginia Thomas Lamphere, BS, RRT-ACCS, RPFT, FAARC Instructor Gwynedd Mercy University Sellerssville, Pennsylvania Joel S Livesay, MS, RRT, RVT Department Chair Spartanburg Community College Spartanburg, South Carolina Glenn R Pippen II, RRT Clinical Education Coordinator

Shelton State Community College Tuscaloosa, Alabama Barry E Ransom, BS, RRT-NPS Director of Clinical Education Rutgers University Newark, New Jersey John A Rutkowski, AS, BA, MBA, MPA, FAARC, FACHE Associate Professor, Respiratory Therapy Program Director County College of Morris Hopatcong, New Jersey Missy Skeens, BA, RRT-NPS, RPFT Program Director/Professor Big Sandy Community & Technical College Paintsville, Kentucky Christopher Paul Trotter, MH, EdS, RRT Associate Professor Respiratory Care Coordinator of Degree Advancement Program Marshall University Huntington, West Virginia Rita F Waller, BS, BSN, MSN Program Director Augusta Technical College North Augusta, South Carolina

CHAPTER

1 Introduction to Critical Respiratory Care David C. Shelledy and Jay I. Peters

© Anna RubaK/ShutterStock, Inc.

OUTLINE Overview Critical Respiratory Care Types of Intensive Care Units (ICUs) Patients Personnel Intensive Care Unit Design Other Units Assessment of the Patient in the ICU Review of the Medical Record Patient History Physical Examination Laboratory Studies Imaging in the ICU Bronchoscopy and Thoracentesis Cardiac Monitoring in the ICU Types of Respiratory Care Provided in the ICU Summary

OBJECTIVES 1. 2. 3.

Define respiratory care and critical care. Summarize the disease states or conditions that often require ICU admission and mechanical ventilatory support. Contrast the types of patients seen in the medical intensive care unit (MICU), surgical intensive care unit

4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23.

(SICU), coronary care unit (CCU), pediatric intensive care unit (PICU), and neonatal intensive care unit (NICU). Explain the differences between Level I, II, III, and IV neonatal levels of care. Describe the types of services provided in a Level I Trauma Center. Explain the types of personnel and their qualifications needed to staff the ICU. Explain the importance of interprofessional practice (IPP) in the ICU. Contrast the design and activities associated with each of the four zones or areas found in the ICU. Explain the differences between an acute care hospital ward, step-down unit, and ICU. Explain the term long-term acute care (LTAC) to include the types of patients seen in an LTAC facility. Explain the difference between a specialty hospital and a skilled nursing facility (SNF). Explain the importance of assessment of the respiratory care patient in the ICU to include types of assessment procedures and methods used. Identify common admitting diagnoses seen in the ICU. Explain the significance of specific physician’s orders in the ICU to include medication orders for respiratory care, laboratory testing, imaging, and special procedures. Describe the elements of the history and physical examination performed in the ICU. Recognize and contrast the signs and symptoms of hypoxia, hypercapnea, respiratory failure, and ventilatory failure. Describe the importance of specific laboratory tests and imaging procedures performed in the ICU. Explain the purpose of bronchoscopy and thoracentesis performed in the intensive care unit. Describe the types of cardiac and hemodynamic monitoring performed in the ICU. Contrast the terms acute respiratory failure and acute ventilatory failure. Recognize the indications for mechanical ventilatory support. Describe the use of airway clearance therapies (ACT) in the ICU. Summarize the types of care often provided by respiratory therapists in the ICU.

KEY TERMS acute respiratory distress syndrome (ARDS) acute respiratory failure (ARF) acute ventilatory failure (AVF) atelectasis bronchoscopy bronchoalveolar lavage (BAL) cardiac arrhythmia cerebral infarction chronic obstructive pulmonary disease (COPD) coma conduction disorders congestive heart failure (CHF) coronary artery disease (CAD) coronary care unit (CCU) critical care endobronchial ultrasound (EBUS) exudate heart failure intensive care unit (ICU) interprofessional education (IPE) interprofessional practice (IPP) intracranial hemorrhage long-term acute care (LTAC) mechanical ventilation mechanical ventilatory support medical intensive care unit (MICU)

musculoskeletal disease myocardial infarction (MI) neonatal intensive care unit (NICU) neuromuscular disease pediatric intensive care unit (PICU) pneumonia pulmonary edema renal failure respiratory care respiratory failure respiratory therapist sepsis shock step-down unit surgical intensive care unit (SICU) thoracentesis tracheostomy transudate trauma center

Overview The purpose of this chapter is to introduce the reader to critical respiratory care and mechanical ventilation. We will review the definitions of respiratory care and critical care, discuss various types of intensive care units, and introduce patient assessment as applied to the intensive care unit (ICU) patient. Types of respiratory care provided in the ICU will also be reviewed, to include ventilatory support, patient monitoring, care plans and protocols, and special procedures.

Critical Respiratory Care Respiratory care may be defined as the healthcare discipline that specializes in the promotion of optimum cardiopulmonary function and health.1 Respiratory care is specifically focused on the assessment, diagnostic evaluation, treatment, and care of patients with deficiencies and abnormalities of the cardiopulmonary system. Thus, the treatment and support of patients in respiratory failure is a core respiratory care competency. Respiratory care may be provided by physicians, nurses, physician assistants, or other healthcare providers. The respiratory therapist is specifically trained and educated to deliver respiratory care to patients across multiple settings, including acute care hospitals and ICUs. Respiratory therapists are trained in cardiopulmonary physiology and pathophysiology, the principles of biomedical engineering, and the application of technology to assist in the provision of patient care services. Respiratory therapists apply scientific principles to prevent, identify, and treat acute or chronic dysfunction of the cardiopulmonary system. Thus, the respiratory therapist must also attend to the prevention of cardiopulmonary disease and the management of patients with chronic disease. The practice of respiratory care extends to the patient, the patient’s family, and public education. Critically ill patients are at high risk for actual or potential life-threatening health problems.2 Critical care is a term used to refer to the care and management of critically ill patients who require sophisticated support, careful and constant monitoring, and complex decision making to ensure that therapy is adjusted as patients’ needs change. Critically ill patients suffer from a wide range of diseases and disorders that often result in multiorgan system failure. Examples include shock, trauma, cardiac disease, hemodynamic instability, renal failure, neurologic disease, liver failure, and acute pulmonary disease. Critically ill patients are often physiologically unstable, requiring comprehensive care and minute-to-minute adjustments in the support provided. While typically delivered in an ICU, critical care may be provided in the prehospital setting, emergency department, or other acute care settings. Critical respiratory care refers to those respiratory care techniques and procedures used in the assessment, diagnosis, management, support, monitoring, and care of critically ill patients. While the types of respiratory care provided in the ICU range

from diagnostic and monitoring procedures (e.g., blood gases, respiratory monitoring), maintenance and management of artificial airways (e.g., suctioning and airway care), and basic respiratory care techniques (e.g., oxygen therapy, aerosolized medication delivery), an essential respiratory care function is the provision of mechanical ventilatory support (also known as mechanical ventilation) to patients suffering from respiratory failure. The role of the respiratory therapist in the ICU includes patient assessment and monitoring, performing basic and advanced respiratory care procedures and techniques, and providing care to patients receiving mechanical ventilatory support. Care often provided by the respiratory therapist in the ICU is summarized in Table 1-1. TABLE 1-1 Types of Respiratory Care Provided in the ICU The role of the respiratory therapist in the ICU includes patient assessment, performance of basic and advanced respiratory care techniques and procedures, care of patients receiving mechanical ventilatory support, respiratory-related diagnostic testing, and performance or assistance with special procedures: ▪ Patient Assessment • Obtain/review history and physical examination. • Obtain/review clinical laboratory testing (e.g., complete blood count [CBC], cardiac markers, electrolytes, oximetry, blood gases, lactate level, coagulation studies, sputum Gram stain, culture and sensitivities, blood urea nitrogen [BUN] and creatinine, urinalysis, analysis of pleural fluid, and cerebrospinal fluid [CSF] analysis). • Obtain/review imaging studies (e.g., radiograph, computed tomography [CT scans], magnetic resonance imaging [MRI], ultrasound, and angiography). • Assess oxygenation, ventilation, and acid–base balance. • Assess for respiratory failure (e.g., acute respiratory distress syndrome [ARDS], pulmonary edema, pneumonia, exacerbation of obstructive disease, neuromuscular disease, and other restrictive pulmonary disease). • Assess patients’ airway and recognize difficult airways. • Assess patients for ventilator initiation. • Assess patients for adjustment in ventilatory support provided (e.g., ventilator mode, trigger effort, rates, volumes, pressures, flows, oxygen concentration, positive end-expiratory pressure/continuous positive airway pressure [PEEP/CPAP], patient–ventilator interaction, and alarm settings). • Perform ventilator waveform analysis. • Assess for patient–ventilator asynchrony. • Evaluate pulmonary mechanics (e.g., compliance and resistance) and work of breathing. • Assess patients for ventilator weaning and discontinuance. • Evaluate neurologic status (e.g., level of consciousness, neuromuscular function, respiratory drive, stroke, seizures, and brain death) • Evaluate cardiac/cardiovascular status (e.g., cardiac arrhythmias, heart failure, coronary artery disease [CAD], hypotension and hypertension [systemic, pulmonary]). • Assess hemodynamics (e.g., preload, afterload, contractility, and cardiac output). • Recognize and assess different types of shock (e.g., anaphylactic, cardiogenic, septic, hypovolemic, and neurogenic shock). • Assess nutritional status.

• Recognize effects of drugs and medications (e.g., sedatives, hypnotics, analgesics, neuromuscular blocking agents, reversal agents, vasoactive drugs, inotropic agents, and diuretics). • Develop, implement, assess, and modify respiratory care plans. ▪ Basic Respiratory Care Procedures in the ICU • Oxygen therapy • Secretion management and airway clearance therapy • Management of bronchospasm and mucosal edema (e.g., bronchodilators) • Lung expansion therapy • Airway care (humidification, suctioning, secretion management, tube position, cuff pressure, and tracheostomy care) ▪ Critical Care and Ventilatory Support • Conventional (invasive) mechanical ventilatory support: ∘ Ventilator initiation ∘ Patient stabilization ∘ Ventilator monitoring ∘ Weaning and ventilator discontinuance • Noninvasive mechanical ventilatory support (initiation, stabilization, monitoring, and discontinuance). • High-frequency ventilation (initiation, stabilization, monitoring, and discontinuance). • Differential/independent lung ventilation. • Recruitment maneuvers. • Prone positioning. • Physiologic monitoring. • Ventilator waveform analysis. • Cardiac and hemodynamic monitoring. • Monitor intracranial pressure (ICP). • Suctioning and airway care. • Administer additional aerosolized agents (e.g., narcotics, antimicrobials, and vasodilators). • Administer airway installations (e.g., lidocaine, cold saline, and topical thrombin). • Advanced cardiovascular life support. • Administer specialty gas mixtures (e.g., helium-oxygen) and inhaled vasodilators (nitric oxide, prostacyclin). • Metabolic studies and nutritional studies (V̇o2, V̇co2, and indirect calorimetry). • Extracorporeal membrane oxygenation (ECMO). • Mechanical circulatory assistance. • Manage specific disease states and conditions (see also Box 1-2). ▪ Diagnostic Testing • Oximetry • Arterial blood gases • Bedside measures of pulmonary function • Cardiac testing (ECG) • Ultrasound (thoracic, cardiac, abdominal, and transesophageal sonography) ▪ Special Procedures • Patient transport. • Bedside bronchoscopy. • BAL (bronchoalveolar lavage). • Insert and manage arterial lines. • Insert and manage central lines. • Thoracentesis. • Insert, manage, and remove chest tubes. • Perform airway intubation, to include use of advanced techniques (e.g., cricoid pressure, specialty visualization devices). • Exchange endotracheal tubes.

• • • •

Airway extubation. Percutaneous tracheostomy. Change tracheostomy tubes. Disaster response.

Types of Intensive Care Units While types of ICUs vary from hospital to hospital, some of the more common types of ICUs are listed in Box 1-1. These include medical intensive care units (MICU), surgical intensive care units (SICU), coronary care units (CCU), pediatric intensive care units (PICU), and neonatal intensive care units (NICU). Small hospitals may have only one or two types of ICUs accepting a variety of patients (e.g., MICU and SICU).3

BOX 1-1 Types of Intensive Care Units ∎

∎

∎

∎

Medical Intensive Care Unit (MICU). The MICU generally accepts a wide variety of critically ill patients, excluding only those patients who can be managed in another available ICU setting, such as surgical intensive care or pediatric intensive care. In smaller hospitals, where no other specialty units are available, pediatric patients and surgical patients are sometimes placed in the MICU. Surgical Intensive Care Unit (SICU). An intensive care unit that primarily serves critically ill postoperative patients and is staffed and managed by surgeons and anesthesiologists with training and specialization in critical care. Coronary Care Unit (CCU). The traditional coronary care unit tends to focus on to providing care to patients following acute myocardial infarction (MI), patients with unstable angina, and those with other serious cardiac arrhythmias. The CCU typically incorporates telemetry or other continuous cardiac monitoring system and is supported by the cardiology service of the hospital. Cardiovascular Intensive Care Unit (CVICU). The types of patients seen in the CVICU vary, depending on the hospital. In hospitals with separate CCU services (see above), the CVICU tends to focus on postoperative care following cardiothoracic or vascular surgery including coronary artery bypass, heart valve replacement, and heart transplants. Other CVICUs may see patients following cardiac arrest and/or MI, and those with cardiac dysrhythmias, or heart failure; interventional cardiology procedures (e.g.,

∎

∎

∎

∎

cardiac catheterization) may be followed by admission to the CVICU. Special procedures, such as hypothermia post–cardiac arrest (now the standard of care in all ICUs for patients who remain unresponsive after return of spontaneous circulation [ROSC]), extracorporeal membrane oxygenation (ECMO), intra-aortic balloon pump (IABP), and use of ventricular assist devices (VADs) may be employed in the CVICU. Respiratory Intensive Care Unit (RICU). Though less common in the United States, RICUs specialize in the care of critically ill patients with pulmonary problems. Examples of patients that may be seen in the respiratory ICU include those with acute exacerbation of chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), severe pneumonia, and patients with other chronic lung conditions suffering from acute respiratory failure. Neonatal Intensive Care Unit (NICU). The NICU provides care for critically ill newborns. Disorders seen in the NICU include respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN), neonatal pneumonia, meconium aspiration, persistent pulmonary hypertension of the neonate (PPHN), sepsis, and bronchopulmonary dysplasia (BPD). Respiratory care provided in the NICU may include provision of a neutral thermal environment, monitoring, surfactant therapy, oxygen therapy, continuous positive airway pressure (CPAP), and ventilatory support. ECMO and inhaled nitric oxide therapy (iNO) are also sometimes provided in the NICU. Pediatric Intensive Care Unit (PICU). The PICU focuses on the care of critically ill children, typically ranging in age from infants to teenagers. Disease states or conditions seen in the PICU include acute respiratory failure, shock, trauma, overwhelming infection, multi-organ system dysfunction, acute neurologic disease, gastrointestinal disorders, liver failure, renal disease, blood disorders, and cardiac disease. Pneumonia, respiratory syncytial virus (RSV), bronchiolitis, epiglottitis, laryngeal tracheobronchitis (i.e., croup), upper airway obstruction, acute pediatric asthma, cystic fibrosis, sepsis, anaphylaxis, poisoning, near drowning, and neurologic or neuromuscular disorders may lead to respiratory failure in pediatric patients. PICU services include basic respiratory care, patient assessment and monitoring, and providing mechanical ventilatory support. Some units also provide ECMO, high-frequency ventilation, and inhaled nitric oxide therapy (iNO). Neurologic Intensive Care Unit (Neuro ICU). The Neuro-ICU focuses on the care of patients with critical, life-threatening neurological disorders such as stroke, cerebral aneurysm, head trauma, traumatic brain injury, intracranial or subarachnoid hemorrhage, encephalitis, meningitis, and subdural

∎

∎

hematoma. Other conditions seen in the Neuro-ICU include status epilepticus, postoperative brain surgery (e.g., tumor removal), spinal cord injury, and neuromuscular disease (e.g., Guillain-Barre syndrome, myasthenia gravis). Postanesthesia Care Unit (PACU). The PACU, also sometimes known as the recovery room, receives patients immediately following surgical operations and anesthesia. Patients generally remain in the PACU for short periods of time until they are stabilized. The PACU provides postoperative observation, monitoring of vital signs, medication administration, intravenous (IV) fluid administration, airway care, oxygen therapy, and extubation in patients ready for removal of the endotracheal tube, if not removed in the operating room. Recovery room nurses also provide the initial management of postoperative pain, treatment for postoperative nausea and vomiting, treatment of postanesthetic shivering, and monitoring of surgical sites for bleeding, swelling, discharge, or other complications. Occasionally, patients in the PACU require mechanical ventilatory support, generally for brief periods of time. Once stable, the PACU patient is transferred back to the general hospital ward or other care unit. In outpatient surgical settings, the patient may be discharged to home. Mobile Intensive Care Unit (Mobile ICU). The term mobile intensive care unit is used to describe an emergency response unit, ambulance, or transport vehicle that includes sophisticated life– support and monitoring technology. Typically, the Mobile ICU is staffed by qualified paramedics who are linked to a medical center via telecommunications technology. In addition, critical care transport may be accomplished using a ground mobile ICU, helicopter, or fixed-wing aircraft. Critical care transport teams may include critical care nurses, critical care flight medics, respiratory therapists, and critical care physicians.

ICUs may be described by the level of care provided.3 Level I ICUs are found in teaching hospitals with an academic mission and provide comprehensive care for patients with a wide variety of disorders. Level II ICUs may be found in large community hospitals that provide comprehensive care but may not have the resources to care for specific types of patients (e.g., multiple trauma). Level III ICUs may be found in smaller hospitals and are able to stabilize critically ill patients, but unable to provide certain types of comprehensive care. Level III ICUs typically have transfer arrangements with more comprehensive units.

Trauma centers are often identified by level based on the kinds of resources available and the types and numbers of patients admitted. For example, a Level I Trauma Center provides total care for every aspect of injury and is characterized by 24-hour in-house coverage by general surgeons, and the rapid availability of specialists (e.g., anesthesiology, radiology, orthopedics, and neurosurgery).4 A Level I Trauma Center serves as a comprehensive regional resource. A Level V Trauma Center, on the other hand, provides basic emergency department services, and may only perform initial patient evaluation, stabilization, and transfer of patients to facilities providing more comprehensive care, as needed.4 Unlike adult critical care units and trauma centers, where Level I indicates the most comprehensive care, newborn infant care complexity goes from Level I, basic newborn care to Level IV, the highest level of regional neonatal intensive care unit (NICU).5 Level I nurseries (well newborn nursery) care for healthy babies, while Level II units provide advanced newborn care (special care nursery). Level II nurseries may provide mechanical ventilatory support until the infant improves or is transferred to a higher-level facility. Level III NICUs provide comprehensive intensive care for very premature infants (i.e., 45 mmHg) resulting in a pH ≤ 7.25. Items to be monitored following the institution of mechanical ventilation include oximetry values (i.e., Spo2), ventilatory parameters (e.g., respiratory rate, tidal volume, I:E ratio, ventilatory pattern, patient-ventilator interaction, airway pressures, and ventilator graphics), cardiac monitoring (e.g., rate, rhythm, and ECG), and hemodynamic monitoring (e.g., arterial blood pressure, fluid intake and output, central line pressures, and measures of cardiac output).

Types of Respiratory Care Provided in the ICU Patients in ICU often have problems that affect oxygenation and/or ventilation. Respiratory failure is a general term indicating an inability of the heart and lungs to maintain adequate tissue oxygenation and/or removal of CO2. ARF can be defined as a sudden decrease in arterial blood oxygen levels with or without carbon dioxide retention. AVF can be defined as a sudden rise in Paco2 with a corresponding decrease in pH. Clinical Focus 1-2 discusses the use of mechanical ventilation in the ICU. ICU patients may suffer from upper respiratory tract infection, pneumonia, acute bronchitis, and asthma exacerbation, exacerbation of COPD, pulmonary hypertension, CHF, pulmonary emboli, cardiac or noncardiac pulmonary, or postoperative pulmonary complications. All of these conditions may lead to ARF, impair gas exchange, and require oxygen therapy, ventilatory support, and the use of PEEP. Respiratory care provided in the ICU may include therapy to improve oxygenation and/or ventilation, provide secretion management and airway care, treat bronchospasm and mucosal edema, or deliver lung expansion therapy to treat or prevent atelectasis. Invasive or noninvasive ventilatory support (i.e., mechanical ventilation) in the ICU should aim to maintain adequate tissue oxygenation, support ventilation and carbon dioxide removal, and maintain a normal or near-normal acid– base balance. Respiratory care provided in the ICU also seeks to maintain adequate circulation, blood pressure, and cardiac output. Monitoring of the patient’s oxygenation status, ventilatory status, and cardiac and hemodynamic function is a central concern. Specific respiratory problems seen in the ICU include bronchospasm and mucosal edema, retained secretions, and airway plugging. These problems may respond to various forms of respiratory care, such as oxygen therapy, administration of aerosolized medications and secretion clearance techniques (e.g., suctioning and airway care, and/or airway clearance therapy [ACT]; see Clinical Focus 1-3). Lung expansion therapy (e.g., incentive spirometry [IS]and various forms of positive airway pressure) may also be of some value to prevent or treat inadequate lung expansion and atelectasis. It must be noted however, that the evidence base for the effectiveness of various ACT and lung expansion therapy techniques does not

provide a high level of support for their use.18, 19 Clinical Focus 1-3 discusses the use of airway clearance therapies in the ICU.

CLINICAL FOCUS 1-3: Airway Clearance Therapies in the ICU Concerns regarding secretion mobilization, ineffective cough, secretion retention, mucous plugging, atelectasis, and the possible development of pneumonia secondary to retained secretions and infection are common in the ICU patient. Excessive airway secretions may be seen in ICU patients with COPD exacerbation, acute and chronic bronchitis, acute asthma, bronchiectasis, pneumonia, and in patients following endotracheal intubation. Impaired cough is common in patients with neuromuscular disease, respiratory muscle weakness, and following abdominal or thoracic surgery. Consequently, airway clearance therapy (ACT) for secretion management has been widely used in the acute care setting, including the ICU. ACT techniques commonly used include chest physiotherapy (CPT), positive expiratory pressure (PEP), intrapulmonary percussive ventilation (IPV), and incentive spirometry (IS) to prevent atelectasis. Airway clearance therapies also include active cycle breathing, forced exhalation technique (FET), high-frequency chest wall compression (HFCWC), and mechanical insufflation–exsufflation. Administration of aerosolized medications (e.g., bronchodilators, mucolytics) and/or bland aerosols have also been routinely used in the ICU setting to aid in secretion mobilization. Current evidence suggests that ACT may be considered in the following types of patients seen in the ICU:18 COPD patients with secretion retention and associated symptoms and an ineffective cough. Patients with neuromuscular disease and ineffective cough (i.e., peak cough flow < 270 L/min) may benefit from cough-assist techniques such as mechanical insufflation-exsufflation. (e.g., Cough-Assist). While the lack of high-level evidence does not support the routine use of ACT, according to the AARC Clinical Practice Guidelines,18,19 it may be considered for certain individuals based on clinical judgment. Answers to the following questions should be considered: 1. Does the patient have difficulty clearing airway secretions? 2. Are retained secretions affecting gas exchange or lung mechanics? 3. What is the potential for adverse effects (vs. benefits) due to ACT? 4. What would be the associated cost of providing ACT? 5. Does the patient have any preferences regarding ACT?

If an individual patient has an inadequate cough and difficulty clearing secretions, retained secretions are affecting gas exchange or lung mechanics (e.g., lung compliance and/or airway resistance), the potential for adverse effects are minimal, and the cost is acceptable, ACT may be appropriate. Patient preferences should also be considered. Goals of ACT therapy may include18, 19: Changes in volume of expectorated sputum Improvements in gas exchange Improvement in the chest radiograph Improvement in symptoms (e.g., dyspnea) Remember: the routine use of ACT techniques for airway clearance in patients without cystic fibrosis is not recommended; the routine use of IS also is not recommended to prevent atelectasis. Further, there is currently no high-level evidence to support the use of bronchodilators, mucolytics, or mucokinetics for airway clearance in hospitalized patients who do not have cystic fibrosis.18,19 Clinical judgment, however, may suggest that ACT and/or the use of aerosolized bronchodilators is appropriate in individual patients in the ICU in order to facilitate secretion management and prevent or treat bronchospasm.18,19

To review, basic respiratory care techniques and procedures often used in the ICU setting include oxygen therapy, secretion management, management of bronchospasm and airway edema, and lung expansion therapy. Procedures and techniques sometimes classified as critical respiratory care include invasive and noninvasive mechanical ventilatory support, physiologic monitoring, cardiac and hemodynamic monitoring, suctioning and airway care, airway intubation, advanced cardiovascular life support, ECMO, and mechanical circulatory assistance. Respiratory care diagnostic tests performed in the ICU include oximetry, arterial blood gases, venous blood gases, and bedside pulmonary function testing. Table 1-1 lists the types of respiratory care commonly provided in the ICU.

Summary Critically ill patients are those at high risk for life-threatening health problems. Critically ill patients are often unstable and require sophisticated support, careful monitoring and rapid adjustment of care based on changes in their condition. Critical care is provided in various types of ICUs using interprofessional teams consisting of specially trained physicians, nurses, respiratory therapists, and other healthcare personnel. Critical respiratory care refers to those respiratory care techniques and procedures used in the assessment, diagnosis, management, support, monitoring, and care of critically ill patients. Respiratory care provided in the ICU includes diagnostic and monitoring procedures, management of artificial airways, basic respiratory care techniques (e.g., oxygen therapy, aerosolized medication delivery), and the provision of mechanical ventilatory support. The treatment and support of patients in respiratory failure is a core respiratory care competency. This includes careful assessment, monitoring, care, and management of patients requiring mechanical ventilation.

Key Points Respiratory care is defined as the healthcare discipline that specializes in the promotion of optimal cardiopulmonary function. Critically ill patients are at high risk for life-threatening health problems. Critical care refers to the care and management of critically ill patients who require sophisticated support and constant monitoring. Conditions sometimes requiring ICU admission and mechanical ventilation include acute and chronic respiratory disease; cardiac, cardiovascular, or circulatory disease; shock; trauma; sepsis; and neuromuscular or neurologic disease. Critical care requires complex decision making to ensure therapy is adjusted as patients’ needs change. Critically ill patients are often unstable and require frequent adjustments in the support provided. Critical respiratory care includes diagnostic and monitoring procedures, management of artificial airways, performing basic and advanced respiratory care, and management of mechanical ventilation. Types of ICUs include medical intensive care units (MICU), surgical intensive care units (SICU), coronary care units (CCU), pediatric intensive care units (PICU), and neonatal intensive care units (NICU). ICUs may be classified by level. A Level I Trauma Center provides the highest level of support for adults and children while a Level III NICU provides the highest level of support for the newborn. Acute care hospitals often have step-down units that provide a lower level of care than the ICU but a higher level of care than general medical and surgical wards. Specially trained physicians, nurses, and respiratory therapists are needed to staff the ICU. Specialty credentials are available for nurses and respiratory therapists who wish to work in the ICU. Interprofessional practice (IPP) occurs when multiple health workers from different professional backgrounds work together with patients, families, and communities to deliver the highest quality of care. Interprofessional practice (IPP) occurs when multiple health workers from different professional backgrounds work together with patients, families, careers, and communities to deliver the highest quality of care. Standards have been recommended for the design of ICUs. Long-term acute care hospitals (LTACs) provide care to patients with serious medical conditions that require an extended hospital stay but no longer require intensive care. Children’s hospitals are specialty hospitals that provide high levels of care to

pediatric and neonatal patients. Certain skilled nursing facilities (SNFs) will accept patients who are ventilator dependent and may require prolonged ventilator weaning. Assessment of the respiratory care patient in the ICU must include evaluation and monitoring of the patient’s oxygenation, ventilation, and circulation. ICU patient assessment should include review of the medical records, history and physical exam, review of laboratory studies, medical imaging, results of cardiac and hemodynamic tests, and monitoring and review of critical care monitoring flowsheets. Physical assessment should be especially attentive to the signs of respiratory distress, hypoxia, and hypercapnia (i.e., ventilatory failure). A wide range of laboratory studies may be ordered to assist in the assessment of the ICU patient. Arterial blood gas studies can quantify the degree of hypoxemia, identify hypoventilation or hyperventilation, and assess acid–base balance. ICU bedside imaging includes portable chest radiographs and bedside sonography (i.e., ultrasound). Monitoring procedures in the ICU include respiratory, cardiac, and hemodynamic monitoring. Special procedures performed in ICU include bedside bronchoscopy and thoracentesis. Respiratory care plans in the ICU may focus on improving oxygenation, ensuring adequate ventilation, providing cardiorespiratory support, and monitoring the patient’s condition. Respiratory care plans in the ICU may also provide for secretion management, airway care, treatment of bronchospasm and airway edema, and/or delivery of lung expansion therapy. Indications for mechanical ventilation include apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems (refractory hypoxemia).

References 1. American Association for Respiratory Care (AARC). Position statement: Definition of Respiratory Care. July 2015. Available at https://www.aarc.org/wp-content/uploads/2017/03/statement-of-definition-of-respiratorycare.pdf. 2. Robertson LC, Al-Haddad M. Recognizing the critically ill patient. Anaesthesia & Intensive Care Medicine. 2013;14(1):11–14. 3. Haupt MT, Bekes CE, Brilli RJ, et al. Guidelines on critical care services and personnel: Recommendations based on a system of categorization of three levels of care. Crit Care Med. 2003;31:2677–2683. 4. American Trauma Society. Trauma center levels explained. Available at http://www.amtrauma.org/? page=traumalevels. Accessed April 5, 2016. 5. Barfield WD. Policy statement: Levels of neonatal care. Pediatrics 2012;130(3); a statement of reaffirmation for this policy was published in Pediatrics 2015;136(5):e1418. Available at http://pediatrics.aappublications.org/content/130/3/587.full. Accessed April 5, 2016. 6. Barrett ML, Smith MW, Elixhauser A, et al. Utilization of Intensive Care Services, 2011. HCUP Statistical Brief #185. December 2014. Rockville, MD: Agency for Healthcare Research and Quality. Available at http://www.hcup-us.ahrq.gov/reports/statbriefs/sb185-Hospital-Intensive-Care-Units-2011.pdf. 7. Neuraz A, Guérin C, Payet C, et al. Patient mortality is associated with staff resources and workload in the ICU: A multicenter observational study. Crit Care Med. 2015;43(8):1587–1594. 8. Kleinpell RM. ICU workforce. Crit Care Med. 2014;42(5):1291–1292. 9. American Association of Critical-Care Nurses (AACN). CCRN Exam Handbook. Available at https://www.aacn.org/certification/preparation-tools-and-handbooks/~/media/aacn-website/certification/getcertified/handbooks/ccrnexamhandbook.pdf?la=en. Accessed April 5, 2016. 10. National Board for Respiratory Care (NBRC). Adult Critical Care Specialty Examination Detailed Content Outline. June 2018. Available at https://www.nbrc.org/wp-content/uploads/2017/08/ACCS-Detailed-ContentOutline-For-Public-Uses.pdf. Accessed August 25, 2018. 11. Ekmekci O, Sheingold B, Plack M, et al. Assessing performance and learning in interprofessional health care teams. J Allied Health. 2015;44(4):236–243. 12. Interprofessional Education Collaborative Expert Panel. Core Competencies for Interprofessional Collaborative Practice: Report of an Expert Panel. 2011. Washington, DC: Interprofessional Education Collaborative. 13. Thompson DR, Hamilton DK, Cadenhead CD, et al. Guidelines for intensive care unit design. Crit Care Med. 2012;40(5):1586–1600. 14. Prin M, Wunsch H. The role of stepdown beds in hospital care. Am J Respir Crit Care Med. 2014;190(11):1210–1216. 15. American Speech-Language-Hearing Association (ASHA). Long-Term Acute Care Hospitals. Available at http://www.asha.org/slp/healthcare/ltac/. Accessed April 5, 2016. 16. Brochard L, Martin GS, Blanch L, et al. Clinical review: Respiratory monitoring in the ICU – a consensus of 16. Crit Care. 2012;16:219. Available at http://ccforum.biomedcentral.com/articles/10.1186/cc11146. Accessed April 5, 2016. 17. Lichtenstein DA. Lung ultrasound in the critically ill. Ann Intens Care. 2014;4:1. Available at http://annalsofintensivecare.springeropen.com/articles/10.1186/2110-5820-4-1. Accessed April 5, 2016. 18. Strickland SL, Rubin BK, Drescher GS, et al. AARC Clinical Practice Guideline: Effectiveness of nonpharmacologic airway clearance therapies in hospitalized patients. Respir Care. 2013;58(12):2187– 2193. Available at http://rc.rcjournal.com/content/58/12/2187.short. 19. Strickland SL, Rubin, BK, Haas, CF; et al. AARC Clinical Practice Guideline: Effectiveness of pharmacologic airway clearance therapies in hospitalized patients. Respir Care. 2015;60(7):1071–1077.

CHAPTER

2 Respiratory Failure Jay I. Peters and David C. Shelledy

© Anna RubaK/ShutterStock, Inc.

OUTLINE Overview Respiratory Failure Types of Respiratory Failure Indications for Mechanical Ventilatory Support Clinical Manifestations of Respiratory Failure Assessment for Respiratory Failure Oxygenation Assessment of Ventilation Alveolar Ventilation and Dead Space Alveolar Ventilation and PaCO2 Assessment of Acid-Base Balance Assessment of Cardiac and Circulatory Status Assessment of Cognitive and Neurologic Status Nutritional Status Prediction of ICU Outcomes Management Principles for Patients in Respiratory Failure Acute Asthma Exacerbation Acute Exacerbation of COPD Acute Respiratory Distress Syndrome Heart Failure Acute Myocardial Infarction Shock Sepsis Trauma Pulmonary Embolus and Deep Vein Thrombosis Neurologic and Neuromuscular Disease Summary

OBJECTIVES 1.

2.

3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.

25. 26. 27. 28. 29.

Define respiratory failure and explain the differences between specific types of respiratory failure (i.e., acute respiratory failure, chronic respiratory failure, hypoxemic respiratory failure, and hypercapnic respiratory failure). Define ventilatory failure and explain the differences between acute ventilatory failure, chronic ventilatory failure, acute ventilatory failure superimposed on chronic ventilatory failure, and impending ventilatory failure. Describe the four primary indications for mechanical ventilation. Recognize the clinical manifestations of acute respiratory failure. Describe types of high-altitude illness that may be life threatening. Recognize causes of ambient hypoxia at normal barometric pressures. Describe problems with the conducting airways that may impair oxygenation and/or ventilation. Contrast the effects of hyperventilation and hypoventilation on arterial oxygen levels. Explain how each of the common causes of reduced oxygen transfer across the lung cause hypoxemia. Contrast the ventilation perfusion relationships described by the terms “shunt,” “dead space,” and “low V∙/Q∙”. Recognize clinical causes of increased capillary shunt, anatomic shunt, low V̇/Q̇, and diffusion limitations in the lung and the resultant effects on oxygenation. Contrast the oxygen therapy requirements and treatment of patients with significant capillary shunt to those with low V̇/Q̇. Interpret levels of hypoxemia based on measurement of PaO2 and SaO2. Assess each component of arterial blood oxygen content in terms of its effect on oxygen delivery to the tissues. Compare different forms of anemic hypoxia due to low hemoglobin or hemoglobin dysfunction. Describe findings associated with acute chest syndrome as a complication of sickle-cell disease. Describe possible causes, clinical manifestations, diagnosis, and treatment of carbon monoxide poisoning. Calculate oxygen delivery to the systemic tissues based on cardiac output and arterial oxygen content. Describe each of the common causes of reduced cardiac output seen in the intensive care unit (ICU). Contrast the causes and treatment of cardiogenic shock and hypovolemic shock. Explain the term distributive shock and give examples of each major type of distributive shock. Summarize the possible causes, clinical manifestations, effects, and treatment of cyanide poisoning. Describe bedside measures of the adequacy of ventilation. Based on patient history and arterial blood gas analysis, recognize acute ventilatory failure, chronic ventilatory failure, acute ventilatory failure superimposed on chronic ventilatory failure, acute alveolar hyperventilation, and chronic alveolar hyperventilation. Recognize causes of respiratory acidosis and alkalosis. Contrast causes of normal anion gap metabolic acidosis and increased anion gap metabolic acidosis. Explain the importance of nutritional assessment for patients in the ICU. Explain the use of scoring tools available in the ICU to predict patient outcomes, including APACHE, SAPS, and SOFA. Summarize the key features of management of patients in respiratory failure due to acute asthma exacerbation, acute exacerbation of COPD, pneumonia, ARDS, shock, trauma, sepsis, cardiac or cardiovascular disease, and neurologic or neuromuscular disease.

KEY TERMS acute alveolar hyperventilation Acute Physiology and Chronic Health Evaluation (APACHE) acute respiratory distress syndrome (ARDS) acute respiratory failure (ARF) acute ventilatory failure (AVF) acute ventilatory failure superimposed on chronic ventilatory failure altitude hypoxia

alveolar dead space ambient hypoxia amyotrophic lateral sclerosis (ALS) anaphylactic shock anatomic dead space anatomic shunt anemic hypoxia anion gap apnea arrhythmia atelectasis botulism bradycardia bradypnea capillary shunt carbon monoxide poisoning carboxyhemoglobin cardiogenic shock chronic alveolar hyperventilation chronic obstructive pulmonary disease (COPD) chronic respiratory failure chronic ventilatory failure circulatory hypoxia congestive heart failure (CHF) continuous positive airway pressure (CPAP) coronary artery disease (CAD) dead space units diffusion limitations distributive shock encephalitis enteral nutrition exacerbation expected maximal renal compensation Glasgow Coma Scale Guillain-Barré syndrome high-altitude cerebral edema (HACE) high-altitude pulmonary edema (HAPE) histotoxic hypoxia hypercapnea hypercapnic respiratory failure hyperventilation hypotension hypoventilation hypovolemic shock hypoxemic respiratory failure ischemic hypoxia Lung Injury Prediction Score (LIPS) meningitis metabolic acidosis metabolic alkalosis methemoglobinenemia myocardial infarction (MI) myasthenia gravis neurogenic shock neuromuscular disease

non-ST segment elevation MI (NSTEMI) parenteral nutrition physiologic dead space pneumonia polycythemia positive end-expiratory pressure (PEEP) pulmonary edema respiratory acidosis respiratory alkalosis sepsis septic shock Sequential Organ Failure Assessment (SOFA) shock Simplified Acute Physiologic Score (SAPS) ST segment elevation MI (STEMI) tachycardia tachypnea tetanus upper airway obstruction vasopressors ventilator-associated pneumonia (VAP) ventilator asynchrony

Overview Respiratory care is specifically focused on the assessment, diagnostic evaluation, treatment, and care of patients with heart and lung problems.1 A major focus of critical respiratory care is the treatment and support of patients in respiratory failure. This chapter will the review definitions of respiratory failure, to include types of respiratory failure and their causes. The assessment of patients with respiratory failure will be described, and the management of specific causes of respiratory failure will be discussed.

Respiratory Failure Normal aerobic metabolism produces carbon dioxide and consumes oxygen. Thus, oxygen (O2) must be transported to the body’s tissues for consumption and carbon dioxide (CO2) transported from the tissues to the lungs to be removed. Respiration refers to the exchange of oxygen and carbon dioxide across the lung (i.e., external respiration) and at the tissue level (i.e., internal respiration). Ventilation, on the other hand, refers to the movement of gas into and out of the lung. Respiratory failure is broadly defined as an inability of the heart and lungs to provide adequate tissue oxygenation and/or carbon dioxide removal.2 Respiratory failure can be caused by problems that reduce the amount of oxygen delivered to the tissues, or interfere with carbon dioxide removal, or both. In other words, respiratory failure can occur due to problems with oxygenation or ventilation. Respiratory failure can be life threatening, and the respiratory care clinician must be able to promptly recognize respiratory failure and take appropriate action. Table 2-1 describes common physiologic causes of respiratory failure. TABLE 2-1 Common Physiologic Causes of Respiratory Failure Oxygenation Problems ▪ Decreased ventilation-to-perfusion ratio (low V̇/Q̇) • Underventilation with respect to pulmonary perfusion ∘ Examples: obstructive lung disease (asthma, emphysema, COPD, cystic fibrosis, bronchiectasis). ∘ Interstitial lung disease (ILD) and pneumonia can also cause low V̇/Q̇. ▪ Pulmonary shunt • No ventilation with respect to pulmonary perfusion ∘ Examples: ARDS, atelectasis, pneumonia, rarely pulmonary edema. ▪ Diffusion problems • Impaired diffusion due to increased diffusion distance, block ∘ Example: early pulmonary fibrosis, which usually causes exercise desaturation. ▪ Hypoventilation • With hypoventilation, increased Paco2 results in a corresponding decrease in Pao2. ▪ Low blood oxygen content • Low Pao2, Sao2, or Hb ∘ Examples: • Low Pao2 may be due to low V̇/Q̇, shunt, diffusion problems, or hypoventilation. • Low hemoglobin (anemia), abnormal hemoglobin (carbon monoxide poisoning) will reduce the blood’s O2-carrying capacity. ▪ Increased pulmonary dead space • Examples: pulmonary embolus, obliteration of the pulmonary capillaries (as in severe emphysema) Ventilation Problems

▪ Acute ventilatory failure (AVF) • A sudden increase in Paco2 with a corresponding decrease in pH; hypoxemia generally is also present. For example, when breathing room air, for every increase in Paco2 of 4 mmHg Pao2 will decrease about 5 mmHg. • Conditions associated with acute ventilatory failure include: ∘ Acute lung injury, ARDS, severe pneumonia ∘ Shock, sepsis, trauma, pneumothorax, head trauma, stroke, spinal cord injury, smoke or chemical inhalation, aspiration, and near-drowning ∘ Sedative or narcotic drug overdose, paralytic drugs, and deep anesthesia ∘ Respiratory muscle fatigue and increased work of breathing due to acute exacerbation of COPD, acute severe asthma, severe obesity, and thoracic deformity ∘ Neuromuscular disease associated with respiratory failure: Guillain-Barré syndrome, amyotrophic lateral sclerosis (ALS), myasthenia gravis, polio, critical illness/steroid myopathy, botulism, and tetanus • Patients recovering from abdominal or thoracic surgery may need mechanical ventilatory support (e.g., postoperative respiratory failure). ▪ Chronic ventilatory failure • A chronically elevated Paco2 with normal or near-normal pH ∘ Examples: chronic bronchitis, severe COPD, obesity–-hypoventilation syndrome. ∘ It should be noted that full compensation for an elevated Paco2 generally does not occur although pH may return to near-normal (see expected compensation).

Types of Respiratory Failure Respiratory failure may be acute or chronic. Acute respiratory failure (ARF) is defined as a sudden decrease in arterial oxygenation with or without carbon dioxide retention (i.e., with or without hypercapnia).2 Patients with acute respiratory failure may have hypoxemia alone or hypoxemia with hypercapnia. Acute respiratory distress syndrome (ARDS) is a special case of acute respiratory failure characterized by severe problems with oxygenation (Box 2-1). Chronic respiratory failure generally is due to chronic lung disease, such as chronic obstructive pulmonary disease (COPD), cystic fibrosis, or pulmonary fibrosis. Chronic respiratory failure can also occur with neuromuscular disease (e.g., amyotrophic lateral sclerosis [ALS], aka Lou Gehrig’s disease), spinal cord injury, obesity– hypoventilation syndrome, or chest wall deformity.

BOX 2-1 Acute Respiratory Distress Syndrome (ARDS) ARDS is a noncardiogenic form of hypoxemic respiratory failure as defined by the ratio of the partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FIO2). In the definition published in 1994, a distinction was made between ARDS and acute lung injury (ALI) as characterized by the

PaO2/FIO2 ratio: ∎ ∎ ∎

∎

Bilateral pulmonary infiltrates on chest x-ray: ARDS and ALI Pulmonary capillary wedge pressure (PCWP) < 18 mmHg: ARDS and ALI PaO2/FIO2 < 300 but > 200: ALI (now classified as mild ARDS – see Berlin definition below) • Equivalent to a PaO2 < 63 mmHg while breathing room air (FIO2 = 0.21) PaO2/FIO2 < 200: ARDS

•

Equivalent to a PaO2 < 42 mmHg while breathing room air (FIO2 = 0.21)

More recently, the Berlin definition of ARDS was adopted; it does not distinguish between ARDS and ALI. The Berlin definition of ARDS is based on symptom timing, chest imaging, and PaO2/FIO2 ratio while receiving at least 5 cm H2O of positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP). This revised definition combines aspects of ALI and ARDS and requires:

1. Identification of respiratory symptoms within 1 week of new or worsening symptoms or a known clinical insult. 2. Bilateral opacities upon chest imaging (chest x-ray or CT scan). 3. Opacities cannot be due to lobar collapse, lung collapse, pulmonary effusion, or pulmonary nodules. 4. Pulmonary edema cannot be due to cardiac failure or fluid overload as assessed by echocardiography or other measures to exclude hydrostatic pulmonary edema (e.g., PCWP < 18 mmHg). 5. PaO2/FIO2 ≤ 300 mmHg with PEEP or CPAP ≥ 5 cm H2O. Further, the Berlin definition of ARDS classifies the degree of hypoxemia based on the PaO2/FIO2 ratio while receiving at least 5 cm H2O PEEP or CPAP:

∎

PaO2/FIO2 ≤ 300 mmHg but > 200 mmHg: mild

∎

PaO2/FIO2 ≤ 200 mmHg but > 100 mmHg: moderate

∎

PaO2/FIO2 ≤ 100 mmHg: severe

If altitude is higher than 1000 m, then correction factor should be calculated as follows: [PaO2/FIO2 × (barometric pressure/760)]. Data from ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012;307(23):2526−2533. doi: 10.1001/jama.2012.5669.

RC Insight Acute conditions generally are sudden in onset and limited in duration, while chronic conditions persist for an extended period of time.

As noted, respiratory failure can occur with hypoxemia and/or hypercapnia. Hypoxemic respiratory failure, also known as “lung failure” or “Type 1 respiratory failure” refers to a primary problem with arterial oxygenation. Hypoxemic respiratory failure is typically caused by problems with gas exchange in the lung. Oxygenation problems in the lung may be caused by poor matching of gas and blood (e.g., pulmonary shunt or low ventilation to perfusion ratios [low V̇/Q̇]), diffusion problems (e.g., early pulmonary fibrosis), and hypoventilation, in which an increased alveolar carbon dioxide tension (PACO2) reduces alveolar and arterial oxygen tensions (i.e., decreased PAO2 and PaO2). Common causes of hypoxemic respiratory failure include atelectasis, pneumonia, and pulmonary edema. Hypoxemic respiratory failure can be identified by measurement of arterial blood oxygen tension (PaO2) or arterial blood oxygen saturation measured directly (SaO2) or via pulse oximetry (SpO2). ARDS is a type of hypoxemic respiratory failure due to noncardiogenic pulmonary edema.2,3 Box 2-2 summarizes the definitions of respiratory failure. Table 2-2 provides guidelines for classifying the severity of hypoxemia based on oximetry and blood gas results. TABLE 2-2 Assessment of Severity of Hypoxemia

Description • • •

Expected Pao2 declines with age. For subjects over the age of 60 years, expected “normal” Pao2 can be estimated as follows: Supine normal Pao2 = 109 – (0.43 × age) ± 8 mmHg Standing normal Pao2 = 104 – (0.27 × age) ± 12 mmHg

aNote also that the normal range is for patients breathing room air. If the patient is receiving supplemental

oxygen therapy, Pao2 in the range of 80–100 mmHg represents corrected hypoxemia. bMany authors list the range of Pao for assessment of hypoxemia as mild: Pao 60–79, moderate: Pao 40– 2 2 2

59, and severe: Pao2 < 40. We would suggest that a Pao2 < 50 represents a medical emergency, which should be treated according to protocols for moderate to severe hypoxemia. cActual Sao will vary with pH, Paco , and temperature. 2 2

BOX 2-2 Types of Respiratory Failure Respiratory failure is a general term that indicates the inability of the heart and lungs to provide adequate tissue oxygenation and/or CO2 removal. Acute respiratory failure may be defined as a sudden decrease in arterial blood oxygen levels (arterial partial pressure of oxygen [PaO2] < 50–60 mmHg; arterial oxygen saturation [SaO2] < 88–90%), with or without carbon dioxide retention (arterial partial pressure of carbon dioxide [PaCO2] > 45 mmHg).

∎ ∎

Hypoxemic respiratory failure (lung failure) refers to a primary problem with oxygenation.1 Hypercapnic respiratory failure (pump failure) refers to a primary problem with ventilation.2 Hypercapnic respiratory failure is also known as ventilatory failure.

Common causes of acute respiratory failure requiring mechanical ventilation include ARDS, aspiration, heart failure, pneumonia, postoperative failure, sepsis, and trauma. Chronic respiratory failure is a long-term condition, usually occurring over a period of months or years. Chronic respiratory failure may be due chronic lung disease, such as COPD, cystic fibrosis, or pulmonary fibrosis. Neuromuscular disease, spinal cord injury, chest wall abnormalities, and obesity–hypoventilation syndrome may also cause chronic respiratory failure. Chronic respiratory failure may be classified as occurring with hypoxia or hypercapnea:

1. Hypoxemic respiratory failure is also known as Type 1 respiratory failure. 2. Hypercapnic respiratory failure is also known as Type 2 respiratory failure.

Hypercapnic respiratory failure, also known as “pump failure,” “Type 2 respiratory failure,” or “ventilatory failure,” refers to a primary problem with ventilation. Ventilation can be defined as the bulk movement of gas into and out of the lungs. As ventilation increases, arterial carbon dioxide levels decrease and vice versa. Thus, arterial carbon dioxide tension (PaCO2) is the single best index of alveolar ventilation. An abnormally elevated PaCO2 (hypercapnea) indicates hypoventilation, while an abnormally reduced PaCO2 (hypocapnea) indicates hyperventilation. Ventilatory failure (aka hypercapnic respiratory failure) can be simply defined as an abnormally elevated PaCO2. An elevated PaCO2 may also be called hypoventilation or hypercapnea. Because CO2 is a volatile acid, when arterial PaCO2 rises abruptly (acute increases), pH falls, and when PaCO2 decreases suddenly, pH rises. Prolonged elevation in PaCO2 (chronic increase) will generally cause retention of bicarbonate by the kidneys, resulting in a near-normal pH (i.e., metabolic compensation), although compensation generally does not completely correct pH

(see expected compensation). Ventilatory failure may be acute, subacute, or chronic. Apnea is the complete cessation of breathing, which represents a severe form of ventilatory failure requiring mechanical ventilatory support if the patient is to survive. Causes of apnea include cardiac arrest; respiratory arrest; narcotic, sedative, or tranquilizer drug overdose; trauma (e.g., near-drowning, electrical shock, head trauma, and chest trauma), high cervical spine injury (e.g., C2, C3, or C4 spinal cord injury), or neuromuscular disease. Administration of anesthesia or paralytic drugs (e.g., atracurium [Tracrium], vercuronium [Norcuron], cisatrocurium [Nimbex], rocuronium [Zemuron], or pancuronium [Pavulon]) may also cause apnea. Acute ventilatory failure (AVF) is defined as a sudden increase in arterial PaCO2 with a corresponding decrease in pH. Acute ventilatory failure may be caused by a decreased respiratory drive, airway obstruction, an increased work of breathing, or respiratory muscle fatigue. Causes of an increased work of breathing and respiratory muscle fatigue include severe pneumonia, ARDS, heart failure (aka congestive heart failure or CHF), and pulmonary edema. Other causes may include shock, trauma, smoke or chemical inhalation, aspiration, and near-drowning. Causes of decreased respiratory drive include general anesthesia, sedative or narcotic drug overdose, head trauma, or stroke. Neuromuscular disease, including Guillain-Barré syndrome, myasthenia gravis, and spinal cord injury may also result in acute ventilatory failure. Acute ventilatory failure superimposed on chronic ventilatory failure is sometimes seen in patients with acute exacerbation of chronic lung disease. Depending on severity, acute ventilatory failure may require mechanical ventilation. Generally speaking, mechanical ventilation should be considered in patients with an acute increase in PaCO2 > 45 mmHg resulting in a pH ≤ 7.25, although no specific cut-points should be arbitrarily imposed. RC Insight A respiratory rate greater than 30 breaths/min with tidal volume of less than 300 mL (adults) is associated with acute ventilatory failure and the need for mechanical ventilation.

Chronic ventilatory failure is defined as a chronically elevated PaCO2, with a normal or near-normal pH owing to metabolic compensation. A common cause of chronic ventilatory failure is COPD, although not all patients with COPD develop

chronic ventilatory failure. Chronic ventilatory failure is also seen in patients with late-stage cystic fibrosis, severe interstitial lung disease, and obesity–hypoventilation syndrome. With the exception of acute exacerbation of chronic lung disease, patients with chronic ventilatory failure generally do not require mechanical ventilatory support unless there is an acute insult. Acute ventilatory failure superimposed on chronic ventilatory failure occurs when a patient with a chronically elevated PaCO2 experiences an acute increase in PaCO2 with a corresponding decrease in pH. For example, a COPD patient with chronic ventilatory failure may acutely develop pneumonia, resulting in a further increase in PaCO2. Patients with acute ventilatory failure superimposed on chronic ventilatory failure may require mechanical ventilatory support. Box 2-3 summarizes types of ventilatory failure sometimes seen in the ICU.

BOX 2-3 Ventilatory Failure Ventilatory failure may be defined as an elevated PaCO2 greater than 45–50 mmHg. Other terms sometimes used to describe an elevated PaCO2 (i.e., ventilatory failure) include hypoventilation, hypercapnea, and respiratory acidosis. Types of ventilatory failure include: ∎ Acute ventilatory failure: a sudden increase in arterial PaCO with a 2 corresponding decrease in pH. ∎ Chronic ventilatory failure: a chronically elevated PaCO with a normal or 2 near-normal pH due to metabolic compensation (although complete compensation generally does not occur—see expected compensation). ∎ Acute ventilatory failure superimposed on chronic ventilatory failure: a chronically elevated PaCO2 followed by an acute increase in PaCO2 and a corresponding decrease in pH. Patients with ventilatory failure are generally hypoxemic if supplemental oxygen is not provided. Apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems requiring PEEP or CPAP are indications for mechanical ventilation.

Impending ventilatory failure is a category in which hypoventilation and hypercapnea are not yet present but are likely to occur in the immediate future if no

action is taken. For example, adult patients with markedly increased respiratory rates (> 35 breaths/min), hyperventilation (i.e., decreased PaCO2), severe distress, accessory muscle use, diaphoresis, and air hunger may rapidly progress to a state of severe hypoventilation and possible respiratory arrest. RC Insight Severe respiratory distress with air hunger, sweating, accessory muscle use, and significantly increased respiratory rate (>35 breaths/min in adults) may signal an impending respiratory arrest.

Indications for Mechanical Ventilatory Support The primary goals of mechanical ventilation are to maintain tissue oxygenation and provide for carbon dioxide removal. Mechanical ventilation supports or replaces the normal ventilatory pump, and thus the primary indication is inadequate or absent spontaneous breathing. Specific indications for mechanical ventilation are: 1. 2. 3. 4.

Apnea Acute ventilatory failure Impending ventilatory failure Severe oxygenation problems (e.g., refractory hypoxemia)

In addition, some patients may receive ventilatory support for problems associated with depressed mental status (e.g., Glasgow Coma Score < 8) or airway protection (e.g., depressed ventilatory status during ICU procedures).

Clinical Manifestations of Respiratory Failure Clinical manifestations of acute respiratory failure include increased heart rate, increased respiratory rate, accessory muscle use, intercostal retractions, nasal flaring (especially in infants and children), diaphoresis, and oxygen desaturation. Excitement, overconfidence, restlessness, anxiety, nausea, headache, and altered mental status may be present, followed by confusion, somnolence, and coma as the patient’s condition deteriorates. Rapid, shallow breathing is a common finding. Severe respiratory failure may be signaled by slowed or irregular breathing, reduced chest expansion, cardiac arrhythmias, and hypotension. Accessory muscle use, intercostal retractions, and asynchronous chest wall-to-diaphragm movement are associated with increased work of breathing. Initially, arterial blood gases may show hypoxemia and hyperventilation (i.e., respiratory alkalosis). As the patient’s illness worsens, this may be followed by hypoventilation, hypercapnea, and respiratory acidosis. Cyanosis is a variable finding and may not be present in patients with anemia. Table 2-3 summarizes the clinical manifestations of hypoxia and hypercapnia. TABLE 2-3 Clinical Manifestations of Hypoxia and Hypercapnia

When the clinical manifestations of respiratory failure are present, the respiratory care clinician should assess the patient’s arterial blood oxygen and carbon dioxide levels. Pulse oximetry provides an inexpensive, fast, safe, and convenient method to assess arterial oxygen saturation (SpO2). Pulse oximetry, however, may not detect certain types of hypoxia, including anemic hypoxia, circulatory hypoxia, ischemic hypoxia, and histotoxic hypoxia, each of which is discussed later in this chapter. Standard pulse oximetry should also not be relied upon in the presence of carbon monoxide poisoning or other abnormalities of the hemoglobin such as methemoglobinenemia, although newer devices are available that can assess oxygen saturation (SpO2), carboxyhemoglobin saturation, and methemoglobin

saturation, as well as oxygen content. Table 2-4 reviews the various types of hypoxia. TABLE 2-4 Types of Hypoxia

Assessment for Respiratory Failure Evaluation of patients in respiratory failure must include a thorough assessment of oxygenation and carbon dioxide removal (i.e., ventilation). Factors to consider in performing this assessment are discussed below.

Oxygenation The oxygenation process begins with the inspired gas and moves to the conducting airways, matching of gas and blood in the lung, diffusion of oxygen across the alveolar-capillary membrane, and loading of the arterial hemoglobin with oxygen. Oxygenated blood must then be transported to the tissues and tissue uptake and cellular utilization must occur. Problems may occur at each step of the oxygenation process resulting in tissue hypoxia. Assessment of patients with oxygenation problems should include evaluation of each of the stages in the oxygenation process beginning with the inspired oxygen concentration, assessment of the conducting airways, and assessment of gas exchange in the lung. Other important factors to review in assessment of oxygenation include blood oxygen content, cardiac output, oxygen delivery, and tissue perfusion. As noted, Table 2-3 reviews the clinical manifestations of hypoxia. Box 2-4 reviews each of the steps in the oxygenation process.

BOX 2-4 Steps in the Oxygenation Process In order for tissue oxygenation to be adequate, the following must occur: ∎ Inspired oxygen tension (PIO ) must be sufficient. PIO is determined by 2 2 barometric pressure (e.g., altitude) and FIO2. ∎ ∎ ∎ ∎ ∎

Oxygen must be conducted to the alveolar level, which requires clear and patent conducting airways. There must be adequate alveolar ventilation (V̇A). Matching of gas and blood in the alveoli and adjacent pulmonary capillaries must occur. Oxygen must diffuse across the alveolar capillary membrane into the blood. The arterial blood oxygen content (CaO2) must be adequate, which requires adequate PaO2, SaO2 (dependent on PaO2, chemical environment of the blood

∎ ∎ ∎

[pH, PaCO2, temperature], and functional Hb), and adequate Hb concentration. Adequate blood oxygen transport must occur to deliver the oxygenated blood to the tissues, which requires adequate CaO2 and cardiac output. The systemic tissue beds must be adequately perfused and oxygen must be unloaded from the blood and move to the tissues. Tissue oxygen uptake and utilization must function properly.

Inspired Oxygen The major factors that affect inspired oxygen tension (PIO2) are inspired oxygen concentration (FIO2) and barometric pressure (PB), where: PIO2 = FIO2 (PB – PH2O) Given a normal FIO2 of 0.2095, a sea level PB of 760 mmHg, and saturated gas at body temperature (PH2O = 47 mmHg), a normal PIO2 can be calculated: PIO2 = FIO2 (PB – PH2O) PIO2 = 0.2095 (760 – 47) = 150 mmHg A decrease in inspired oxygen concentration (FIO2) or a decrease in barometric pressure (PB) will reduce inspired oxygen tension (PIO2) and may cause ambient hypoxia. Altitude hypoxia is a special case of ambient hypoxia due to reduced PB at altitude. Barometric pressure progressively declines with increasing altitude, and acute altitude sickness is common in people who abruptly travel to above 8200 feet of elevation.4 For example, the altitude in Vail, Colorado is approximately 8500 feet and the barometric pressure is approximately 565 mmHg, resulting in a PIO2 of about 110 mmHg (assuming normal lung function) and a PaO2 in the range of 55 to 75 mmHg, with a SpO2 of 90% to 95%. Recall that a normal PIO2 is 150 mmHg at sea level, resulting in a normal PaO2 in the range of 80 to 100 mmHg. Patients with chronic lung disease may experience hypoxemia at sea level, and possible further decreases in PaO2 should be anticipated when such patients are considering travel to higher-altitude locations. Abrupt ascent to very high altitudes (e.g., > 11,400 feet)

can be dangerous for even healthy individuals, and a gradual ascent to allow for acclimation is recommended. As a point of interest, Colorado State Highway 82 allows people to drive across the U.S. Continental Divide at Independence Pass, an altitude of 12,095 feet. The world’s largest optical astronomy observatory is located at the summit of Mauna Kea in Hawaii, which has a peak elevation of 13,800 feet. High-altitude illness may affect hikers, skiers, mountain climbers, or others traveling to high-altitude locations. Types of high-altitude illness include acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), and highaltitude cerebral edema (HACE); HAPE and HACE are associated with higher elevations (> 10,000 feet), although they may occur at lower altitudes (e.g., 8000 feet).4 Symptoms of AMS include headache, loss of appetite, nausea, vomiting, sleep disturbance, fatigue, and exertional dyspnea.5 In general, symptoms occur within the first day following ascent to high altitude and subside in a day or two. Treatment of severe AMS includes oxygen therapy and medications for prevention or treatment of symptoms (e.g., ibuprofen [Advil, Motrin], acetazolamide ([Diamox], and dexamethasone [Decadron]); moving the patient to a lower altitude may be necessary.5 High-altitude cerebral edema (HACE) and high-altitude pulmonary edema (HAPE) represent life-threatening medical emergencies. HAPE may occur with or without AMS and the incidence, although relatively uncommon, increases with altitude and the rate of ascent.6 HAPE generally occurs at higher elevations (> 10,000 feet) and may be more likely in patients with preexisting pulmonary hypertension or left-to-right cardiac shunts (e.g., septal defects).6 Treatment of HAPE includes rest, warmth, oxygen therapy, and descent, particularly from very high altitude (e.g., > 13,000 feet).6 Expiratory positive airway pressure (EPAP) may be helpful and continuous positive airway pressure (CPAP) has been used, although the evidence for effectiveness is only anecdotal.6 Lightweight, portable hyperbaric oxygen (HBO) chambers can be lifesaving in remote locations where evacuation may be difficult or delayed.6 The need for hospitalization and admission to the ICU will vary, depending on the patient’s condition. HACE is an extreme and relatively uncommon form of AMS associated with elevations greater than 10,000 feet.5 Symptoms of HACE include trouble walking (i.e., ataxic gait), irritability, confusion, drowsiness, lethargy, and progressive decline

of mental function followed by coma.5 Urgent treatment of HACE should include oxygen therapy and moving the patient to a lower altitude as soon as possible. Dexamethasone and oxygen should be given immediately, although rapid descent should not be delayed.5 HACE and HAPE may occur together in some patients, further complicating treatment. Hospitalization, ICU admission, measures to reduce intracranial pressure (ICP), intubation, and mechanical ventilatory support may be required. Survivors generally have a full recovery, although persistent neurologic deficits may occur in a few. Aircraft often fly at altitudes up to 40,000 feet, which requires that aircraft cabins be pressurized, typically to simulate a cabin altitude of between 5000 and 8000 feet.7 Individuals with lung disease may experience hypoxemia due to the reduced barometric pressure (PB) unless provided supplemental oxygen in flight.7 Emphysema patients with lung bullae are also at risk for the development of pneumothorax as the aircraft ascends to altitude and cabin pressure decreases.7 While ambient FIO2 remains constant at 0.2095 up to 60 miles of altitude, barometric pressure declines rapidly. For example, PB at 30,000 feet is only about 226 mmHg resulting in a PIO2 of only about 38 mmHg. Aircraft decompression due to mechanical failure, accident, or attack at high altitude can result in severe hypoxemia (i.e., PaO2 < 40 mmHg), rapid loss of consciousness, and death if supplemental oxygen is not provided quickly. Thus, altitude hypoxia is a serious threat in the case of cabin pressure loss at altitudes above 12,500 to 14,000 feet. In addition to altitude hypoxia, explosive aircraft decompression may cause lung trauma when air exits the cabin at a faster rate than the lung can be decompressed.7 Loose objects may become projectiles, further increasing the risk of trauma. Altitude-induced decompression sickness can occur when pilots and passengers are exposed to altitudes of greater than 18,000 feet in unpressurized aircraft cabins.8 Altitude decompression sickness may occur at altitudes as low as 5000 feet in unpressurized aircraft if the flight is preceded by self-contained underwater breathing apparatus (SCUBA) diving within the previous 24 hours.8 Altitude decompression sickness can also occur following rapid inflight aircraft decompression. Decompression sickness is due to nitrogen bubble formation in joints (the “bends”), skin, lungs, and nervous system (i.e., brain, spinal cord, and peripheral nerves). Treatment includes descent from altitude, oxygen therapy, and, in severe cases,

HBO. Causes of ambient hypoxia related to a reduced FIO2 at normal barometric pressure include confinement in an enclosed space such as a mine, submarine, or airtight container without fresh gas replacement. Children using refrigerators or airtight storage chests for play are at special risk. Industrial or mining accidents may expose victims to asphyxiant gases, which in high concentrations may displace oxygen and cause ambient hypoxia. Initial treatment includes moving victims to a location with adequate ventilation and oxygen therapy. Further treatment will depend on the severity and duration of hypoxia; cardiopulmonary resuscitation, hospitalization, and ICU admission may be required. Conventional oxygen therapy will increase FIO2 while hyperbaric therapy will increase barometric pressure (PB); both increase PIO2 and, in turn, arterial oxygen tension (PaO2) and saturation (SaO2).

Conducting Airways The conducting airways extend from the external nares down to and including the terminal bronchioles. The conducting airways may be further subdivided into the upper airways (above the carina) and lower airways (below the carina). Conducting airway problems that may affect oxygenation and/or ventilation include airway obstruction, increased secretions, airway mucosal edema, and bronchospasm. Causes of upper airway obstruction include upper respiratory tract infection, upper airway edema, tumor, abscess, foreign body inhalation, and laryngeal abnormalities (e.g., vocal cord paralysis, laryngeal tumor, subglottic stenosis, and edema). Laryngeal edema may be caused by infection (e.g., croup, epiglottitis), artificial airways, trauma, or inhalation of noxious gases or flames. Angioedema (swelling under the skin caused by allergic reaction) may also result in laryngeal edema. Obstructive sleep apnea (OSA) is caused by a decrease in upper airway muscle tone during sleep resulting in soft tissue obstruction and periods of apnea. Tracheal stenosis, tracheal tumor, or other tracheal abnormalities (e.g., tracheomalacia, goiter pressing on trachea) may also cause obstruction. Lower airway obstruction may be caused by airway inflammation, mucosal edema, excess secretions, mucus plugging, and bronchospasm. Bronchospasm, mucosal edema, and secretions also increase airway resistance. Chronic obstructive pulmonary disease (COPD), chronic

bronchitis, emphysema, asthma, cystic fibrosis, and bronchiectasis all cause lower airway obstruction. Treatment of problems with the conducting airways will vary, depending on the location and cause. Partial upper airway obstruction may increase work of breathing, reduce ventilation, and impair oxygenation; complete obstruction represents an immediately life-threatening emergency. Lower airway obstruction may increase airway resistance, increase work of breathing, reduce gas flow, and lead to uneven or absent ventilation with respect to perfusion resulting in decreased arterial oxygen levels (i.e., ↓PaO2, ↓SaO2).

Alveolar Ventilation Adequate alveolar ventilation is required to bring oxygen rich inspired gas into the alveoli for gas exchange in the lung. The primary determinants of alveolar oxygen tension (PAO2) are inspired oxygen tension (PIO2) and alveolar carbon dioxide tension (PACO2) as represented in the alveolar air equation:

Normally, there is complete equilibration between the alveoli and adjacent capillaries in the lung for CO2 and PACO2 and PaCO2 are equal. Substituting PaCO2 for PACO2 and assuming a normal respiratory quotient (R) of 0.80, the alveolar air equation can be simplified:

As demonstrated by the alveolar air equation, an increase in PaCO2 (hypoventilation) will cause PAO2 to decrease while a decrease in PaCO2 (hyperventilation) will cause PAO2 to increase. Alveolar oxygen tension (PAO2) has a direct effect on arterial oxygen tension; as PAO2 increases or decreases, so does PaO2, although the relationship between PAO2 and PaO2 varies with differences in inspired oxygen concentrations (i.e., FIO2) and changes in alveolar ventilation with

respect to perfusion (V̇/Q̇). Recall also that the single best clinical index of alveolar ventilation is PaCO2 and as alveolar ventilation decreases, PaCO2 increases (and vice versa).

Effect of Hyperventilation on Oxygenation An increase in alveolar ventilation will cause PACO2 and PaCO2 to decrease. This, in turn, will result in an increase in PAO2 and (most likely) an increase in PaO2. This relationship explains why hyperventilation provides a moderately beneficial response to hypoxemia and may result in an increase in PaO2. In general, the initial physiologic response to acute hypoxemia is an increased heart rate and increased respiratory rate. An increase in heart rate increases cardiac output and oxygen delivery to the tissues. An increase in respiratory rate increases alveolar ventilation, reduces arterial and alveolar PCO2 and thus increases alveolar and arterial PO2. Hyperventilation secondary to hypoxemia is a commonly encountered condition associated with acute respiratory failure. In addition to acute hypoxemia, other common causes of hyperventilation include anxiety, pain, early sepsis, neurologic disorders, pulmonary emboli, and metabolic acidosis. Clinical Focus 2-1 provides an example of the effect of hyperventilation on PAO2 and PaO2.

CLINICAL FOCUS 2-1 Effects of Hyperventilation and Hypoventilation on Oxygenation The simplified alveolar air equation describes the relationship between alveolar oxygen tension (PAO2), inspired oxygen tension (PIO2), and arterial carbon dioxide tension (PaCO2): PAO2 = PIO2 – PaCO2 × 1.25 Based on this relationship, as PaCO2 increases, PAO2 and PaO2 will decrease in a somewhat predictable fashion. Hyperventilation will increase alveolar and, in turn, arterial oxygen tension while hypoventilation will have the opposite effect. Question 1. The Effect of Hyperventilation on Oxygenation Given a patient who is hyperventilating (PaCO2 = 18 mmHg) while breathing room air due to a metabolic acidosis, use the simplified alveolar air equation to estimate the effect of the hyperventilation on alveolar oxygen tension (PAO2). The resultant alveolar oxygen tension can be estimated as follows:

1. PAO2 = PIO2 – PaCO2 × 1.25 This is the simplified alveolar air equation where PAO2 is the partial pressure of alveolar oxygen, PIO2 is the partial pressure of inspired oxygen, and PaCO2 × 1.25 is the partial pressure of carbon dioxide adjusted by a factor to account for the respiratory quotient (assumes R = 0.80). 2. PAO2 = FIO2 (PB – PH2O) – (PaCO2 × 1.25) This expansion of the simplified alveolar air equation allows for calculation of PIO2 where PIO2 = FIO2 (PB – PH2O). 3. PAO2 = 0.21 (760 – 47) – (18 × 1.25) 4. PAO2 = 150 – 22.5 = 128 mmHg Thus, hyperventilation resulting in a PaCO2 of 18 mmHg will cause PAO2 to increase to 128 mmHg. Assuming a normal room air alveolar to arterial oxygen tension gradient (PAO2 – PaO2) of 10 mmHg, the resultant PaO2 would be about 118 mmHg: 1. PAO2 = 128 mmHg This is the calculated alveolar oxygen tension based on the simplified alveolar air equation. 2. PaO2 = PAO2 – (PAO2 – PaO2) PAO2 – PaO2 is also known as the A-a gradient. For subjects breathing room air (FIO2 = 0.21), the normal A-a gradient is about 10 mmHg with a normal range of 5–15 mmHg. 3. PaO2 = PAO2 – (PAO2 – PaO2) = PAO2 – A-a gradient = 128 – 10 = 118 mmHg Hyperventilation is a normal physiologic response to hypoxia and can have a small, but sometimes beneficial effect in terms of increasing PAO2 and in turn PaO2. Two of the most common early responses to hypoxia are an increased heart rate (tachycardia) and increased respiratory rate (tachypnea). An increase in heart rate increases oxygen delivery to the tissues by increasing cardiac output. An increase in respiratory rate increases alveolar ventilation and reduces PACO2 and PaCO2 and thus increases PAO2 as illustrated in the example above. Question 2. The Effect of Hypoventilation on Oxygenation Given a patient breathing room air, with otherwise normal lung function whose PaCO2 increases from 40 mmHg to 80 mmHg due to an acute narcotic drug overdose, calculate the effect of this acute hypoventilation on alveolar and arterial oxygen tensions. The resultant alveolar oxygen tension can be estimated as follows:

1. PAO2 = PIO2 – PaCO2 × 1.25 → 2. PAO2 = FIO2 (PB – PH2O) – PaCO2 × 1.25 → 3. PAO2 = 0.21 (760 – 47) – 80 × 1.25 → 4. PAO2 = 150 – 100 = 50 mmHg Thus, hypoventilation resulting in an increase in PaCO2 to 80 mmHg will cause PAO2 to decrease to 50 mmHg. Assuming a normal room air A-a gradient of 10 mmHg, the patient’s resultant PaO2 would be about 40 mmHg: 1. PAO2 = 50 mmHg This is the calculated alveolar oxygen tension based on the simplified alveolar air equation. 2. PaO2 = PAO2 – (PAO2 – PaO2) For subjects breathing room air (FIO2 = 0.21), the normal A-a gradient is about 10 mmHg with a normal range of 5–15 mmHg. 3. PaO2 = PAO2 – (PAO2 – PaO2) = PAO2 – A-a gradient = 50 – 10 = 40 mmHg Thus, hypoventilation may cause severe hypoxemia, even with otherwise normal lungs. Possible causes of acute, severe hypoventilation include trauma, sedative or narcotic drug overdose, central nervous system or neuromuscular disease, and acute cardiopulmonary disease. Assuming normal lung function, if the patient described above had his or her ventilation restored to normal (PaCO2 = 40 mmHg), the patient’s PAO2 and PaO2 should also return to normal. The “Rule of 4 and 5,” which states that for each increase of 4 mmHg in PaCO2, PaO2 will fall about 5 mmHg, provides a quick way to estimate the effect of increases in PaCO2 on PaO2 in patients breathing room air.

Effect of Hypoventilation on Oxygenation While hyperventilation can result in a small improvement in arterial oxygenation, hypoventilation can significantly reduce arterial oxygen levels. For example, an acute increase in alveolar and arterial PCO2 to 80 mmHg (from a normal PCO2 of 40 mmHg) would cause a decrease in alveolar PO2 by about 40 mmHg, as illustrated in Clinical Focus 2-1. Thus, acute alveolar hypoventilation is a common cause of hypoxemia in patients with compromised respiratory drive (e.g., sedative or narcotic drug overdose, head trauma), reduced ventilatory capacity (e.g., diaphragmatic fatigue

due to increased work of breathing), or neurologic disease effecting ventilation (e.g., spinal cord injury, Guillian-Barré syndrome). RC Insight When breathing room air, an increase in PaCO2 of 4 mmHg will reduce PaO2 about 5 mmHg. This is known as the Rule of 4 and 5.

Matching of Gas and Blood (V̇/Q̇) The most common causes of reduced oxygen transfer across the lung are hypoventilation (discussed above), ventilation–perfusion mismatch (i.e., low V̇/Q̇ and right-to-left shunt), and diffusion limitations. Of these, the relationship between alveolar ventilation (V̇A) and pulmonary capillary blood flow (Q̇), often referred to as the matching of gas and blood or V̇/Q̇, may have the most significant impact on the transfer of oxygen across the lung. In the normal lung, the relationship between ventilation and perfusion varies by lung region or zone (e.g., apices, middle portion, and bases) and patient position (e.g., upright vs. supine). Ideally, alveolar ventilation matches pulmonary capillary perfusion and V̇/Q̇ = 1. However, in the normal upright subject, there is more blood flow to the dependent (inferior) regions of the lung, and less blood flow to the nondependent (superior) regions due to gravity. In supine patients lying flat, there is more blood flow to the posterior portions of the lung, while in patients lying on one side, there is greater blood flow to the side that is dependent or “down.” In a similar fashion, prone patients have increased blood flow to the anterior portions of the lung, and prone positioning is sometimes used in ARDS patients to improve oxygenation. Thus, V̇/Q̇ varies with lung zone and position. For example, in an upright subject, V̇/Q̇ > 1 in the apices of the lung, while V̇/Q̇ < 1 in the bases (Figure 2-1). Figure 2-2 illustrates the effects of position on ventilation and perfusion.

FIGURE 2-1 The Effects of Gravity on Ventilation and Perfusion in the Upright Lung.

Description

FIGURE 2-2 The Effects of Gravity and Position on V̇/Q̇. In the upright lung at rest, the bases receive more perfusion (Q̇) with respect to ventilation (V̇), while the apices receive less perfusion (Q̇) with respect to ventilation. In the supine position, blood flow is greater in all posterior regions of the lung. In the prone position (not shown), blood flow would be greater in the anterior portions of the lung.

Description There are a number of possible relationships between ventilation and perfusion in alveolar units: 1. Ventilation matches perfusion (ideal normal, V̇/Q̇ = 1) 2. Underventilation with respect to perfusion (low V̇/Q̇ where V̇/Q̇ < 1.0 but > 0) 3. Absent ventilation with respect to perfusion (shunt units [aka perfusion without ventilation], V̇/Q̇ = 0) 4. Overventilation with respect to perfusion (V̇/Q̇ > 1.0) 5. Ventilation without perfusion (dead space units, V̇/Q̇ = n/0 or undefined) In addition, in the absence of ventilation, the normal physiologic response is to reduce or eliminate perfusion. This may result in alveoli with no ventilation and no perfusion, known as “silent units.” Figure 2-3 illustrates the possible relationships between ventilation and perfusion in alveolar units in the lung.

FIGURE 2-3 Ventilation and Perfusion in the Lung. There are six possible relationships between ventilation and perfusion for alveolar units in the lung. Where ventilation matches capillary perfusion, V̇/Q̇ = 1. With underventilation with respect to perfusion, V̇/Q̇ < 1 but > 0 (low V̇/Q̇). Capillary shunt occurs in cases of perfusion without ventilation and V̇/Q̇ = 0. Where ventilation exceeds perfusion, V̇/Q̇ > 1. Ventilation without perfusion (alveolar dead space) represents an extreme case, where V̇/Q̇ = V̇/0 = ∞ (or undefined). In the absence of ventilation, the normal physiologic response is to reduce or eliminate perfusion, which may result in alveoli with no ventilation and no perfusion, known as “silent units.”

Description In patients with respiratory failure, V̇/Q̇ abnormalities represent pathophysiologic changes, which may cause hypoxemia. Disease states or conditions associated with specific V̇/Q̇ abnormalities are listed below. Figure 2-4 illustrates the effects of breathing room air (FIO2 = 0.21) and 100% O2 on normal lung units and in the presence of low V̇/Q̇, and capillary shunt due to atelectasis or alveolar filling (e.g., consolidative pneumonia, pulmonary edema).

FIGURE 2-4 (A) Normal Ventilation. (B) Underventilation to Perfusion, (C) Alveolar Filling. (D) Atelectasis.

Description Description Causes of low V̇/Q̇ (underventilation with respect to perfusion; V̇/Q̇ < 1 but > 0) include: Asthma Bronchiectasis Bronchospasm Bronchiolar mucosal edema COPD (emphysema, chronic bronchitis) Cystic fibrosis Decreased tidal volume Focal pneumonia Partial airway obstruction

Regional increases in fibrotic tissue Retained secretions Hypoxemia due to underventilation with respect to perfusion (V̇/Q̇ < 1 but > 0) often responds well to the administration of low to moderate concentrations of oxygen. For example, patients with asthma, emphysema, chronic bronchitis, COPD, bronchiectasis, and cystic fibrosis often do well with low-flow oxygen therapy (e.g., nasal cannula). In patients with low V̇/Q̇, an increase in oxygen concentration of 1% will increase PaO2 at least 5 mmHg. Causes of pulmonary capillary shunt (perfusion without ventilation; V̇/Q̇ = 0) include: ARDS Atelectasis (including microatelectasis) Complete airway obstruction Consolidative pneumonia Pneumothorax (large) Pulmonary edema (with complete alveolar filling) Patients with significant pulmonary capillary shunt (aka physiologic shunt) may experience refractory hypoxemia in which even high concentrations of oxygen are ineffective. Possible causes of refractory hypoxemia include significant atelectasis, consolidative pneumonia, ARDS, and pulmonary edema. With refractory hypoxemia due to significant pulmonary capillary shunt (V̇/Q̇ = 0), an increase in oxygen concentration ≥ 10% will increase PaO2 < 5 mmHg. These patients may require moderate to high oxygen concentrations, PEEP or CPAP, and mechanical ventilatory support. Causes of overventilation with respect to perfusion (high V̇/Q̇); V̇/Q̇ > 1) include: Decreased lung perfusion Decreased cardiac output Acute pulmonary hypertension Ventilation in excess of perfusion Positive-pressure ventilation Causes of alveolar dead space (ventilation without perfusion; V̇/Q̇ = ∞ or undefined) include:

Pulmonary embolus (with complete occlusion of pulmonary vessel) Obliteration of the pulmonary capillaries (e.g., emphysema) As noted, V̇/Q̇ will change with patient position. With unilateral lung disease, if the supine patient is turned laterally to place the disease affected side down, the resultant increased perfusion of the “bad” lung may cause worsening hypoxemia. Placing the “good” lung down may result in a temporary increase in PaO2, however, this should be avoided if there is any possibility of compromising the good lung due to drainage (e.g., secretions or hemorrhage) from the diseased lung to the “good” lung by gravity.

Shunt Shunt represents an extreme situation in which V̇/Q̇ = 0. Shunts can be anatomic (both intrapulmonary and extrapulmonary anatomic shunt) or physiologic (see pulmonary capillary shunt above). Clinically, it is often difficult to distinguish a physiologic shunt from a very severe V̇/Q̇ mismatch. A small amount of anatomic shunt is normal; however certain anatomic anomalies can result in increased shunt.

Physiologic Shunt (Pulmonary Capillary Shunt) Physiologic right-to-left shunts occur when alveoli are perfused but not ventilated (V̇/Q̇ = 0). Common causes of physiologic shunt include atelectasis and conditions that cause alveolar filling (e.g., consolidative pneumonia, ARDS). As noted above, patients with significant physiologic shunt may experience refractory hypoxemia.

Anatomic Shunt An anatomic shunt occurs when blood travels from the right side of the heart to the left side of the heart via anatomic structures that bypass the alveoli. Normally, a small amount of venous blood is carried from the bronchial veins, Thebesian veins, and pleural veins to the left side of the heart where it mixes with oxygenated blood from the pulmonary circulation. This normal venous admixture (i.e., anatomic shunt) represents 2%–5% of the cardiac output and explains why arterial oxygen tension (PaO2) is slightly less than pulmonary capillary oxygen tension (Pc´O2). An abnormal anatomic shunt can occur with certain congenital cardiac defects (e.g., cardiac septal defects, tetralogy of Fallot) or cases of persistent fetal circulation

(e.g., patent ductus arterious [PDA] or patent foramen ovale). Large anatomic shunts may cause severe hypoxemia that is refractory to oxygen administration.

Impaired Diffusion (Diffusion Limitations) Diffusion of oxygen across the alveolar–capillary membrane can be impaired (known as diffusion limitation) due to mismatch of ventilation and perfusion, a reduction in the available surface area for diffusion, or an increase in diffusion distance. Interstitial lung disease (ILD) may cause inflammation, edema, and interstitial fibrosis and thus increase the distance oxygen must travel from the alveolus to the adjacent pulmonary capillary. Other causes of diffusion problems include pulmonary vascular disease, emphysema, and alveolar or interstitial edema. With impaired diffusion, hypoxemia may only occur during exercise; hypoxemia due to a diffusion defect is typically reversible by the administration of low to moderate concentrations of oxygen.

Indices of O2 Transfer Certain measures are sometimes used to assess the effectiveness of gas exchange across the lung. These include PaO2, SpO2, SaO2, A-a oxygen gradient, PaO2/FIO2 ratio (aka P/F ratio), and A-a ratio. In addition, it is possible to calculate intrapulmonary shunt using the clinical shunt equation. Hypoxemia refers to low arterial blood oxygen levels as defined by measurement of PaO2 and/or oxygen saturation (SaO2 or SpO2). When breathing room air, a normal PaO2 is from 80 to 100 mmHg resulting in an oxygen saturation (SaO2 or SpO2) of 96% to 98%. Mild, moderate, and moderately severe in severe hypoxemia may then be defined as a 60 < PaO2 < 80 mmHg, PaO2 < 60 mmHg, PaO2 < 50 mmHg, and PaO2 < 40 mmHg, respectively. Clinical Focus 2-2 illustrates the calculation of several indices of oxygenation and provides examples of normal and abnormal values.

CLINICAL FOCUS 2-2 Indices of O2 Transfer Across the Lung Clinically, the effectiveness of gas exchange and oxygen transfer across the lung can be assessed by measurement of arterial oxygen tension (PaO2), pulse

oximetry (SpO2), and direct measurement of arterial oxygen saturation (SaO2). Other indices of the effectiveness of gas transfer include calculation of the alveolar to arterial oxygen tension difference ([PAO2 – PaO2], aka A-a gradient and P(A-a)O2), arterial oxygen tension to fractional concentration of inspired oxygen ratio (PaO2/FIO2, aka P/F ratio), and ratio of alveolar to arterial oxygen tension (PaO2/PAO2, aka a/A ratio). In addition, intrapulmonary shunt fraction (Q̇S/Q̇T) can be calculated using the clinical shunt equation. The questions below use the following inputs: PB: barometric pressure FIO2: fractional concentration of oxygen Hb: hemoglobin concentration (grams/100 mL blood) PaO2: partial pressure of oxygen in the arterial blood (mmHg) SaO2: arterial oxygen saturation CaO2: arterial blood oxygen content (mL O2 per 100 mL blood) PaCO2: partial pressure of carbon dioxide in the arterial blood P

O2: partial pressure of oxygen in the mixed venous blood

S

O2: mixed venous oxygen saturation

C O2: mixed venous blood oxygen content (vol% or mL O2 per 100 mL blood) Q̇S/Q̇T: shunt fraction Cc´O2: pulmonary capillary O2 content (mL O2 per 100 mL blood) Pc´O2: partial pressure of oxygen in the pulmonary capillary blood Question 1. What are normal values for PaO2, SpO2, SaO2, A-a oxygen gradient (PAO2 – PaO2), PaO2/FIO2 ratio, A-a ratio, and Q̇s/Q̇ T? Answer: Normal values for patients breathing room (FIO2 = 0.21) are listed for indices of oxygenation. Expected (normal) values when breathing 100% oxygen (FIO2 = 1.0) are listed for comparison for several indices. PaO2: 80–100 mmHg (FIO2 = 0.21); PaO2: 543–583 mmHg (FIO2 = 1.0) Expected PaO2 values decline with age. SpO2: 96%–98% (FIO2 = 0.21); SpO2 = 100% (FIO2 = 1.0) SaO2: 96%–98% (FIO2 = 0.21); SaO2 = 100% (FIO2 = 1.0) A-a oxygen gradient (PAO2 – PaO2): Normal A-a gradient is 10 mmHg with a range of 5–15 mmHg (FIO2 = 0.21); when breathing 100% O2 (FIO2 = 1.0); normal A-a gradient increases to about 100 mmHg with a range of 80–120

mmHg. PaO2/FIO2 ratio: Assuming normal values breathing room air, PaO2/FIO2 = 100/0.21 = 476 with range of 380–500 mmHg (FIO2 = 0.21); breathing 100% oxygen, a normal PaO2/FIO2 = 563/1.0 = 563 (FIO2 = 1.0). PaO2/PAO2 ratio: 0.80 with a range of 0.77 to 0.82 (FIO2 = 0.21); normal PaO2/PAO2 ratio breathing 100% O2 is about 0.85 (FIO2 = 1.0). Q̇S/Q̇T: Normal shunt fraction is 0.02 to 0.05 (2% to 5% shunt). Question 2. Clinically, what values for common indices suggest problems with oxygenation and/or gas transfer across the lung? Answer: 1. PaO2 values associated with oxygenation problems while breathing room air (FIO2 = 0.21): 60–79 mmHg: mild hypoxemia 50–59 mmHg: moderate hypoxemia 40–49 mmHg: moderate to severe hypoxemia < 40 mmHg: very severe hypoxemia Most clinicians are not overly concerned as long as PaO2 ≥ 60 mmHg while the patient is breathing room air. PaO2 values normally decline with age. PaO2 < 543 mmHg while breathing 100% oxygen (FIO2 = 1.0) is below normal. 2. SpO2 and SaO2 values while breathing room air (FIO2 = 0.21) associated with oxygenation problems: 91%–95%: mild hypoxemia 85%–90%: moderate hypoxemia 75%–84%: moderate to severe hypoxemia < 75%: very severe hypoxemia Most clinicians are not overly concerned as long as SaO2 ≥ 90%. SpO2 and SaO2 in normal subjects should be 100% while breathing 100% oxygen (FIO2 = 1.0). SpO2 and SaO2 values are affected by the chemical environment of the blood (e.g., temperature, PaCO2, and pH) and decreased with hemoglobin impairment (e.g., carboxyhemoglobin, methemoglobin). SpO2 and SaO2 values also decline with age. 3. A-a oxygen gradient (PAO2 – PaO2)

When breathing room air (FIO2 = 0.21): PAO2 – PaO2 > 15 mmHg in healthy young adults suggests possible oxygenation problems. PAO2 – PaO2 increases with age; at age 60 years, PAO2 – PaO2 should be ≤ 25 mmHg. When breathing 100% O2 (FIO2 = 1.0): (PAO2 – PaO2) ÷ 20 provides a rough estimate of physiologic shunt for patients breathing 100% oxygen. PAO2 – PaO2 > 100–120 mmHg while breathing 100% oxygen suggests oxygenation problems. 4. PaO2/FIO2 ratio < 380 mmHg while breathing room air (FIO2 = 0.21) suggests oxygenation problems. While breathing supplemental O2 with PEEP ≥ 5 cm H2O: PaO2/FIO2 ratio ≤ 300 mmHg but > 200 mmHg suggests mild oxygenation problems. PaO2/FIO2 ratio ≤ 200 mmHg but > 100 mmHg suggests moderate oxygenation problems. PaO2/FIO2 ratio ≤ 100 mmHg suggests severe oxygenation problems. PaO2/PAO2 ratio < 0.77 suggests oxygenation problems. 5. Q̇S/Q̇T > 5% suggests oxygenation problems due to increased intrapulmonary shunt where:

Question 3. Given an adult patient in the ICU receiving invasive mechanical ventilatory support with 5 cm H2O of PEEP and the following data, calculate each of the oxygenation indices described above, where: PB = 760 mmHg FIO2 = 0.50 Hb = 10 g PaO2 = 50 mmHg SaO2 = 0.88 CaO2 = 1.34 × Hb × SaO2 + 0.003 × PaO2 = (1.34 × 10 × 0.88) + (0.003 × 50) = 11.94 vol% PaCO2 = 40 mmHg

P O2 = 36 mmHg S O2 = 0.66 C O2 = 1.34 × Hb × S O2 + 0.003 × P O2 = (1.34 × 10 × 0.66) + (0.003 × 36) = 8.95 vol% 1. What is the patient’s calculated A-a oxygen gradient (PAO2 – PaO2)? Calculate PAO2: PAO2 = (PB – PH2O) × FIO2 – PaCO2 × 1.25 PAO2 = (760 – 47) × 0.50 – 40 × 1.25 = 306.5 mmHg This is a normal PAO2 in a patient breathing 50% O2 at sea level. Calculate A-a oxygen gradient (PAO2 – PaO2): PAO2 – PaO2 = 306.5-50 = 256.5 mmHg A normal PAO2 – PaO2 in a patient at sea level breathing 21% O2 is about 10 mmHg while a normal PAO2 – PaO2 in a normal patient breathing 100% O2 is about 100 mmHg. A normal PAO2 – PaO2 when breathing 50% O2 would be about 60 mmHg. An A-a gradient (PAO2 – PaO2) of 256.5 mmHg is much greater than would be expected and indicates abnormal gas exchange. 2. What is the patient’s calculated PaO2/ PAO2 ratio? PaO2/PAO2 = 50/306.5 = 0.16 A normal PaO2/ PAO2 ratio is about 0.80 (range of 0.77–0.82); a value of 0.16 is very low, probably due to a large intrapulmonary shunt. 3. What is the patient’s calculated PaO2/FIO2 ratio? PaO2/ FIO2 = 50/0.50 = 100 An ideal normal PaO2/FIO2 ratio is > 380 with a clinical range of 300–500; PaO2/ FIO2 < 300 while receiving supplemental oxygen and 5 cm H2O PEEP represents abnormal gas exchange; PaO2/FIO2 ≤ 100 represents severe hypoxemia. 4. What is the patient’s calculated shunt fraction (Q̇S/Q̇T)? Estimate Pc´O2 and Sc´O2. Assume PAO2 = Pc´O2 = 306.5 mmHg (see question 3-1 above). Estimate Sc´O2 based on estimated PO2. Pc´O2 of 306.5 would achieve 100% saturation of the Hb. Pc´O2 = 306.5 → Sc´O2 = 1.0. Calculate Cc´O2.

Cc´O2 = 1.34 × Hb × Sc´O2 + 0.003 × Pc´O2 Cc´O2 = (1.34 × 10 × 1.0) + 0.003 × 306.5 = 14.32 vol% Calculate shunt fraction. Q̇S/Q̇T = (Cc´O2 – CaO2) ÷ (Cc´ – C O2) Q̇S/Q̇T = (14.32 – 11.94) ÷ (14.32 – 8.95) Q̇S/Q̇T = 0.44 or 44% A normal, physiologic shunt is 3%–5%. A right-to-left shunt of 44% is very high.

Blood Oxygen Content When evaluating a patient in respiratory failure, it is important to consider all aspects of the oxygenation process. As noted above, PaO2 may be reduced due to problems with inspired oxygen tension or concentration (e.g., altitude or ambient hypoxia), problems with the conducting airways (e.g., obstruction, airway edema, or tumor), hypoventilation (e.g., sedative or narcotic drug overdose, head trauma, or neuromuscular disease), problems with the matching of gas and blood (e.g., low V̇/Q̇, shunt) or diffusion limitations. While the severity of hypoxemia is often assessed by evaluation of arterial oxygen tension (PaO2) and saturation (SaO2 and/or SpO2), it is important to consider all factors that affect the arterial blood oxygen content (CaO2): CaO2 = 1.34 × Hb × SaO2 + 0.003 × PaO2 Where: CaO2 is amount of O2 carried by 100 mL of blood (mL O2/100 mL blood [aka vol%]). Hb is the hemoglobin level of the blood in grams per 100 mL of blood (reported as grams per deciliter [g/dL]). Normal hemoglobin is about 15 g/dL. 1.34 is the factor that expresses the maximum Hb-O2 carrying capacity at 100% saturation (1.34 mL O2 per 1 g Hb). 1.34 × Hb × SaO2 = total amount of O2 carried by the Hb (i.e., HbO2) in mL O2/100 mL blood. 0.003 is the Bunsen solubility coefficient for oxygen that allows for calculation of the amount of O2 dissolved in the plasma (mL O2 /100 mL plasma).

O2 dissolved in the blood plasma (mL O2 /100 mL plasma) = 0.003 × PaO2. Assuming normal Hb-O2 affinity, and normal values for Hb (15 g/dL), PaO2 (100 mmHg), and SaO2 (0.97), the amount of oxygen carried by the Hb (HbO2) would be: HbO2 = 1.34 × Hb × SaO2 = 1.34 × 15 × 0.97 = 19.5 mL O2/100 mL blood At these same normal values, the O2 dissolved in the plasma would be: Plasma O2 = 0.003 × PaO2 = 0.003 × 100 mmHg = 0.3 mL O2/100 mL blood Inserting these normal values into our equation for CaO2: CaO2 = 1.34 × Hb × SaO2 + 0.003 × PaO2 CaO2 = 1.34 × 15 × 0.97 + 0.003 × PaO2 = 19.8 mL O2/100 mL blood or 19.8 vol% Thus, normal CaO2 is about 20 mL O2/100 mL blood (or 19.8 vol% to be exact). Examination of the formula for CaO2 illustrates the importance that Hb and SaO2 play in maintaining adequate arterial blood oxygen content and, in turn, oxygen delivery to the tissues. Thus, factors that effect Hb or SaO2 may have a significant effect on CaO2 and O2 delivery to the tissues as described below.

Factors that Affect O2 Saturation Arterial oxygen saturation (SaO2) is primarily determined by the PaO2 and Hb-O2 affinity. As PO2 increases, SO2 also increases as described by the sigmoid-shaped oxyhemoglobin (HbO2) disassociation curve (Figure 2-5). PaO2 values > 60 mmHg will normally result in SaO2 values > 90% and increases in PaO2 above 60 mmHg result in only modest increases in SaO2. For example, an increase in PaO2 from 60 mmHg to 100 mmHg only increases SaO2 from 90% to 97%. While a normal PaO2 of 100 mmHg results in a SaO2 of about 97%, an increase in PaO2 > 150 to 200 mmHg is required to achieve a SaO2 of 100%. Thus, PaO2 > 60 mmHg will place most patients on the “flat part” of the HbO2 disassociation curve where large changes in PaO2 result in relatively small changes in SaO2 (Figure 2-5). This explains why a clinical goal of PaO2 > 60 mmHg but ≤ 100 mmHg for most patients in respiratory

failure usually provides an acceptable SaO2. The HbO2 disassociation curve also illustrates why achieving a PaO2 above 100 mmHg provides little benefit in terms of oxygen saturation. In addition, to achieve a PaO2 > 100 mmHg at normal barometric pressures may require administration of excessive concentrations of oxygen (e.g., FIO2 . 0.50 to 0.60) and risk of the associated complications (e.g., oxygen toxicity, oxygen-associated hypercarbia in chronic CO2 retainers).

FIGURE 2-5 Oxyhemoglobin Dissociation Curve.

Description Arterial oxygen levels corresponding with PaO2 < 60 mmHg place the patient on the “steep part” of the HbO2 disassociation curve where small changes in PaO2 result in relatively large changes in SaO2 (Figure 2-5). For example, a decrease in PaO2 from 60 mmHg to 40 mmHg results in a decrease in SaO2 from about 90% to 75%.

As another point of reference, an arterial PaO2 of 40 mmHg represents moderate to severe hypoxemia, while a venous PO2 of 40 mmHg is normal. As noted, a PaO2 of 40 mmHg will normally result in an SaO2 of about 75%, and modest increases in PaO2 above 40 mmHg will result in large increases in SaO2 – as expected on the steep part of the HbO2 disassociation curve. Hb-O2 affinity is affected by the chemical environment of the blood, which may increase or decrease Hb-O2 affinity as follows: Decreased Hb-O2 affinity (right shift in the HbO2 disassociation curve): increased temperature (e.g., fever), increased PaCO2 (e.g., hypoventilation), reduced pH (e.g., acidosis). With decreased Hb-O2 affinity (i.e., right shift), SaO2 is less at a given PaO2. Increased Hb-O2 affinity (left shift in HbO2 disassociation curve): decreased temperature (e.g., hypothermia), decreased PaCO2 (e.g., hyperventilation), increased pH (e.g., alkalosis). With increased Hb-O2 affinity (i.e., left shift), SaO2 is greater at a given PaO2. Figure 2-6 illustrates the effects of a “right shift” and “left shift” of the HbO2 disassociation curve.

FIGURE 2-6 Factors That Affect the Oxyhemoglobin Disassociation Curve Position. DPG = diphosphoglycerate.

Description

Factors that Affect the Hemoglobin As noted above, the majority of the oxygen carried in the blood is carried by the hemoglobin (Hb). A reduced Hb level (e.g., blood loss or anemia) may significantly reduce CaO2, while an elevated Hb level (e.g., polycythemia) will increase CaO2. For example, even with a normal PaO2 of 100 mmHg and SaO2 of 97%, a reduction in Hb from a normal value of 15 g/dL to 7.5 g/dL will reduce CaO2 from about 20 mL O2/100 mL blood to about 10 mL O2/100 mL blood. To put that value in perspective, normal mixed venous blood oxygen content (Cv̄O2) is about 15 mL O2/100 mL blood. Clinical Focus 2-3 illustrates normal arterial oxygen content and the effects of anemia and polycythemia on CaO2.

CLINICAL FOCUS 2-3 Effect of Hemoglobin (Hb) on Arterial Oxygen Content (CaO2) Hemoglobin levels can have a profound effect on arterial oxygen content. The clinician should always review the patient’s hemoglobin as part of the routine assessment of oxygenation status, keeping in mind the effect of hemoglobin levels on CaO2. Question 1. Given a patient with a normal hemoglobin (Hb = 15 g/dL), normal arterial oxygen tension (PaO2 = 100 mmHg), and normal arterial oxygen saturation (SaO2 = 0.97), what would be the resultant CaO2? Hb = 15 g/100 mL of blood (Normal range is 12–16 females and 14–18 in males.) PaO2 = 100 mmHg (Normal clinical range is 80–100 mmHg.) SaO2 = 0.97 (Normal range is 0.95–0.97.) Answer: This patient’s arterial oxygen content (CaO2) in mL of O2 per 100 mL of blood (aka vol%) would be: CaO2 = 1.34 × Hb × SaO2 + 0.003 PaO2 CaO2 = 1.34 × 15 × 0.97 + 0.003 (100) CaO2 = 19.5 mL O2/100 mL blood + 0.3 mL O2/100 plasma CaO2 = 19.8 mL O2/100 mL blood or 19.8 vol%—a normal value Question 2. Given a patient with severe anemia (Hb = 5 g/dL), normal arterial oxygen tension (PaO2 = 100 mmHg), and normal arterial oxygen saturation (SaO2 = 0.97), what would be the resultant CaO2? Hb = 5 g/100 mL of blood (Normal range is 12–16 females and 14–18 in males.) PaO2 = 100 mmHg (Normal clinical range is 80–100 mmHg.) SaO2 = 0.97 (Normal range is 0.95–0.97.) Answer: This patient’s arterial oxygen content (CaO2) would be: CaO2 = 1.34 × Hb × SaO2 + 0.003 PaO2 CaO2 = 1.34 × 5 × 0.97 + 0.003 (100) CaO2 = 6.5 mL O2/100 mL blood + 0.3 mL O2/100 plasma CaO2 = 6.8 mL O2/100 mL blood or 6.8 vol%.

Thus, even if arterial oxygen tension and saturation are normal, anemia can have a profound effect in reducing arterial oxygen content. This patient has severe anemic hypoxia. Causes of anemia include blood loss, excessive red blood cell destruction, and decreased red blood cell formation. Question 3. Given a patient with chronic lung disease and polycythemia (Hb = 20 g/dL), reduced arterial oxygen tension (PaO2 = 50 mmHg), and reduced arterial oxygen saturation (SaO2 = 0.85), what would be the resultant CaO2? Hb = 20 g/100 mL of blood (Normal range is 12–16 females and 14–18 in males.) PaO2 = 50 mmHg (Normal clinical range is 80–100 mmHg.) SaO2 = 0.85 (Normal range is 0.95–0.97.) Answer: This patient’s arterial oxygen content (CaO2) would be: CaO2 = 1.34 × Hb × SaO2 + 0.003 PaO2 CaO2 = 1.34 × 20 × 0.85 + 0.003 (50) CaO2 = 22.78 mL O2/100 mL blood + 0.15 mL O2/100 plasma CaO2 = 22.93 mL O2/100 mL blood or 22.93 vol% Thus, even though this patient has moderate hypoxemia based on his arterial oxygen tension (PaO2 = 50) and saturation (SaO2 = 0.85), his arterial oxygen content is actually above normal. Primary polycythemia may be caused by a gene mutation (e.g., polycythemia vera). Secondary polycythemia is often a response to chronic hypoxemia due to chronic lung disease (e.g., COPD). Living at high altitude may also cause polycythemia. As shown in this example, an elevated Hb can compensate for a reduced PaO2 and SaO2 in patients with chronic lung disease and in people living at higher elevation.

Anemic hypoxia refers to a significant decrease in arterial blood oxygen content due to low hemoglobin or hemoglobin dysfunction. The symptoms of anemic hypoxia are similar to other forms of hypoxia and include dyspnea, fatigue, tachycardia, and tachypnea. An increase in cardiac output is a typical physiologic response, and may result in a full bounding pulse, palpitations, angina, and a loud “roaring” in the ears due to increased blood flow. It’s important to note that patients with anemic hypoxia may not exhibit cyanosis and verification of anemic hypoxia requires measurement

of hemoglobin, hematocrit, and/or red blood cell count (RBC). Anemia may be caused by decreased RBC formation, excessive RBC destruction, or blood loss. Decreased RBC formation may be caused by nutritional deficits (e.g., iron deficiency), bone marrow disorders (e.g., aplastic anemia), bone marrow suppression (e.g., chemotherapy or radiation therapy), hormone deficiencies, or chronic inflammatory disease.9 Excessive RBC destruction may be genetic (e.g., sickle-cell disease) or acquired (e.g., malaria).9 Blood loss may be due to trauma, surgery, or gastrointestinal tract bleeding. RC Insight A hemoglobin (Hb) of less than 13.5 g/dL or hematocrit (HCT) value of less than 41% in men or a Hb value of less than 12 g/dL or HCT of less than 36% in women is consistent with a diagnosis of anemia.

Platelet disorders and certain drugs (e.g., aspirin, heparin, warfarin [Coumadin]) may cause bleeding due to inadequate blood clot formation. Newer blood thinners used to prevent stroke (e.g., apixaban [Eliquis], dabigatran [Pradaxa], edoxaban [Savaysa], and rivaroxaban [Xarelto]) may also cause bleeding. Platelet disorders sometimes seen in the ICU include thrombocytopenia (low platelet count) due to bone marrow disease (e.g., leukemia), aplastic anemia, exposure to toxic chemicals (e.g., pesticides, arsenic), and certain medications (e.g., diuretics, sulfa drugs, and chloramphenicol).10,11 Other possible causes of platelet disorders include viral disease (e.g., molds, rubella, chickenpox, and acquired immunodeficiency syndrome [AIDS]), autoimmune disease (e.g., immune thrombocytopenia), enlarged spleen (e.g., severe liver disease), and disseminated intravascular coagulation (DIC).10,11 Disease states or conditions sometimes associated with the development of DIC include sepsis, trauma, certain cancers, complications of pregnancy, transfusion reactions, and venomous snake bites (e.g., rattlesnake bites).10,11 Evaluation of patients for anemic hypoxia requires the measurement of Hb, HCT, and/or RBC count. As noted, anemia can have a profound effect on arterial oxygen content, even if arterial oxygen tension and saturation are normal. It should also be noted that cyanosis is a poor guide to the severity of hypoxemia in anemic patients. This is because cyanosis requires at least 5 g of desaturated Hb. Thus, a patient with a Hb level of only 8 g/dL would require SaO2 to fall below 38% before there was

at least 5 g of desaturated Hb: 8 g Hb total – 5 g desaturated Hb = 3 g saturated Hb (HbO2) → SaO2 = 3 g HbO2/8 g Hb total = 0.375 or 37.5% Decreased hemoglobin levels reduce the oxygen-carrying capacity of the blood; oxygen therapy is indicated for anemic hypoxia, though it will have limited benefit until the hemoglobin levels are restored. Treatment of anemia is dependent upon the cause. Blood transfusion may be considered when Hb < 10 g/dL or hematocrit < 30%; Hb < 7 to 8 g/dL provides a clear indication for blood transfusion.9,10 As noted, Clinical Focus 2-3 provides an example of the effects of anemia on CaO2. RC Insight Patients with severe anemia may experience profound hypoxia without cyanosis.

Sickle-cell disease (aka sickle-cell anemia) is an inherited blood disorder caused by the presence of sickle-cell hemoglobin (HbS). With sickle-cell disease, the RBCs become curved into a sickle or crescent shape. HbS can crystalize in the RBCs, and fragile RBCs may rupture, form clots, or clump. Most of the complications of sicklecell disease are caused by microvascular occlusion or clot formation.9 The most common symptom is episodes of acute pain, which can be treated by analgesics, fluids, and oxygen therapy. Hypoxia, dehydration, and acidosis may occur, and complications may include development of vaso-occlusive crises, infection, and stroke.9 Cardiac, liver, bone, or neurologic complications may occur, including acute chest syndrome with chest pain, hypoxemia, and pulmonary infiltrates on imaging. Acute chest syndrome may be accompanied by the development of pneumonia, pulmonary thrombosis, pulmonary infarction, and multisystem organ failure. Treatment of acute chest syndrome includes hospitalization, O2 therapy, antibiotics, and consideration of emergent exchange blood transfusion.9 Polycythemia is defined as an abnormally high red blood cell count and is associated with Hb > 16.0 g/dL in women (or HCT > 48%) and Hb > 16.5 g/dL (or HCT > 49%) in men.12 Polycythemia may be primary (e.g., due to a gene mutation) or secondary. Secondary polycythemia is often a response to chronic hypoxemia,

living at high altitude, or chronic exposure to carbon monoxide. Patients with chronic lung disease (e.g., chronic respiratory failure) often have low PaO2 and SaO2. An elevated hemoglobin due to polycythemia may compensate for chronically decreased PaO2 and SaO2 by increasing CaO2. As noted, Clinical Focus 2-3 provides an example of the effects of polycythemia on CaO2. It is also important to note that cyanosis can occur without profound tissue hypoxia in polycythemic patients. On the other hand, with anemia, profound hypoxia can occur without cyanosis. Carbon monoxide poisoning causes an increase in carboxyhemoglobin (HbCO), a dysfunctional form of hemoglobin that reduces hemoglobin’s oxygen-carrying capacity by displacing oxyhemoglobin (HbO2) and decreasing SaO2.13 For example, an HbCO of 30% will limit the maximum possible SaO2 to 70%, which will cause severe hypoxia. Causes of carbon monoxide poisoning include exposure to improperly functioning heating systems, exhaust from motor vehicles or gaspowered generators in poorly ventilated spaces, and inhalation of smoke from fires. The clinical manifestations of carbon monoxide poisoning include headache, nausea, dizziness, weakness, and discomfort. Severe poisoning may cause unconsciousness, seizures, cardiopulmonary collapse, and death. Diagnosis of carbon monoxide poisoning should include measurement of HbCO levels via cooximetry. Conventional pulse oximeters and some blood gas machines do not include co-oximetry and do not detect HbCO; resultant reported oxygen saturation values can be incorrect. Newer pulse oximetry devices are now available that allow for the measurement of HbCO, although use of a blood gas analyzer that includes co-oximetry is preferred. Treatment of carbon monoxide poisoning includes administration of high concentrations of oxygen. The half-life of HbCO while breathing room air at normal barometric pressure is about 5 hours; this is reduced to 60 to 90 minutes when breathing 100% oxygen at normal barometric pressure. In severe cases (HbCO > 25%–40%), hyperbaric oxygen (HBO) administration may be rapidly instituted (if available); HBO may be considered in pregnant women when HbCO > 20%.13 With hyperbaric oxygen administration at 100% O2 at 3 atmospheres (ATA) of pressure, the half-life of HbCO is reduced to about 30 minutes. HBO allows for a significant increase in CaO2 by increasing the amount of oxygen dissolved in plasma. For

example, at normal barometric pressure, a normal PaO2 of 100 mmHg results in a plasma O2 concentration of only about 0.3 mL per 100 mL of blood. Breathing 100% oxygen at normal barometric pressures may raise the PaO2 up to as much as 500 mmHg in the presence of normal lung function. However, even with a PaO2 of 500 mmHg, plasma O2 concentration would reach only 1.5 mL/100 mL of blood. HBO with 100% O2 at 3 ATA, however, may raise plasma O2 as high as 6.8 mL/100 mL blood.13 To summarize, HBO is indicated in the treatment of carbon monoxide poisoning when CoHb > 25% (> 20% in pregnancy) and in all patients with evidence of myocardial ischemia, severe metabolic acidosis, or altered mental status. Moderate to severe carbon monoxide poisoning may cause myocardial ischemia, which should be assessed by electrocardiogram (ECG); cardiac biomarkers should be assessed in patients with a history of cardiac disease or evidence of ischemia on ECG.13 Patients with impaired mental status or coma may need to be intubated to protect the airway and mechanical ventilation should be provided if needed. RC Insight Carboxyhemoglobin levels (HbCO) of 20% to 40% will cause moderate to severe hypoxia. HbCO of 50% or more may cause seizures, coma, cardiopulmonary collapse, and death.

Methemoglobinemia occurs with the presence of methemoglobin (metHb). Congenital methemoglobinemia is a relatively rare hereditary disease.14 Acquired methemoglobinemia can be caused by certain antibiotics (e.g., dapsone, sulfa drugs), local anesthetics (e.g., benzocaine, lidocaine, and prilocaine), inhaled nitric oxide (NO), certain chemicals such as nitrates, nitrobenzene, aniline dyes, and certain other chemical agents.14 Symptoms of mild methemoglobinemia include headache, fatigue, and dyspnea. High levels of metHb may cause respiratory depression, unconsciousness, shock, seizures, and death. Routine pulse oximetry is inaccurate in the presence of metHb. Diagnosis is confirmed by co-oximetry followed by the Evelyn–Malloy method, a photoelectric technique for determination of MetHb in blood. MetHb levels above 20% usually cause clinical symptoms, and levels above 40% may be fatal.14 Treatment includes removal or discontinuing use of the suspected causal agent. Intravenous methylene blue may be administered in the presence of symptoms.14 Hyperbaric oxygen therapy (HBO) and/or exchange

transfusion may be considered in cases of severe methemoglobinemia.14

Oxygen Delivery For adequate oxygen delivery to the tissues to occur, there must be an adequate arterial oxygen content (CaO2) and the oxygenated blood must be pumped to the systemic tissue beds, which requires a sufficient cardiac output (Q̇T) and adequate tissue perfusion. Oxygen delivery to the tissues can be calculated as follows: ḊO2 = CaO2 × Q̇T where: ḊO2 = O2 delivery (mL O2/min); normal ḊO2 is about 1000 mL O2/min. CaO2 = arterial O2 content (mL O2/100 mL blood); normal CaO2 is 19.8 mL O2/100 mL blood (aka 19.8 vol%) or about 20 vol%. Q̇T = cardiac output (mL/min); normal resting Q̇T is about 5 L/min (5000 mL/min) with a range of 4–8 L/min. Calculation of ḊO2 is shown in Box 2-5. Oxygen delivery may be reduced because of a decrease in CaO2 or Q̇T. Common causes of reduced CaO2 seen in the ICU include reductions in PaO2 and SaO2 due to lung disease and anemia, blood loss, or dysfunctional Hb (e.g., metHb or COHb).

BOX 2-5 Calculation of Oxygen Delivery to the Tissues Given the following normal values for O2 content (CaO2) and cardiac output (QT), calculate a normal O2 delivery to the tissues. ∎ ∎

Normal CaO2 = 19.8 mL O2/100 mL blood or approximately 20 mL O2/100 mL blood QT = 5 L/min or 5000 mL/min 1. ḊO2 = CaO2 × QT 2. ḊO2 = O2 content (mL O2/100 ml blood) × cardiac output (mL/min) 3. 4. ḊO2 1000 mL O2/min

Normal O2 delivery to the tissues is about 1000 mL O2 per minute.

Reduced cardiac output is a sometimes-overlooked cause of tissue hypoxia due to inadequate circulation (aka circulatory hypoxia). Cardiac disease and hypovolemia can cause a reduction in cardiac output. Cardiac output (Q̇T) is determined by heart rate (HR) and stroke volume (SV) where: Q̇T = HR × SV Heart rate is affected by many factors and may be abnormally elevated (HR > 100 = tachycardia) or decreased (HR < 60 = bradycardia). In general, tachycardia increases cardiac output, while bradycardia reduces cardiac output, although tachycardia may also reduce cardiac output due to decreased ventricular filling time. Common causes of tachycardia seen in the ICU include pain, anxiety, and hypoxemia, although severe hypoxia can cause bradycardia. Other common causes of tachycardia include anemia, blood loss, hypovolemia, hypotension, shock, cardiac disease, and certain medications (e.g., epinephrine, isoproterenol [Isuprel], dopamine [Intropin], and atropine). Causes of bradycardia include ischemic heart disease, acute MI, trauma, arrhythmia (e.g., heart block), certain medications (e.g., parasympathomimetics, sympatholytics [beta-blockers], opioids, sedatives, and digitalis), and severe hypoxia.15 Patients with obstructive sleep apnea, excessive vagal activity (e.g., vasovagal responses due to carotid sinus stimulation), increased intracranial pressure, or infectious disease (e.g., Lyme disease, Rocky Mountain spotted fever) may also experience bradycardia.15 Stroke volume is determined by cardiac preload, afterload, and cardiac contractility. Preload is simply the volume of blood in the ventricles at end diastole. Preload can be affected by changes in venous return, total blood volume, intrathoracic pressure, and other factors. Afterload is the force the ventricles must contract against and is determined by arterial blood pressure, systemic vascular resistance (SVR), and other factors. Cardiac contractility is the force of ventricular contraction, which is affected by sympathetic nerve activity, circulating catecholamines (e.g., epinephrine), inotropic drugs (e.g., digitalis, milrinone [Primacor], dopamine [Intropin], and dobutamine [Dobutrex]) and other factors. Common causes of reduced cardiac output seen in the ICU include ischemic heart

disease, myocardial infarction (MI), cardiac arrhythmias, heart failure, hypovolemia, or late septic shock. Hypertension, cardiac valvular disease, cardiomyopathies (diseases of the heart muscle), and mechanical ventilatory support with PEEP may also reduce cardiac output. Shock is caused by circulatory failure resulting in decreased oxygen delivery (ḊO2) to the tissues and cellular and tissue hypoxia. Hypotension due to reduced cardiac output and/or inadequate circulating blood volume is a common feature resulting in inadequate systemic tissue perfusion; cellular and organ damage may occur. Increased tissue oxygen consumption or problems with tissue O2 uptake and utilization may cause or worsen shock states. Clinical findings in patients with shock include low blood pressure ([BP] < 90/60 mmHg or mean arterial pressure [MAP] < 65 to 70 mmHg); altered mental status; decreased urine output (oliguria); cool, clammy skin (except in early septic shock, where extremities may be flushed with increased blood flow); and metabolic acidosis. Cardiogenic shock is caused by low cardiac output while hypovolemic shock is caused by inadequate intravascular volume due to blood or fluid loss. Obstructive shock is due to a mechanical problem outside of the heart affecting cardiac output and/or blood pressure. Septic shock, neurogenic shock, and anaphylactic shock are all forms of distributive shock in which inappropriate peripheral vasodilation results in decreased systemic vascular resistance and low blood pressure. Sepsis is a contributing factor in up to half of all deaths in hospitalized patients, with up to 50% mortality in patients with septic shock.16 Box 26 provides definitions and examples of each of these types of shock. Clinical Focus 2-4 provides an example of a patient with shock resulting in circulatory hypoxia.

BOX 2-6 Categories of Shock Categories of shock often seen in the ICU include: ∎ Cardiogenic shock – low blood pressure (< 90/60 mmHg) due to low cardiac output. Common causes include MI, cardiac arrhythmia (ventricular tachycardia, supraventricular tachycardia, ventricular fibrillation, and bradycardia), tear, or rupture (myocardium, septum, and valve tendons). ∎ Obstructive shock – a form of shock sometimes grouped with cardiogenic shock resulting in low blood pressure (< 90/60 mmHg) due to obstruction of

∎

∎

blood flow from the heart or major vessels. Causes include pulmonary embolus, severe obstruction of the tricuspid or pulmonary valve, and pericardial tamponade. Hypovolemic shock – low blood pressure (< 90/60 mmHg) due to decreased intravascular volume. Common causes include blood loss due to trauma or internal bleeding or loss of fluids due to vomiting, diarrhea, burns, or excessive sweating. Distributive shock – inappropriate peripheral vasodilation resulting in decreased systemic vascular resistance and low blood pressure. Specific types of distributive shock include: • Septic shock – a form of distributive shock resulting in low blood pressure (< 90/60 mmHg) due to decreased systemic vascular resistance as a result of an overwhelming infection. Common causes include gramnegative sepsis, though other bacteria or fungi may cause septic shock. The resulting hypotension is due to inappropriate peripheral vasodilation caused by toxins released by the offending microorganism. With early septic shock, Q̇T may be elevated; Q̇T may be depressed with late septic shock. • Neurogenic shock – a form of distributive shock resulting in low blood pressure (< 90/60 mmHg) and occasionally, bradycardia. Causes include head trauma, brain injury, and cervical or thoracic spinal cord injury, which may result in a loss of sympathetic stimulation, vasodilation, and a decrease in peripheral vascular resistance. • Anaphylactic shock – a form of distributive shock resulting in low blood pressure (< 90/60 mmHg) due to an allergic reaction to a drug or other substance (e.g., insect stings, certain foods such as peanuts, shellfish, tree nuts, eggs, and dairy products, or latex).

CLINICAL FOCUS 2-4 Circulatory Hypoxia A 65-year-old female patient with a history of heart failure is exhibiting the clinical signs and symptoms of hypoxia. She has been admitted to the hospital and the following information has been collected: FIO2 = 0.35–0.40 (approximate) via nasal cannula at 4 L/mini PaO2 = 80 mmHg SaO2 = 0.95 Hb = 12

CaO2 = 15.5 mL O2/100 mL of blood BP = 55/40 mmHg (Normal range is 90–130/60–90.) Question 1. Describe the patient’s oxygenation status. Answer: The partial pressure of oxygen (PaO2 = 80 mmHg) and oxygen saturation (SaO2 = 0.95) are within normal range, though the patient is receiving supplemental oxygen, which suggests corrected hypoxemia. The Hb is normal for a female patient and the resultant CaO2 is 15.3 mL O2 per 100 mL arterial blood. Considering only the arterial blood oxygen levels, one might assume this is corrected hypoxemia, and the patient is being adequately oxygenated. However, the patient is exhibiting the clinical manifestations of tissue ischemia and the blood pressure is very low. Question 2. Assume that we are able to measure the patient’s cardiac output (Q̇T) and it is only 2.5 L/min (i.e., 50% of normal). Now estimate the patient’s O2 delivery (D˙O2). D˙O2 = CaO2 × Q̇T D˙O2 = 15.5 mL O2/100 mL blood × 2500 mL/min D˙O2 = 387.5 mL O2/minute Answer: Normal D˙O2 is about 1000 mL O2/min; thus, this patient’s oxygen delivery is only about 40% of a normal value due to the reduced cardiac output. The patient is experiencing circulatory hypoxia (also known as stagnant hypoxia). Circulatory hypoxia can occur even in the presence of a normal arterial PaO2, SaO2, and CaO2. The oxygen concentration delivered via nasal cannula ranges from about 24%–40% at oxygen flows of 1–5 L/min, and varies with the patient’s ventilatory pattern (i.e., rate, tidal volume, and inspiratory flow). A rough estimate of delivered oxygen concentration can be estimated as follows:i FIO2 = 20% + (4 × oxygen flow [L/min]) i Wedzicha JA, Miravitlles M, Hurst JR, et al. Management of COPD exacerbations: a European Respiratory

Society/American Thoracic Society guideline. Eur Respir J. 2017;49:1600791 [https://doi.org/10.1183/13993003.00791-2016]

RC Insight The need for vasopressors to maintain mean arterial pressure > 65 mmHg and lactate > 2 mmol/L after

adequate fluid resuscitation is consistent with the presence of septic shock.16

In summary, oxygen delivery (ḊO2) is a function of arterial blood oxygen content (CaO2) and cardiac output (Q̇T). Tissue hypoxia, anaerobic metabolism, and lactic acid production may occur in cases where oxygen delivery is insufficient to meet tissue oxygen requirements.

Tissue Oxygen Uptake and Utilization Peripheral perfusion and oxygenation can be compromised by low cardiac output, low blood pressure, and blockage or disruption of blood flow to a particular tissue bed. Peripheral artery disease including emboli, atherosclerosis, injury, infection, or fibrosis can impair regional tissue bed perfusion. In cases where regional blood flow is disrupted, regional tissue oxygenation may be compromised. For example, ischemic stroke may cause cerebral hypoxia. Once the oxygenated blood is delivered to the peripheral tissues, the hemoglobin must be unloaded, and oxygen must diffuse out of the red blood cell, across the capillary cell membrane, across the extracellular space, and then across the tissue cell membrane and into the intracellular space for cell utilization. Extreme left shifts in the oxyhemoglobin dissociation curve due to severe alkalosis, marked hyperventilation, hypothermia, and carbon monoxide poisoning may interfere with unloading of the hemoglobin. The diffusion distance from the capillary to the tissue cells is generally small; however, for cells located far from the capillaries, or when capillary flow is reduced or absent, there may be problems with oxygen’s diffusion to the peripheral tissue cells. Oxygen tissue extraction can be estimated by calculation of the oxygen extraction ratio (O2 ER): O2 ER = (CaO2 – Cv̄O2) ÷ CaO2, where: CaO2 is arterial oxygen content; normal 20 vol% (20 mL O2/100 mL blood). Cv̄O2 is mixed venous oxygen content; normal is 15 vol% (15 mL O2/100 mL blood).

A normal O2 ER would be calculated as: O2 ER = (CaO2 – Cv̄O2) ÷ CaO2 = (20 vol% – 15 vol%) ÷ 20 vol% = 0.25 or 25% Normal O2 ER is 25% with a range of 25% to 30%.17 Put another way, normal tissue oxygen delivery (ḊO2) is about 1000 mL/min, whereas normal tissue oxygen consumption (V̇O2) at rest is about 250 mL/min (i.e., 25% of the ḊO2). Thus, the tissues normally extract about 25% of the oxygen delivered to the tissues by the arterial blood. Oxygen not extracted by the tissues from the systemic capillary blood returns to the lung as reflected in mixed venous oxygen content (Cv̄O2). Low cardiac output or high tissue oxygen utilization will cause the O2 ER to increase. Tissue oxygen utilization can be blocked due to cyanide poisoning, resulting in histotoxic hypoxia. Cyanide may be produced in domestic fires (e.g., fires involving polyurethane, other plastics, synthetic rubber, wool, or silk) or due to certain industrial processes or medical treatments (e.g., sodium nitroprusside or amygdalin [Laetrile] administration).18 Signs and symptoms of cyanide poisoning include headache, anxiety, confusion, vertigo, coma, and seizures; vomiting, abdominal pain, and renal failure may occur. Victims may describe a metallic taste in the mouth, and a bitter, almond odor. Tachycardia and hypertension may be followed by bradycardia and hypotension. The clinician may observe a bright cherry-red color to the skin and venous oxygen levels may be elevated because oxygen is not taken up by the tissues. Treatment of cyanide poisoning may include high-concentration oxygen therapy and intubation to secure the airway; resuscitation and mechanical ventilatory support may be required. Cyanide antidotes are available and administered intravenously. Mixed venous blood samples can be obtained from a pulmonary artery (SwanGanz) catheter and are sometimes used to assess patients’ oxygenation in the ICU. Mixed venous blood may be analyzed to obtain the partial pressure of oxygen (Pv̄O2), oxygen saturation (Sv̄O2), and oxygen content (Cv̄O2), and to allow for the calculation of arterial-venous oxygen content difference (CaO2 – Cv̄O2). Normal arterial and mixed venous oxygen values are listed in Table 2-5. Mixed venous oxygen levels can be useful to assess aspects of tissue oxygenation as described below.

TABLE 2-5 Mixed Venous Oxygen Levels

A mixed venous blood sample is obtained from a pulmonary artery (Swan-Ganz) catheter and contains venous blood that has been returned to the right side of the heart via the superior and inferior vena cava. A blood sample may be drawn from the distal port of the pulmonary artery catheter and analyzed to determine oxygen levels. Normal values, as well as clinically acceptable values, are listed.

Decreased mixed venous oxygen levels (Pv̄O2, Sv̄O2, Cv̄O2) may be caused by: Arterial hypoxemia Decreased cardiac output Increased tissue oxygen consumption Increased physical activity (anxiety, pain, and fighting the ventilator) Seizures Postoperative shivering Elevated temperature (hyperthermia, fever) Increased metabolic demand due to critical illness such as ARDS or septic shock

Feeding regimens with excessive glucose Increased mixed venous oxygen levels (Pv̄O2, Sv̄O2, and Cv̄O2) may be caused by: Increased cardiac output Decreased tissue oxygen consumption Decreased level of physical activity (rest, sleep, and sedation) Skeletal muscle relaxation (e.g., sedative or narcotic medications, paralytic drugs) Hypothermia Cyanide poisoning Mechanical ventilation reducing the oxygen cost of breathing CaO2 – Cv̄O2 may increase with arterial hypoxemia, decreased cardiac output, increased tissue oxygen consumption, seizures, shivering, and hyperthermia. CaO2 – Cv̄O2 may decrease with increased cardiac output, skeletal muscle relaxation, peripheral shunt, cyanide poisoning, and hypothermia. To summarize, the oxygenation process requires adequate arterial blood oxygen content and sufficient oxygen delivery to the tissues. Common causes of decreased arterial oxygen content include diminished inspired oxygen, lung disease (e.g., V̇/Q̇ mismatch, intrapulmonary capillary shunt, and diffusion limitation), cardiovascular right-to-left shunt (e.g., anatomic cardiac shunt), and hypoventilation. ḊO2 may also be reduced because of decreased cardiac output (e.g., cardiac disease or hypovolemia) or anemia. Tissue perfusion must be adequate and disordered regional perfusion may result in tissue hypoxia. Finally, cellular oxygen uptake and utilization must be effective. Box 2-4 reviews the steps in the oxygenation process.

Assessment of Ventilation Ventilation is simply the bulk movement of air into and out of the lungs. Problems with ventilation may be indicated by findings from the patient’s history (e.g., dyspnea, cough, sputum production, wheezing, and history of chest illness), physical exam (e.g., increased respiratory rate, irregular ventilatory pattern, accessory muscle use, and abnormal breath sounds), bedside pulmonary function testing (e.g., decreased tidal volume, increased or decreased minute ventilation, and decreased expiratory flowrates) or the results of imaging and laboratory studies (e.g., chest x-ray, oximetry, and arterial blood gases). An understanding of the various components of

ventilation is required in order to perform a complete assessment and is discussed below. Ventilation can be subdivided into tidal volume (VT), respiratory rate (f), and minute ventilation (V̇E) where: VT × f = V̇E Respiratory rate varies with age and level of activity. A normal adult’s spontaneous respiratory rate ranges from 12 to 20 breaths/min while infants may have a normal respiratory rate in the range of 30 to 40 breaths/min. Respiratory rates in children can range from 18 to 30 breaths/min and vary with age. Tachypnea in adults is defined as a respiratory rate greater than 20 breaths/min. Tachypnea is often a response to anxiety, severe pain, hypoxemia, acute pulmonary disease, cardiac insufficiency, and metabolic acidosis. Rapid shallow breathing is a common finding in patients with acute respiratory failure. Tachypnea (especially f > 35 breaths/min) combined with severe distress, air hunger, diaphoresis, and accessory muscle use may signal an impending respiratory arrest requiring intubation and mechanical ventilatory support. Bradypnea refers to an abnormally slow respiratory rate that may be caused by excessive sedation, anesthesia, narcotic drug overdose, excessive alcohol consumption, head trauma, increased intracranial pressure, neurologic disease, hypothermia, or cardiogenic shock. Abnormal ventilatory patterns associated with specific disease states and conditions include Biot’s breathing (rapid, shallow breathing with periods of apnea sometimes seen with stroke or trauma), Cheyne-Stokes breathing (cyclical increases and decreases in tidal volume with periods of apnea sometimes seen with cardiac or neurologic disease, sedation, or acid-base disturbances), and Kussmaul breathing (increased depth of breathing associated with diabetic ketoacidosis). Spontaneous tidal volume, minute ventilation, and respiratory rate can be easily measured at the bedside using a handheld respirometer. This is commonly performed in intubated patients being considered for discontinuance or weaning from mechanical ventilatory support. Normal adult values for spontaneous respiratory rate, tidal volume, and minute ventilation, along with minimally acceptable values associated with adequate spontaneous ventilation, are listed below:

f = 12 breath/min (normal range 12–20 breaths per minute [bpm]); f < 30 and > 6 breaths/min associated with adequate spontaneous breathing. VT = 500 mL (normal range 400–700 mL [about 7 mL/kg IBW]; VT > 5 mL/kg associated with adequate spontaneous breathing. V̇E = 6 L/min (normal range 5–10 L/min). V̇E < 10 L/min associated with adequate spontaneous breathing; higher values may be associated with distress. Other bedside measures of pulmonary function sometimes used to assess the adequacy of spontaneous ventilation and the need for mechanical ventilatory support (along with acceptable values) include rapid, shallow breathing index (RSBI): f/ VT < 105, maximum voluntary ventilation (MVV) ≥ 2 × V̇E, vital capacity (VC) > 10–15 mL/kg, measures of ventilatory muscle strength (maximum inspiratory pressure – MIP < –20 to –30 cm H2O; maximum expiratory pressure – MEP ≥ +60 cm H2O); measures of ventilatory workload (e.g., static total compliance and airway resistance measured while on the ventilator), and measures of respiratory drive (e.g., airway occlusion pressure 0.1 s [PO.1] after the start of inspiratory flow; PO.1 < 4 to 6 cm H2O). The 20 – 30 – 40 Rule suggests institution of mechanical ventilation when VC < 20 mL/kg, MIP > –30 cm H2O, and MEP < 40 cm H2O. RC Insight In spontaneously breathing patients, a respiratory rate > 30 breaths/min combined with a spontaneous tidal volume of ≤ 300 mL is associated with ventilatory failure and the need for mechanical ventilatory support.

Alveolar Ventilation and Dead Space While tidal volume, minute ventilation, and respiratory rate provide gross measures of ventilation, alveolar ventilation determines the effectiveness of ventilation and removal of carbon dioxide. The volume of gas in the conducting airways does not participate in gas exchange and is known as anatomic dead space (VD anat), while alveoli that are ventilated but not perfused make up the alveolar dead space (VD alv). With emphysema, alveolar capillaries may be destroyed by the toxic effects of cigarette smoking, resulting in an increase in alveolar dead space. With pulmonary embolus, when there is complete obstruction of the pulmonary vessel, alveolar dead space will increase. Anatomic dead space plus alveolar dead space is known as

physiologic dead space (VD phys). In normal subjects, physiologic dead space is approximately the same as anatomic dead space. With dead space causing disease, such as emphysema, physiologic dead space will be greater than anatomic dead space. Physiologic dead space to tidal volume ratio (VD/VT) can be calculated fairly easily at the bedside (using the Enghoff modification of the Bohr equation) by simultaneously collecting an arterial blood sample for measurement of PaCO2, and measurement of mean exhaled carbon dioxide tension (PĒCO2) where: VD/VT = (PaCO2 – PĒCO2) ÷ PaCO2 Inserting normal values for PaCO2 and PĒCO2, this becomes: VD/VT = (PaCO2 – PĒCO2) ÷ PaCO2 = (40 – 28) ÷ 40 = 0.30 or 30% Measurement of dead space to tidal volume ratio (VD/VT) allows for the calculation of physiologic dead space volume (VD phys) where: VD = VD/VT × VT Inserting normal values for VD/VT and tidal volume (VT) allows for the calculation of normal physiologic dead space volume (VD phys): VD phys = VD/VT × VT = 0.30 × 500 mL = 150 mL The normal range for VD/VT is about 0.20 to 0.40 (i.e., 20% to 40% dead space ventilation), although patients receiving mechanical ventilatory support with positive pressure often have a VD/VT approaching 0.50 (i.e., 50% dead space ventilation). A normal mean exhaled carbon dioxide tension (PĒCO2) is 28 mmHg with a range of about 24 to 32 mmHg. It should be noted that some newer mechanical ventilators (e.g., the Dra¨ger XL ventilator [Dra¨ger Medical, Telford, Pennsylvania]) are equipped with integrated CO2 and volume measurement capabilities that may allow for accurate calculation of VD/VT without requiring a separate device to measure PĒCO2.19 Alveolar ventilation per breath (VA) is the portion of ventilation that participates in gas exchange (i.e., effective ventilation) and can be calculated by subtracting

physiologic dead space (VD phys) from tidal volume (VT): VA per breath = VT – VD phys Alveolar ventilation per minute (V̇A) is simply tidal volume (VT) minus physiologic dead space (VD phys) times respiratory rate (f): V̇A per minute = (VT – VD phys) × f Inserting normal values for VT, VD phys, and f, we can calculate normal alveolar ventilation per minute (V̇A): V̇A = (VT – VD phys) × f = (500 mL – 150 mL) × 12 = 4200 mL/min = 4.2 L/min Box 2-7 summarizes terms used to describe ventilation, while Clinical Focus 2-5 further illustrates the effects of dead space ventilation.

BOX 2-7 Terms Used to Describe Ventilation Tidal volume (VT) is the volume of gas exhaled passively following a normal inspiration (aka exhaled tidal volume). ∎ Normal adult tidal volume is about 500 mL or approximately 7 mL/kg of ideal body weight (IBW).a ∎ Normal range for adult tidal volume is about 400 to 700 mL. ∎ Children have a smaller V , and infants have a much smaller V . T T

• • • • ∎ ∎ ∎

VT increases in children with age. VT for a normal full-term newborn is about 15–20 mL. VT for a 5-year-old child may be about 100 mL, depending on his or her size. By age 12–16, VT begins to approach adult values.

Inspiratory tidal volume (VT-I) is the volume of gas inhaled normally flowing a passive expiration. Expiratory tidal volume (VT-E) is the volume of gas exhaled passively following a normal inspiration. Normally VT-I and VT-E are almost identical, though there is often a very small variation due to differences in oxygen consumption (V̇O2) and carbon dioxide

production (V̇CO2). Respiratory rate (f) is the number of breaths taken by the patient per minute. ∎ Normal respiratory rate for an adult is approximately 12 breaths/min (range of about 12 to 18 or 20 breaths/min). ∎ Tachypnea refers to an elevated respiratory rate while bradypnea refers to an abnormally slow respiratory rate. ∎ Normal respiratory rates in infants and children are higher. • Normal newborn’s respiratory rate is between 30 and 60 breaths/min. Minute ventilation (V̇E) is simply the tidal volume (VT) times the respiratory rate or frequency (f): V̇E = VT × f ∎

Normal adult minute ventilation is approximately 6 L/min (range of about 5– 10 L/min). Alveolar ventilation is the volume of gas reaching alveoli that are both ventilated and perfused. Dead space ventilation is that portion of ventilation that does not participate in gas exchange (i.e., ventilation without perfusion). Types of dead space include anatomic, alveolar, physiologic, and mechanical dead space. Anatomic dead space (VD anat) is the volume of gas in the conducting airways. ∎

Anatomic dead space is made up of the airways from the external nares (nostrils) down to and including the terminal bronchioles. ∎ Normal anatomic dead space is approximately 1 mL per pound of ideal body weight (about 150 mL in a normal adult) ∎ Anatomic dead space will vary based on the patient’s size. Alveolar dead space (VD alv) is the volume of ventilation received by alveoli that are ventilated but not perfused. ∎ V D alv may be increased with emphysema (where the capillaries are destroyed from the toxic effects of cigarette smoking). ∎ Pulmonary embolus with complete occlusion of the vessel is sometimes cited as an example of increased VD alv. Severe V̇/Q̇ problems may occur with partial occlusion of a pulmonary vessel due to pulmonary embolus. Physiologic dead space (VD phys) is total functional dead space including alveolar dead space and anatomic dead space: VD phys = VD anat + VD alv ∎

In normal subjects, VD VD phys ≅ VD anat.

∎

With dead space causing diseases (e.g., emphysema/pulmonary embolus), VD phys > VD anat. Dead space to tidal volume ratio (VD/VT): Physiologic dead space can be measured fairly easily at the bedside using the Bohr equation*, which requires arterial blood gas analysis for measurement of PaCO2 and collection of expired gas from which mean exhaled carbon dioxide tension (PĒCO2) is measured. This allows for calculation of the dead space to tidal volume ratio (VD/VT), and in turn the calculation of physiologic dead space: Dead spaced to tidal volume ratio =

Physiologic dead space = VD/VT × VT Using normal values for PaCO2 (40 mmHg), PĒCO2 (28 mmHg), and VT (500 mL), we can calculate the normal dead space to tidal volume ratio (VD/VT) and dead space volume:

A normal VD/VT ranges from about 0.20 to 0.40 (20%–40% dead space ventilation), though it’s not unusual to have a VD/VT of up to 0.50 (50% dead space ventilation) in mechanically ventilated patients with normal lungs. aFormulas for estimating ideal body weight (IBW) vary (e.g., Broca formula, Devine formula, Hamwi

formula). The ARDSNet uses the term “predicted body weight” (PBW) where: Males: PBW (kg) = 50 + 2.3 (height (in) – 60) Females: PBW (kg) = 45.5 + 2.3 (height (in) – 60) The ARDSNet recommendation is based on the Devine formula for IBW calculation (i.e., PBW = IBW; see www.ardsnet.org).

CLINICAL FOCUS 2-5 Dead Space Ventilation Alveolar ventilation refers to the volume of gas reaching alveoli that are ventilated AND perfused. Dead space refers to that portion of ventilation that

does not participate in gas exchange (i.e., ventilation without perfusion). In general, there are four types of dead space seen in the ICU: anatomic, physiologic, alveolar, and mechanical. Question 1. Define types of dead space and give examples of things that will affect each type. Answer: Anatomic dead space (VD anat) refers to the volume of gas in the conducting airways. Anatomic dead space is made up of the airways from the external nares (nostrils) down to and including the terminal bronchioles. Normal anatomic dead space is approximately 1 mL per pound of ideal body weight. This is about 150 mL in a normal adult; however anatomic dead space will vary based on the patient’s size. Alveolar dead space (VD alv) refers to the volume of ventilation received by alveoli that are ventilated but not perfused. An important cause of an increase in alveolar dead space is emphysema (where the capillaries are destroyed from the toxic effects of cigarette smoking). Pulmonary embolus (PE) is sometimes cited as a good example of dead space causing disease. With PE, severe V̇/Q̇ problems may occur with partial occlusion of a pulmonary vessel and when there is complete occlusion of the vessel alveolar dead space will increase. Physiologic dead space (VD phys) refers to the total functional dead space and consists of the alveolar dead space plus the anatomic dead space: VD phys = VD anat + VD phys Mechanical dead space refers to the volume of rebreathed gas due to a mechanical device. Examples of mechanical dead space include the volume of rebreathed gas associated with an oxygen facemask. Large bore tubing is sometimes placed between the patient “Y” (aka patient “wye”) and the endotracheal tube or tracheostomy tube in intubated patients. This added volume of rebreathed gas is another form of mechanical dead space. The addition of mechanical dead space may cause an increase in PaCO2 if there is no change in the patient’s tidal volume or respiratory rate. Question 2. Explain the relationship between anatomic and physiologic dead space and list things that might increase physiologic dead space. Answer: In normal subjects, VD phys ≅ VD anat. With dead space causing diseases (e.g., emphysema/pulmonary embolus), VD phys > VD anat. Thus, possible causes of increased physiologic dead space include pulmonary emphysema and pulmonary embolus. Question 3. Explain how to calculate physiologic dead space in the clinical

setting. Answer: Physiologic dead space can be measured fairly easily at the bedside using the Bohr equation*, which requires arterial blood gas analysis for measurement of PaCO2 and collection of expired gas from which mean exhaled carbon dioxide tension (PĒCO2) is measured. This allows for calculation of the dead space to tidal volume ratio (VD/VT) and in turn the calculation of physiologic dead space:

Using normal values for PaCO2 (40 mmHg), PĒCO2 (28 mmHg), and VT (500 mL), we can calculate the normal dead space to tidal volume ratio (VD/VT) and dead space volume:

A normal VD/VT ranges from about 0.20 to 0.40 (20%–40% dead space ventilation), though it’s not unusual to have a VD/VT of up to 0.50 (50% dead space ventilation) in mechanically ventilated patients with normal lungs. Question 4. Given VT = 600 mL, PaCO2 = 40 mmHg, and PĒCO2 = 20 mmHg, calculate VD/VT and VD. Answer:

* Note that the original Bohr equation used alveolar CO2 tension (i.e., Paco2) in place of Paco2. Estimating Paco2 requires an end-tidal gas sample; in normal subjects PACO2= Paco2.

Alveolar Ventilation and PaCO2 Normally, alveolar CO2 tension (PACO2) is equal to arterial PaCO2 and the relationship between alveolar ventilation and PaCO2 is defined by the following equation: V̇A = (0.863 × V̇CO2) ÷ PaCO2, where: V̇A is alveolar ventilation in L/min. V̇CO2 is carbon dioxide production in mL/min (normally about 200 mL/min, although this varies with metabolic rate and diet). PaCO2 is the partial pressure of arterial carbon dioxide in mmHg. 0.863 is a conversion factor. Thus, normal ventilation can be defined as a PaCO2 of 35–45 mmHg; hypoventilation corresponds to a PaCO2 > 45 mmHg while hyperventilation corresponds to a PaCO2 < 35 mmHg. Clinical Focus 2-6 further illustrates the relationships between PaCO2, V̇CO2, and V̇A.

CLINICAL FOCUS 2-6 Alveolar Ventilation and Arterial Carbon Dioxide Tension The relationship between alveolar ventilation and arterial carbon dioxide is defined by the following equation: V̇A = (0.863 × V̇CO2) ÷ PaCO2, where: V̇A is alveolar ventilation in L/min; normal is about 4.2 L/min with a range of about 4–5 L/min. V̇CO2 is carbon dioxide production in mL/min; normal CO2 is about 200 mL/min. PaCO2 is the partial pressure of arterial carbon dioxide in mmHg; normally alveolar CO2 tension (PACO2) is equal to PaCO2 and is about 40 mmHg with a range of 35–45 mmHg. 0.863 is a conversion factor. It is important to consider this relationship when evaluating a patient’s ventilatory status.

Question 1. Given the following information on a patient receiving mechanical ventilatory support, calculate the resultant PaCO2: CO2 production (V̇CO2) = 200 mL/min (in the normal range) Alveolar ventilation (V̇A) of 4.3 L/min (in the normal range) Answer: V̇A = (0.863 × V̇CO2) ÷ PaCO2 → PaCO2 = (0.863 × V̇CO2) ÷ V̇A → PaCO2 = (0.863 × 200 mL/min) ÷ 4.3 L/min = 40 mmHg Question 2. What would happen to the patient’s PaCO2 if alveolar ventilation increased to 6.2 L/min, assuming no change in CO2 production? CO2 production (V̇CO2) = 200 mL/min Alveolar ventilation (V̇A) = 6.2 L/min Answer: V̇A = (0.863 × V̇CO2) ÷ PaCO2 → PaCO2 = (0.863 × V̇CO2) ÷ V̇A → PaCO2 = (0.863 × 200 mL/min) ÷ 6.2 L/min = 28 mmHg Thus, an increase in alveolar ventilation in this patient from 4.3 L/min to 6.2 L/min would cause the patient’s PaCO2 to decrease from 40 mmHg to 28 mmHg. Question 3. If this patient had an increase in metabolic rate due to fever or increased muscle activity, such as fighting the ventilator, what would happen to the patient’s PaCO2? Answer: Increased metabolic rate will increase CO2 production (V̇CO2). If there is no compensatory increase in alveolar ventilation, PaCO2 will increase. For example, given a patient with a normal alveolar ventilation of 4.3 L/min, normal CO2 production (V̇CO2) of 200 mL/min, and normal arterial CO2 (PaCO2) of 40 mmHg (see Question 1 above), what would happen to the patient’s PaCO2 if CO2 production increased to 300 mL/min with no change in alveolar ventilation? PaCO2 = (0.863 × V̇CO2) ÷ V̇A PaCO2 = (0.863 × 300 mL/min) ÷ 4.3 L/min = 60 mmHg Thus, an increase in V̇CO2 to 300 mL/min with no change in alveolar ventilation would cause the PaCO2 to rise to 60 mmHg.

Assessment of ventilation in patients receiving mechanical ventilatory support should also include the possibility of air leaks in the system. For example, under normal circumstances, inspired tidal volume and expired tidal volume are equal, except for very small differences due to differences in oxygen consumption (V̇O2 – normally about 250 mL/min) vs. carbon dioxide production (V̇CO2 – normally about 200 mL/min). During mechanical ventilation, air leaks may occur around improperly inflated or damaged endotracheal or tracheostomy tube cuffs, ventilator circuits, or out of the lung through the pleural space via chest tubes used to treat pneumothorax. In these cases, measurement of inspired versus expired tidal volume may help verify air leaks and locate the source. Clinical Focus 2-7 provides a discussion of inspired vs. expired tidal volumes.

CLINICAL FOCUS 2-7 Inspired and Expired Tidal Volume: The Effects of Oxygen Consumption (V˙O2), Carbon Dioxide Production (V˙CO2), and Air Leaks Question 1. What are normal adult values for V̇O2, V̇CO2, exhaled tidal volume (VE), and respiratory rate (f)? Answer: Normal V̇O2 is about 250 mL/min. Normal V̇CO2 is about 200 mL/min. Normal exhaled tidal volume is about 500 mL or about 7 mL/kg IBW. Normal respiratory rate is about 12 breaths/min. These values vary with size, gender, and level of activity. Question 2. If tidal volume, respiratory rate, oxygen consumption, and carbon dioxide production are normal, what would be the difference in inhaled and exhaled tidal volume? Answer: If V̇O2 is 250 mL/min and V̇CO2 is 200 mL/min, then the difference is: V̇O2 – V̇CO2 = 250 mL/min – 200 mL/min = 50 mL/min If the respiratory rate was 12 breath/min, the difference would be about 4 mL per breath: 50 mL/min ÷ 12 breaths/min = 4.2 mL/per breath

Thus, inspired tidal volume would be about 4.2 mL greater than expired tidal volume, a very small amount. Normal inspired tidal volume (VI) is typically slightly greater than expired tidal volume (VE). This will, of course vary as O2 consumption and CO2 production varies. For example, if V̇O2 = V̇CO2 there should be no difference in inspired and expired tidal volumes Clinically, the difference (if any) probably is unimportant, and we assume inspired and expired tidal volume to be the same. Question 3. Are there any circumstances in which differences in inspired and expired tidal volume are clinically important? Answer: Mechanically ventilated patients may exhibit a measurable difference between inspired and expired tidal volume. Examples include air leaks around the endotracheal tube and pneumothorax. For example, an intubated adult patient receiving mechanical ventilation in the intensive care unit may have inspired tidal volume of 600 mL and an expired tidal volume of only 400 mL due to a large air leak. Possible causes include: Cuff leak. The endotracheal tube cuff may not seal the airway resulting in a cuff leak. Gas delivered to the endotracheal tube will exit the patient’s mouth and not be measured by the ventilator’s volume sensing system. Pneumothorax with chest tubes. Patients receiving mechanical ventilation who experience a pneumothorax will often have chest tubes inserted into the pleural space to remove fluid and gas. If there is a tear in the lung tissue, gas delivered by the ventilator during inspiration may exit via the tear into the pleural space and then out the chest tube and measured inspiratory tidal volume will be greater than expiratory tidal volume.

To summarize, assessment of ventilation may begin with review of the patient’s history and physical, being on the alert for signs and symptoms of ventilatory failure. Bedside measures of pulmonary function are sometimes used to assess a patient’s readiness for discontinuance of mechanical ventilatory support. These include spontaneous tidal volume, respiratory rate, minute ventilation, rapid, shallow breathing index, vital capacity and measures of ventilatory muscle strength, workload, and respiratory drive. However, clinically, the single best index of effective ventilation is measurement of PaCO2.

Assessment of Acid-Base Balance

Patients in respiratory failure often experience acid-base disturbances resulting in an abnormal hydrogen ion concentration ([H+]) as assessed by arterial or venous blood pH (recall that pH = –log [H+]). pH is primarily determined by the relationship between plasma HCO3−, which is the major blood base, and PCO2, which is the major volatile blood acid. Simply expressed, pH is a function of the ratio of the plasma bicarbonate concentration ([HCO3−]) to the carbonic acid concentration ([H2CO3]), which may be calculated based on the PCO2 (where [H2CO3] = 0.03 × PCO2), as expressed by the Henderson-Hasselbach equation:

The relationship between pH, HCO3−, and PaCO2 can be further simplified as follows:

Plasma bicarbonate is primarily regulated by the kidneys and is considered to be the “metabolic” component of acid-base balance, while PaCO2 is primarily dependent on the level of alveolar ventilation and is considered to be the “respiratory” component of acid-base balance. Acid-base disturbances are best assessed by obtaining an arterial blood sample and analyzing arterial pH and PaCO2 and calculating other measures related to acidbase balance including plasma bicarbonate (HCO3−) and base excess (BE) or base deficit (BD). A normal arterial pH is 7.40 with a range of 7.35–7.45, while a normal PaCO2 is 40 mmHg with a range of 35–45 mmHg. A normal arterial plasma HCO3− is 24 mEq/L (range of 22–28 mEq/L), while a normal base excess or deficit is 0 (± 2). In the absence of an arterial blood sample, venous blood may be used to assess a patient’s acid-base balance, with the knowledge that venous pH is 0.02 to 0.04 pH units lower than arterial blood, venous PCO2 is approximately 3 to 8 mmHg higher

than arterial blood, and HCO3− concentration is generally 1 to 2 mEq/L higher than arterial blood.20 Venous blood samples are also commonly used to measure total CO2 (TCO2), which is typically about 2 mEq/L per liter greater than calculated arterial HCO3−.20 Specifically, TCO2 = HCO3− + H2CO3 = HCO3− + PCO2 × 0.03. It should be noted, however, that local ischemia can sometimes cause unpredictable changes in the pH of venous blood drawn peripherally. An acidosis refers to an arterial pH < 7.35, which may be caused by an increase in respiratory acid (i.e., increased PaCO2) or a decrease in metabolic base (i.e., decreased plasma bicarbonate [HCO3−], or both. An alkalosis refers to an arterial pH > 7.45, which may be caused by decreased PaCO2, increased HCO3−, or both. Causes of an acidosis or alkalosis may be classified as “respiratory” or “metabolic,” as described below. It should also be noted that, strictly speaking, the terms alkalosis and acidosis refer to general conditions affecting the extracellular fluid pH, while the terms acidemia and alkalemia refer to pH abnormalities of the blood.

Respiratory Acidosis and Alkalosis Carbon dioxide is a volatile acid and consequently respiratory acidosis may be defined as an elevated PaCO2 > 45 mmHg (i.e., hypoventilation) and respiratory alkalosis defined as a decreased PaCO2 < 35 mmHg (i.e., hyperventilation) [recall that CO2 in water forms carbonic acid (H2CO3), which then dissociates into hydrogen ions (H+) and bicarbonate ions (HCO3−): CO2 + H2O → H2CO3 → H+ + HCO3−]. Respiratory acidosis may also be described as hypoventilation, hypercapnia, hypercapnic respiratory failure, and ventilatory failure. Causes of respiratory acidosis include: Increased work of breathing resulting in decreased ventilation Decreased lung compliance (e.g., atelectasis, pneumonia, pulmonary edema, ARDS, fibrotic lung disease, and pneumothorax) Decreased chest wall compliance (e.g., obesity, chest wall deformity, and kyphoscoliosis) Increased airway resistance (e.g., upper airway obstruction, airway tumor, asthma, COPD exacerbation, bronchospasm, airway secretions, and mucosal edema)

Decreased respiratory drive (e.g., sedative or narcotic drugs, brainstem lesions, head trauma, morbid obesity, sleep apnea, or metabolic alkalosis) Neurologic disease resulting in decreased ventilation (e.g., spinal cord injury, amyotrophic lateral sclerosis [ALS], poliomyelitis, Guillain-Barré syndrome, myasthenia gravis, botulism, muscular dystrophy, and critical care myopathy) The normal compensation mechanism for a respiratory acidosis is a renalmediated increase in hydrogen ion secretion resulting in an elevated plasma HCO3− and a calculated base excess (BE) > +2.0 mEq/L. A respiratory acidosis may be further classified as uncompensated (acute), partly compensated (subacute), or fully compensated (chronic) based on the presence and degree of renal compensation as assessed by the plasma HCO3− and base excess or deficit. The following conventional nomenclature results: Uncompensated (acute) respiratory acidosis: ↓pH, ↑PaCO2, normal HCO3−, and BE/BD ± 2 Partly compensated (subacute) respiratory acidosis: ↓pH, ↑PaCO2, ↑HCO3−, and BE > +2 Fully compensated (chronic) respiratory acidosis: normal pH, ↑PaCO2, ↑HCO3−, and BE > +2 mEq/L For every 10-mmHg acute increase in PaCO2 (i.e., acute respiratory acidosis), HCO3− will increase about 1 mEq/L.20 This small increase in HCO3− occurs rapidly due to the formation and disassociation of carbonic acid and does not represent renal compensation. For example, an acute increase in PaCO2 from 40 to 50 mmHg (a 10-mmHg increase) will result in an immediate increase in HCO3− from 24 mEq/L (normal) to 25 mEq/L; this does not represent renal compensation. A chronic increase in PaCO2 of 10 mmHg, on the other hand, will cause the kidneys to increase H+ secretion resulting in an increase in plasma HCO3− of about 4 to 5 mEq/L.20 This is sometimes referred to as expected maximal renal compensation, and may take 3 to 5 days to complete. It also should be noted that renal compensation generally does not result in a completely normalized pH. Thus, there is a predictable change in pH for a given change in PaCO2 and the magnitude of change observed can help determine if the change is acute or chronic. RC Insight

With acute increases in PaCO2, pH will decrease 0.008 units for every 1-mmHg increase in PaCO2. With chronic increases in PaCO2, pH will decrease 0.003 units for every 1-mmHg increase in PaCO2.

An abnormal decrease in PaCO2 represents a respiratory alkalosis, also known as hyperventilation, which can be acute, subacute, or chronic. Causes of respiratory alkalosis include: Hypoxemia (e.g., hyperventilation secondary to hypoxemia) Pain and anxiety resulting in increased ventilation Fever Early sepsis, which typically includes increased temperature, increased heart rate, and increased respiratory rate Hyperventilation syndrome Hepatic encephalopathy (may also lead to liver coma and hypoventilation) Other neurologic disorders (e.g., head trauma, infection, and stroke) that may cause hyperventilation Lung receptor stimulation (e.g., pulmonary embolus, pneumonia, and pulmonary edema) Metabolic acidosis (e.g., ketoacidosis, lactic acidosis, kidney failure, and salicylate toxicity) Pregnancy Excessive mechanical ventilatory support (i.e., iatrogenic hyperventilation) Compensation for a respiratory alkalosis occurs by decreased renal secretion of hydrogen ions and urinary loss of HCO3−, resulting in a decreased plasma HCO3− and a base deficit (BD) < –2.0 mEq/L. Conventional classification of respiratory alkalosis based on pH, PaCO2, HCO3−, and BD/BE follows: Uncompensated respiratory alkalosis: ↑pH, ↓PaCO2, normal HCO3−, and BE/BD ± 2 Partly compensated respiratory alkalosis: ↑pH, ↓PaCO2, ↓HCO3−, and BD < –2 Fully compensated respiratory alkalosis: normal pH, ↑PaCO2, ↑HCO3−, and BD < –2 Acutely, HCO3− will decrease about 2 mEq/L for every 10-mmHg acute decrease in PaCO2. This small decrease in HCO3− occurs immediately due to a decrease in the formation and disassociation of carbonic acid and does not represent renal compensation. For example, an acute decrease in PaCO2 from 40 to 30 mmHg (a 10mmHg decrease) will result in a rapid decrease in HCO3− from 24 mEq/L (normal) to

22 mEq/L; again, this does not represent renal compensation. The expected renal compensation for a chronic respiratory alkalosis is a decrease in plasma HCO3− of 4 to 5 mEq per liter for every 10-mmHg decrease in PaCO2.20 For example, the expected renal compensation for a chronic decrease in PaCO2 from 40 to 30 mmHg would be a decrease in HCO3− from 24 mEq/L (normal) to about 19 to 20 mEq/L (a 4- to 5-mEq/L decrease in HCO3−). As discussed earlier in this chapter, clinical nomenclature often used to describe alterations in ventilation as assessed by increased values for PaCO2 includes the following terms: Acute ventilatory failure is defined as a sudden increase in PaCO2 with a corresponding decrease in pH (i.e., uncompensated respiratory acidosis). [Recall that when breathing room air, a rise in PaCO2 of 4 mmHg will cause a decrease in PaO2 of 5 mmHg. Thus, acute ventilatory failure may result in acute hypoxemia.] Chronic ventilatory failure is defined as a chronically elevated PaCO2 with a normal or near-normal pH owing to metabolic compensation (i.e., compensated or partly compensated respiratory acidosis). Acute ventilatory failure superimposed on chronic ventilatory failure occurs when a patient with a chronically elevated PaCO2 (e.g., COPD with chronic CO2 retention) experiences an acute additional increase in PaCO2 with a corresponding decrease in pH. Impending ventilatory failure is a term used in cases where an elevated PaCO2 is not yet present but is likely to occur in the immediate future if no action is taken (e.g., severe hypoventilation and/or respiratory arrest are imminent). Clinical terminology sometimes used to describe an abnormally decreased PaCO2 includes the following expressions: Acute alveolar hyperventilation is defined as a sudden decrease in PaCO2 with a corresponding increase in pH (i.e., uncompensated respiratory alkalosis). Chronic alveolar hyperventilation is defined as a chronically decreased PaCO2 with a normal or near-normal pH (i.e., compensated or partly compensated respiratory alkalosis). Acute alveolar hyperventilation superimposed on chronic ventilatory failure, as may occur with patients whose baseline condition is chronic ventilatory failure and an acute insult results in a mild relative hyperventilation

such as may occur with worsening hypoxia.

Metabolic Acidosis and Alkalosis Metabolic acidosis may be defined as a decrease in the concentration of plasma HCO3− < 22 mEq/L. As noted earlier, the terms acidosis and alkalosis refer to general conditions associated with changes in body hydrogen ion concentration ([H+]) and bicarbonate concentration ([HCO3−]), while the terms acidemia and alkalemia refer specifically to blood hydrogen ion concentration (i.e., pH) and HCO3−. Metabolic acidosis may be caused by ingestion of acids, increased fixed acid production, decreased renal excretion of acids, or loss of HCO3−. Assessment of the anion gap (AG) can be useful in determining if an acidosis is caused by an increase in fixed acids or a loss of HCO3−. The anion gap may be calculated as follows, based on the plasma concentrations of major electrolytes: Anion gap (mEq/L) = [Na+] – ([Cl−] + [HCO3−]) A normal anion gap is approximately 3 to 10 mEq/L, although this varies depending on the laboratory technology in use and should be adjusted down in the presence of reductions in serum albumin.21 Sources sometimes report a normal AG range of 8 to 16 mEq/L; newer ion-selective electrode laboratory technology, however, may result in an normal AG range of 3 to 11 mEq/L or 3 to 10 mEq/L. Each laboratory should determine its own normal range, and clinicians should consult the clinical laboratory at their institution. Specifically, for every decrease in the albumin of l g/dL, add 2.5 mEq/L to the anion gap, where corrected AG = AG + 2.5 × [4measured serum albumin]. Causes of a normal anion gap acidosis include loss of HCO3−, failure to reabsorb HCO3−, or ingestion of certain substances such as ammonium chloride or hyperalimentation. For example, loss of HCO3− can occur due to diarrhea or pancreatic fistula, while proximal (Type 2) renal tubular acidosis can result in a failure to reabsorb HCO3−.21 Other causes of a normal anion gap acidosis include distal (Type 1) renal tubular acidosis, hypoaldosteronism (Type 4 renal tubular acidosis), posttreatment ketoacidosis, ureteral diversion (as a part of surgery to remove the bladder), administration of carbonic anhydrase inhibitors such as acetazolamide (Diamox), intravenous hyperalimentation, and ingestion of toluene (a

solvent in some types of paint thinner).21 With a normal anion gap metabolic acidosis, chloride ion concentration ([Cl−]) will increase; an alternative term used to describe this type of acidosis is hyperchloremic metabolic acidosis. Causes of increased anion gap acidosis (AG > 11 mEq/L) include ingestion of acids, increased fixed acid production, or decreased renal excretion of acids as described below:21 Ingestion of acids. Examples of acids that can be ingested resulting in an increased anion gap metabolic acidosis include methanol, ethylene glycol, aspirin (salicylic acid), or toluene. Products that contain methanol and ethanol glycol include automotive antifreeze, windshield wiper fluid, and certain chemical solvents, cleaning fluids, and industrial products. Aspirin overdose is occasionally seen in children. Toluene is found in certain glues, adhesives, acrylic paints, paint thinners, and other products that may be ingested intentionally (e.g., glue sniffing) or accidentally. Ingestion of acids typically causes an increased anion gap acidosis (AG > 11 mEq/L). Increased fixed acid production. Lactic acidosis and ketoacidosis will cause an increase in fixed acid production resulting in an increased anion gap acidosis. Lactic acidosis is a result of anaerobic metabolism and lactic acid production due to insufficient cellular oxygen levels (e.g., tissue hypoxia). Cardiac arrest, cardiac failure, hypovolemia, sepsis, or other types of shock are common causes of lactic acidosis seen in the intensive care unit. Diabetic ketoacidosis is associated with uncontrolled diabetes mellitus. Alcoholic ketoacidosis is caused by excessive alcohol consumption. Fasting or starvation may also cause the formation of ketones resulting in an acidosis. Decreased renal excretion of acids. Kidney failure may cause inadequate excretion of fixed organic and inorganic acids. Increased hydrogen ion retention, decreased plasma HCO3− , and an increased anion gap acidosis may result. Kidney failure may cause an increased anion gap acidosis such as occurs with failure to excrete acid or a normal anion gap acidosis as may occur with renal tubular acidosis and failure to reabsorb HCO3−. Box 2-8 summarizes causes of increased anion gap and normal anion gap metabolic acidosis.

BOX 2-8 Causes of Normal Anion Gap and Increased Anion Gap Metabolic Acidosis

Anion gap (AG) may be calculated as follows: AG = [Na+] – ([Cl−] + [HCO3−]) Inserting normal serum electrolyte values, this becomes: AG = [Na+] – ([Cl−] + [HCO3−]) = [140 mEq/L] – ([105 mEq/L] + [24 mEq/L]) = 11 mEq/L The normal range for anion gap is often reported as 8 to 16 mEq/L; however, newer laboratory methods may result in a normal AG range of 6 to 12 mEq/L or as low as 3 to 9 mEq/L. Clinicians should check with their medical laboratory for the appropriate AG range for their institution.

Causes of Increased Anion Gap Acidosisa ∎ Ketoacidosisb (e.g., diabetes mellitus [diabetic ketoacidosis], fasting, starvation, and alcoholic ketoacidosis) ∎ Lactic acidosis (e.g., acute, severe hypoxia, shock, and tissue hypoperfusion) ∎ Most patients with renal failurec (retention of hydrogen ions, sulfate ions, phosphate, and urate ions) ∎ Salicylate (aspirin) overdose • Acetaminophen used chronically may cause an increased anion gap acidosis due to pyroglutamic acid accumulation, particularly in malnourished patients with chronic illness. ∎ Pyroglutamic acid (5-oxoproline) accumulation associated with genetic glutathione synthetase deficiency or acquired glutathione depletion ∎ Ingestion of methanol (methyl alcohol [wood alcohol], antifreeze, and solvents) ∎ Ingestion of ethylene glycol (automotive radiator antifreeze, brake fluid) ∎ Ingestion of large quantities of propylene glycol (newer automotive antifreeze, airport de-icers, and cosmetic products) ∎ Ingestion of toluene, a solvent used in paint thinners and for other industrial uses (Metabolic acidosis is an early finding or seen with impaired kidney function.) Causes of Normal Anion Gap Acidosis ∎

Diarrhea (loss of HCO3−)

∎

Pancreatic fistula (loss of HCO3−)

∎

Distal (Type 1) renal tubular acidosisd Proximal (Type 2) renal tubular acidosis (failure to reabsorb HCO3−)

∎ ∎ ∎

Hypoaldosteronism (Type 4 renal tubular acidosis)d Posttreatment ketoacidosisb

∎ ∎ ∎ ∎ ∎

Ureteral diversion (e.g., ileal loop) performed as part of surgery to remove the bladder Ingestion or administration of ammonium chloride (sometimes used to treat severe metabolic alkalosis) Administration of carbonic anhydrase inhibitors (e.g., acetazolamide [Diamox], a diuretic sometimes used to treat metabolic alkalosis) Intravenous hyperalimentation Ingestion of toluene (late finding or with good kidney function) aLow albumin may cause a decrease in anion gap (AG). To adjust for this, some suggest calculation of

“corrected anion gap” = AG + 2.5 × (4 – measured albumin). If the corrected AG > 16 → increased anion gap acidosis is present; if corrected AG < 16 → normal anion gap acidosis is present. bDuring the treatment phase of diabetic ketoacidosis, the anion gap may return to normal. cWith renal failure, some patients may have a normal anion gap though most do not. dType 1 renal tubular acidosis (RTA) or hypoaldosteronism (Type 4 RTA) is generally present with a

normal anion gap. Adapted from Scott JB, Walsh BK, Shelledy DC. Blood gas analysis, hemoximetry and acid-base balance. In: Shelledy DC, Peters J (eds.), Respiratory Care Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016:281–346. Data from Scott, JB, Walsh, BK, Shelledy, DC. Blood Gas Analysis, Hemoximetry and Acid-Base Balance. In Shelledy, DC, Peters, J. Respiratory Care Patient Assessment and Care Plan Development: 1st ed., Burlington: Jones & Bartlett Learning, 2016:281-346.

The management of patients with metabolic acidosis depends on the cause. For example, lactic acidosis due to severe systemic hypotension requires attention to restoring blood pressure, circulation, and tissue oxygenation. The treatment of ketoacidosis resulting from uncontrolled diabetes mellitus may require administration of insulin and correction of fluid and electrolyte abnormalities.22 Treatment of a metabolic acidosis due to diarrhea may require rehydration, attention to electrolyte abnormalities, and assessment and treatment of the underlying cause (e.g., viral or bacterial infection).21 Treatment of distal renal tubular acidosis (Type 1) may include bicarbonate therapy (aka alkali therapy).23 Alkali therapy has also been suggested in patients with metabolic acidosis due to chronic kidney disease.24 Administration of sodium bicarbonate (NaHCO3) in patients with acute, severe metabolic acidosis is controversial, although it should be considered in cases where HCO3− and pH are very low (e.g., pH < 7.1).21 Treatment of metabolic acidosis should aim to restore extracellular pH to a more

normal value. In general, a metabolic acidosis will improve rapidly once the underlying cause has been resolved. Hyperventilation is the normal compensatory response for a metabolic acidosis and may be helpful in improving arterial pH. Spontaneously breathing patients with good lung function may able may be able to hyperventilate to achieve a PaCO2 as low as 8 to 12 mmHg. A ventilatory response that is less than expected may be due to lung disease, muscle weakness, or impaired respiratory drive. RC Insight With metabolic acidosis, most patients will hyperventilate to reduce PaCO2 to match the last two digits of the pH. For example, a pH of 7.25 should result in a PaCO2 of 25 mmHg. This is the expected respiratory compensation for a metabolic acidosis.

Metabolic alkalosis may be defined as an increase in the concentration of plasma HCO3− > 28 mEq/L. Metabolic alkalosis may be caused by: Gastrointestinal tract loss of hydrogen ions (e.g., vomiting, nasogastric tube suction, and unusual cases of diarrhea with potassium loss) Renal loss of hydrogen ions (e.g., loop or thiazide diuretics, genetic renal tubular disorders, post hypercapnic increase in HCO3− followed by mechanical ventilation, primary aldosteronism, hypochloremia, hypokalemia, or hypercalcemia) Intracellular shift of hydrogen ions (e.g., hypokalemia) Contraction of blood volume (e.g., fluid loss or loop or thiazide diuretics) Administration of base (e.g., intravenous administration of base [e.g., NaHCO3], ingestion of NaHCO3 or citrate salts in the presence of inadequate renal function) or use of crack cocaine, which contains NaHCO3 Treatment of metabolic alkalosis should be aimed at the underlying cause. For example, gastrointestinal tract loss of hydrogen ions due to vomiting may be addressed by administration of antiemetic medications. Nasogastric (NG) suction resulting in a loss of hydrochloric acid from the stomach may be discontinued. If it has occurred, administration of base may be discontinued. Renal loss of hydrogen ions may be addressed by treating the specific cause (e.g., correction of electrolyte abnormalities, discontinuance of loop or thiazide diuretics, restoration of blood volume and renal perfusion, or adjustment of the level of mechanical ventilatory

support provided).25 Renal excretion of excess HCO3− can be improved by correction of factors that impair renal function (e.g., electrolyte disturbances, hypovolemia).25 Patients who have been overventilated resulting in a posthypercapnic alkalosis can be treated by selection of more appropriate ventilator settings. For patients with kidney disease, renal dialysis using a low bicarbonate bath concentration can rapidly improve an metabolic alkalosis.25 In cases of severe metabolic alkalosis, where kidney function is compromised and dialysis is not an option, administration of ammonium chloride or a dilute solution of hydrochloric acid may be considered using available formulas for dosage calculation.25 Box 2-9 summarizes the causes of metabolic alkalosis.

BOX 2-9 Causes of Metabolic Alkalosis ∎

GI tract loss of hydrogen ions • Vomiting (loss of HCI – stomach acid) • Nasogastric (NG) tube suction (loss of HCI via NG tube) • Unusual cases of diarrhea with potassium lossa ∎ Renal loss of hydrogen ions • Loop or thiazide diuretics (loss of CI−, K+, and fluid volume) • Genetic renal tubular disorder (e.g., Bartter and Gitelman syndromes) • Posthypercapnic increase in ↑ HCO3− (e.g., chronic ventilatory failure) followed by mechanical ventilation and a relative hyperventilation • Excess mineralocorticoid (e.g., primary aldosteronism) • Hypochloremia (↓ CI−, ↑ H+ secretion, ↑ HCO3− reabsorption)

• •

∎

∎

Hypokalemia (↓K+, ↑ H+ secretion, ↑ HCO3− reabsorption)

Hypercalcemia due to ingestion of calcium-containing substances (milkalkali syndrome) Intracellular shift of hydrogen ions + pulls potassium from cells in • Hypokalemia – decreased plasma K + exchange for H Contraction of blood volume • Hypovolemia resulting in a relative ↑ HCO3− ○ Fluid loss (bleeding, excessive sweating) ○ Loop or thiazide diureticsb

∎

Administration of base • Sodium bicarbonate (NaHCO3) administration for severe metabolic acidosis • Ingestion of base (NaHCO3, citrate salts) in the presence of inadequate renal function • Crack cocaine or free base cocaine (contain NaHCO3) GI: gastrointestinal HCI: hydrochloric acid CI−: chloride ions K+: potassium ions H+: hydrogen ions HCO3−: bicarbonate ions NaHCO3: sodium bicarbonate

a Lower GI-tract secretions are alkaline, and diarrhea more commonly causes a metabolic acidosis.

Unusual cases of diarrhea (e.g., laxative abuse) with potassium loss may cause a metabolic alkalosis. b Loop or thiazide diuretics may cause hypokalemia. Potassium diuretics (e.g., amiloride [Midamor],

spironolactone [Aldactone], and eplerenone [Inspra]) may conserve K+. Adapted from Scott JB, Walsh BK, Shelledy DC. Blood gas analysis, hemoximetry and acid-base balance. In: Shelledy DC, Peters J (eds.), Respiratory Care Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016:281-346. Data from Scott, JB, Walsh, BK, Shelledy, DC. Blood Gas Analysis, Hemoximetry and Acid-Base Balance. In Shelledy, DC, Peters, J. Respiratory Care Patient Assessment and Care Plan Development: 1st ed., Burlington: Jones & Bartlett Learning, 2016:281-346.

Combined and Mixed Acid-base Disorders Respiratory and metabolic disorders often coexist in critically ill patients. For example, a patient with acute ventilatory failure and severe hypoxemia may experience a combined metabolic and respiratory acidosis (e.g., lactic acidosis with hypercapnia). The normal response to hypoxemia is hyperventilation and patients may experience a combined respiratory and metabolic alkalosis when hyperventilation is accompanied by a gastrointestinal tract or renal loss of hydrogen ions (e.g., NG suction, vomiting, or hypokalemia). With a combined respiratory and metabolic acidosis or combined respiratory and metabolic alkalosis, the pH may reach extreme values. It is also sometimes useful to estimate maximal compensation for an acid-base

disturbance. If compensation is submaximal, a coexisting disorder may be present. In other cases, compensation may be more than expected. In such cases, a secondary condition is likely. For example, expected respiratory compensation for a severe metabolic acidosis would include hyperventilation to a level roughly corresponding to the last two digits of the pH. If the pH fell to 7.25 due to a metabolic acidosis, the expected respiratory compensation would result in an arterial PaCO2 of approximately 25 mmHg. If the patient was only able to hyperventilate resulting in a PaCO2 of 35 mmHg, a secondary condition that limits ventilation may be present, such as ventilatory muscle fatigue, decreased pulmonary compliance, or obstructive disease. Box 2-10 summarizes methods for estimating the maximal expected compensation for metabolic and respiratory acid-base disorders.

BOX 2-10 Expected Compensation for Metabolic and Respiratory AcidBase Disorders Respiratory Acidosis ∎

Normal metabolic compensation for a respiratory acidosis is renal retention of HCO3−.

∎

For an acute respiratory acidosis, a 10-mmHg increase in PaCO2 will increase HCO3− about 1 mEq/L. This reaction occurs within minutes and does not represent metabolic compensation. With maximal expected metabolic compensation for a chronic respiratory acidosis, a 10-mmHg increase in PaCO2 will increase HCO3− about 4 to 5 mEq/L. This increase in HCO3− may take 3 to 5 days to be completed by the kidneys.

∎

Respiratory Alkalosis ∎ Normal metabolic compensation for a respiratory alkalosis is renal excretion of HCO3−. ∎

∎

For an acute respiratory alkalosis, a 10-mmHg decrease in PaCO2 will decrease HCO3− about 2 mEq/L. This does not represent metabolic compensation. With maximal expected metabolic compensation for a chronic respiratory alkalosis, a 10-mmHg decrease in PaCO2 will decrease HCO3− about 4 to 5 mEq/L. This decrease in HCO3− may take 3 to 5 days to be completed by the

kidneys. Metabolic Acidosis ∎ Normal respiratory compensation for a metabolic acidosis is a decrease in PaCO2. ∎

∎

Uncompensated metabolic acidosis is rare and generally only occurs if there is also respiratory center depression, mechanical inability to hyperventilate, or other pulmonary or neuromuscular problems. Respiratory compensation for metabolic acidosis typically results in a decrease in PaCO2 of about 1.2 mmHg for each 1-mEq/L decrease in HCO3−. This decline in PaCO2 usually begins within 30 minutes and is complete within 12 to 24 hours. • The lowest possible expected PaCO2 in compensation for a metabolic acidosis is in the range of 8 to 12 mmHg, which assumes excellent lung function. Most patients with lung disease will be unable to hyperventilate to this extreme in compensation for metabolic acidosis.20 Winter’s formula may also be used to calculate expected respiratory compensation for a metabolic acidosis where:20 • Expected PaCO2 = (1.5 × HCO3−) + 8 ± 2.

•

∎

∎

An alternative to Winter’s formula has also been suggested: 20 • Expected PaCO2 = HCO3− + 15.20

∎

A quick estimate of the expected respiratory compensation for a metabolic acidosis is simply the last two digits of the pH: • For example, the expected respiratory compensation for a metabolic acidosis resulting in a pH of 7.20 would be a PaCO2 of 20 mmHg.

Metabolic Alkalosis ∎

Normal respiratory compensation for a metabolic alkalosis is an increase in PaCO2.

∎

Uncompensated metabolic alkalosis is unusual, unless the patient is receiving mechanical ventilatory support that does not allow for a rise in PaCO2.

∎

Expected respiratory compensation for metabolic alkalosis typically results in an increase in PaCO2 of about 0.7 mmHg for each 1-mEq/L increase in HCO3−.

• •

This increase in PaCO2 is usually rapid and begins within minutes. The maximum expected PaCO2 in compensation for a metabolic alkalosis rarely exceeds 55 mmHg.

∎

Expected respiratory compensation for a metabolic alkalosis can be calculated as follows: • Expected PaCO2 = (0.7 × HCO3−) + 20 ± 2

∎

A quick estimate of the expected respiratory compensation for a metabolic alkalosis is simply the last two digits of the pH. • For example, the expected respiratory compensation for a metabolic alkalosis acidosis resulting in a pH of 7.55 would be a PaCO2 of 55 mmHg.

Assessment of Cardiac and Circulatory Status Assessment of cardiac and circulatory status includes noting specific cardiac and cardiovascular related findings on history, physical examination, and diagnostic testing (e.g., laboratory studies, imaging). For example, chest pain or discomfort, palpitations, dyspnea, orthopnea, or decreased exercise tolerance may suggest cardiac disease. A past history of cardiac problems, such as MI or heart failure, or high blood pressure should be noted. In addition, ECG, bedside imaging (e.g., ultrasound), and specific additional measures of hemodynamic function are often acquired in the intensive care setting. Physical assessment should include measurement of heart rate (HR), characteristics of the pulse, and blood pressure. Causes of tachycardia (HR > 100 bpm) include anxiety, fear, fever, hypoxia, anemia, blood loss, hypovolemia, hypotension, shock, heart disease, and certain drugs and medications (e.g., epinephrine, dopamine, and cocaine). Bradycardia (HR < 60 bpm) can be caused by severe hypoxia, severe acidosis, cardiac disease, vagal stimulation, heart block, and certain medications such as beta-blockers. An irregular pulse is associated with cardiac arrhythmia. A weak, thready pulse may suggest diminished blood flow. Hypovolemia, hypotension, shock, MI, heart failure, and poor or blocked peripheral perfusion all may reduce or diminish the pulse. A full, bounding pulse is associated with increased activity (e.g., fighting the ventilator) or distress (e.g., hypoxemia, early septic shock). Abnormalities of the pulse include pulsus bisferiens, pulsus parvus, pulsus paradoxus, and pulsus alternans, all of which can suggest specific types of cardiac disease (Box 2-11).

BOX 2-11 Abnormalities of the Pulse, Heart Rate and Rhythm Tachycardia: Heart rate greater than 100 bpm. Common causes seen in the ICU include hypoxia, anemia, blood loss, hypovolemia, hypotension, shock, uncontrolled pain, fever, and cardiac disease. Cardiac arrhythmias such as sinus tachycardia, supraventricular tachycardia, and ventricular tachycardia are also common in the ICU setting. Certain medications, such as sympathomimetics, anticholinergic drugs, and xanthenes may cause tachycardia. Cocaine use and abuse may also cause tachycardia. Tachycardia is often associated with procedures performed in the ICU including endotracheal suctioning, and manipulation of tracheostomy tubes or tracheostomy tube ties. Bradycardia: Heart rate less than 60 bpm. Causes of bradycardia seen in the ICU include severe hypoxia, severe acidosis, cardiac disease, vagal stimulation, heart block, and administration of certain medications such as beta-blockers, digitalis, calcium channel blockers, and certain antiarrhythmic agents. Other possible causes of sinus bradycardia include hyperkalemia, hypothyroidism, and hypothermia. Diminished pulse: Causes of a weak or diminished pulse include hypovolemia, hypotension, shock, MI, heart failure, or poor or blocked peripheral perfusion such as may occur with clots or atherosclerosis. A weak, thready pulse is associated with diminished cardiac output. Bounding pulse: A full, bounding pulse is associated with exercise, increased levels of muscular activity (e.g., fighting the ventilator in the ICU), or distress (e.g., increased heart rate and force of cardiac contraction in compensation for hypoxemia, early septic shock). Pulsus bisferiens: A pulse characterized by two systolic peaks and associated with aortic regurgitation. Hypertropic cardiac myopathy, large patent ductus arteriosis, mitral valve prolapse, and hyperdynamic circulatory states (such a septic shock) have been associated with pulsus bisferiens. Pulsus parvus: A small, weak pulse that seems to rise and fall slowly in magnitude. Associated with aortic stenosis and increased peripheral vascular resistance. Pulsus paradoxus: Decrease in force (not rate) almost to the point of disappearance during inspiration (only). Constrictive pericarditis, pericardial effusion, and cardiac tamponade are important causes. Hypvolemic shock, heart failure, increased venous return on inspiration, severe emphysema, and asthma have been associated with pulsus paradoxus. It is significant if inspiratory blood pressure (systolic) falls more than 20 mmHg on inspiration. Pulsus alternans: Strong beats alternating with weak beats. Left ventricular failure is the most important cause. Severe hypertension, cardiac tamponade,

severe aortic regurgitation, and coronary artery disease have been associated with pulsus alternans. Adapted from McCarthy M, Shelledy DC. Physical assessment. In: Shelledy DC, Peters J (eds.), Respiratory Care Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016:137-186. Data from McCarthy, M, Shelledy, DC. Physical Assessment. In Shelledy, DC, Peters, J. Respiratory Care Patient Assessment and Care Plan Development: 1st ed., Burlington: Jones & Bartlett Learning, 2016:137186.

Systemic hypertension (sustained systolic pressure ≥140 mmHg or sustained diastolic pressure ≥ 90 mmHg) may be primary (aka essential) hypertension or secondary hypertension. Primary hypertension does not have a clearly identifiable cause, but is often associated with smoking, obesity, sedentary lifestyle, hyperlipidemia, excessive salt intake, alcohol abuse, vitamin D deficiency, or mental health issues (e.g., depression or type A behavior).26 Patients seen in the ICU may suffer from a number of problems associated with persistent or chronic hypertension, including ventricular hypertrophy, heart failure, MI, ischemic stroke, hemorrhagic stroke, and kidney disease.26 Treatment of primary hypertension includes lifestyle changes (e.g., salt restriction, weight loss, diet modification, and exercise) and may include use of a antihypertensive drugs (e.g., thiazide diuretics, calcium channel blockers, angiotensin-converting enzyme [ACE] inhibiters, or angiotensin II receptor blockers [ARBs]) as monotherapy or in combination.26 Secondary hypertension may be due to renovascular disease (e.g., renal artery stenosis), kidney disease (acute or chronic), primary aldosteronism (excessive adrenal secretion of aldosterone), or sleep apnea syndrome, as well as a number of less common causes (e.g., oral contraceptives, Cushing syndrome, or endocrine disease).27 Treatment of secondary hypertension includes addressing the specific cause. Acute, severe hypertension (diastolic pressure > 120 mmHg) may be life threatening. Patients with renal artery stenosis or following discontinuance of hypertensive therapy in patients with chronic, poorly controlled hypertension are at risk for the development of acute, severe hypertension. A hypertensive emergency is associated with very high arterial blood pressures, usually greater than 220/140 mmHg accompanied by signs and symptoms of organ dysfunction (e.g., myocardial

ischemia, MI, cerebral ischemia or infarction, renal failure, and pulmonary edema).28,29 Causes of hypertensive emergencies may be cardiac (e.g., aortic dissection, acute MI, and unstable angina), neurologic (e.g., stroke, hemorrhage, and hypertensive encephalopathy) or trauma (e.g., head trauma, severe burns).28,29 Other causes include postoperative bleeding, eclampsia, and uncontrolled epistaxis.28,29 Clinical manifestations of a hypertensive emergency may include headache, confusion, hypertensive retinopathy, nausea and vomiting, seizures, heart failure, and renal failure.29 Initial treatment of a hypertensive emergency should include ICU admission, continuous monitoring, and may include administration of antihypertensive medications such as intravenous labetalol (Normodyne) or nitroprusside (Nitropress).29 Hypotension can be defined as a sustained arterial blood pressure < 90/60 mmHg. Causes of hypotension include decreased cardiac output, peripheral vasodilation, or low circulating fluid volume. Specific causes of hypotension often seen in the ICU include sepsis, blood loss, heart disease, and shock. Clinical findings in patients with shock include low blood pressure, decreased urine output, cool, clammy skin, altered mental status, and metabolic acidosis. Cardiogenic shock is caused by low cardiac output while hypovolemic shock is caused by inadequate intravascular volume due to blood or fluid loss. Distributive shock is caused by inappropriate peripheral vasodilation. Types of distributive shock include septic shock, neurogenic shock, and anaphylactic shock. Treatment of shock includes aggressive fluid replacement and treatement of the underlying cause. For example, drugs to improve cardiac function may be administered in the treatment of cardiogenic shock. The electrocardiogram (ECG or EKG) provides a great deal of information including heart rate and rhythm, recognition of premature beats (e.g., premature atrial contraction [PACs], premature junctional complexes [PJCs], and premature ventricular contractions [PVCs]), and identification of other arrhythmias (e.g., heart block, atrial flutter or fibrillation, ventricular tachycardia, ventricular flutter or fibrillation, and asystole). The ECG is also very useful in assessment of patients with myocardial ischemia and acute MI. Symptoms of acute MI include chest pain not fully relieved by rest or nitroglycerin, anxiety, and nausea. Physical findings associated with acute MI include pallor, diaphoresis, and tachycardia. ST segment elevation MI (STEMI) typically shows ST segment elevation followed by T-wave

inversion and then Q wave development over a period of several hours if the heart muscle is not reperfused.30,31 Non-ST segment elevation MI (NSTEMI) typically shows ST segment depression and/or T-wave inversion in two or more leads without Q-wave development.30,31 Laboratory assessment of cardiac biomarkers (e.g., elevated troponins T and I ; elevated CKMB) when combined with the signs and symptoms of MI and related ECG changes confirm the diagnosis.31 Management of cardiac arrhythmias will depend on the cause and the patient’s clinical condition and may include the use of anti-arrhythmia medications, cardiac pacemakers to treat bradyarrhythmias, and electrical cardioversion or radiofrequency ablation to treat certain tachyarrhythmias. Advanced cardiac life support (ACLS) protocols to treat asystole and ventricular fibrillation include the appropriate use of cardiac defibrillation.

Assessment of Cognitive and Neurologic Status Critically ill patients in respiratory failure may suffer from a wide variety of cognitive and neurologic problems. Recall that the brain is very sensitive to inadequate oxygen levels and that hypoxia may cause excitement, restlessness, anxiety, disorientation, or confusion. Occasionally, hypoxia may cause overconfidence, impaired judgment, and/or euphoria resulting in inappropriate or dangerous behavior. Severe hypoxia may cause somnolence, loss of consciousness, convulsions, and coma. Trauma, narcotic or sedative drugs, hypoxia, hypotension, and shock all may affect brain function and level of consciousness (LOC). The ICU patient’s LOC may range from awake and alert, to lethargic, stuporous, semicomatose, and comatose. The patient may be oriented to place, person, time, and situation or be confused, disoriented, delirious, or unresponsive. Delirium can be defined as an acute confusional state that generally develops in a short period of time and may fluctuate over time. Delirium is commonly seen in the ICU and is typically caused by medication side effects, substance intoxication, or specific medical conditions (e.g. encephalopathy, sepsis, and organ failure). Steps that may help reduce the incidence of delirium include providing clocks, calendars, and windows with outside views. Visits from family and friends, early mobilization, and the use of physical and occupational therapy along with avoidance of medications associated with delirium

(e.g., benzodiazepines, barbiturates, opioids [meperidine (Demerol)], antihistamines, dihydropyridine calcium channel blockers, and certain antibiotics) may be helpful. Hypoxemia may contribute to or worsen delirium. The Glasgow Coma Scale (Box 2-12) is sometimes used to quantify level of consciousness in the ICU, with scores ranging from 3 points (e.g., brain death) to fully conscious at 15 points. As a rough guide, Glasgow Coma Scores of less than 8 suggest the possible need for endotracheal intubation for protection of the airway. The Ramsey Sedation Scale (Box 2-13) or the Richmond Agitation-Sedation Scale (Box 2-14) are sometimes used in the ICU to rate patients’ level of sedation and/or agitation. Box 2-15 summarizes additional scoring tools sometimes used in the ICU.

BOX 2-12 Glasgow Coma Scale The Glasgow Coma Scale ranges from a low score of 3 points (e.g., brain death) to a maximum score of 15 points (e.g., fully conscious). A patient who spontaneously opens his or her eyes, responds in an oriented manner to verbal stimuli, and obeys motor commands would have a score of 15 points. Points are assigned for eye opening, verbal response, and motor response as listed below. Observation Score Eye opening Spontaneous

4

In response to voice

3

In response to pain

2

None

1

Verbal response Oriented response

5

Confused response

4

Inappropriate words

3

Incomprehensible words

2

None

1

Motor response Obeys commands

6

Localizes

5

Withdraws

4

Flexes (decorticate)

3

Extends (decerebrate)

2

None

1

Adapted from Centers for Disease Control and Prevention. Glasgow Coma Scale. (May 2003). Available at http://www.cdc.gov/masscasualties/pdf/glasgow-coma-scale.pdf. Data from Center for Disease Control. Glascow Coma Score. Last updated May, 2003. Retrieved from http://www.bt.cdc.gov/masscasualties/pdf/glasgow-coma-scale.pdf.

BOX 2-13 Ramsey Sedation Scale The Ramsey Sedation Scale rates the patient’s sedation/agitation level from minimal sedation/high agitation (scale score = 1) to maximum sedation (scale score = 6). A score of 2 points would be preferred in most patients. Level Response 1 Anxious, agitated, and restless 2 Cooperative, oriented, and tranquil 3 Responding to commands only 4 Asleep, brisk response to stimulus 5 Asleep, sluggish response to stimulus 6 Unarousable Adapted from Ramsay MAE. How to use the Ramsay score to assess the level of ICU sedation. Available at http://www.sedationconsulting.com/oldsite/about/principals/171-how-to-use-the-ramsay-score-to-assessthe-level-of-icu-sedation. Data from Ramsay MAE. How to use the Ramsay score to assess the level of ICU sedation. Available at http://www.sedationconsulting.com/oldsite/about/principals/171-how-to-use-the-ramsay-score-to-assessthe-level-of-icu-sedation.

BOX 2-14 The Richmond Agitation-Sedation Scale The Richmond Agitation-Sedation Scale provides another method to quantify a patient’s sedation. The scale range is +4 points (no sedation/combative) to –5 points (unarousable) as described below. The preferred score for most patients is 0 (alert and calm). Score +4

Term Combative

+3

Very agitated

+2

Agitated

+1

Restless

Description Overtly combative, violent, and immediate danger to staff Pulls or removes tube(s) or catheter(s), aggressive Frequent nonpurposeful movement, fights ventilator Anxious but movements not aggressive or

0 –1

Alert and calm Drowsy

–2

Light sedation

–3

Moderate sedation

–4

Deep sedation

–5

Unarousable

vigorous Not fully alert, but has sustained awakening (eye opening/eye contact) to voice (≥ 10 seconds) Briefly awakens with eye contact to voice (≤ 10 seconds) Movement or eye opening to voice (but no eye contact) No response to voice, but movement or eye opening to physical stimulation No response to voice or physical stimulation

Adapted from Richmond Agitation-Sedation Scale (RASS). Available at http://www.icudelirium.org/docs/RASS.pdf. Accessed March 25, 2015. Data from Richmond Agitation-Sedation Scale (RASS). Available at http://www.icudelirium.org/docs/RASS.pdf. Accessed March 25, 2015.

BOX 2-15 Predictive Scoring Tools Used in the ICU The Acute Physiology and Chronic Health Evaluation (APACHE) scoring system was developed to predict severity of illness and mortality in ICU patients and is available in four versions (I to IV). APACHE II scores are calculated based on the patient’s age, Glasgow Coma Score, body temperature, mean arterial blood pressure, heart rate, respiratory rate, oxygenation status (PAO2 – PaO2 [FIO2 > 0.50] or PaO2 [FIO2 < 0.50], arterial pH or HCO3−, serum K+, serum Na+, serum creatinine, hematocrit, white blood cell count (WBC), and the presence or absence of specific chronic health problems (liver cirrhosis, severe COPD, hypercapnia, use of oxygen in the home, pulmonary hypertension, regular dialysis, immunocompromised conditions, or the evidence of heart disease). APACHE II scores range from 0 to 100 points, with approximate mortality predicted as follows: Score

Predicted Mortality (postoperative)

0–4

1%–4%

5–9

3%–8%

10–14

7%–15%

15–19

12%–24%

20–24

30%–40%

25–29

35%–55%

30–34

73%

35–100

85%–88%

While the APACHE II remains in use, newer versions (APACHE III and APACHE IV) add additional variables. For example, the APACHE IV uses 129 variables collected during the initial 24 hours of ICU stay and is useful in prediction of mortality and length of ICU stay. Three versions of the Simplified Acute Physiologic Score (SAPS) are available. The SAPS 3 score is calculated based on the patient’s age, temperature, systolic blood pressure, heart rate, Glasgow Coma Score, WBC, platelet count, blood pH, creatinine, bilirubin level, oxygenation status (PaO2 [or PaO2/FIO2 if receiving mechanical ventilation]), length of stay before ICU admission, comorbidities, intrahospital location before ICU admission, use of vasoactive drugs before ICU admission, nature of ICU admission (planned or unplanned), reason for admission (e.g., cardiovascular, neurologic, hepatic, or digestive), surgical status (scheduled, emergency, or no surgery), anatomical site of surgery, and presence and type of acute infection (nosocomial, respiratory). The SAPS scores are easier to calculate than APACHE; however they do not predict length of stay. Sequential Organ Failure Assessment (SOFA) scores predict ICU mortality based on the level of dysfunction of six organ systems: respiratory (PaO2/(FIO2), cardiovascular (hypotension level, vasoactive medication), neurologic (Glasgow Coma Score), renal (creatinine or urine output, whichever is worse), coagulation (platelet count), and hepatic (bilirubin). SOFA scores may be useful to assess the level of organ dysfunction and identify patients at risk of dying from sepsis, although the SOFA may be used on all ICU patients. The quick SOFA (qSOFA) uses an abbreviated scoring system and has been suggested for use in sepsis patients outside of the ICU. The Lung Injury Prediction Score (LIPS) assigns points for the presence of specific factors associated with the development of ARDS. These include the presence of shock, aspiration, sepsis, pneumonia, orthopedic spine surgery, acute abdominal surgery, cardiac surgery, aortic vascular surgery, traumatic brain injury, smoke inhalation, near-drowning, lung contusion, multiple fractures, alcohol abuse, obesity, hypoalbuminemia, chemotherapy, FIO2 > 0.35 or O2 therapy > 4 L/min, tachypnea > 30 breaths/ min, SaO2 or SpO2 < 95%, and diabetes mellitus. LIPS > 4 was predictive for the development of ARDS. The Nutrition Risk in the Critically Ill (NUTRIC) scoring algorithm was developed to identify critically ill patients most likely to benefit from aggressive nutrition therapy. The NUTRIC scoring system incorporates predictors of mortality (age, Apache II, or SOFA), measures related to acute and chronic inflammation (interleukin-6 [IL-6], procalcitonin [PCT], C-reactive protein [CRP], and comorbidities), measures related to acute starvation (decreased oral intake, pre-ICU hospital admission), and measures related to chronic starvation (weight loss over the last 6 months, BMI < 20). Nutrition Risk Screening 2002 (NRS 2002) provides a screening tool for nutritional risk. Specifically, the NRS 2002 screens for impaired nutritional status (i.e., undernutrition) and disease severity. Percent recent weight loss, change in food intake, and BMI are scored from 0 to 3, where 0 = normal nutritional status and 3 indicates severely impaired nutritional status. Severity of illness is scored from 0 to 3 where 0 indicates normal nutritional requirements, 1 indicates mild severity of disease (e.g., hip fracture or chronic illness such as COPD), 2 indicates moderate severity of disease (e.g., severe pneumonia, major abdominal surgery, or stroke), while 3 indicates severe disease (e.g., head injury, ICU patients with APACHE ≥ 10). Total NRS 2002 scores > 3 and ≥ 5 define patients at “nutrition risk” and “high nutrition risk,” respectively.

Common neurologic symptoms seen in the ICU include headache, altered

perception (e.g., hallucinations), confusion, somnolence, seizures, loss of consciousness, and coma. Neurologic disease seen in the ICU setting includes stroke, head trauma, intracerebral hemorrhage, subarachnoid hemorrhage, and bacterial meningitis. Stroke may result from cerebral venous thrombosis (e.g., ischemic stroke) or vessel dissection (e.g., hemorrhagic stroke). The presence of muscle weakness, tremors, or paralysis also suggest neurologic disease. Neurologic syndromes that may lead to ventilatory failure include spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis (ALS), West Nile virus (which may cause encephalitis or meningitis), poliomyelitis, post-polio syndrome, Guillain-Barré syndrome, and myasthenia gravis. Botulism and tetanus may also lead to ventilatory failure requiring mechanical ventilation. Neurologic assessment identifies cognitive, sensory, motor, and coordination deficits. A complete neurologic examination includes assessment of the patient’s mental status; cranial nerves; motor examination (muscle tone, muscle strength, and muscle wasting); reflexes (pupillary reaction, tendon reflexes); posture, balance, and coordination; sensory examination (pain, touch); peripheral nerves; conduction; and movement of specific muscle groups. ICU patients often experience moderate to severe pain due to intubation, mechanical ventilation, trauma, surgical procedures, and invasive diagnostic or therapeutic interventions.32 Treatment of pain should seek to optimize patient comfort without resulting in oversedation. Visual analog scales or numeric scales may be used to assess pain in patients who are able to communicate. For example, a patient may be asked to rate his or her level of pain from 0 (no pain) to 10 (the worst possible pain). Pain assessment tools based on observation of pain-related behaviors and physiologic indicators can be used in critically ill patients who are unable to communicate. These include the Behavioral Pain Scale (BPS) and the Critical Care Pain Observation Tool (CPOT) (Box 2-16). Pain control for patients receiving mechanical ventilation often includes IV opioids such as fentanyl (Duragesic), morphine (Roxanol), or hydromorphone (Dilaudid).32 Remifentanil (Ultiva), a short-acting opioid, may be used in patients when extubation is anticipated soon or for patients requiring frequent neurologic assessments.32 Assessment of patients receiving opioids should include observation for specific side effects, which may include depressed consciousness, depressed respiratory drive, hallucinations,

hypotension, histamine release, peripheral vasodilation, nausea and vomiting, ileus and constipation, urinary retention, pruritus (skin itching), and increased intracranial pressure (ICP).32

BOX 2-16 Critical Care Pain Observation Tool (CPOT)

Reproduced from Stites M. Observational pain scales in critically ill adults. Crit Care Nurs. 2014,34:14-15. Data from Stites M. Observational pain scales in critically ill adults. Critical Care Nurse 2014, 34:14-15. American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2013804 http://www.aacn.org/wd/Cetests/media/C1333.pdf. Accessed July 24, 2018.

Mental health issues such as anxiety, depression, other mood disorders, or sleep

disturbances are commonly seen in the ICU. Patients may exhibit alterations in attitude, mood, or affect including anger, hostility, fearfulness, worry, or sadness. Wherever possible, care should be taken to promote communication with the patient, involving the patient in care decisions, and provision of a supportive, pleasant environment.

Nutritional Status Patients seen in the ICU with respiratory failure may be experiencing a catabolic stress state, systemic inflammatory response, infection, multisystem organ system failure, and increased morbidity and mortality associated with critical illness.33 Nutritional therapy may be helpful in reducing the metabolic response to stress, improving immune response and preventing oxidative cellular injury.33 Nutritional assessment in the ICU should include determination of nutritional risk using a standardized assessment tool such as the NRS 2002 or NUTRIC score (see also Box 2-15 and Box 2-17).33

BOX 2-17 Nutritional Risk Screening Scoring systems have been developed to assess critically ill patients’ nutritional risk. The NUTRIC Score assigns points based on the patient’s age, APACHE II score, SOFA score, number of comorbidities, days from the hospital to ICU admission, and IL-6 (interleukin 6) values as follows: Variable Age

APACHE II

SOFA

Range

Points

< 50

0

50–74

1

≥ 75

2

< 15

0

15–19

1

20–27

2

≥ 28

3

< 6

0

6–9

1

≥ 10

2

Number of comorbidities

Days from hospital to ICU admission

IL-6

0–1

0

≥ 2

1

< 1

0

≥ 1

1

< 400

0

≥ 400

1

If IL-6 is available, a score in the range of 6 to 10 indicates the patient is likely to benefit from aggressive nutrition therapy. If IL-6 is not available, a score in the range of 5 to 9 indicates the patient is likely to benefit from aggressive nutrition therapy. Scores of < 6 (with IL-6) or < 5 (without IL-6) suggest low risk of malnutrition. Data from Heyland DK, Dhaliwal R, Jiang X, Day AG. Identifying critically ill patients who benefit the most from nutrition therapy: the development and initial validation of a novel risk assessment tool. Crit Care. 2011;15(6):R268.

Providing nutritional support in critically ill patients entails the delivery of calories, protein, electrolytes, vitamins, minerals, trace elements, and fluids. Enteral nutrition refers to the delivery of liquid food mixtures given through a tube into the stomach or small bowel (i.e., tube feeding). Enteral nutrition allows food to be digested and absorbed normally by the gastrointestinal tract. Enteral nutrition may be provided using a NG tube or a tube directly inserted into the stomach (e.g., percutaneous endoscopic gastrostomy [PEG]) or small intestine (e.g., percutaneous endoscopic jejunostomy [PEJ]). Parenteral nutrition refers to nutritional support provided intravenously. Occasionally, parenteral nutrition is used as an adjunct to enteral nutrition. While enteral nutrition is generally preferred, there is currently no evidence that enteral nutrition provides an advantage in terms of mortality when compared to parental nutrition in critically ill patients.34 Enteral nutrition, however, may reduce the risk of infection when compared to parenteral nutrition.34 Unless contraindicated, providing enteral feeding to critically ill patients early in the course of their illness (e.g., within 48 to 72 hours of ICU admission) may be beneficial; providing early enteral nutrition may be especially beneficial in patients who are malnourished.34 Enteral nutrition should be avoided in patients who are hemodynamically unstable due to inadequate fluid resuscitation and those with gastrointestinal tract disease (e.g., bowel obstruction, ileus, gastrointestinal bleeds, and severe vomiting or diarrhea).34 In addition, initial enteral nutrition should avoid providing excessive

caloric intake. In cases where enteral nutrition is contraindicated, parenteral nutrition may be necessary. Early parenteral nutrition in the ICU is generally avoided and parenteral nutrition may be deferred in otherwise adequately nourished patients until 1 or 2 weeks have passed.33,34 On the other hand, malnourished patients may benefit from the initiation of parenteral nutrition within the first few days of ICU admission.34 Contraindications to parental nutrition include hyperglycemia, electrolyte disturbances, fluid overload, hyperosmolality (e.g., diabetic hyperosmolar syndrome), and lack of intravenous access.34 Calculation of the desired caloric and protein intake is based on the patient’s approximate body weight. An initial goal may be to provide 8 to 10 kcal/kg/d initially and then 18 to 25 kcal and 1.5 g of protein/kg/d after 5 to 7 days.34 Obesity is a major health problem in the United States and overweight and obese patients are at increased risk for the development of heart disease, hypertension, stroke, sleep apnea, type 2 diabetes, cancer, liver disease, gallbladder disease, osteoarthritis, high total cholesterol, and high triglycerides. Obese patients are often seen in the ICU and may have an increased work of breathing and may be difficult to wean from mechanical ventilation. Measurement of the patient’s height and weight are used to calculate the body mass index (BMI) where a BMI of 25 to 29.9 indicates the patient is overweight and a BMI ≥ 30 indicates that the patient is obese. Unless contraindicated, enteral nutrition is preferred for obese patients in the ICU and dosing generally should be the same as that for an adequately nourished critically ill patient.34

Prediction of ICU Outcomes Various assessment tools are used in the intensive care unit to predict patient outcomes such as mortality and ICU length of stay (See Box 2-15). These include APACHE, SAPS, the Mortality Prediction Model (MPM0), SOFA, and LIPS. Some of these scoring systems are available in multiple versions (e.g., APACHE I-IV, SOFA 1-3, quick SOFA [aka qSOFA]). Of scoring systems available, the APACHE IV is generally the most accurate in predicting mortality but requires the input of a large number of variables.35 The SAPS 3 and SOFA scoring systems are easier to use, in that they require less data for their calculations. In addition, the SOFA may be useful

in identifying septic patients at risk of dying.35 For example, a SOFA score of 2 in hospitalized patients with suspected infection suggests an overall 10% mortality risk.36 qSOFA scores are based on a very abbreviated data set, including respiratory rate ≥ 22/min, altered mental status, and systolic blood pressure ≤100 mmHg. The LIPS is used to predict the development of ARDS.35 In addition, the NUTRIC and NRS 2002 tools are used for assessment of nutritional risk. Each of these scoring systems is described in Box 2-15.

Management Principles for Patients in Respiratory Failure Management of patients in respiratory failure includes support of oxygenation, ventilation, circulation, and acid-base balance. Patient should be assessed carefully for oxygenation and ventilatory status, and most patients will require oxygen therapy. For those patients in whom ventilatory failure is likely to occur (i.e., impending ventilatory failure) in the immediate future, invasive or noninvasive ventilatory support may be initiated prior to the development of an acute, severe respiratory acidosis. Patients in acute ventilatory failure and a corresponding respiratory acidosis often require mechanical ventilatory support. Assessment and support of cardiac and circulatory function must also be provided. In addition to providing cardiopulmonary support, a cornerstone of the care of patients in respiratory failure is the identification and treatment of the underlying cause. A brief description of major causes of respiratory failure follows.

Acute Asthma Exacerbation Acute, severe asthma exacerbation represents a potentially life-threatening condition requiring careful assessment, appropriate treatment, and monitoring and may require hospitalization and ICU admission. Characteristics of asthma include airway hyperreactivity, airway inflammation, and reversible airflow obstruction. Clinical manifestations include cough, wheezing, and episodes of dyspnea, although wheezing may not always be present. Chest pain and/or chest tightness may also be present. Symptoms often worsen at night and in the early morning. Tachypnea, accessory muscle use, severe dyspnea (e.g., orthopnea), diaphoresis, tachycardia, and peak expiratory flow (PEF) or forced expiratory volume in 1 second (FEV1.0) < 50% of baseline signify severe asthma exacerbation.37,38 It should be noted that some patients have difficulty perceiving their asthma symptoms, and routine selfmonitoring of PEF can be especially helpful in these cases. In the acute care setting, the chest radiograph may be used to evaluate the patient for infiltrates and comorbidities, and exclude alternative diagnoses. Complete blood count (CBC) with differential may be helpful in certain cases (e.g., to screen for eosinophilia or anemia). Pulse oximetry and arterial blood gas analysis are especially useful to

evaluate hypoxemia and ventilatory status. Hyperventilation is common with acute asthma exacerbation resulting in a decreased PaCO2; an increasing PaCO2 is an ominous sign. FEV1.0 measurement is the best method to assess the severity of an asthma exacerbation and to monitor response to therapy.37,38 Patients at high risk of death due to acute asthma include those with an asthmarelated history of intubation, ICU admission, recent hospitalization or emergency department visits, and those with comorbid cardiovascular or chronic lung disease.37,38 Other important risk factors for fatal asthma exacerbation include failure to prescribe and use inhaled steroids, recent or current use of oral steroids, and use of more than one canister of short-acting β2-agonist per month. Poor adherence to an asthma action plan and/or asthma medications, illicit drug use, and mental health problems (e.g., depression) are additional risk factors.37,38 Emergency department and hospital-based care of acute asthma includes initial assessment (brief history, physical exam, PEF or FEV1, SpO2); oxygen therapy, administration of inhaled short-acting β2-agonist, or systemic corticosteroid administration; repeat assessment (physical assessment, PEF or FEV1); continued therapy, as indicated (e.g., inhaled short-acting β2-agonist, corticosteroid administration, O2, and possible addition of ipratropium [Atrovent]); and a follow-up decision regarding discharge (good response), hospitalization (incomplete response), or ICU admission (poor response) based on the patient’s response.37,38 Status asthmaticus refers to severe bronchospasm that is unresponsive to routine therapy. Although status asthmaticus may occur very rapidly, more often it is preceded by progressive dyspnea, increasing bronchodilator use, and worsening symptoms over a period of hours to days.39 Magnesium sulfate administered IV has been suggested for patients who do not respond to conventional therapy or whose asthma exacerbation is life threatening.37,38 Other nonstandard therapies include the use of inhalational anesthetic agents, and administration of helium–oxygen gas mixtures.39 In asthma patients unresponsive to conventional therapy, an increase in PaCO2 may signal the development of severe respiratory failure and the need for mechanical ventilatory support.39 While some patients may benefit from the use of noninvasive positive pressure ventilation (NPPV), it is often very poorly tolerated by patients with acute asthma. Unlike NPPV in the treatment of COPD exacerbation,

there is limited evidence for its effectiveness with acute asthma.39 Depressed mental status, slowed spontaneous respiratory rate, hypoxemia despite supplemental oxygen therapy, and development of respiratory acidosis suggest the need for intubation and invasive mechanical ventilation.37 It should be noted that endotracheal intubation may initially cause bronchoconstriction to worsen. Mechanical ventilation of patients with severe asthma can be extremely challenging and may require the use of paralytic agents to control ventilation.39 Lower tidal volumes should applied in the range of 6 to 8 mL/kg, in order to reduce airway pressures and avoid barotrauma.37 Ventilator rates of 10 to 12 breaths/min with inspiratory flow rates of 60 to 80 L/min should provide an adequate I:E ratio and expiratory time to allow for complete exhalation in the face of airway obstruction and avoid air trapping.37 Ventilator settings for tidal volume, respiratory rate, inspiratory flow, and trigger sensitivity are adjusted to ensure patient-ventilator synchrony, reduce the work of breathing, and achieve adequate oxygenation and ventilation while ensuring Pplateau ≤ 30 cm H2O. Oxygen concentrations should be adjusted to achieve SpO2 ≥ 90%. Permissive hypercapnia may be required in order to ensure airway pressures are not excessive. Box 2-18 outlines the routine, in-patient, and ICU care of patients with asthma exacerbation.

BOX 2-18 In-patient Care of Patients with Acute Exacerbation of Asthma Routine Management of Asthma The routine management of asthma includes patient education, avoidance of triggers, use of rescue bronchodilators for acute episodes, and regular use of anti-inflammatory medications for the control of moderate to severe asthma. Before and after bronchodilator therapy, pulmonary function testing is used to document reversibility of airway obstruction. Bronchoprovocation testing may be useful in patients who are difficult to diagnose (e.g., those in whom cough is the only symptom of obstruction). Skin testing is sometimes used to identify household or other antigens and blood tests for increased IgE or eosinophilia may be useful. Most patients with persistent asthma can maintain good control of their asthma with proper symptom monitoring, a written asthma action plan, avoidance of asthma triggers, and appropriate rescue and controller medications.

Management of Acute Asthma Exacerbation: Assessment

Review of the Medical Record and Patient Interview: Assess for severity of exacerbation and risk factors associated with death from asthma. ∎ Asthma history • Level of dyspnea (mild, moderate, or severe?) • Previous history of exacerbation? • Previous emergency department visits (≥ 3 in the past year?) • Previous hospitalizations (≥ 2 in the past year?) • ICU admission and/or intubation for asthma? • Use of β2-adrenergic agonist MDI canisters (>2 per month?) Difficulty perceiving asthma symptoms or severity of exacerbations Written action plan (in place and followed?) Sensitivity to Alternaria (a fungus associated with hay fever and allergic asthma)? ∎ Social history • Low socioeconomic status or inner-city resident? • Illicit drug use? • Major psychological/mental health problems? ∎ Comorbidities? ∎ Cardiovascular disease, chronic lung disease, or chronic psychiatric disease? Physical Assessment ∎ Breathlessness at rest? Ability to talk in sentences, phrases, or only words due to dyspnea? ∎ Alertness (agitated, drowsy, or confused?) ∎ Tachypnea (f >30 is severe)? ∎ Tachycardia (HR >120 is severe)? Pulsus paradoxus? ∎ Accessory muscle use? ∎ Wheezing? (Absence of wheeze may signal an imminent respiratory arrest.) Pulmonary Function: PEF percent predicted or percent personal best (for asthma) ∎ ≥ 70%: mild severity ∎ 40%–60%: moderate severity ∎ 95% and/or PaO 80 to 100 on room air – normal 2 2

• • •

∎

SpO2 90-95% and/or PaO2 ≥ 60 but < 80 – moderate

∎

SpO2 < 90% and/or PaO2 < 60 – severe

∎

PaCO2 30 breaths/min • Accessory muscle use • No change in mental status • Hypoxemia corrected with low concentrations (28% to 35%) of oxygen therapy • PaCO2 increased compared to baseline or in the range of 45 to 60 mmHg

∎

Life-threatening Acute Respiratory Failure • Respiratory rate > 30 breaths/min • Accessory muscle use • Acute change in mental status • Hypoxemia not responsive to > 40% oxygen therapy • PaCO2 increased compared to baseline or > 60 mmHg or pH ≤ 7.25

Data from Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017. Available at: http://www.goldcopd.org Accessed January 15, 2017.

The in-hospital treatment of acute exacerbation of COPD includes oxygen therapy, bronchodilator administration, systemic corticosteroids, antibiotics, and other therapies.39−41 In the absence of acute or impending ventilatory failure, low-flow (0.5 to 4 L/min) oxygen therapy via nasal cannula to achieve a SpO2 of 88% to 92% and a PaO2 of 60 to 70 mmHg is suggested.39−41 If the patient’s ventilatory pattern is irregular or rapid, shallow breathing is present, a high-flow air-entrainment mask to deliver 24% to 28% oxygen may be considered. High concentrations of oxygen should be avoided because of the risk of further increasing PaCO2 (i.e., oxygenassociated hypercapnia). Most patients with acute exacerbation of COPD respond well to low to moderate concentrations of oxygen therapy. If a higher FIO2 is needed to correct hypoxemia, the clinician should suspect other problems such as severe pneumonia, ARDS, pulmonary edema, or pulmonary emboli.41 Bronchodilator therapy generally consists of administration of a short-acting β2-

agonist with or without a short-acting anticholinergic medication. The administration of systemic corticosteroids may improve patient outcomes and reduce length of stay. Intravenous or oral prednisone, 30 to 60 mg once daily for 5 to 7 days, is suggested.41,41 The dose may then be tapered for another 7 days; however, tapering generally is unnecessary for therapy of less than 3 weeks.40,41 As an alternative, oral prednisolone, 30 to 40 mg per day for 10 to 14 days, may be given.40,41 Antibiotics can shorten recovery time and duration of hospitalization, and reduce the risk of early relapse or treatment failure. Antibiotics should be considered for 5 to 7 days in patients who meet one or more of the following criteria:40,41 Increased dyspnea, increased sputum volume, and increased sputum purulence, OR Increased sputum purulence and increased sputum volume, OR Increased sputum purulence and increased dyspnea, OR Ventilatory failure requiring mechanical ventilatory support. Mechanical ventilatory support may be necessary for patients with severe exacerbation of COPD in respiratory failure. Indications for noninvasive mechanical ventilation include the presence of at least one of the following: acute respiratory acidosis (PaCO2 ≥45 mmHg and pH ≤ 7.35); severe dyspnea with clinical signs of respiratory muscle fatigue, increased work of breathing or both; and/or persistent hypoxemia notwithstanding supplemental oxygen therapy.40 Patients unable to tolerate NPPV and those who fail an NPPV trial are candidates for invasive mechanical ventilation. Indications for invasive mechanical ventilation include patients who have experienced a respiratory or cardiac arrest, patients with diminished consciousness, those with agitation inadequately controlled by sedation, massive aspiration, persistent vomiting, inability to remove respiratory secretions, hemodynamic instability, ventricular or supraventricular arrhythmias, and lifethreatening hypoxemia.39−41 Most patients requiring mechanical ventilatory support should begin with NPPV delivered by facemask, nasal mask, or nasal pillows. NPPV settings include use of a spontaneously triggered mode with a backup control respiratory rate (i.e., assist/control mode) and inspiratory pressure in the range of 8 to 20 cm H2O.41 Expiratory pressure may set be set to deliver a PEEP in the range of 3 to 5 cm H2O. Patients who cannot be successfully and adequately ventilated with NPPV, or those

who have contraindications to NPPV may require intubation and invasive ventilation. The initial ventilator settings for invasive ventilatory support of patients with acute exacerbation of COPD include assist-control ventilation with a tidal volume in the range of 6 to 8 mL/kg, a backup rate of 12 to 14 breaths/min, and a low to moderate initial oxygen concentration.42,43 Care should be taken to ensure adequate expiratory time to avoid air trapping and auto-PEEP. FIO2 is adjusted to achieve an adequate SpO2 and PaO2. Intubation and invasive mechanical ventilation are clearly indicated in COPD patients with life-threatening respiratory failure.42,43 Failure of noninvasive ventilation, continuing hypoxemia in the presence of supplemental oxygen therapy, and severe respiratory acidosis suggest the need for invasive mechanical ventilation. We suggest employment of a volume-targeted mode, either assist-control (A/C) ventilation or synchronized intermittent mandatory ventilation (SIMV). Tidal volume can be initiated in the range of 6 to 8 mL/kg with a ventilator rate of 10 to 16 breaths/min, and inspiratory flow 60 L/min.42 Inspiratory flow rate may be increased in order to decrease inspiratory time, ensure adequate expiratory time, and reduce the risk of dynamic hyperinflation. For A/C ventilation, trigger sensitivity is initiated at –1 to 2 cm H2O (pressure trigger) or 2 L/min (flow trigger).42 For SIMV, similar initial ventilator rate, inspiratory flow, and trigger sensitivity may be used. The addition of 5 to 10 cm of water pressure support ventilation (PSV) to SIMV mode may improve patient comfort and reduce the work of breathing. FIO2 is adjusted to the lowest level needed to achieve a SpO2 ≥ 92% (and/or PaO2 ≥ 60 mmHg). PEEP may be beneficial in patients with expiratory airflow limitation starting at 5 cm H2O and adjusting, based on the presence of auto PEEP and trigger effort (applied PEEP should be less than auto PEEP).42,43 Ventilator settings are then adjusted to ensure patient-ventilator synchrony, reduce the work of breathing, and achieve adequate oxygenation and ventilation while ensuring Pplateau ≤ 30 cm H2O. Attention should also be paid to maintaining an appropriate fluid balance and the use of diuretics for any fluid overload.40,41 The patient’s nutritional needs should be assessed and provided. Comorbid conditions such as pneumonia, cardiovascular disease (e.g., ischemic heart disease, heart failure, hypertension, and atrial fibrillation), lung cancer, renal failure, liver failure, osteoporosis, diabetes, or anxiety and depression should be evaluated and treated as appropriate.40,41

Pneumonia Pneumonia is an infection of the lung parenchyma, usually caused by bacterial or viral infection. Community-acquired pneumonia (CAP) is acquired at home, work, or school.44 Nosocomial pneumonia (aka hospital-acquired pneumonia [HAP]) is typically seen 48 to 72 hours after hospital admission.44 Ventilator-associated pneumonia (VAP) is a form of nosocomial pneumonia that occurs following intubation and institution of mechanical ventilatory support. Pneumonia acquired in other health care settings (e.g., nursing homes, long-term care units) is referred to as healthcare-associated pneumonia (HCAP).44 Severity of illness with pneumonia may range from mild to life threatening. Common bacterial causes of CAP include Haemophilus influenzae, Legionella spp., Staphylococcus aureus, Streptococcus pneumoniae, and (occasionally) gramnegative bacilli.44 Common causes of viral CAP include influenza, parainfluenza, respiratory syncytial virus (RSV), adenovirus, and human metapneumovirus.44 Atypical community-acquired pneumonias may be caused by Mycoplasma pneumoniae, Chlamydia psittaci, or Coxiella burnetii.44 Critically ill patients, ventilator patients, and those with compromised immune systems are especially vulnerable for the development of nosocomial pneumonia. Nosocomial pneumonia may be caused by gram-positive bacteria, gram-negative bacteria, and viral, fungal, or (very rarely) parasitic infections. Gram-positive causes of nosocomial pneumonia include S. pneumoniae and S. aureus, while gramnegative causes of nosocomial pneumonia include H. influenzae, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Acinetobacter baumannii.44 Methicillin-resistant Staphylococcus aureus (MRSA), drug-resistant Streptococcus pneumoniae (DSRP), and multidrug-resistant (MDR) gram-negative bacteria are difficult-to-treat causes of nosocomial pneumonia.44 Patients in the ICU may have compromised immune systems that predispose them to the development of fungal, viral, or parasitic nosocomial infection. It is believed that nosocomial infection occurs when the balance of viral or bacterial burden and host immune function tips in favor of infection. Nosocomial pneumonia occurs following the introduction of contaminated material into the lower respiratory tract and the most common source of infection is aspiration of contaminated secretions from the oropharynx or gastrointestinal tract. Critically ill

patients with depressed levels of consciousness or altered respiratory tract anatomy are at special risk for aspiration. Alcohol or drug intoxication, neurologic illness, seizures, head trauma, administration of sedative or narcotic medications, and the presence of NG tubes, endotracheal tubes, and tracheostomy tubes predispose patients to aspiration. Patients with conditions that interfere with proper swallowing (e.g., stroke, Parkinson’s disease, and ALS) are also at risk for the development of aspiration pneumonia. Administration of medications to reduce gastric acidity may facilitate the colonization of the oropharynx and gastric contents with gram-negative bacteria that may be aspirated resulting in a nosocomial pneumonia.44 Respiratory care equipment such as ventilator circuits, humidifiers, and nebulizers may also serve as environmental reservoirs for bacteria. The diagnosis of pneumonia is based on clinical signs and symptoms, imaging studies, and laboratory data. Common symptoms of CAP include a productive cough, shortness of breath, chest pain, fever, chills, and malaise. Many, but not all, patients develop fever. Physical examination may reveal crackles upon auscultation, signs of consolidation (e.g., E-a egophony, bronchial breath sounds, tactile vocal fremitus, and dullness to percussion), and mucopurulent or watery sputum (bacterial pneumonia and atypical pneumonia, respectively). Tachypnea, tachycardia, and other signs of respiratory failure may be present. Diagnosis should include a chest xray and CBC. White blood cell count (WBC) is often, but not always increased and a left shift with immature cells may be present. The presence of an infiltrate on imaging and corresponding clinical and microbiologic features confirm the diagnosis. Occasionally, bronchoscopy, bronchoalveolar lavage, and/or thoracentesis may be useful. HAP, VAP, and HCAP are diagnosed based on findings of a new or progressive infiltrate on chest x-ray, worsening hypoxemia, fever, and/or elevated WBC count. An increase in serum procalcitonin (PCT) has been associated with bacterial infection while a decrease in PCT has been associated with viral disease.44 ICU patients should have sputum and blood cultures performed and intubated patients should have their tracheal aspirate tested. Gram stains and cultures are also specifically indicated in patients with pleural effusion, cavitary infiltrates, severe COPD, other chronic respiratory disease, and alcohol abuse. Urinary antigen tests (UATs) are available for detection of Legionella and S. pneumoniae.44

Treatment of CAP is often begun empirically, based on the suspected causative agent. For hospitalized patients with CAP, beginning combination therapy with a βlactam antibiotic and a macrolide antibiotic is suggested.44 ICU patients may require a β-lactam antibiotic often in combination with a macrolide or quinolone antibiotic.44 MRSA may require the addition of vancomycin (Vancocin) or linezolid (Zyvox).44 Antimicrobial therapy should be started in patients with suspected nosocomial pneumonia who have a new or progressive infiltrate on chest x-ray and at least two of the following: fever (> 38°C), abnormally increased or decreased WBC (i.e., leukocytosis or leukopenia), and purulent secretions.44 Combined therapy with a βlactam antipseudomonal penicillin or cephalosporin in combination with an aminoglycoside or quinolone antimicrobial agent have been suggested.44 Endotracheal tube or bronchoscopic secretion cultures may be helpful in identifying the specific causative organism. Mechanical ventilation should be considered in pneumonia patients with severe respiratory failure in order to maintain oxygenation, ventilation, and acid-base balance. We suggest either volume-targeted A/C or SIMV with PSV for most patients. Tidal volume and respiratory rate are adjusted to maintain minute ventilation, while ensuring that airway pressures are not excessive (i.e., plateau pressure ≤ 30 cm H2O). In general, an initial tidal volume of 8 mL/kg with a ventilator rate of 14 to 16 breaths/min and inspiratory flow rate of 60 to 80 L/min will achieve an adequate initial level of ventilation. Individual patient needs must be assessed, including the patient’s acid-base status, and ventilator settings adjusted accordingly. Unless previous blood gases and an associated FIO2 are available, it is usually best to initiate the FIO2 at 1.0 (100% O2) and then adjust based on oximetry and arterial blood gases. An initial PEEP setting of 5 to 10 cm H2O is a good place to start. For most patients, a lung protective ventilation strategy is then employed (see Acute Respiratory Distress Syndrome below).

Acute Respiratory Distress Syndrome As noted earlier in this chapter, ARDS is a type of hypoxemic respiratory failure often described as noncardiogenic pulmonary edema. The Berlin definition of ARDS requires the presence of new or worsening respiratory symptoms following a known

clinical insult, bilateral infiltrates on chest imaging, and marked hypoxemia.3,45 More specifically, ARDS is identified based on chest imaging findings, timing, origin of the observed pulmonary edema, and the degree of oxygenation defect (Box 2-1). Chest radiograph or computed tomography (CT) scan findings with ARDS include bilateral chest opacities that are NOT due to lobar or lung collapse or lung nodules. It is also important to verify that the observed pulmonary edema is not entirely attributable to increased hydrostatic pressure (e.g., not due to heart failure or fluid overload) as verified by echocardiography or PCWP < 18 mmHg.43,45,46 It should be noted, however, that ARDS and heart failure can occur in the same patient. RC Insight ARDS is an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue, hypoxemia, and bilateral radiographic opacities associated with increased venous admixture, increased physiological dead space, and decreased lung compliance.45

ARDS is a serious, potentially fatal disorder that interferes with oxygen getting from the alveoli into the pulmonary capillaries and, in turn, to the arterial blood for distribution. Over 10% of the patients seen in the ICU and over 20% of patients receiving mechanical ventilation may meet the criteria for ARDS.46 The ratio of the PaO2 to FIO2 while receiving at least 5 cm H2O of PEEP or CPAP is used to determine the severity of the oxygenation problem and disease: PaO2/FIO2 ≤ 300 but > 200: mild PaO2/FIO2 ≤ 200 but > 100: moderate PaO2/FIO2 ≤ 100: severe ARDS is caused by diffuse alveolar damage to the lungs from injury or disease, such as pneumonia, inhalation of toxic chemicals, aspiration of gastric contents, lung transplantation, septicemia, septic shock, or severe trauma.46 Other possible causes include massive transfusion and hematopoietic stem cell transplant.46 ARDS has also been associated with certain types of drug overdose such as aspirin, cocaine, opioid drugs, and tricyclic antidepressants.46 Other risk factors for the development of ARDS include alcohol abuse, tobacco use, acute pancreatitis, obesity, neardrowning, and cardiopulmonary bypass.46 Table 2-6 summarizes common factors

associated with the development of ARDS. The LIPS is sometime used to predict which patients will develop ARDS (Box 2-14). TABLE 2-6 Factors Associated with the Development of ARDS Pulmonary Factors

Extrapulmonary Factors

Aspiration

Drug overdose

Inhalational injury

Hematopoietic stem cell transplant

Lung transplant

Massive transfusion

Near-drowning

Pancreatitis

Pneumonia

Sepsis

Pulmonary contusion

Severe burns Severe trauma Shock Transfusion-related lung injury

Data from Fanelli V, Vlachou A, Ghannadian S, et al. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thoracic Dis. 2013;5(3):326–334. doi:10.3978/j.issn.20721439.2013.04.05.

The primary pathophysiologic effect of ARDS is increased pulmonary capillary permeability resulting in leaky capillaries. This allows excess fluid to move from the pulmonary circulation into the interstitial and then alveolar spaces. As ARDS progresses, an abnormal accumulation of fluid, protein, and fibrin in the alveoli occurs resulting in stiff, heavy, and difficult to expand lungs. Pulmonary compliance is reduced, work of breathing increases, and arterial oxygen levels fall. The resultant hypoxemia may persist, even following the application of mechanical ventilation and PEEP. Management of ARDS includes correction of hypoxemia, support of ventilation and circulation, and careful patient monitoring. Most ARDS patients will require intubation and mechanical ventilation.47 Initially, very high oxygen concentrations may be required, although FIO2 should be reduced to 0.60 or 0.50 (i.e., 50% to 60%) as soon as feasible in order to avoid oxygen toxicity.47 Ventilator management for ARDS patients should incorporate low tidal volume

ventilation (i.e., lung protective ventilation) to avoid ventilator-associated lung injury. Most ARDS patients are first intubated and ventilation is begun using a full ventilatory support mode. Initial tidal volume is set at 8 mL/kg of predicted body weight (PBW) and the initial respiratory rate is set to achieve an adequate minute ventilation.48 Tidal volume is then reduced to 7 mL/kg and then 6 mL/kg and respiratory rate increased to maintain minute ventilation over the next 1 to 3 hours.47,48 Additional tidal volume adjustments may be made based on plateau airway pressure (Pplateau) with the goal of maintaining Pplateau ≤ 30 cm H2O. PEEP improves oxygenation by facilitating alveolar recruitment and reducing endexpiratory alveolar collapse. PEEP strategies vary and a number of different methods to titrate PEEP have been suggested, including “open lung ventilation,” which combines low tidal volumes with high PEEP to maximize alveolar recruitment. Other strategies have suggested the use of pressure-volume curves to adjust PEEP levels to either maximize lung compliance or adjust the PEEP to achieve ventilation slightly above (e.g., 2 cm H2O) the lower inflection point on the pressure-volume curve. A good strategy for most patients is to adjust the PEEP to the lowest level that results in an adequate PaO2 with an FIO2 ≤ 0.60. The ARDS net protocol also provides a method to adjust PEEP based on FIO2 using a simple table. Other strategies to improve oxygenation during mechanical ventilation of ARDS patients include the use of recruitment maneuvers, inverse ratio ventilation with prolonged inspiratory times, and prone positioning, which has been shown to improve oxygenation in these patients.47−49 Fighting the ventilator, pain, anxiety, and fever will increase oxygen consumption. Proper sedation and pain management and treatment of fever with antipyretics (e.g., acetaminophen) can reduce oxygen consumption and help ensure the patient tolerates mechanical ventilation. Excessive sedation, on the other hand, can be harmful and use of sedation scales (e.g., Richmond Agitation-Sedation Scale [RASS]) and routinely waking patients each day may be beneficial. The use of neuromuscular blocking agents probably should be reserved for patients with persistent ventilator asynchrony or severe oxygenation problems and for relatively short periods of time.47,48 Monitoring of the patient’s ventilatory parameters (e.g., pressures, flows, and volumes), oximetry and ECG should be included, and the ventilator settings should be adjusted to reduce or eliminate patient-ventilator

asynchrony. Hemodynamic monitoring may be accomplished by use of a central venous catheter or pulmonary artery catheter, although catheter-related complications are significantly more common with the use of a pulmonary artery catheter.47 A conservative approach to fluid management may help reduce pulmonary edema; however, a conservative approach should not be at the expense of maintaining an adequate systemic blood pressure and tissue perfusion.47 Supportive care for ARDS patients includes nutritional support; control of blood glucose levels; rapid treatment of nosocomial pneumonia, if it occurs; prevention of deep vein thrombosis (DVT); and prevention of gastrointestinal tract bleeding.47 Enteral nutritional support is preferred, unless contraindicated, and overfeeding should be avoided. Anemia should be corrected if the Hb < 7 g/dL, although transfusion has been associated with increased mortality in ARDS patients.47 Complications associated with the ARDS include pulmonary barotrauma, delirium, nosocomial pneumonia, deep vein thrombosis, gastrointestinal bleeds, and catheterrelated infections.50 Mortality due to ARDS increases with the severity of disease and estimates range from 26% to 58%.50 Mortality rates for ARDS have declined in recent years and death is generally not due to respiratory failure, but rather to secondary complications such as sepsis or multiorgan system failure. Patients who do survive may experience cognitive deficits, depression, anxiety, or posttraumatic stress disorder. Physical disabilities and a reduction in lung function are also common.50

Heart Failure Heart failure occurs due to a structural or functional impairment in which the ventricles are unable to adequately fill or eject blood.51−53 Common causes of heart failure include myocardial, pericardial, endocardial, or valvular heart disease; disorders of the great vessels and certain metabolic disorders may also cause heart failure.51 Low-output heart failure results in reduced cardiac output and inadequate systemic blood flow. “Congestive heart failure” (CHF) is an older term used for heart failure and refers to the heart’s inability to maintain adequate blood circulation. Heart failure may be left-sided, right-sided or both. Left-sided heart failure may be

systolic or diastolic. Left ventricular failure (aka left-sided systolic failure) refers specifically to failure of the left side of the heart to adequately pump blood out to the body; left ventricular ejection fraction (LVEF) is used to classify the degree of left ventricular dysfunction. Left-sided diastolic failure (aka diastolic dysfunction) occurs when the left ventricle becomes stiff and does not fill properly during diastole. Right ventricular failure refers to failure of the right side of the heart to adequately pump blood to the lungs. Left ventricular failure is a common cause of right ventricular failure due to blood backing up in the pulmonary circulation, and then to the right side of the heart. Cor pulmonale is a form of right-sided heart failure associated with chronic lung disease and characterized by right ventricular hypertrophy and dilatation caused by increased pulmonary artery pressures due to chronic hypoxia and increased pulmonary vascular resistance. Heart failure can be specifically characterized as ischemic (e.g., acute MI), nonischemic (e.g., idiopathic cardiomyopathy), or valvular (e.g., mitral regurgitation).52 It should be noted that while cardiomyopathy (disease of the heart muscle) or left ventricular dysfunction may lead to heart failure, the terms are not synonymous.51 Left ventricular myocardial dysfunction, however, is the most common cause of heart failure seen in the ICU.51 Specific causes of congestive heart failure and cardiomyopathy are found in Box 2-20.

BOX 2-20 Causes of Heart Failure and Cardiomyopathy Heart failure (aka congestive heart failure) refers to a clinical syndrome in which there is impairment of ventricular filling or impairment of ejection of blood resulting in inadequate blood flow to body tissues and organs. Cardiomyopathy specifically refers to diseases of the heart muscle. Specific causes of heart failure include: ∎ Coronary artery disease (CAD) • Myocardial ischemia • Myocardial infarction ∎ Pressure or volume overload • Hypertension • Fluid overload • Aortic valvular stenosis or aortic insufficiency

∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

Mitral valve regurgitation Obesity Diabetes Certain toxins (e.g., cocaine, ethanol, doxorubicin, and methamphetamine) Hereditary conditions (e.g., hypertrophic cardiomyopathy) Viral myocarditis Amyloidosis Other metabolic-endocrine conditions (e.g., thiamine deficiency) Certain idiopathic conditions (e.g., idiopathic dilated cardiomyopathy)

Data from Gaglianello NA, Mahr C, Benjamin IJ. Heart failure and cardiomyopathy. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:55–66.

Development of heart failure is associated with coronary artery disease (CAD), chronic hypertension, cardiomyopathy, and cardiac valvular disease (e.g., aortic stenosis). Chronic systemic hypertension is a common cause of heart failure. Episodes of heart failure may be triggered by excessive salt intake, worsening hypertension, acute MI, development of arrhythmias, pulmonary embolus, infection, anemia, and certain drugs.51−53 Respiratory distress, fatigue, peripheral edema (e.g., swelling in the legs, ankles, and ascites), and weight gain due to fluid retention are common findings and patients may develop acute pulmonary edema (i.e., cardiogenic pulmonary edema).51−53 Treatment of heart failure is dependent on the cause and may include diuretics to treat fluid retention and the use of specific pharmacologic agents to improve cardiac function (e.g., angiotensin-converting enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], beta-blockers, digoxin [Lanoxin]).52,53 General measures may include salt restriction, avoidance of nonsteroidal anti-inflammatory drugs, and preventative immunizations including influenza and pneumococcal pneumonia vaccines. Patients prone to the development of ventricular arrhythmias may benefit from the placement of an implantable cardiac defibrillator.52,53 Intraventricular conduction delays may be treated by cardiac resynchronization therapy (e.g., biventricular pacing).52,53 Anticoagulation therapy may be considered in the presence of atrial fibrillation.52,53 Mechanical circulatory assistance using a ventricular assist

device (VAD) may be considered as a bridge to heart transplant or for those ineligible for heart transplantation.52 Acute decompensated heart failure (ADHF) is a potentially life-threatening problem that may be caused by left ventricular dysfunction, valvular heart disease, or elevated cardiac filling pressures.54 ADHF causes acute respiratory distress and severe dyspnea, and is usually, but not always, associated with the development of acute pulmonary edema. Treatment of ADHF may include careful assessment, ECG monitoring and pulse oximetry, oxygen therapy, noninvasive ventilatory support, diuretic therapy, and assessment for vasodilator administration to correct elevated filling pressures and/or left ventricular afterload.54 Invasive mechanical ventilatory support with PEEP may be required in some patients. As noted, heart failure patients may develop acute pulmonary edema, resulting in severe hypoxemia and respiratory failure. Such patients may require moderate to high concentrations of oxygen therapy and patients in severe respiratory failure may require invasive mechanical ventilatory support.

Acute Myocardial Infarction Acute MI occurs when part of the heart muscle is damaged or dies due to lack of blood flow. The most common cause of acute MI is blockage of one of the coronary arteries by a blood clot. Coronary artery disease with plaque buildup may lead to the development of an MI. The site of the blockage of myocardial blood supply will determine which parts of the heart are affected. There are three broad types of acute coronary syndromes and MI based on ECG findings. These acute coronary syndromes include STEMI, NSTEMI, and unstable angina. STEMI typically shows ST segment elevation followed by T-wave inversion and then Q-wave development over a period of several hours if cardiac reperfusion has not occurred.30,31,55 Initial treatment of STEMI should include assessment for the clinical manifestations of MI, immediate administration of aspirin, oxygen therapy, establishment of IV access, and initiation of cardiac monitoring.55,56 ACLS protocols are implemented, if indicated (e.g., in the presence of ventricular arrhythmia).30,31,55 An ECG should be performed within 10 minutes of arrival in the health care facility to verify STEMI.55,56 Cardiac biomarkers (e.g., troponins T and I), electrolytes, hemoglobin/hematocrit and coagulation studies should be obtained.55,56 Patients

should be evaluated for percutaneous coronary intervention (PCI) or the administration of fibrinolytic agents in patients who cannot receive rapid PCI (i.e., within 120 minutes).55,56 Angina may be treated with sublingual nitroglycerin (Nitrostat) tablets and morphine sulfate administered for anxiety and discomfort. Arrhythmias should be managed as appropriate, and a beta-blocker given to prevent recurrent ischemia and ventricular arrhythmias.55,56 The NSTEMI ECG typically shows ST segment depression and/or T-wave inversion in two or more leads without Q-wave development. ECG changes that do not include ST segment elevation in combination with elevated cardiac biomarkers (i.e., elevated troponins) indicate NSTEMI.55,57 Unstable angina primarily differs from NSTEMI in that myocardial ischemia does not result in sufficient cardiac damage to cause elevated cardiac troponins. Because cardiac troponins may not be initially elevated, it may be difficult to distinguish between NSTEMI and unstable angina early in the course of care. The initial treatment of NSTEMI and unstable angina are similar to that of STEMI, with the exception of fibrinolytic therapy, which should not be given to patients with NSTEMI or unstable angina. Initial treatment of NSTEMI and unstable angina should include relief of ischemic pain (nitroglycerin, morphine), oxygen therapy, support of hemodynamic status, antithrombotic therapy (e.g., aspirin, anticoagulant therapy), and beta-blocker therapy to prevent recurrent ischemia and prevent life-threatening arrhythmias.55,57 Additional treatment may include cardiac catheterization (PCI), coronary artery bypass graft, or a conservative medical strategy depending on the patient’s condition and estimation of risk.55,57

Shock As noted earlier in this chapter, shock is generally caused by circulatory failure and results in systemic hypotension, decreased oxygen delivery to the tissues, and cellular and tissue hypoxia. Types of shock include cardiogenic, hypovolemic, obstructive, and distributive shock. In early stages of shock, heart rate may increase in compensation. As shock progresses, patients may experience dyspnea, restlessness, diaphoresis, and cool clammy skin.58,59 Hypotension, oliguria, and metabolic acidosis may then lead to tissue hypoxia, organ damage, multiorgan failure, and death.

Cardiogenic shock is caused by decreased cardiac output and management consists of efforts to restore systemic blood pressure, improve cardiac output, and treat the underlying cause. Causes of cardiogenic shock include acute MI, cardiac arrhythmias (e.g., ventricular tachycardia, supraventricular tachycardia, ventricular fibrillation, and bradycardia), pericardial tamponade, and tear or rupture of the mitral valve or ventricular septum.58,59 Systemic hypotension, a reduced cardiac index (CI < 1.8 L/min/m3), and an increased pulmonary capillary wedge pressure (PCWP > 18 mmHg) are typical findings with cardiogenic shock.51,58,59 Treatment of cardiogenic shock may include vasopressors (e.g., norepinephrine, epinephrine, phenylephrine [Sudafed], and dopamine) and inotropic drugs (e.g., dobutamine, milrinone) to increase cardiac output and blood pressure.51,59 Antiarrhythmic agents, specifically beta-blockers, have been recommended in postMI patients for the prevention of sudden cardiac death.60 Nonpharmacologic treatment of cardiac arrhythmias may include defibrillation or cardioversion, or insertion of a cardiac pacemaker.51,59 Mechanical circulatory assistance to improve cardiac output may be provided via intra-aortic balloon pump (IABP) or ventricular assist device (VAD).59 Hypovolemic shock is caused by inadequate intravascular volume due to blood or fluid loss; patient management aims to restore circulating blood volume and treat the underlying cause. Establishing vascular access quickly and aggressive volume replacement should be undertaken, guided by careful assessment of the patient.58,61 Blood loss may be due to bleeding from injuries (e.g., blunt or penetrating trauma) or internal bleeding, such as from the gastrointestinal tract (e.g., esophageal varices). Common causes of fluid loss include severe burns, diarrhea, vomiting, and excessive sweating. Laboratory testing may include CBC, blood chemistry, kidney function tests, and assessment of cardiac biomarkers. Imaging studies to assess possible sources of bleeding (e.g., radiograph, CT scan, and ultrasound) may be performed. Endoscopy may be helpful in assessing gastrointestinal bleeds. A primary goal of in-hospital treatment is intravenous replacement of blood and fluids. Drugs to improve cardiac output and blood pressure may be required (e.g., dopamine, dobutamine, epinephrine, and norepinephrine).61 Obstructive shock may be caused by decreased cardiac output due to an extra cardiac problem, such as pulmonary embolism, severe pulmonary hypertension,

tension pneumothorax, pericardial tamponade, constrictive pericarditis (e.g., inflammation of the pericardium resulting in scarring), or restrictive cardiomyopathy (e.g., diabetic cardiomyopathy, amyloidosis).58 Right ventricular failure due to severe pulmonary hypertension or pulmonary embolism are the most common causes of obstructive shock seen in the ICU. Distributive shock occurs when inappropriate peripheral vasodilation results in decreased systemic vascular resistance and low blood pressure. Neurogenic shock, anaphylactic shock, and septic shock are all forms of distributive shock. Neurogenic shock may occur in patients with traumatic brain injury or spinal cord injury.58 Anaphylactic shock is most commonly due to an allergic reaction to insect stings, foods, or certain drugs. Bronchospasm is a common accompanying problem. Transfusion reactions, snake bites, spider bites, and heavy metal poisoning may also cause anaphylactic shock. Septic shock is the most common form of shock seen in the ICU and is due to sepsis, as described below.

Sepsis Sepsis is an inflammatory response to infection that may lead to shock, multiorgan failure, and death. Specifically, sepsis may be defined as a “life-threatening organ dysfunction caused by a dysregulated host response to infection.”16,36,43 Sepsis may be caused by gram-positive bacteria, gram-negative bacteria, or fungi. Patients at increased risk of developing sepsis include all those admitted to the ICU, older patients, immunosuppressed patients, and patients with community-acquired pneumonia, bacteremia, diabetes, or cancer. SOFA scores can be calculated to predict mortality based on the level of organ dysfunction (Box 2-17).36 The SOFA specifically includes factors associated with respiratory, hematologic, liver, renal, brain, and cardiovascular function. ARDS, acute renal failure, and disseminated intravascular coagulation (DIC) are three of the more common forms of organ dysfunction seen with sepsis.62 Clinical manifestations of sepsis often include findings associated with infection, hypotension, tachycardia, fever, and leukocytosis.62 Initially, the skin may be warm and flushed due to increased cardiac output. As shock develops, the skin may become cold and clammy and the patient may experience altered mental status or become obtunded. Other findings may include decreased capillary refill, oliguria,

absent bowel sounds (i.e., ileus due to hypoperfusion), and other manifestations of shock. Lab findings with sepsis may include arterial hypoxemia, increased serum lactate (> 2 mmol/L), increased plasma C-reactive protein, and increased creatinine.62 As noted, sepsis may lead to septic shock, which can be identified by the presence of persistent hypotension requiring vasopressor administration in order to maintain blood pressure. Septic shock is the most common form of shock seen in the ICU. Specifically, septic shock has the following characteristics:36,58,62 Criteria for sepsis present (i.e., organ dysfunction and infection, such as bacteremia) Vasopressors required to maintain mean arterial pressure ≥ 65 mmHg, despite adequate fluid resuscitation Serum lactate levels > 2 mmol/L or > 18 mg/dL Treatment of sepsis should include prompt identification and treatment of the site(s) of infection, and support of oxygenation, ventilation, and circulation.62 Intravenous access should be established and intravenous antibiotic therapy begun. Sputum, urine, and blood cultures should be performed. Intravenous fluids may be required in patients with intravascular hypovolemia in order to improve blood pressure.62 Vasopressors (e.g., norepinephrine, phenylephrine) may be required to maintain arterial blood pressure in the presence of septic shock.62 Patients with refractory shock may also require inotropic therapy (e.g., dobutamine) and severely anemic patients may require blood transfusions.62 Institution of mechanical ventilatory support may be required in the presence of severe respiratory failure (e.g., ARDS, severe pneumonia).

Trauma Traumatic injuries seen in the intensive care unit range from trauma due to motor vehicle accidents, falls, gunshot wounds, stabbings, domestic violence, industrial accidents, fires, explosions, electrical shock, near-drowning, and boating accidents, to name just a few. Traumatic injuries seen in the ICU include chest trauma, cervical spine injury, long bone fractures, burns, head trauma, and abdominal injuries. While all forms of trauma are serious, chest trauma and head trauma are of particular concern. Thoracic trauma accounts for about one-fourth of trauma fatalities and is a

complicating factor in another half of trauma associated fatalities.63 The two most common causes of chest trauma are motor vehicle accidents and falls, although assaults, stabbings, gunshot wounds, and sports injuries also account for a significant number of patients seen with chest trauma.63 Rib fractures are among the most common types of fractures seen in trauma cases. Flail chest is present if five or more ribs in a row are fractured or three or more ribs are broken in two or more places. Pneumothorax, lung contusion, and hemothorax are common findings with chest trauma. Penetrating cardiac trauma from stabbings or bullet wounds is a leading cause of death in urban environments. Blunt myocardial injury including pericardial tamponade may also occur as a result of blunt chest trauma. Other less common complications of chest trauma include subclavian vascular injury, diaphragmatic rupture, tracheobronchial tears, aortic injury, and esophageal rupture.63 The most common causes of death due to trauma are blood loss, cardiopulmonary arrest, and multiple organ dysfunction.63 Airway obstruction is a major cause of death among trauma patients and assessing and securing the airway is essential.63 Shock associated with trauma may be caused by hemorrhage, third spacing (as may occur with burns), pericardial tamponade, myocardial contusion, or tension pneumothorax.63 Following initial patient stabilization, a thorough assessment to determine the severity and extent of injuries is required. Treatment is then directed at specific problems, while ensuring that support is provided for oxygenation, ventilation, and circulation. Mechanical ventilation is often required in patients admitted to the ICU due to trauma. Ventilator management can be challenging, depending on the type and severity of the patient’s illness. Patients with pulmonary contusions or ARDS or those developing a severe pneumonia following injury are ventilated using a low tidal volume strategy to reduce airway pressures and avoid ventilator-induced lung injury. PEEP is often required for patients with refractory hypoxemia. Care must be taken to ensure hemodynamic stability, adequate oxygen delivery, and organ perfusion. Mechanical ventilation with positive pressure and PEEP will raise intrathoracic pressures and may worsen hypotension in patients with shock. In these cases, ventilation strategies to reduce mean airway pressure and use of the lowest PEEP required to maintain adequate oxygenation may be helpful.

Patients with traumatic pneumothorax need to be monitored carefully for the possible development of tension pneumothorax. Smoke inhalation may result in airway inflammation and pulmonary complications. Burn patients can be very challenging to manage and are best cared for in specialized burn centers. Carbon monoxide poisoning sometimes occurs in patients exposed to smoke and fires and must be recognized and treated with aggressive oxygen therapy.

Head Trauma Traumatic brain injury (TBI) is caused by a sudden blow to the head or penetrating head injury and may result in loss of consciousness or coma. Severe TBI may be defined as a brain injury resulting in a coma of > 6 hours and a Glasgow Coma Score of 3 to 8 (see Box 2-12).64 Common civilian causes of TBI include falls and motor vehicle accidents, while blasts are the leading cause of TBI amongst military personnel in war zones. Moderate to severe TBI can result in cognitive deficits, problems with speech and language, and sensory, perceptual, and/or visual disturbances. Patients with head trauma and TBI may experience apnea, alterations of respiratory rate (e.g., tachypnea, bradypnea, and irregular breathing), hyperventilation or hypoventilation (e.g., ventilatory failure).64 Hypoxia and hypotension are often present in these patients. These patients often have other traumatic injuries to the chest, limbs, or spinal cord. Initial assessment should include neurologic assessment and assessment of oxygenation, vital signs, and laboratory studies (e.g., CBC, electrolytes, glucose, coagulation, blood alcohol level, and urine toxicology)64 CT imaging should be performed to assess for the presence of skull fractures, intracranial hematomas, or cerebral edema.64 Oxygen therapy, blood pressure support, and the management of increased intracranial pressure (if present) should begin. Surgical treatment may be required for intracerebral hemorrhage, hematoma, or depressed skull fractures. ICU management of the patient with TBI includes maintenance of blood pressure, oxygen therapy, prevention of deep vein thrombosis, and care to minimize intracranial pressure (ICP < 20 mmHg).64 Intubation is indicated in patients with a Glasgow Coma Score ≤ 8.64 Patients with TBI requiring mechanical ventilatory support should be ventilated in a manner to ensure adequate oxygenation and avoid

hypotension and hypercarbia.65 Hyperventilation has been shown to reduce ICP. Currently, hyperventilation is not recommended in the first 24 to 48 hours following traumatic brain injury.64 Patients with cerebral edema due to head trauma may benefit from moderate hyperventilation (e.g., PaCO2 30 to 35 mmHg) later in the course of their care. A lung-protective strategy in TBI patients may elevate PaCO2 and compromise cerebral perfusion, and should be avoided, if possible.64,65 Acute spinal cord injury may be caused by diving accidents, motor vehicle accidents, gunshot wounds, or other traumatic accidents. Patients with acute spinal cord injury require ICU admission and careful assessment and monitoring to ensure adequate oxygenation, ventilation, and circulatory status. Acute spinal cord injury may precipitate respiratory failure and/or hemodynamic instability. For example, cervical spine injury may cause diaphragmatic paralysis requiring immediate ventilatory support. Neurogenic shock may develop resulting in hypotension and bradycardia. Other complications of acute spinal cord injury include the development of pulmonary edema, pneumonia, and DVT resulting in pulmonary embolism.

Pulmonary Embolus and Deep Vein Thrombosis Venous thromboembolism includes deep vein thrombosis (DVT) and pulmonary embolism. DVT typically begins in the calf veins; however DVT can occur in the upper extremities (e.g., subclavian or axillary vein thrombosis).11,29 Clinical manifestations of DVT in any extremity include pain and swelling. Upper extremity DVT can cause facial swelling, blurred vision, and dyspnea.11,29 Laboratory confirmation of plasma D-dimer elevation is a sensitive indicator of DVT.11,29 Imaging tests for DVT include ultrasonography or, less commonly, CT venography and magnetic resonance (MR) angiography. Treatment of DVT includes systemic anticoagulation if the patient’s risk of bleeding is thought to be acceptably low.29 Placement of an inferior vena caval filter to block clot migration to the lungs may be considered in certain patients. Pulmonary embolus occurs when a deep vein thrombosis is dislodged and travels via the vena cava to the right heart and then out via the pulmonary artery to the lungs. A pulmonary embolus will increase pulmonary arterial pressure and pulmonary vascular resistance. This may, in turn, cause an increase in right

ventricular end-diastolic pressure. Pulmonary embolus will also cause a decrease in perfusion of portions of the lung, resulting in V̇/Q̇ mismatch and arterial hypoxemia. If blood flow to specific respiratory units is completely blocked, ventilation without perfusion occurs (i.e., increased pulmonary dead space). Pulmonary embolus can be asymptomatic or symptoms may be severe, including shock and sudden death. Clinical manifestations of acute pulmonary embolus include dyspnea, pleuritic chest pain, tachypnea, and tachycardia. In the case of massive pulmonary embolism, patients may experience anginal chest pain and syncope. Adventitious breath sounds may include inspiratory crackles, expiratory wheezing, and pleural rub. Typical arterial blood gases display hypoxemia, hyperventilation, and acute respiratory alkalosis, although some patients may have normal blood gas values. Plasma D-dimer level is elevated in most patients.11 Chest imaging may reveal atelectasis, pleural effusion, and pulmonary infiltrates, although the chest x-ray may be normal.11 A web-shaped infiltrate without air bronchograms in the peripheral lung field (Hampton hump) or decreased vascularity (i.e., Westermark sign) are sometimes seen with pulmonary infarction.11,29 CT angiography provides excellent visualization of the pulmonary artery and a negative CT scan excludes the diagnosis of pulmonary embolus.11,29 Echocardiography may be helpful in the diagnosis of pulmonary embolus in patients with hypotension or shock by allowing for the evaluation of thrombi in the right heart or pulmonary artery and indirectly confirming right ventricular dysfunction.11,29 Initial treatment of acute pulmonary embolus should include ensuring the patient is oxygenated and stable. Pulmonary embolism may cause hemodynamic instability and hypotension requiring vasopressor or inotropic drug administration. Patients in severe failure may require mechanical ventilatory support. Treatment of acute pulmonary embolus should include anticoagulant therapy (e.g., heparin or fondaparinux [Arixtra]) followed by warfarin therapy.11,29 In cases of hypotension, shock or right ventricular dysfunction, thrombolytic therapy with recombinant tissuetype plasminogen activator (rt-PA) should be considered.11,29 In cases of massive pulmonary embolus in which thrombolytic therapy is contraindicated, surgical removal may be considered.11 Patients at high risk of developing venous thromboembolism include those who are expected to be immobilized for several days (e.g., following major surgery) and

patients with a previous venous thromboembolism. Prevention of venous thromboembolism in high-risk patients may include prophylactic anticoagulant therapy (e.g., heparin, rivaroxaban [Xarelto]) and intermittent pneumatic compression of the lower legs.

Neurologic and Neuromuscular Disease Neurologic disorders, such as stroke, head trauma, spinal cord injury, central nervous system tumor, meningitis, or encephalitis may cause or precipitate the development of respiratory failure.66 Neuromuscular disease may impair neuromuscular transmission to the ventilatory muscles and result in muscle weakness, which may be acute, chronic, intermittent or progressive.66 Examples of neuromuscular diseases that may cause respiratory failure include certain genetic disorders (e.g., Duchenne muscular dystrophy), degenerative disorders (e.g., ALS), and autoimmune diseases (e.g., Guillain-Barré syndrome, multiple sclerosis [MS], and myasthenia gravis).66 Cerebral vascular diseases that may cause or precipitate the development of respiratory failure include ischemic stroke, cerebral infarction, cerebrovascular hemorrhage, cerebrovascular thrombosis, hypertensive encephalopathy, and cerebral vascular aneurysm.66 Spinal cord injury with damage to one or both of the phrenic nerves at the level of C3 to C5 may result in paralysis of the right, left, or both hemidiaphragms, resulting in respiratory failure. Infectious diseases that may cause respiratory failure include bacterial meningitis, encephalitis, polio, and Clostridium infection (e.g., tetanus and botulism). Coma is a neurologic disorder often seen in the ICU in which the patient is unresponsive, even with vigorous stimulation. Coma may be caused by a large number of conditions including meningitis, encephalitis, sedative or narcotic drug overdose, hypo-/hyperglycemia, hypo-/hypernatremia, hypercalcemia, hepatic or uremic encephalopathy, and brainstem ischemia.67 Severe hypoxia, carbon monoxide poisoning, methemoglobinemia, and cyanide poisoning may also cause coma. Other causes of coma include disseminated intravascular coagulopathy (DIC), sepsis, and pancreatitis.67 Coma is not uncommon after resuscitation following cardiac arrest. Comatose patients are at risk for aspiration and soft tissue airway obstruction requiring endotracheal intubation for maintenance and protection of the airway. Comatose patients may also require mechanical ventilatory support due to

apnea or hypoventilation. Severe brain injury can result in a coma-like vegetative state known as unresponsive wakefulness syndrome.67 Such patients may require tracheotomy is in order to secure their airway and manage secretions; the most common cause of death in these patients is pneumonia.66,67 Brain death refers to irreversible cessation of brain function, often associated with an episode of acute, severe hypoxia. Criteria for establishing brain death includes apnea, unreactive pupils, absent reflex eye movements, and unresponsiveness to sensory stimuli including pain.66,67 Neuromuscular diseases impair neuromuscular function and may result in loss of ventilatory muscle strength, absent or ineffective cough, problems with airway protection, and the development of acute respiratory failure.68−71 Certain neuromuscular diseases directly affect muscle contraction. These include muscular dystrophies (e.g., Duchenne muscular dystrophy, myotonic dystrophy) and myopathies (e.g., critical illness myopathy, rhabdomyolysis, and polymyositis).68 For example, Duchenne muscular dystrophy is an inherited (genetic) disease resulting in muscle weakness beginning at age 2 or 3 and progressively worsening as the child grows older, often resulting in wheelchair confinement by the time the child is 12 years old.68 Respiratory care in these patients should be staged, based on specific criteria including vital capacity.68 Initially, volume recruitment and use of mechanical insufflation-exsufflation to assist cough may suffice. As the patient’s condition declines, nocturnal noninvasive ventilation may be needed.68 Further decline may lead to daytime noninvasive ventilation.68 Eventually, the patient may require tracheostomy and invasive ventilation.68 Respiratory failure is the most common cause of death, although with improvements in respiratory and cardiac care, patients may survive into their 30s and older.68 Critical illness myopathy causes muscle weakness and is associated with corticosteroid administration, use of neuromuscular blocking agents, hyperglycemia, hyperthyroidism, and systemic inflammatory response; weaning such patients from mechanical ventilation may be delayed.69 Critical illness polyneuropathy is specifically associated with severe sepsis, and may persist for years, although some patients do recover over time.69 Some neuromuscular diseases affect the neuromuscular junction, decreasing the transmission of nerve impulses to the peripheral muscles. Examples include

myasthenia gravis, Lambert-Eaton syndrome, tetanus, botulism, and organophosphate poisoning.69 Other neuromuscular diseases, such as GuillainBarré syndrome, affect the peripheral nerves resulting in paralysis.69 Guillain-Barré syndrome causes progressive (often, but not always ascending) muscle weakness and flaccid paralysis of the arms and legs; involvement of the diaphragm may occur requiring mechanical ventilatory support in up to 30% of cases.69 Patients with Guillain-Barré should be monitored frequently for impending respiratory failure by measurement of spontaneous vital capacity (VC), maximum inspiratory pressure (MIP), and maximum expiratory pressure (MEP). Institution of mechanical ventilation should be considered in the presence of respiratory distress, concerns regarding airway patency, and a reduction in bedside pulmonary function values (e.g., VC < 20 mL/kg, MIP > –30 cm H2O, and MEP < 40 cm H2O). Signs of significant bulbar weakness (i.e., impairment of the upper airway muscles) may also indicate the need for intubation and the institution of mechanical ventilatory support. Guillain-Barré is typically self-limiting and patients requiring mechanical ventilation can be weaned when the vital capacity and maximum inspiratory pressure (MIP) return to acceptable values.69 In addition to supportive care, intravenous gammaglobin or plasmapheresis may be helpful.69 Most patients begin to recover after about 4 weeks following disease onset and generally recover with little or no continuing disability.69 Myasthenia gravis and multiple sclerosis (MS) may cause relapsing, chronic respiratory muscle weakness.69−70 Myasthenia gravis is an autoimmune disease that generally improves with the administration of anticholinesterase medications (e.g., edrophonium [Tensilon], pyridostigmine [Mestinon], or neostigmine [Prostigmin]).70 Common symptoms include blurred vision, double vision, and droopy eyelids, although some patients present with difficulty swallowing (dyphagia), trouble speaking certain words (dysarthria), shortness of breath, or limb weakness.70 A myasthenic crisis represents a life-threatening neurological emergency and impending respiratory failure that occurs in 15% to 20% of patients.70 A myasthenic crisis may be precipitated by infection, surgery, excessive anticholinesterase medication administration, or worsening of the disease; intubation and mechanical ventilatory support may be required.70 Edrophonium (Tensilon) is a short-acting anticholinesterase medication. The “Tensilon test” has been used in the past to

assist in the diagnosis of myasthenia gravis and to discriminate between a myasthenic and a cholinergic crisis. With a myasthenic crisis, the patient should improve following administration of edrophonium. If, on the other hand, the patient’s condition worsens following the administration of edrophonium, a cholinergic crisis associated with over administration of anticholinesterase medications (e.g., pyridostigmine) may be present.70 The use of the Tensilon test is not recommended due to concerns regarding test reliability.72 Prednisone (Deltasone) may be helpful for short-term improvement of muscle weakness; long-term treatment may include immunosuppressive medications such as azathioprine (Imuran) and mycophenolate mofetil (CellCept).70,72 Plasmapheresis and intravenous immunoglobulin (IVIG) therapy are sometimes used for patients who do not respond to immunomodulating medications and in cases of myasthenic crisis with respiratory failure.70,72 Multiple sclerosis (MS) is also thought to be an autoimmune disorder; however, the exact cause is unknown. MS is a central nervous system disease that damages the myelin sheath of nerves and disrupts nerve transmission from the brain to the other parts of the body.71 While many patients experience only mild symptoms limited to muscle weakness in their extremities and difficulty with coordination and balance, some may have difficulty walking or standing and become wheelchair bound.71,73 Many patients with mild MS do not require additional therapy. In advanced cases, patients may be unable to write, speak, or walk and partial or complete paralysis may occur. Specific medications may be effective in reducing exacerbations and the progression of physical disability. However, patients with severe MS may require tracheotomy and intermittent or continuous mechanical ventilatory support.71,73 Amyotrophic lateral sclerosis (ALS, aka Lou Gehrig’s disease) is a chronic and relentlessly progressive motor neuron disease resulting in degeneration and death of motor neurons and progressive voluntary muscle weakness, which eventually leads to respiratory failure.69 Noninvasive ventilatory (NIV) support may be effective in prolonging life in patients with ALS, although mean survival time is generally only about 3 to 5 years after diagnosis.69

Neurologic Disease Caused by Infection or Bacterial Toxins Neurologic diseases caused by infection include encephalitis, meningitis, and

polio.66,70 Tetanus and botulism are caused by neurotoxins produced by certain gram-positive Clostridium bacteria. Encephalitis refers to inflammation of the brain parenchyma (i.e., brain tissue) resulting in neurologic dysfunction. Encephalitis is a relatively rare disease, usually caused by viral infection (e.g., enteroviruses, herpes simplex, and rabies virus), although encephalitis may be caused by bacteria, fungi, and parasites as well as noninfectious causes.74,75 Symptoms may include headache, fever, confusion, drowsiness, stiff neck and back, nausea, and vomiting. Encephalitis can be life threatening and result in muscle weakness, paralysis, loss of consciousness, unresponsiveness, stupor, coma, and seizures. Meningitis is inflammation of the meninges that cover the brain and spinal cord. Meningitis is most commonly caused by bacterial infection (e.g., Streptococcus pneumonia, Neisseria meningitides, Haemophilus influenza, and Borrelia burgdorferi [Lyme disease]), although viral, fungal, or parasitic infections may also cause meningitis.74,75 Noninfectious causes of meningitis include lupus, certain cancers, and traumatic injury. Pneumococcal meningitis (caused by S. pneumoniae) is the most common and serious form of bacterial meningitis in adults and is potentially fatal.74,75 Symptoms of bacterial meningitis in adults include severe headache, fever, nausea, vomiting, and light sensitivity. Confusion, delirium, decreased levels of consciousness, lethargy, seizures, and coma may occur. Critically ill patients require ICU admission and support of oxygenation, ventilation, and circulation. Treatment of encephalitis and meningitis includes therapy aimed at specific causes (e.g., viral, bacterial, fungal, and postinfectious encephalomyelitis), monitoring, and supportive care. In certain cases, anticonvulsants may be used to treat seizures, while corticosteroids may be helpful to reduce cerebral edema. For example, initial treatment of acute bacterial meningitis should include diagnostic lumbar puncture and blood cultures followed immediately by administration of dexamethasone and antimicrobial therapy.74,75 Poliomyelitis is caused by the poliovirus. While polio may cause paralysis requiring mechanical ventilation, the use of the polio vaccine has eliminated the disease in the United States and many other countries. Post-polio syndrome, however, can appear years after the initial infection and may cause tiredness, muscle weakness, and other neurologic symptoms.75 Botulism is caused by ingestion of food contaminated with Clostridium botulinum,

which produces the botulinim nerve toxin that causes paralysis.70,76 Botulism may also be caused by certain strains of C. butyricum and C. baratii. Although rare, botulism is a potentially fatal disease that causes visual disturbances, difficulty swallowing, and muscle weakness.70,76 If untreated, botulism may progress to muscle paralysis and ventilatory failure. In addition to foodborne botulism, wound infection may cause wound botulism, which is sometimes associated with IV drug abuse.76 Infants (and rarely adults) may consume botulinum bacterial spores, which then produce the toxin in the intestines resulting in infant botulism (or adult intestinal botulism in adult cases).76 Treatment of botulism includes supportive care and administration of antitoxin. Vomiting may be induced and/or enemas given in an attempt to clear contaminated food from the gut.76 Wound infection may be treated surgically followed by administration of antibiotics.76 Severe botulism may cause paralysis and ventilatory failure requiring ICU admission, intensive care, and mechanical ventilatory support for weeks or even months.76 Tetanus (aka lockjaw) is caused by bacterial spore infection (C. tetani spores), which upon incubation produce a toxin that results in uncontrolled skeletal muscle contractions.77 Wound contamination with tetanus spores in dirt, feces, or saliva, puncture wounds, burns, and crush injuries may all cause tetanus infection.77 Neonatal tetanus may be caused by umbilical stump infection.77 The incubation period for spore germination varies, depending on the type and site of the wound, with an average incubation of about 10 days.77 Toxins produced interfere with the release of neurotransmitters and affect the brain, spinal cord, and sympathetic nervous system.77 Uncontrolled muscle contractions follow, especially in jaw, neck, and to lesser extent the abdominal muscles; seizures may also occur. Other symptoms include abdominal rigidity, generalized muscle spasms, and hypersensitivity to sensory stimuli. Severe tetanus infection is a life-threatening medical emergency requiring ICU admission, immediate administration of human tetanus immunoglobulin (or equine tetanus antitoxin), airway maintenance, and (if needed) mechanical ventilatory support.77 Antibiotics, administration of the tetanus toxoid vaccinee, sedation, and muscle relaxants to control muscle spasms and aggressive wound care should be implemented.

Ventilatory Support in Patients with Neurologic or Neuromuscular Disease

Bedside assessment of respiratory muscle strength and spontaneous breathing should be performed in the evaluation of neuromuscular disease patients and mechanical ventilatory support provided when ventilatory failure appears to be inevitable (i.e., impending ventilatory failure; see Assessment of Ventilation above). Noninvasive mechanical ventilatory support may be considered in patients who do not require emergent intubation. Patients in whom noninvasive ventilation is contraindicated, and those requiring intubation for protection or maintenance of the airway, should receive conventional invasive mechanical ventilation. Initiation of invasive mechanical ventilation in patients with neurologic or neuromuscular disease can be typically accomplished by use of a volume control mode (assistant–control [A/C] or SIMV) with an initial tidal volume of approximately 8 mL/kg of ideal (predicted) body weight, a respiratory rate of 12 to 16 breaths/min, and a resultant minute ventilation of approximately 100 mL per kg of IBW per minute.65 Initial inspiratory peak flow may be set at 60 to 80 L/min with a decelerating (down ramp) flow waveform to achieve an I:E ratio of 1:2 or better. Initial ventilator sensitivity may set at –0.5 to –1.5 cm H2O (pressure trigger) or 1 to 2 L/min (flow trigger) and adjusted to ensure minimal trigger effort without autocycling. Pressure support starting at 5 cm H2O may be added when using SIMV in order to reduce the work of breathing during spontaneous breaths. Initial oxygen concentration is selected based on the patient’s condition, and previous blood gas or oximetry results. If little is known about the patient or the patient’s condition is grave, the initial oxygen concentration can be set at 100%. Initial PEEP is typically set at 0 to 5 cm H2O and PEEP and FIO2 are adjusted to achieve the lowest FIO2 that results in adequate arterial oxygenation (e.g., SpO2 > 90%, PaO2 > 60 mmHg). Patients with neuromuscular disease, head trauma, or spinal cord injury may have otherwise normal lungs. These patients may require only low to moderate concentrations of oxygen and may benefit from the use of slightly larger tidal volumes (e.g., 8 to 10 mL/kg) with PEEP (5 cm H2O) in order to prevent the development of atelectasis.65 Ventilator settings are then adjusted to ensure patientventilator synchrony, reduce the work of breathing, and achieve adequate oxygenation and ventilation while ensuring Pplateau ≤ 30 cm H2O. Patients with concurrent acute restrictive pulmonary disease (e.g., ARDS, pneumonia) may require a lung-protective ventilatory strategy (see Acute Respiratory Distress

Syndrome above). Certain patients (e.g., bacterial meningitis, cerebral edema, and intracranial hemorrhage) with dangerously elevated intracranial pressure may be briefly hyperventilated in order to achieve a PaCO2 between 26 and 30 mmHg in order to produce cerebral vasoconstriction and reduce ICP.65 Hyperventilation is not recommended for patients with stroke or traumatic brain injury, as it may reduce local cerebral perfusion.78

Postoperative Patients Some postoperative surgical patients may require a period of mechanical ventilatory support following general anesthesia and major surgery. Strategies for mechanical ventilation of the postoperative patient will vary depending on the patient’s condition and type of surgery performed. For example, many otherwise healthy patients may be extubated in the operating room. Patients with upper abdominal or thoracic surgery, however, are more likely to suffer postoperative pulmonary complications, including the possible development of acute respiratory failure. Postoperative heart surgery patients are often ventilated overnight following surgery, although some centers now have implemented early extubation protocols following heart surgery. Patients who have undergone a long intraoperative procedure, received heavy sedation and/or paralytic drugs, and those with chronic illnesses (e.g., COPD, cardiac disease) may need continued intubation for protection of the airway and a period of postoperative mechanical ventilatory support. Similarly, patients who undergo extensive oropharyngeal surgery often remain intubated until airway edema subsides. ICU patients who are critically ill prior to surgery may be returned to the intensive care unit directly from the operating room. Ventilation strategies for postoperative patients will vary depending on the patient’s condition. For example, a lung protective strategy may be required for patients with reduced pulmonary compliance (e.g., ARDS) while patients with normal lungs may be ventilated with slightly larger tidal volumes. Mechanical ventilation, especially with PEEP, increases mean pulmonary and intrathoracic pressures, and may reduce venous return; strategies to ensure adequate cardiac output may be needed.

Summary Respiratory failure can be life threatening, and the respiratory care clinician must be able to promptly recognize respiratory failure and take appropriate action. Common causes of hypoxemic respiratory failure include atelectasis, pneumonia, and pulmonary edema. ARDS is a special case of acute respiratory failure characterized by severe problems with oxygenation. The oxygenation process requires adequate arterial blood oxygen content and sufficient oxygen delivery to the tissues. Common causes of decreased arterial oxygen content include diminished inspired oxygen, lung disease (e.g., V̇/Q̇ mismatch, capillary shunt, and diffusion defect), cardiovascular right-to-left shunt, hypoventilation, and hemoglobin problems (e.g., anemia, carboxyhemoglobinemia). Oxygen delivery may also be reduced because of decreased cardiac output and reduced tissue perfusion. Disordered regional tissue perfusion may result in tissue hypoxia. Last, cellular oxygen uptake and utilization must be effective. Assessment of ventilation may begin with a review of the patient’s history and physical, being on the alert for the clinical manifestations of ventilatory failure. Bedside measures of pulmonary function are sometimes used to assess the patient’s readiness for discontinuance of mechanical ventilatory support. These include spontaneous tidal volume, respiratory rate, minute ventilation, rapid, shallow breathing index, vital capacity and measures of ventilatory muscle strength, workload, and respiratory drive. Clinically, however, the single best index of effective ventilation is measurement of PaCO2. Common disease states or conditions that may cause or precipitate the development of acute respiratory failure include acute asthma, exacerbation of COPD, pneumonia, ARDS, shock, trauma, sepsis, cardiac or cardiovascular disease, neurologic or neuromuscular disease, and other specific problems requiring specialized medical and/or surgical care.

Key Points A major focus of critical respiratory care is the treatment and support of patients in respiratory failure. Respiratory failure is broadly defined as an inability of the heart and lungs to provide adequate tissue oxygenation and or carbon dioxide removal. Acute respiratory failure is defined as a sudden decrease in arterial oxygenation with or without carbon dioxide retention. Hypoxemic respiratory failure, also known as “lung failure,” refers to a primary problem with arterial oxygenation. Hypercapnic respiratory failure, also known as “pump failure” or “ventilatory failure,” refers to a primary problem with ventilation. Acute ventilatory failure is defined as a sudden increase in arterial PaCO2 with a corresponding decrease in pH. Chronic ventilatory failure is defined as a chronically elevated PaCO2, with a normal or near-normal pH due to metabolic compensation. Acute ventilatory failure superimposed on chronic ventilatory failure is sometimes seen in patients with acute exacerbation of chronic lung disease. Impending ventilatory failure is a category in which hypoventilation and hypercapnea are not yet present but are likely to occur in the immediate future if no action is taken. Mechanical ventilation supports or replaces the normal ventilatory pump, and the primary indication for mechanical ventilation is inadequate or absent spontaneous breathing. Specific indications for mechanical ventilation are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. Altitude hypoxia is caused by reduced barometric pressure at altitude. High-altitude illness may affect hikers, skiers, mountain climbers, or other travelers to high-altitude locations. Potentially life-threatening types of high altitude illness include high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). Individuals with lung disease may experience hypoxemia when flying in commercial aircraft due to the normally reduced barometric pressure in the cabin. Problems with the conducting airways that may impair oxygenation and/or ventilation include airway obstruction, increased secretions, airway mucosal edema, and bronchospasm. Hyperventilation can result in a small improvement in arterial oxygenation, while hypoventilation can significantly reduce arterial oxygen levels. The most common causes of reduced oxygen transfer across the lung are hypoventilation, ventilation-perfusion mismatch (low V̇/Q̇ and right-to-left shunt),

and diffusion limitations. Common causes of low V̇/Q̇ in the lung include asthma, emphysema, chronic bronchitis, bronchiectasis, cystic fibrosis, COPD, bronchospasm, mucosal edema, retained secretions, and regional increases in fibrotic lung tissue. Causes of increased capillary shunt in the lung include ARDS, atelectasis, complete airway obstruction, consolidative pneumonia, large pneumothorax, and pulmonary edema. Patients with hypoxemia due to underventilation with respect to perfusion (low V̇/Q̇) often respond well to the administration of low to moderate concentrations of oxygen, while those with significant shunt do not. Patients with hypoxemia due to significant capillary shunt may require moderate to high oxygen concentrations, PEEP, CPAP, and/or mechanical ventilatory support. Large anatomic shunts (e.g., cardiac septal defects) may cause severe hypoxemia, which is refractory to oxygen administration. In patients breathing room air, mild, moderate, moderately severe, and severe hypoxemia are defined as a PaO2 of < 80 mmHg, < 60 mmHg, < 50 mmHg, and < 40 mmHg, respectively. The arterial blood oxygen content is determined by the hemoglobin level, arterial oxygen saturation, and PO2. Anemic hypoxia refers to a significant decrease in arterial blood oxygen content due to low hemoglobin or hemoglobin dysfunction (e.g., increased carboxyhemoglobin, methemoglobinemia). Patients with severe anemia may experience profound hypoxia without cyanosis. Acute chest syndrome is a complication of sickle cell disease associated with chest pain, hypoxemia, and pulmonary infiltrates on imaging. Secondary polycythemia is often a response to chronic hypoxemia, living at high altitude, or chronic exposure to carbon monoxide. Carbon monoxide poisoning may be caused by exposure to improperly functioning heating systems, exhaust from motor vehicles or gas-powered generators in poorly ventilated spaces, and inhalation of smoke from fires. Severe carbon monoxide poisoning may cause unconsciousness, seizures, cardiopulmonary collapse, and death. Increased HbCO is not detectable by standard pulse oximetry and requires cooximetry, which may not be included with routine blood gases. Treatment of carbon monoxide poisoning includes administration of high concentrations of oxygen. In severe cases, hyperbaric oxygen administration may be indicated. Methemoglobinemia can be caused by certain antibiotics, local anesthetics, inhaled nitric oxide, and certain chemicals. High levels of methemoglobin can

cause respiratory depression, unconsciousness, shock, seizures, and death. Oxygen delivery to the tissues can be calculated by multiplying arterial oxygen content times cardiac output. Reduced cardiac output is a sometimes overlooked cause of tissue hypoxia due to inadequate circulation (aka circulatory hypoxia). Common causes of reduced cardiac output seen in the ICU include ischemic heart disease, MI, cardiac arrhythmias, congestive heart failure, hypovolemia, and late septic shock. Shock is caused by circulatory failure resulting in decreased oxygen delivery to the tissues and causing cellular and tissue hypoxia. Shock may be an overlooked cause of tissue hypoxia due to inadequate circulation (aka circulatory hypoxia). Cardiogenic shock is caused by low cardiac output, while hypovolemic shock is caused by inadequate intravascular volume due to blood or fluid loss. Septic shock, neurogenic shock, and anaphylactic shock are all forms of distributive shock in which inappropriate peripheral vasodilation results in decreased systemic vascular resistance and low blood pressure. Extreme left shifts in the oxyhemoglobin dissociation curve due to severe alkalosis, marked hyperventilation, hypothermia, or carbon monoxide poisoning may interfere with unloading of oxygen from the hemoglobin at the tissue level. Normal tissue oxygen delivery is about 1000 mL/min, normal tissue oxygen consumption is about 250 mL/min, and normal tissue oxygen extraction is about 25% of the oxygen delivered to the tissues by the arterial blood. Cyanide poisoning may be caused by cyanide produced in domestic fires, certain industrial processes, or certain medical treatments. Clinical manifestations of cyanide poisoning include headache, anxiety, confusion, vertigo, coma, seizures, vomiting, abdominal pain, and renal failure. Cyanide poisoning causes histotoxic hypoxia in which tissue oxygen utilization is blocked. Treatment may include administration of cyanide antidotes, high concentration of oxygen therapy, intubation to secure the airway, and mechanical ventilatory support. Decreased mixed venous oxygen levels can be caused by arterial hypoxemia, decreased cardiac output, or increased oxygen consumption. Ventilation is simply the bulk movement of gas into and out of the lungs. Bedside spirometry is sometimes used in the ICU to assess the adequacy of ventilation by measuring the patient’s spontaneous tidal volume, respiratory rate, and minute ventilation. Other bedside measures sometimes used to assess the adequacy of spontaneous ventilation include measurement of vital capacity (VC), maximum voluntary ventilation (MVV), maximum inspiratory pressure (MIP), and calculation of the rapid, shallow breathing index (RSBI).

Alveolar ventilation is simply tidal volume minus dead space times respiratory rate. Emphysema or pulmonary embolus may increase alveolar dead space. The single best index of alveolar ventilation in the clinical setting is measurement of arterial PCO2. Arterial PCO2 is inversely proportional to alveolar ventilation and directly proportional to carbon dioxide production. Carbon dioxide production is determined by metabolic rate and diet. Arterial blood gas studies are especially useful in evaluating the degree of hypoxemia, as well as the presence of a metabolic or respiratory acidosis or alkalosis. Causes of respiratory acidosis include increased work of breathing resulting in decreased ventilation, decreased respiratory drive, and neurologic or neuromuscular disease resulting in decreased ventilation. Causes of respiratory alkalosis include hypoxemia, pain, anxiety, fever, early sepsis, lung receptor stimulation, and in compensation for metabolic acidosis. Causes of a normal anion gap metabolic acidosis include loss of HCO3−, failure to reabsorb HCO3−, or ingestion of certain substances. Causes of an increased anion gap metabolic acidosis include ingestion of acids, increased fixed acid production, or decreased renal excretion of acid. Causes of metabolic alkalosis include gastrointestinal tract loss of hydrogen ions, renal loss of hydrogen ions, intracellular shift of hydrogen ions, contraction of blood volume, and administration of base. Assessment of the respiratory failure patient’s cardiac and circulatory status includes noting specific cardiac and cardiovascular related findings on history, physical examination, and diagnostic testing. Assessment of the respiratory failure patient’s cognitive and neurologic status includes observation for common neurologic symptoms seen in the ICU, neurologic physical assessment, and use of specific tools such as the Glasgow Coma Scale and Behavioral Pain Scale. Patients in the ICU with respiratory failure requiring nutritional assessment may be experiencing a catabolic stress state, systemic inflammatory response, infection, multisystem organ failure, and increased morbidity and mortality associated with critical illness. Nutritional support in critically ill patients entails the delivery of calories, protein, electrolytes, vitamins, minerals, trace elements, and fluids. Enteral nutrition is given through a tube into the stomach or small bowel; parenteral nutrition is supplied intravenously. Scoring tools available in the ICU to predict patient outcomes include the APACHE, SAPS, and SOFA. Patients may experience respiratory failure due to acute asthma exacerbation,

acute exacerbation of COPD, pneumonia, ARDS, shock, trauma, sepsis, cardiac or cardiovascular disease, neurologic or neuromuscular disease, or other specific problems requiring specialized medical and/or surgical care.

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50. Siegel MD. Acute respiratory distress syndrome: Prognosis and outcomes in adults. In: Parsons PE, Finlay G (eds.). UpToDate. December 2016. 51. Yancy CW, Su M, Bozkurt B, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive summary. ACCF/AHA Practice Guideline. Circulation. 2013;128:1810–1852. 52. Gaglianello NA, Mahr C, Benjamin IJ. Heart failure and cardiomyopathy. In: Benjamin IJ, Griggs RC, Wings EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine 9th ed. Philadelphia, PA: ElsevierSaunders; 2016:55–66. 53. Colucci WS. Overview of the therapy of heart failure with reduced ejection fraction. In: Gottlieb SS, Yeon SB (eds.). UpToDate. December 2016. 54. Colucci WS. Treatment of acute decompensated heart failure: Components of therapy. In: Gottlieb SS, Hoekstra J, Yeon SB (eds.). UpToDate. December 2016. 55. Cinquegrani MP. Coronary heart disease. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:87–109. 56. Reeder GS, Kennedy HL. Overview of the acute management of ST elevation myocardial infarction. In: Cannon CP, Hoekstra J, Saperia GM (eds.). UpToDate. December 2016. 57. Breall JA, Aroesty JM, Simons M. Overview of the acute management of unstable angina and non-ST elevation myocardial infarction. In: Cannon CP, Hoekstra J, Cutlip D, Saperia GM (eds.). UpToDate. December 2016. 58. Gaieski DF, Mikkelsen ME. Definition, classification, etiology, and pathophysiology of shock in adults. In: Parsons PE, Finlay G (eds.). UpToDate. December 2016. 59. MedlinePlus. Cardiogenic shock. Bethesda, MD: National Library of Medicine; May 5, 2016. Available at https://medlineplus.gov/ency/article/000185.htm. Accessed January 27, 2017. 60. Podrid PJ, Ganz LI. Role of antiarrhythmic drugs for ventricular arrhythmias in patients with a prior myocardial infarction. In: Gersh BJ, Downey BC (eds.). UpToDate. December 2016. 61. MedlinePlus. Hypovolemic shock. Bethesda, MD: National Library of Medicine; October 16, 2017. Available at https://medlineplus.gov/ency/article/000167.htm. Accessed January 27, 2017. 62. Schmidt GA, Mandel J. Evaluation and management of suspected sepsis and septic shock in adults. In: Parsons PE, Sexton DJ, Hockberger RS, Finlay G (eds.). UpToDate. December 2016. 63. Raja A, Zane RD. Initial management of trauma in adults. In: Moreira ME, Grayzel J (eds.). UpToDate. December 2016. 64. Hemphill III JC, Phan N. Management of acute severe traumatic brain injury. In: Aminoff MJ, Moreira ME, Wilterdink JL (eds.). UpToDate. December 2016. 65. Hou P, Baez AA. Mechanical ventilation of adults in the emergency department. In: Walls RM, Grayzel J (eds.). UpToDate. December 2016. 66. Marshall FJ. Neurologic evaluation of the patient. In: Benjamin IJ, Griggs RC, Wings EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:960–964. 67. Chmayssani M, Vespa PM. Disorders of consciousness. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:965–970. 68. Darras BT. Clinical features and diagnosis of Duchenne and Becker muscular dystrophy. In: Patterson MC, Firth HV, Dashe JF (eds.). UpToDate. December 2016. 69. Jackson CE. Neuromuscular diseases: Disorders of the motor neuron and plexus and peripheral nerve disease. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:1077–1086. 70. Ciafaloni E. Neuromuscular junction disease. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:1098– 1101. 71. Cross AH. Demyelinating and inflammatory disorders. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016:1069–1076. 72. Bird SJ. Treatment of myasthenia gravis. In: Shefner JM, Targoff IN, Dashe JF (eds.). UpToDate. December 2016. 73. National Institute of Neurological Disorders and Stroke (NINDS). Multiple sclerosis. Available at https://www.ninds.nih.gov/Disorders/All-Disorders/Multiple-Sclerosis-Information-Page. Accessed January

27, 2017. 74. Tunkel AR, Janvier MA, Nath A. Infections of the head and neck. In: Benjamin IJ, Griggs RC, Wing EJ, Fitz JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: ElsevierSaunders; 2016:853-866. 75. National Institute of Neurological Disorders and Stroke (NINDS). Meningitis and encephalitis. Available at https://www.ninds.nih.gov/Disorders/All-Disorders/Meningitis-and-Encephalitis-Information-Page. Accessed January 27, 2017. 76. Centers for Disease Control and Prevention (CDC). Botulism. Available at https://www.cdc.gov/botulism/. Accessed January 27, 2017. 77. Centers for Disease Control and Prevention (CDC). Tetanus. Available at https://www.cdc.gov/tetanus/clinicians.html. Accessed January 27, 2017. 78. Smith ER, Amin-Hanjani S. Evaluation and management of elevated intracranial pressure in adults. In: Aminoff MJ, Wilterdink JL (eds.). UpToDate. December 2016.

CHAPTER

3 Principles of Mechanical Ventilation Gregory A. Holt, Sheila A Habib, and David C. Shelledy

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction to Mechanical Ventilation Ventilation Spontaneous Breathing Negative Pressure Breathing Positive Pressure Breathing Invasive Versus Noninvasive Ventilation Ventilator Principles Input Power and Control Systems Ventilator Variables: Breath Trigger Ventilator Variables: Breath Cycle Operator Interface Ventilator Classification or Taxonomy Ventilator Modes Continuous Mandatory Ventilation Intermittent Mandatory Ventilation Positive End-Expiratory Pressure Continuous Positive Airway Pressure Pressure Support Ventilation Airway Pressure Release Ventilation Automatic Tube Compensation Proportional Assist Ventilation Dual Modes and Adaptive Control High-Frequency Ventilation Neurally Adjusted Ventilatory Assist Ventilator Parameters

Flow Waveforms Inspiratory Pause FIO2 PEEP/CPAP Alarms Humidification Sigh Breaths Effects of Mechanical Ventilation on Organ Systems Pulmonary System Cardiovascular System Renal System Gastrointestinal System Central Nervous System Complications of Mechanical Ventilation Pulmonary Extrapulmonary Organ Systems

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30.

Summarize the history of events that led to modern mechanical ventilation. Contrast the differences between positive and negative pressure ventilation. Recognize differences in patient interface when considering invasive and noninvasive mechanical ventilation. Define the timing points that constitute a breath and calculate the respiratory rate from TI and TE. Describe alveolar and dead space ventilation and calculate V̇E and V̇A. Interpret changes in volume, airflow, and alveolar and intrapleural pressure over the course of a single breath. Describe the differences between an iron lung and a chest cuirass. Identify the components of a ventilator circuit and the mechanical events during lung inflation and deflation during delivery of a positive pressure breath. Describe the effects of alterations in lung mechanics (CST and RAW) on volume and pressure in volume and pressure-control modes. Predict changes in peak inspiratory pressure and plateau pressure when either CST or RAW are altered. Define PEEP and describe its influence on gas exchange and hemodynamics. Describe the variables of interest in an optimal PEEP study. Define pressure support ventilation (PSV) and describe its influence on the work of breathing (WOB). Define CPAP, BiPAP, AutoPAP, ASV, CFLEX, EPR, IPAP, and EPAP. Describe patient scenarios that will lead to increased mean airway and peak inspiratory pressures. Describe the variables that can be trigger inspiration during mechanical ventilation. Describe the variables that can cycle a breath from inspiration to expiration. Contrast the differences between PC-AC and VC-AC. Contrast the differences between PC-IMV and VC-IMV. Describe the rationale for prone positioning ARDS patients. Describe lung protective strategies for mechanical ventilation. Define APRV and compare this mode to BiPAP. Describe the use of automatic tube compensation (ATC). Define PAV and describe its use. Identify dual modes of ventilation. Define PRVC and VAPS. Describe each of the four types of high-frequency ventilation (HFV). Contrast the trigger variable used in NAVA to conventional mechanical ventilation. Describe inspiratory flow waveforms used in mechanical ventilation. Determine the ventilator variables that affect PaO2, pH, and PaCO2.

31. 32. 33. 34. 35. 36. 37. 38. 39.

Identify the alarms that require clinician adjustment and the levels of priority assigned. Describe the rationale for a sigh breath. Explain the effects of positive pressure ventilation on the lung. Explain the effects of positive pressure ventilation on the cardiac/cardiovascular system. Describe the central nervous system (CNS), renal, and gastrointestinal effects of positive pressure ventilation. Explain the importance of appropriate sedation protocols during weaning from mechanical ventilation. Describe the influence of PaCO2 on intracranial pressure (ICP). Identify the effects of sleep disruption on the ICU patient. List the complications of mechanical ventilation and explain each.

KEY TERMS acidosis acute lung injury (ALI) acute respiratory distress syndrome (ARDS) afterload airway pressure release ventilation (APRV) airway resistance (RAW) alkalosis alveolar volume amyotrophic lateral sclerosis (ALS) assist control (A/C) atelectotrauma atrial natriuretic peptide (ANP) automatic positive airway pressure (autoPAP) automatic servo ventilation (autoSV) automatic tube compensation (ATC) autoPEEP bilevel positive airway pressure (BiPAP) breath cycle breath trigger continuous positive airway pressure (CPAP) dead space volume (VD) expiratory positive airway pressure (EPAP) expiratory time (TE) extrinsic PEEP flow cycle flow-time scalar fraction of inspired oxygen (FIO2) high-frequency jet ventilation (HFJV) high-frequency oscillatory ventilation (HFOV) high-frequency percussive ventilation (HFPV) high-frequency positive pressure ventilation (HFPPV) hyperventilation hypoventilation inspiratory positive airway pressure (IPAP) inspiratory time (TI) inspiratory to expiratory ratio (I:E) intracranial pressure (ICP) intrinsic PEEP iron lung lung compliance (CL)

mean airway pressure (MAP) minute alveolar volume minute ventilation (V̇E) negative pressure ventilation neurally adjusted ventilatory assist (NAVA) noninvasive positive pressure ventilation (NPPV) oxygen content in arterial blood (CaO2) oxygen content in mixed venous blood (CV̄O2) oxygen delivery (ḊO2) oxygen saturation in arterial blood (SaO2) oxygen saturation in mixed venous blood (Sv–O2) partial pressure of alveolar oxygen (PaO2) partial pressure of arterial oxygen (PaO2) partial pressure of mixed venous oxygen (Pv̄O2) peak airway pressure (PAW) peak inspiratory pressure (PIP) plateau pressure (Pplateau) positive end-expiratory pressure (PEEP) positive pressure ventilation preload pressure control (PC) pressure-regulated volume control (PRVC) pressure support ventilation (PSV) pressure–time scalar proportional assist ventilation (PAV) pulmonary vascular resistance (PVR) synchronized intermittent mandatory ventilation (SIMV) tidal volume (VT) time cycling total cycle time (Ttot) transmural wall pressure ventilator-associated lung injury (VALI) ventilator-associated pneumonia (VAP) ventilator-induced lung injury (VILI) ventilator mode volume-assured pressure support (VAPS) volume control (VC) volume of carbon dioxide production (V̇CO2) volume of oxygen uptake (V̇O2) volume support (VS) volutrauma work of breathing (WOB)

Introduction to Mechanical Ventilation The development of respiratory care progressed through history from Galen’s observations on the respiratory and circulatory systems in the 2nd century to the early 20th century, when great strides in pulmonary physiology were made. The Drinker Respirator, which provided negative pressure ventilation, was introduced in 1928, and a commercial version of this “iron lung” was offered by John Emerson in 1932. In the 1940s and 1950s, polio epidemics were sweeping across Europe and the United States. Worldwide, 500,000 people per year were either paralyzed or had died from the disease.1 These negative pressure ventilators were sometimes employed in large halls dedicated to providing support to polio victims (Figure 3-1). The iron lung did not require an artificial airway and was simple and easy to use. Problems included difficulty with patient access, patient immobility, and large and bulky equipment.

FIGURE 3-1 The Iron Lung in Use During the Polio Epidemic. ©Dennis MacDonald/age fotostock / Alamy Stock Photo; BOTTOM: ©Science History Images / Alamy Stock Photo.

In 1952, a polio outbreak in Copenhagen (following a 1951 international convention on polio) resulted in 50 new admissions every day and an 87% mortality rate. Medical students were called upon, and nearly 1500 provided manual bagmask positive pressure ventilation totaling 165,000 hours with a drop in mortality to approximately 25%.2 The development of the modern intensive care unit (ICU) providing mechanical ventilatory support can be traced directly to the impact of this single disease, polio. The use of positive pressure ventilation grew along a similar timeline and rapidly became the predominant form of ventilatory support in use. Patient-triggered, pressure-cycled ventilators (e.g., Bird respirators) and flow-sensitive breathing valves (e.g., the Bennett valve) based on technology developed during World War II

were further developed in the 1950s and 1960s (Figure 3-2). Volume ventilators began to become available, first as time-triggered devices, and later with patienttriggered options. Space requirements and patient access were obvious advantages of these new ventilators over the “iron lung.” The volume ventilators of the 1960s and early 1970s allowed clinicians to set a precise tidal volume (VT) and backup respiratory rate to guarantee a minimum minute ventilation. It took longer to understand the mechanisms of ventilator-induced lung injury and the balance between atelectasis, pulmonary overdistension, and barotrauma. The mechanisms of ventilator-induced lung injury (VILI) are due, in part, to the release of cellular inflammatory mediators associated with the use of large tidal volumes and pressures. This has led to a reduction in applied tidal volumes from 10 to 15 mL/kg used since the mid-1970s to the 4 to 8 mL/kg currently employed.3,4 Additional methods to reduce ventilator-associated lung injury include appropriate application of positive end-expiratory pressure (PEEP), lung recruitment strategies, permissive hypercapnia, the introduction of newer modes of pressure limited ventilation, and the addition of noninvasive ventilation (NIV) to the decision tree for respiratorycompromised patients.



FIGURE 3-2 Bird and Bennett Pressure Respirators. The Bennett PR-2 was time or patient triggered to inspiration, pressure limited, and flow cycled to expiration. The Bird Mark 7 was time or patient triggered to inspiration and pressure cycled to expiration.

The mechanical ventilator of the 21st century employs sophisticated technology to detect and shape the breath with sensitivity and responsiveness providing clinicians with a myriad of control features. The goal of mechanical ventilation continues to be support of the oxygenation and ventilation of patients in respiratory failure. The resolution of the underlying disease process, the anticipated timing of resolution, and the expected outcomes guide the type of mechanical ventilation and delivery interface selected. For example, a patient with an acute exacerbation of congestive heart failure (CHF) may benefit from noninvasive positive pressure ventilation (NPPV) via full face mask until pharmacologic agents have had a chance to produce favorable outcomes. A patient with amyotrophic lateral sclerosis (ALS) requiring long-term care may elect tracheostomy and continuous full ventilatory support. Engineers developing these devices work closely with physiologists, pulmonary physicians, and respiratory therapists to match function to the pathologies before them. The purpose of this chapter is to introduce the principles of mechanical ventilation to the reader.

Ventilation The primary function of the respiratory system is to ensure adequate tissue oxygenation and carbon dioxide removal. Ventilation is cyclic in nature and composed of an inspiratory and expiratory phase whereby volumes of alveolar gas are moved from ambient air to the alveoli and back. The gases of interest are nitrogen, oxygen, and carbon dioxide. Dependent on the fuel substrate for ATP production and the general health of the individual, volume of oxygen uptake (V̇O2) and volume of carbon dioxide output (V̇CO2) are normally about 250 mL O2/min and 200 mL CO2/min. Nitrogen, an inert gas, generally does not cross the alveolarcapillary (AC) membrane to any appreciable degree unless the subject is exposed to higher than atmospheric pressures. The ventilatory cycle combines a single inspired volume of air with a single expired volume of air. The time it takes for this event is termed the total cycle time. The total cycle time (Ttot) is equal to the inspiratory time (TI) plus the expiratory time (TE) where Ttot = TI + TE. The inspiratory time occurs when inspiratory gas flow moves from zero to peak and back to zero at the end of inspiration (Figure 3-3). The expiratory time begins at the end of inspiration with airflow at zero and continues until the start of the next inspiratory cycle. Generally, the expiratory time is longer than inspiratory time and may include a brief pause with airflow remaining at zero. In mechanical ventilation, it is important to understand the timing of the ventilatory cycle and its relationship with the inspiratory-to-expiratory ratio (I:E ratio) (Box 3-1).

FIGURE 3-3 Determination of Respiratory Cycle Time Using a Flow–Time Curve. Here, the inspiratory time (TI) is 2 seconds, the expiratory time (TE) is 4 seconds, and the total cycle time (Ttot) is 6 seconds. The TI continues as long as inspired flow is above 0. TE begin at the end of TI and continues to the next inspired breath. Creative Media Services, UT Health. Data from Creative Media Services, UT Health.

Description

BOX 3-1 Components of the Breath The timing of a single breath is divided into the time for inspiration (TI) and the time for exhalation (TE). The total cycle time (Ttot) is given by the equation: Ttot = TI + TE The inspiratory to expiratory ratio is expressed: I:E For example, if TI = 2 seconds and TE = 4 seconds, then Ttot = 6 seconds, or 6 sec = 2 sec + 4 sec The I:E ratio is 2 : 4 or reduced, 1 : 2, and the respiratory rate (f) is given by the equation:

Ventilation can be defined as the bulk movement of gas into and out of the lungs. A normal adult tidal volume (VT) is about 500 mL (range 400–700 mL) or 7 mL/kg of ideal body weight (IBW, aka predicted body weight [PBW]). A normal adult respiratory rate (f) is about 12 breaths/min (range 12 to 20) and a normal adult minute ventilation (V̇E) is about 6 L/min (range 5 to 10 L/min), where: V̇E = VT × f = 500 mL/breath × 12 breath/min = 6000 mL/min or 6 L/min Only about 70% of the inspired VT will reach the alveoli to participate in gas exchange, and this is the alveolar ventilation per breath (VA) and per minute (V̇A) (Box 3-2). The remaining 30% (about 150 mL/breath) fills the conducting airways, which extend from the external nares down to (and including) the terminal bronchioles. The volume of gas in the conducting airways is about 1ml/lb IBW and represents the anatomic dead space (VD ant). There may also be alveoli that are ventilated but not perfused and the is the alveolar dead space (VD alv). Physiologic dead space (VD phys) is simply VD ant + VD alv, which represents all the inspired gas that does not participate in gas exchange. Thus, alveolar ventilation is simply tidal volume minus dead space times respiratory rate:

BOX 3-2 Minute Ventilation and Alveolar Ventilation Minute exhaled ventilation (V̇E) is given by the equation: V̇E= f × VT Minute alveolar ventilation (V̇A) is given by the equation: V̇A = f × (VT – VD) For example, if f = 12 breaths/min, VT = 500 mL/breath and VD = 150 mL/breath, then:

V̇A = (VT – VDphys) × f = (500 mL– 150 mL) × 12 breath/min = 4200 mL/min or 4.2 L/min A major purpose of ventilation is removal of CO2. Normal CO2 production (V̇CO2) is about 200 mL/min and the normal partial pressure of carbon dioxide in the arterial blood (PaCO2) is 40 mmHg. There is a direct relationship between alveolar ventilation, CO2 production, and arterial PaCO2: V̇A = (0.863 × V̇CO2) ÷ PaCO2 = (O.863 × 200) ÷ 40 = 4.3 L/min (very close to 4.2 L/min above) Thus, as V̇A increases, PaCO2 decreases and vice versa. As V̇CO 2 increases (e.g., increased metabolic rate, fever), V̇A must increase if PaCO2 is to remain constant.

Spontaneous Breathing At rest, the autonomic centers for respiratory control within the nucleus of the tractus solitarius are active and responsive to afferent feedback from chemoreceptor and mechanoreceptor systems.5 The phases of inspiration and exhalation during quiet breathing pass without conscious awareness. The timing of inspiration and exhalation will vary from moment to moment, dependent on sleep/wake state and activity. The inspired flow rate will also vary, but given a VT of 500 mL/breath and an inspiratory cycle time of 1 second, the average inspired flow rate is 0.5 L/sec and extrapolated to 1 minute, 30 L/min. Voluntary (cortical) control of breathing is asserted during many normal activities, including laughing, singing, speaking, and playing a wind instrument. Larger-thannormal tidal volumes and flow rates occur with cough, sneeze, sigh, and extremes of arterial acidosis or exercise. These flow rates, tidal volumes, and

inspiratory/expiratory times are the result of central nervous system (CNS) outflow, either autonomic or under conscious control. When cortical and/or medullary centers produce an inspiratory activating signal, a series of action potentials first encounters the phrenic motoneurons of the cervical spinal cord between the third and fifth cervical vertebrae and travel down the right and left phrenic nerve. These nerves innervate the right and left hemidiaphragm. When contraction is initiated, the diaphragm descends towards the abdominal cavity. The degree of motion is dependent on the level of activation. When the diaphragm contracts and descends, there is a decrease in the intrapleural and intrathoracic pressures. During quiet respiration, the intrapleural pressure may range from –5 cm H2O at passive end expiration to –10 cm H2O during inspiration. This 5-cm H2O pressure change, when coupled with normal lung-thorax system compliance of 100 mL/cm H2O, is sufficient to achieve a normal tidal volume of 500 mL/breath. With normal spontaneous breathing, alveolar pressure is below atmospheric (negative) during inspiration and above atmospheric (positive) during expiration. Normal intrapleural pressures are slightly below atmospheric at end expiration and decrease (become more negative) during inspiration. These pressure changes allow for inspiratory and expiratory gas flow. Figure 3-4 illustrates the changes in volume, alveolar pressure (Palv), intrapleural pressure (Ppl), and gas flow during inspiration and expiration.

FIGURE 3-4 Single Breath Analysis Curves. Note that as the alveolar and intrapleural pressures decrease during inspiration, air flow and volume increase achieving an inspiratory tidal volume of about 0.5 L. As these pressures return to their normal baseline, gas is exhaled. Creative Media Services, UT Health.

Description

Negative Pressure Breathing Mechanical ventilation can either be invasive or noninvasive, depending on the airway adjunct and needs of the patient, and either positive or negative pressure. Today, almost all mechanical ventilation is provided by positive pressure. Beginning in the late 1920s, early examples of ventilatory support, however, were based on the use of negative pressure (Clinical Focus 3-1). The iron lung (Figure 3-1) was in high demand during polio outbreaks around the world. The principle of operation was relatively simple: the patient was placed on a stretcher within a metal tube with head exposed to room air. A leather seal around the neck closed the system, and a bellows attached to a mechanical pivot like the drive mechanism of a locomotive alternately decreased the chamber pressure below atmospheric (inspiration) and then returned the chamber pressure to baseline (expiration). The transrespiratory system pressures were transmitted to the airways and as airway pressure dropped below atmospheric, the patient inspired. Exhalation followed as the airway, intrapleural, and transrespiratory system pressures were reversed.6 The large space within the chambers did not prevent spontaneous respiration, and it was possible to make observations on the patient’s ventilatory progress. These ventilators saved thousands of lives during the polio epidemics. The Emerson iron lung was produced from the 1930s into the 1970s. The chest curaisse, body suit (Pulmowrap), and Portalung are other devices used to provide negative pressure ventilation. The Biphasic Cuirass Ventilator (United Hayek) uses a plastic shell coupled to a negative-pressure generator (Figure 3-5). Hayek Medical uses the term “biphasic” in its description of using both an active inspiratory (negative pressure) and expiratory (positive pressure) phase in its operation.7 It has been used in a variety of patients with and without an endotracheal (ET) tube. The device also functions as a bronchial hygiene device with capabilities of high-frequency chest wall oscillation and generation of a negative/positive pressure as a cough assist device.8

FIGURE 3-5 The Biphasic Cuirass Ventilator. Courtesy of United Hayek Industries Inc.

CLINICAL FOCUS 3-1 Negative Pressure Ventilation Your patient is a 4-year-old boy diagnosed with spinal muscle atrophy (SMA) since birth. He is chronically hypercarbic and a decision must be made concerning tracheostomy and mechanical ventilation. The parents are adamantly opposed to tracheostomy. The patient’s respiratory rate (f) is 28 breaths/min, blood pressure (BP) is 135/68, and heart rate (HR) is 105. He is diaphoretic and appears to be in distress. The most recent arterial blood gas (ABG) on room air (RA) is: pH PaCO2

7.31 65 mmHg

PaO2

55 mmHg

HCO3−

32 mEq/L

SaO2

89%

A decision to institute negative pressure ventilation was agreed upon. The Hayek chest cuirass was used and set to –18 cm H2O to maintain a VT between 100 to 130 mL/breath (patient weight is 14 kg and the estimated VT desired was

8 mL/kg). The ventilator was set in a respiratory synchronization mode with a backup rate of 18 breaths/min. Supplemental O2 was bled into the system at 4 L/min. Within the next 2 hours, the patient seemed more comfortable. An ABG drawn at 15 minutes post negative pressure ventilation initiation is shown in (A) and at 2 hours in (B):

The plan was to reduce the backup rate as the patient’s spontaneous rate increased. Urine output and renal function would be monitored. PETCO2 and O2 by pulse oximetry would be monitored continuously and ABGs would be drawn in the morning and as needed (PRN). The parents seemed happy. Questions: 1. How would you classify each of the three ABGs? 2. Was the chest cuirass successful in reversing the ventilatory failure? 3. Do you anticipate a continued decrease in the bicarbonate level? Answers: 1. Blood gas classification Initial: Partially compensated respiratory acidosis with moderate hypoxemia. A. Compensated respiratory acidosis with normoxemia. B. Within normal limits (WNL). 2. Yes. 3. Possibly. If the PaCO2 rises, the HCO3− may increase. If the PaCO2 does not change, the HCO3− may decrease a bit as the pH moves closer to 7.40.

Positive Pressure Breathing Positive pressure ventilation rapidly gained in popularity with improvements in design and function. In the 1960s and 1970s, ventilators became much more sophisticated

and required specially trained personnel to operate them safely and effectively (Figure 3-6). Expansion of respiratory therapist educational programs coincided with an upswing in the use of positive pressure ventilators. These devices required a sealed airway via a cuffed endotracheal or tracheostomy tube (although mask ventilation was possible). After advancing the endotracheal tube past the glottis (intubation) with its tip above the level of the carina, the cuff is inflated against the wall of the trachea. The endotracheal tube is fixed in position to provide reasonable assurance against it becoming dislodged and resuscitation bag ventilation is maintained until ready to connect the patient to the positive pressure ventilator.

FIGURE 3-6 Pressure and Volume Ventilators Introduced in the 1940s Through the Early 1970s. Top left, the Bird Mark 7 (introduced in 1958) and Bird Mark 8 (introduced in 1959). Top right, the Bennett TV-2P (introduced in 1948) and Bennett PR-2 (introduced in 1963). Bottom left, Bennett MA-1 volume ventilator (introduced in 1967) and Servo 900 (introduced in 1971). Bottom right, the Ohio 560 (introduced in the 1970s). Reproduced from Kacmarek RM. The Mechanical Ventilator: Past, present, and future. Respir Care. Aug 2011;56(8):1170–1180; doi: 10.4187/respcare.01420

The function of the ventilator is to provide a volume of gas to the patient with such sufficiency as to supply the alveoli and arterial system with oxygen and support carbon dioxide removal. While various patient circuit configurations have been employed, in its most simplified form the ventilator is attached to the patient by two limbs of tubing joined at a “Y” connection. The inspiratory limb carries gas from the ventilator to the “Y” connector and endotracheal tube. The volume of air meant for the lungs does not flow past the “Y” connector through the expiratory limb as there is an expiratory valve that closes the exhalation limb during the inspiratory phase. Once the inspiratory volume is delivered, the expiratory limb is opened to exhaust the volume of gas leaving the lungs. The inspiratory tidal volume may be humidified and enriched with supplemental oxygen. During inspiration, as gas flows into the lung, the airway pressure will rise. The airway pressure is dependent on both the machine’s set parameters and the compliance and resistance of the lungs being ventilated. Generally, the larger the tidal volume, the greater the peak pressure. Similarly, the lower the lung compliance, the greater the peak and plateau pressure. Figure 3-7 illustrates a typical ventilator patient circuit.

FIGURE 3-7 An Example of a Mechanical Ventilator Patient Circuit. This circuit shows the inspiratory (green) and expiratory (gray) limbs that serve as a conduit of respirable gases between the ventilator (shown in gray) and the patient connection. A heated humidifier with attached water reservoir line is shown and heated internal wires maintain ventilator circuit temperature and reduce condensation.

Description Respiratory clinicians adjust variables including flow, volume, time, and pressure to provide optimal gas exchange while minimizing the risk of barotrauma. Ventilator adjustments can be complex and require advanced training and experience. Untrained or inexperienced personnel should not make changes in mechanical ventilation parameters, as serious patient safety concerns may arise. In any situation in which the ventilator does not appear to be functioning correctly, immediately disconnecting the patient from the ventilator and providing manual ventilatory support using a manual resuscitator bag is strongly encouraged. While the patient is being supported using a manual resuscitator bag with supplemental oxygen, the respiratory therapist can then troubleshoot the ventilator to identify the problem. Figure 3-8 provides an example of ventilator graphics depicting the pressure curves associated with positive pressure volume ventilation with an end-expiratory

pause. All pressures reflect proximal airway pressure (PAW), either measured directly or indirectly. Older systems use a pressure monitoring line consisting of a length of noncompliant tubing that extends from the ventilator to the proximal airway “Y” connector. Most modern ventilators today sense the pressure where expired gas returns to the ventilator via the expiratory limb of the circuit or within the internal ventilator circuit near the point where gas leaves the internal circuit and enters the inspiratory limb of the external circuit.

FIGURE 3-8 Airway Pressure During Volume-Controlled Ventilation: The Pressure vs Time Scalar. Peak inspiratory pressure (PIP) is the highest pressure reached during inspiration. An end inspiratory breath hold allows for measurement of plateau pressure (Pplateau). The difference between PIP and Pplateau represents airway resistance (RAW). PEEP is positive end-expiratory pressure. Introduction of an end expiratory pause allows for the measurement of autoPEEP.

Description

Peak Inspiratory Pressure The peak inspiratory pressure (PIP) is the highest proximal airway pressure

attained during the inspiratory phase. During pressure-control ventilation, PIP is determined by the ventilator settings. During volume-control (VC) ventilation, PIP can be influenced by set tidal volume (VT), inspiratory flow, inspiratory flow waveform, resistance of the ventilator circuit/endotracheal tube, and lung mechanics (compliance and resistance). Proximal airway pressure may also increase during forced exhalation, as noted with cough (Box 3-3). Maintaining PIP < 35 cm H2O should reduce the risk of pulmonary barotrauma.

BOX 3-3 Factors that Increase Peak Inspiratory Pressure (PIP) ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

Increased peak inspiratory flow Increased set tidal volume (VT) Increased airway resistance Decreased total compliance Increased PEEP Kinked or obstructed ET tube Fighting the ventilator Coughing

Plateau Pressure (Pplateau) In the VC mode, plateau pressure (Pplateau) is measured during an inspiratory hold maneuver, typically one second or less in duration (see again Figure 3-8). At the end of inspiration, with Pplateau activated, the ventilator will continue to block the exhalation valve as the airway pressure decreases from a peak value (PIP) to the plateau level. Under static conditions, Pplateau reflects alveolar pressure and the difference between PIP and Pplateau reflects airway resistance (Raw), which can be easily calculated during VC ventilation:

Pplateau is determined by elastic lung tissue recoil in the absence of airflow and allows for the calculation of static total compliance (CST) during VC ventilation:

Baseline Pressure and PEEP The pressure waveform depicted in Figure 3-8 drops to a baseline or resting airway pressure during expiration. If the baseline pressure is the same as ambient pressure, the baseline is recorded as zero. If the baseline pressure during the expiratory phase is above ambient pressure, it is known as positive end-expiratory pressure (PEEP). PEEP has been used since the early days of positive pressure ventilation to maintain alveolar volumes during expiration and to improve oxygenation. Initially, PEEP was applied by simply submersing the distal end of the expiratory limb of the ventilator circuit below the surface of a water container. Early PEEP valve systems were developed (Figure 3-9) and attached to the ventilator and filled with a volume of water. The weight of the water over the ventilator’s exhalation valve created positive airway pressure during the expiratory phase proportional to the height of the water column in centimeters. A water column 5 cm in height would result in PEEP of 5 cm H2O. Today’s ventilators use much more sophisticated systems incorporating servo-adjusted solenoid valves and pressure sensors to actively monitor and maintain airway pressures. PEEP set intentionally to improve lung volumes and oxygenation is known as extrinsic PEEP.

FIGURE 3-9 The Water-Filled PEEP Column. Courtesy Dr. Greg Holt.

AutoPEEP or Intrinsic PEEP Air trapping (aka dynamic hyperinflation) can occur with incomplete emptying of the lung during expiration. Patients with obstructive lung disease are particularly prone to the development of air trapping during mechanical ventilation, especially if expiratory times are inadequate. Terms used for this air trapping during positive

pressure ventilation include autoPEEP, or intrinsic PEEP. AutoPEEP is not observable during positive pressure ventilation on the patient’s pressure-time curve without the use of an expiratory pause maneuver. Most modern ventilators allow for the introduction of an expiratory pause to evaluate autoPEEP Turning once again to Figure 3-8, note that as the pressure curve proceeds to the right, the pressure increases during an expiratory hold maneuver. This increased pressure is the autoPEEP or intrinsic PEEP caused by air trapping during the expiratory phase. This dynamic hyperinflation can lead to higher mean airway pressures and possible cardiovascular side effects (e.g., decreased venous return, decreased stroke volume, and decreased cardiac output). Patients with chronic obstructive pulmonary disease (COPD) are especially likely to develop autoPEEP

Optimal PEEP As noted, the purpose of PEEP is to improve and maintain lung volumes and improve oxygenation in patients with acute restrictive pulmonary disease (e.g., pneumonia, acute respiratory distress syndrome [ARDS], pulmonary edema). A small amount of PEEP (3 to 5 cm H2O) has been suggested for most mechanically ventilated patients to prevent end-expiratory alveolar collapse; this is sometimes referred to as “physiologic PEEP.” High levels of extrinsic PEEP can increase the transmural wall pressures of the low-pressure great vessels (superior and inferior vena cava) and the right and left ventricle. Compression of the vena cava can diminish venous return and ventricular compression may affect diastolic filling. High levels of extrinsic PEEP combined with high levels of intrinsic PEEP (air trapping or autoPEEP) may further reduce venous return. This assumes normal lung compliance as the transmural wall pressure effects are not as easily observed through noncompliant lungs. One approach to optimizing PEEP titrates the PEEP level based on oxygen delivery (ḊO2). Recall that oxygen delivery is simply cardiac output times arterial oxygen content (ḊO2 = Q̇T × CaO2). To achieve the optimal PEEP level, PEEP is increased incrementally followed by measurement of cardiac output or related parameters (blood pressure, mixed venous oxygen levels). The optimal PEEP level is the level that optimizes ḊO2. Other approaches to optimizing PEEP levels include compliance-titrated PEEP and the use of pressure–volume curves to help set the

PEEP level. PEEP studies can be performed by comparing increases in set (extrinsic) PEEP to cardiac output. Clinical Focus 3-2 provides an example of a PEEP study used to determine optimum PEEP. Caution should be exercised in using high levels of PEEP in the setting of hypotension, hypovolemia, increased intracranial pressure (ICP), or pulmonary embolism.9

CLINICAL FOCUS 3-2 Optimal PEEP Study An optimal PEEP study is requested for a patient on mechanical ventilation with settings: Mode: PC-AC FIO2: 100% PIP: 28 cm H2O RR: 16 bpm PEEP: +12 cm H2O Recent ABG results: pH 7.30 PaCO2 60 mmHg PaO2 45 mmHg HCO3− 29 mEq/L Hg 10 g/dL The patient’s ventilator indicates a delivered VT of 400 mL, and there are no spontaneous respirations. The patient has increasing patchy infiltrates on chest x-ray. A PEEP study has been ordered, and you have developed the following table. All measures were made at an FIO2 of 100% with a Hb of 10 g/100 mL blood. The results displayed were obtained after 10 minutes at each PEEP level.

Description Questions: 1. How would you interpret the patient’s initial (recent) ABG? 2. What level of PEEP could be considered optimal? 3. What are other variables that can be used to develop an optimal PEEP study? Answers: 1. The recent blood gas shows a partially compensated respiratory acidosis with moderate to severe hypoxemia. 2. At PEEP of 18 cm H2O the BP, SaO2, CO, and D˙O2, and C(a-v)O2 are acceptable and CST is at its highest value (48) suggesting that this represents the best or optimal PEEP level. Although D˙O2 is highest at the next PEEP level (20 cm H2O), blood pressure, cardiac output, and compliance decrease and C(a-v)O2 increases. 3. Many variables can be used to help determine optimal PEEP. They include hemodynamic measures, lung mechanics, and indices of oxygenation and ventilation (e.g., BP, CO, CI, D˙O2, Pv–O2, Sv–O2, C(a-vO2), PaO2, SaO2, P(Aa), PaO2/FIO2, CST, PaCO2 – PETCO2, and shunt fraction [Q̇S/Q̇T]). ABG, arterial blood gas; BP, blood pressure; CO, cardiac output; CST, static compliance; PC-AC, pressure control-assist control; PCWP, pulmonary capillary wedge pressure; PEEP, positive end-expiratory pressure; PIP, peak inspiratory pressure; RR, respiratory rate.

Mean Airway Pressure (Paw) In addition to the effect of PEEP on venous return, the respiratory care clinician should consider other variables that affect mean airway pressure (Paw) during mechanical ventilation with positive pressure. A 2003 paper on mathematical

modeling of mean airway pressure used PEEP, I:E ratios, and Pplateau to make determinations of mean airway pressures.10 This article suggests using a target airway pressure to recruit alveoli rather than using arterial blood gas analysis, PETCO2, and oximetry alone for ventilator adjustments. The increased focus on the balance of I:E ratios and PEEP with particular attention to inspiratory time (TI) to manage PAW over PEEP settings was the intent of the paper.10 A less stringent method forwards the equation Paw = ½ (PIP – PEEP) × (TI / Ttot) + PEEP. The effect of PEEP is direct, and a 1 cm H2O PEEP increase causes a 1 cm H2O rise in Paw. Factors that increase TI will increase Paw. Changes in pulmonary mechanics (e.g., low lung compliance and high airflow resistance) also may contribute to an increased Paw. Variables that can influence mean airway pressure are described in Box 3-4.

BOX 3-4 Factors That May Increase Mean Airway Pressure ( ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

)

Increased inspiratory time Increased I:E ratio Decreased expiratory time Increased tidal volume Increased extrinsic PEEP AutoPEEP Decreased spontaneous breathing Down-ramp (decreasing) inspiratory flow pattern Low lung compliance High airway resistance (RAW)

Invasive vs. Noninvasive Ventilation Before comparing the similarities and differences between invasive and noninvasive ventilation, we should revisit the goal of mechanical ventilation: to support oxygenation and CO2 removal. Mechanical ventilation requires a trigger (breath initiation), a limit (size of the breath), and a cycle (transition of inspiration to expiration). The forms the trigger, limit, and cycle variables take are dependent on the device, the patient’s condition, and the level of expertise of the respiratory care

clinician. Similarities between invasive and noninvasive ventilation (NIV) include positive pressure breath delivery and the ventilator’s airway pressure and flow sensing capabilities. Many new noninvasive devices can measure volume directly. Size and cost of ventilators designed for invasive vs noninvasive use are major differences between the two. For example, simple NIV devices for the treatment of obstructive sleep apnea (OSA) may cost as little as $600 and fit on a nightstand, while a sophisticated critical care ventilator may cost $35,000 or more and require significant space at the bedside. NIV requires a spontaneously breathing patient with an adequate respiratory drive, while a critical care ventilator can ventilate apneic patients with acute or chronic respiratory failure. Another difference between NIV and invasive ventilation is the interface between the patient and the ventilator. Both methods require a sealed airway to deliver positive pressure, but invasive ventilation requires an endotracheal or tracheostomy tube be placed with the cuff inflated.

Noninvasive Ventilation NIV can be used to provide ventilatory support to patients with a wide variety of conditions, which may be acute or chronic. For example, in the acute care setting, NIV is often used to support patients with acute exacerbations of COPD. Extubation to NIV has also been recommended for certain patients at risk of extubation failure. NIV is also sometimes used in patients with chronic neuromuscular disease. NIV for the treatment of obstructive sleep apnea will be briefly discussed below. NIV has seen great strides in technology and mask interface devices in the treatment of obstructive sleep apnea (OSA) since the mid-1990s. Companies such as ResMed, Respironics, and Fisher-Paykel have invested resources into research and development of better patient-sensing capabilities, improved mask comfort and fit, and new modes of NIV. For example, Respironics developed an expiratory pressure release technology (CFLEX) adjustable from 0 to 3, with 3 providing the greatest drop in exhaled pressure. CFLEX may improve patient comfort and compliance. ResMed followed closely with EPR (expiratory pressure release) that has an adjustable, set pressure drop at the start of exhalation. The relief of patient anxiety associated with the higher pressures sometimes necessary to control OSA was the driving force behind CFLEX and EPR

development. If higher pressures (e.g., > 12 cm H2O) were used in OSA therapy, patients often complained of difficulty exhaling against the pressure. Bilevel positive airway pressure (BiPAP) would be sometimes instituted (Box 3-5), but this added to the cost of the device. A variation on BiPAP was developed, the spontaneous-timed (S/T) mode. With BiPAP S/T (trademark Respironics), inspiratory and expiratory pressures were set along with a backup rate. If the device measured zero inspiratory flow for a set period, the inspiratory positive airway pressure (IPAP) breath would be delivered (i.e., time triggered to inspiration). BiPAP S/T could provide support for some cases of complex sleep apnea (defined as at least 50% of all respiratory events being central in origin); however, the IPAP breath could fall short of preventing sleep arousal as seen via EEG and O2 desaturation. If the IPAP pressures were increased to cover the reduced machine delivered tidal volume, the patient could arouse and awaken to some very high pressures.

BOX 3-5 Bilevel Positive Airway Pressure (BiPAP) for OSA ∎ ∎

BiPAP can be expressed as a combination of IPAP over EPAP. IPAP can reach 30 cm H2O.

∎

EPAP is usually 4 to 8 cm H2O below IPAP.

∎

EPAP is set to abolish obstructive apneas. IPAP is set to improve the inspiratory flow wave characteristics and abolish hypopneas and snoring.

∎

IPAP: inspiratory positive airway pressure; EPAP: expiratory positive airway pressure.

The next generation of NIV to treat central sleep apnea and forms of complex sleep apnea was automatic-servo ventilation (auto-SV, trademark Respironics) and later adaptive-servo ventilation (trademark ResMed). Auto-SV was considered a respiratory assist device, similar to BiPAP S/T with pressure support. Auto-SV would “view” the patient’s rate and volume when the device was initiated (patient awake) and mimic that pattern during the night. If the tidal volumes fell short, pressure support would be added to increase volume (Figure 3-10) The auto-SV would increase pressures to cover obstructive respiratory events with an adjustable range

of pressures; the rate could be set or left in an auto-detection mode and the level of pressure support could be set as a fixed number or range for auto-adjust. These added features, however, result in a cost approximately 5 times the cost of a basic CPAP device.

FIGURE 3-10 Automatic-Servo Ventilation. Pressure support is automatically adjusted to minimize fluctuations in VT and prevent airway obstruction. If central apneas arise, the backup rate will deliver IPAP-associated breaths.

Description Automatic positive airway pressure or autoPAP is a device that continues to be ordered for OSA treatment. The pressure range for autoPAP is adjustable from 4 to 20 cm H2O. By algorithm, the device can detect a reduced or absent inspiratory flow and stepwise increase the delivered pressure. There are problems, however, associated with autoPAP. Primary among them is the inability to detect central versus obstructive sleep apnea. Some units will not increase pressure over 10 cm

H2O unless there is a secondary indication of obstructive respiratory events, such as the acoustical vibration of snoring. A known problem of positive pressure therapy noted during a CPAP titration study for OSA is the potential for central apnea generation at higher pressures. A second problem and more likely occurrence is a subtherapeutic pressure range set on autoPAP. Picking the autoPAP pressure range without the benefit of a CPAP titration study is a guess. If the pressure range is left at its initial setting, 4 to 20 cmH2O, the patient (especially a very tall patient) may inspire with a greater flow than delivered and a feeling of air hunger may result. If the patient on the same settings with OSA is asleep, the autoPAP will respond to his or her apnea by detection and will increase pressure provided. Over time, the patient will either get to the point where the attained pressure allows for ventilation or the patient may arouse and roll to his or her side, where the device lowers the pressure to a new baseline. Put another way, sleep-disordered breathing is required to reach the appropriate therapeutic pressure. The patient may also awaken and feel that the device is not working at all. This could result in reduced compliance. Ideally, the clinician should know the appropriate pressures for each patient that treat OSA while supine, on the patient’s side, and in REM sleep. The autoPAP device could then be set with a minimum pressure treating OSA while on the patient’s side with the idea that the pressures may not be too far from controlling OSA while in supine REM sleep. Minimally, the clinician should follow any patient on autoPAP with overnight oximetry to assess therapeutic effectiveness. Suggested indications for autoPAP are noted in Box 3-6.

BOX 3-6 Indications for Automatic Positive Airway Pressure (autoPAP) 1. 2. 3. 4. 5.

Initial therapy to treat OSA prior to CPAP titration AutoPAP trial after significant weight change to adjust CPAP pressure Patient c/o aerophagia (air swallowing) while on CPAP As primary therapy if optimal pressures are known: side, supine, REM As primary therapy in patients with mild OSA and low BMI

BMI, body mass index; CPAP, continuous positive airway pressure; OSA, obstructive sleep apnea; REM, rapid eye movement sleep

Invasive Ventilation Invasive positive pressure ventilation opens a wide array of ventilatory capabilities using sophisticated critical care ventilators. The goals remain the same, including assuring oxygenation needs are met and supporting ventilation until the patient can return to his or her baseline ventilatory status. Modern critical care ventilators have sophisticated alarms and monitoring systems, advanced graphic displays, and a wide array of modes available ranging from conventional volume-control continuous mandatory ventilation (VC-CMV) to pressure-control continuous mandatory ventilation (PC-CMV), to inverse ratio ventilation, to various permutations of intermittent mandatory ventilation (IMV), to various volume targeting schemes (e.g., pressure-regulated volume control [PRVC], volume support [VS], and adaptive pressure control [APC]). Modern critical care ventilators also often have many adjunct features and modes including automatic tube compensation (ATC), airway pressure release ventilation (APRV), proportional assist ventilation (PAV), or adaptive support ventilation (ASV), as well as the capability to provide NIV. Many of these modes will be introduced later in this chapter. The ventilation of the patient with acute respiratory failure superimposed on chronic respiratory failure is described in Clinical Focus 3-3.

CLINICAL FOCUS 3-3 Acute Ventilatory Failure Superimposed on Chronic Ventilatory Failure Mrs. Ortiz is a 78-year-old female with a 110 pack-year history of smoking. She has been diagnosed with COPD and her “normal” arterial blood gas consists of pH 7.36, PaCO2 55 mmHg, and PaO2 60 mmHg on room air. Her HCO3− is calculated to be 30 mEq/L. She develops pneumonia and presents to the emergency department in respiratory distress. Her ABG results in the ED are: pH 7.21, PaCO2 70 mmHg, and PaO2 45 mmHg, with HCO3− 34 mEq/L. Her condition worsens, and she is intubated and placed on mechanical ventilation. Her ventilation is supported to maintain arterial blood gases similar to her baseline: compensated respiratory acidosis with mild hypoxemia. Intravenous antibiotics are administered until resolution of the pneumonia. Mrs. Ortiz is weaned from mechanical ventilation, extubated, and discharged. To summarize, Mrs. Ortiz’s “normal” baseline can be described as chronic ventilatory failure (compensated respiratory acidosis) and mild hypoxemia.

Following acute exacerbation of his COPD, she developed acute on chronic ventilatory failure with a partially compensated respiratory acidosis and severe hypoxemia. Following treatment, resolution of her pneumonia and ventilator discontinuance, she has returned to her baseline status of chronic ventilatory failure. Mrs. Ortiz might have taken another path if the development of worsening respiratory failure had progressed more slowly allowing for further renal compensation of a worsening PaCO2. In this second example, the original ABG is followed by worsening ventilatory status with renal compensation, then respiratory failure, and finally, mechanical ventilation is initiated with overventilation.

Description Questions: 1. Review the ABGs and determine their classifications for A, B, C, and D. 2. When mechanical ventilation is instituted and the PaCO2 is “normal” at 40 mmHg, what is causing the apparent metabolic alkalosis? 3. Would it have been more appropriate to ventilate this patient to her baseline PaCO2 of 55 mmHg? Answers: 1. A. Compensated respiratory acidosis with mild hypoxemia (chronic ventilatory failure); B. Compensated respiratory acidosis with moderate hypoxemia (chronic ventilatory failure); C. Partially compensated respiratory acidosis with moderate hypoxemia (acute ventilatory failure superimposed on chronic ventilatory failure); D. While this looks like an uncompensated metabolic alkalosis with mild hypoxemia, it is a relative hyperventilation with respect to

the patient’s baseline PaCO2 of 55, resulting in alkalosis. The ventilatory settings should be adjusted. 2. This patient’s “normal” baseline PaCO2 is 55 mm Hg resulting in a pH of 7.36 (see initial ABG - A). If the initial ventilator settings result in a PaCO2 of 40, the pH will increase as noted (see ABG Mechanical Ventilation - D). The ventilator settings have created a relative hyperventilation with respect to the patient’s baseline PaCO2 of 55 resulting in an alkalosis. 3. Yes. The targeted PaCO2 should have been the patient’s “normal” baseline (i.e., PaCO2 = 55).

Ventilator Initiation Indications for mechanical ventilation and ventilator initiation are described in Chapters 5 and 6. Once the decision to provide ventilatory support is made, mechanical ventilation is initiated within specific parameters. Typically, orders will be given for mode, FIO2, VT (or PIP), respiratory rate, PEEP, and pressure support. Some institutions allow for ventilator initiation and adjustments per protocol. Initial ventilator settings are keyed into the ventilator’s control interface. The respiratory therapist typically chooses the patient-trigger method, trigger effort, inspiratory time or flow, and flow waveform (VC modes), and adjusts settings to ensure patient– ventilator synchrony and effective ventilation. Alarm settings are entered, and patient response as assessed. Assessment to ensure successful achievement of ventilatory support goals begins immediately. This will include patient appearance, breath sounds, and assessment of ventilator volumes, pressures, and flows. Assessment of oxygenation (SpO2), ventilation (respiratory rate, VT, V̇E, arterial blood gases, and end-tidal CO2), and cardiovascular status (HR, BP, ECG) should follow. Clinicians should be reminded that when mechanical ventilation does not appear to be functioning properly, the ventilator should be disconnected, and bag ventilation resumed until proper ventilator operation and airway patency can be confirmed. Initial problems sometimes encountered when the patient is placed on the ventilator may be due to pain and anxiety, inadequate oxygenation or ventilation, cardiac/cardiovascular problems, or improper ventilator settings. Solutions may be as simple as altering the ventilator settings, sedation (anxiety) and analgesia (pain), or suctioning to remove

secretions from the airway. Airway problems include secretions, obstruction, or bronchospasm, all of which may cause triggering of high-pressure alarms in the VC mode and decreased VT in the PC mode. For example, the endotracheal tube may be out of position, kinked, or partially occluded. Breath sound assessment and attempting to pass a suction catheter can sometimes identify the cause. Other serious problems include pneumothorax, pulmonary edema, pulmonary embolus, or cardiovascular compromise. Once the patient is stable, comfortable, and adequately oxygenated and ventilated, a regular program of assessment, monitoring, and care is instituted.

Ventilator Principles Input Power and Control Systems Mechanical ventilators must incorporate a power source to perform the work required, known as the input power. Power sources may be pneumatic or electric. Pneumatically powered ventilators connect to an external high-pressure gas source, while electrically powered ventilators use electricity to power internal compressors, blowers, pistons, or bellows. Ventilator control systems use pneumatic valves, electrical circuits, or microprocessor controls to regulate oxygen concentrations and gas flow to the patient.

Pneumatically Powered Ventilators Pneumatically powered ventilators require a compressed gas source, either air or oxygen or both. Older pneumatic ventilators were powered using only one compressed gas source. These older pneumatically powered ventilators (e.g., Bird Mark 7, Bennett PR-2) incorporated needle valves, flexible diaphragms, ceramic valves, pneumatic bleed-down cartridges, flow-sensitive valves, and Venturi devices to perform the various functions required to ventilate patients. These devices could be powered by 100% oxygen, which could be diluted using an on/off venture device to provide 100% O2 or a moderate concentration oxygen (40% to 60%). These ventilators also could be powered by compressed air to provide 21% oxygen or blended gas to provide a precise FIO2. Modern pneumatically powered ventilators require two 50-psi compressed gas sources (air and oxygen) and incorporate microprocessor-controlled valves to provide the desired oxygen concentration and gas flows to the patient. These are known as pneumatically powered microprocessor-controlled ventilators.

Electrically Powered Ventilators The first truly sophisticated modern critical care ventilators were electrically powered and controlled and incorporated internal air compressors, blowers, bellows, or pistons to deliver gas to the patient. These ventilators were introduced in the 1960s and 1970s and allowed for precise control of FIO2, delivered tidal volume, respiratory rate, and inspiratory flow or time. PEEP was an integrated feature and the ventilators could be used to provide patient- or time-triggered ventilation (assist/control or A/C).

By the 1970s, intermittent mandatory ventilation (IMV) and synchronized intermittent mandatory ventilation (SIMV) became common options. Classic electrically powered ventilators included the MA-1, Ohio 560, Emerson 3PV and IMV Emerson, and Bear series (e.g., Bear-1, Bear-2, Bear-3). These ventilators could be described as single circuit, in which the gas power source was sent directly to the patient, or double circuit, in which the gas power source was directed to a bellows housed within a canister. Single-circuit devices included the rotary piston, IMV Emerson, and the Bear series. Double-circuit systems, such as the MA-1 and Ohio 560, used a blower or compressor to push a bellows containing mixed gas upward; the gas within the bellows would then be delivered to the patient (blower-bellows system). These ventilators were extremely efficient, safe, and reliable and allowed for the development of the sophisticated approach to critical care and support of the patient in respiratory failure that we see today.

Control Systems Most modern critical care ventilators today are microprocessor controlled and require a 120-volt continuous electrical supply with stepped-down resistors reducing voltage to control various onboard ventilator systems. Most ventilators possess a battery backup designed to continue ventilation until a substitute power supply is provided (generator backup). Some deep-cycle gel batteries can last 10 hours, but many systems are not designed to support ventilation for more than 2 hours. There have been reported cases of ventilator failure due to batteries beyond their useful life not accepting a charge and faulty battery level indicators. If backup electrical power systems do not respond immediately, the clinician should resume bag ventilation using a manual resuscitator bag. Most modern critical care ventilators also require high-pressure gas sources, both oxygen and compressed air in most cases. Like backup electrical supply, some mechanical ventilators possess onboard gas compressors capable of driving ventilator functions. The usual case is connecting both oxygen and air to 50-psi sources. Piped in medical gas supply systems are built into the walls of hospitals with multiple air and oxygen outlets in each modern ICU room. Large, liquid oxygen systems and powerful medical gas air compressors provide the sources for compressed air and oxygen. Ventilators incorporate pressure regulation devices and solenoid controllers to

provide the desired air/O2 mix to deliver the desired FIO2 and gas flow to the patient. These pressure/flow regulation devices may incorporate a pneumatic diaphragm, electromagnetic valve, poppet/plunger valve, or microprocessor-controlled proportional solenoid valves.4 The control system of a mechanical ventilator generally uses a combination of pressure and electrical/microprocessor-controlled systems to shape and deliver the breath. Control systems may be open loop or closed loop. An open-loop system does not incorporate a feedback signal to assure a specific ventilator parameter has been met. For example, a ventilator in which a microprocessor control system is used to set a specific tidal volume may have no feedback system to adjust gas flow in the presence of a change in actual delivered tidal. A closed-loop system uses a microprocessor-controlled feedback system to adjust gas flow based on measured values. For example, with a closed-loop system the operator may set a specific tidal volume. The ventilator then compares the actual delivered volume to the set value and adjusts gas delivery based on the comparison. Adaptive targeting for tidal volume using pressure support or pressure control provides an example of a closedloop control system known as adaptive pressure control (APC). APC is available as pressure-regulated volume control (PRVC, Getinge Servo-i), auto flow (Dräger Evita Infinity v500), adaptive-pressure ventilation (APV, Hamilton G5), and volume control plus (VC+, Puritan Bennett). Most ventilators incorporate a control panel or a user interface, which may include mechanical or virtual knobs, buttons, and switches to adjust various ventilator parameters. Adjustments may include mode, FIO2, VT or pressure control level, respiratory rate, inspiratory flow or inspiratory time, PEEP, pressure support, ventilator alarms, and ventilator graphic displays. Figure 3-11 provides an example of a modern critical care ventilator’s user interface.

FIGURE 3-11 Example of a Ventilator User Interface with Alphanumeric, Waveform, and Loop Displays. Reproduced with permission from Chatburn RL. Fundamentals of Mechanical Ventilation. Cleveland, OH: Mandu Press Ltd. 2003

Description Few critical care ventilators use purely pneumatic controls, but they do play a role in ventilators used for patient transport and in the hyperbaric environment. For example, the ParaPAC Ventilator (Figure 3-12) is a pneumatically powered and controlled, time and manual triggered, flow and pressure limited, and time-cycled ventilator with spontaneous breathing capability.11 This ventilator is well-suited as a transport ventilator since it does not require an external electrical power source or battery. It can be made magnetic resonance imaging (MRI) compatible, but has shown limitations in the hyperbaric environment (flow rates 10 mL/kg) and high PEEP with volume cycling resulted in increased risk of ventilator-associated lung injury (VALI) and increased mortality. Studies since have shown that alternative ventilatory strategies including pressure-controlled ventilation, permissive hypercapnia, prone position ventilation, inverse ratio ventilation, airway pressure release ventilation, dual-control modes, and high-frequency forms of mechanical ventilation can be effective with ARDS patients.15 Current treatment of ARDS includes treatment of the underlying cause, early use of antibiotics for pneumonia or sepsis, and the use of smaller tidal volumes (VT 4 to 8 mL/kg IBW) delivered at low pressures (≤ 30 cm H2O) from the ventilator (aka lung protective ventilation).

Flow Cycling Most modern critical care ventilators incorporate the option to provide pressuresupport ventilation (PSV). Pressure support may be used as a standalone mode in which each breath is patient triggered, pressure limited, and flow cycled, or as an option with the use of intermittent mandatory ventilation (IMV) or synchronized intermittent mandatory ventilation (SIMV). As a standalone mode, PSV levels are adjusted to ensure adequate tidal volumes (VT 4 to 8 mL/kg) and satisfactory

respiratory rates (f ≤ 25 breaths/min). For ventilator weaning, the PSV level can be reduced gradually, in a stepwise fashion, based on the patient’s response. With IMV or SIMV, mandatory breaths are delivered at a preset rate, allowing for spontaneous breathing to occur in between mandatory breaths. Mandatory breaths are typically pressure controlled or volume controlled. Spontaneous breaths may be pressure augmented by providing low to moderate levels of pressure support. In combination with IMV or SIMV, pressure support is generally used as an adjunct to overcome the imposed WOB (WOBI) due to the artificial airway. As noted above, PSV levels to overcome WOBI during spontaneous breathing are generally in the range of 5 to 15 cm H2O. As described earlier, flow cycling is dependent on a decrease in inspiratory flow rate, often as a set percentage of a peak inspiratory flow. For example, if flow cycling is set to 25% of the peak flow, the ventilator will cycle to exhalation as the inspiratory flow rate diminishes by 75%. Flow cycling generally functions well with variable breathing patterns as may occur with spontaneous ventilation. Flow cycling is sometimes subject to difficulties during ventilation of restrictive and obstructive lung disease. For example, the effects of flow cycling on TI will vary with pulmonary mechanics. With restrictive lung disease (e.g., decreased lung compliance), early termination of the inspiratory phase may occur due to a rapidly diminished inspiratory flow rate. With obstructive lung disease, prolongation of the inspiratory phase may occur due to a more slowly decreasing expiratory flow.16 Accommodation of these problems can be made through patient assessment, waveform analysis, modification of the inspiratory rise time, and adjustment of ventilator flow termination criteria (e.g., expiratory sensitivity [ESENS] or expiratory trigger sensitivity [ETS]). Patient–ventilator synchrony and timing issues of flow cycling in the compromised patient require a knowledgeable respiratory care clinician. Figure 3-15 illustrates typical flow, pressure, and volume–time curves seen with patient-triggered, flow-cycled, pressure-support ventilation.

FIGURE 3-15 Flow, Pressure, and Volume–Time Curves During Pressure Support Ventilation. Pressure support is patient triggered (note the pressure drop that begins inspiration) and flow cycled (note the decreasing flow waveform and near square-wave pressure waveform). Hess DR, Kacmarek RM. Essentials of Mechanical Ventilation, 2nd ed. New York, NY: McGraw Hill; 2002.

Description Some ventilators offer an option that incorporates flow cycling with a volume target (e.g., volume support ventilation [VS]) in which the ventilator automatically adjusts ventilator cycling based on previous breath analysis in order to maintain tidal volume.17

Operator Interface Ventilator controls currently use combinations of buttons, switches, and microprocessor-generated touch-screen simulations of control knobs or icons and the occasional multifunction dial for the adjustment of ventilator functions. Fifty years ago, ventilators like the Puritan Bennett MA-1 were introduced with rheostat/potentiometer operated dials to adjust tidal volume, rate, and FIO2. PEEP systems were soon added followed by reservoir bags, H-valves, and then demand

flow systems for IMV. For many years, Hollywood continued to display the MA-1 in its hospital scenes with the attached bellows spirometer moving up and down simulating positive pressure ventilation. Today’s ventilators display breath-to-breath numerical changes, sophisticated graphics with adjustable time scales, pressure– volume curves, and a host of screen options and views to adjust and monitor ventilation. The myriad of possible screen adjustments varies as widely as the manufacturers of mechanical ventilators. In general, the user interface is divided into sections of machine set parameters, patient-measured variables, alarm settings, and graphics. Pressures (PIP, Paw, and PEEP), volumes (inspiratory VT, expiratory VT, and V̇E, both spontaneous and machine delivered), flow and time variables (peak flow, respiratory rate [f], I:E ratio, and TI) can be displayed both numerically and via user-defined graphics. Some ventilators have gone to “smart” graphic displays of lung function to provide easy recognition of changes in lung compliance or airways resistance (Figure 3-16).

FIGURE 3-16 Lung Mechanics as Displayed on the Dräger Evita V500. At a glance, the respiratory therapist can make observations of worsening RAW and CL as given numerically and a thickening outline of the major airways and lungs and chest wall. (1 mbar = 1.02 cm H2O) © Dragerwerk AG & Co. KGaA. Image reprinted with permission.

Ventilator Classification or Taxonomy Using Chatburn’s strategy for ventilator classification, the 10th maxim refers to the determination of a ventilator mode (Box 3-7).14 The mode of ventilation is determined by the control variable, breath sequence, and targeting scheme employed. The common control variables are pressure or volume for the primary breath. The primary breath is defined as either the spontaneous breath in continuous spontaneous ventilation (CSV), the mandatory breath in continuous mandatory ventilation (CMV), or the mandatory breath in intermittent mandatory ventilation (IMV). With CSV, all breaths are spontaneous. With CMV, all breaths are mandatory. With IMV, spontaneous breaths are interspersed with mandatory breaths. Using the breath sequence of either CSV, CMV, or IMV coupled with the control variable of either pressure or volume, the clinician can describe the basic mode of ventilation being employed. Using this system, there are five basic modes of ventilation available: Volume-control–continuous mandatory ventilation (VC-CMV). This mode is commonly referred to as assist/control volume ventilation. Volume-control–intermittent mandatory ventilation (VC-IMV). This mode is commonly referred to as IMV or SIMV volume ventilation (aka V-SIMV). Pressure-control–continuous mandatory ventilation (PC-CMV). This mode is commonly referred to as assist/control pressure-control ventilation (PCV). Pressure-control–intermittent mandatory ventilation (PC-IMV). This mode is commonly referred to as SIMV pressure-control ventilation (aka P-SIMV). Pressure-control–continuous spontaneous ventilation (PC-CSV). The most common form of this mode is standalone pressure-support ventilation (PSV). The next step in ventilator classification is a determination of the ventilator breath targeting scheme, for both the primary breath and, if applicable, the secondary (spontaneous) breath. The targeting scheme distinguishes one ventilatory pattern from another and is the method used by the ventilator to reach specific parameters. The lowercase letters shown below (s, d, r, a, b, o, and i) describe seven different targeting schemes currently used by modern mechanical ventilators:14 Set-point (s) targeting schemes allow the operator to set all waveform parameters. In volume-control mode, the operator sets volume and flow waveforms. In pressure-control mode, the operator sets the pressure waveform.

Dual (d) targeting schemes refer to the possibility of within-breath variations of volume or pressure control. Servo (r) targeting schemes utilize ventilator-sensing technology to adjust supporting pressures based on the patient’s inspiratory effort. Adaptive (a) targeting schemes can use signal averaging of previous tidal breaths coupled with auto-adjusting (e.g., pressure) variables to make alterations to maintain the desired patient ventilatory parameters. For example, the ventilator may automatically adjust pressure to achieve an average VT over several breaths. Biovariable (b) targeting schemes allow the ventilator to introduce some deviation from the set point of the control variable (pressure or volume) to mimic the variability seen in normal, spontaneous respiration. Optimal (o) targeting schemes allow ventilator auto-adjustments that may alter variables such as respiratory rate, flow, or volume to improve on anticipated outcomes (e.g., lowered WOB). Intelligent (i) targeting schemes use “artificial intelligence programs such as fuzzy logic, rule-based expert systems, and artificial neural networks” to respond to changing patient lung compliance, resistance, or effort. Figure 3-17 provides a simplified taxonomy for classifying ventilator modes.

FIGURE 3-17 A Simplified Taxonomy for Classifying Modes.

Reproduced from Mireles-Cabodevila, E., Hatipoglu, U., Chatburn, R. A rational framework for selecting modes of ventilation. From: Respir Care. 2013;58(2):348-366.

Description Different ventilator manufacturers often use different proprietary names for specific modes as illustrated in Table 3-1. Hopefully, time and consensus will find resolution to the conflict between proprietary names and actual function.18 TABLE 3-1 Ventilator Modes Available on Common ICU Ventilators: Manufacturer’s Mode Name (Classification) Covidien PB840 A/C volume control (VC-CMVs*) SIMV volume control with pressure support (VC-IMVs, s) SIMV volume control with tube compensation (VCIMVs, r) A/C pressure control (PC-CMVs) A/C volume control plus (PC-CMVa) SIMV pressure control with pressure support (PCIMVs, s) SIMV pressure control with tube compensation (PCIMVs, r)

Bilevel with pressure support (PC-IMVs, s) Bilevel with tube compensation (PC-IMVs, r) SIMV volume control plus with pressure support (PCIMVa, s) SIMV volume control plus with tube compensation (PC-IMVa, r) Spontaneous pressure support (PC-CSVy) Spontaneous tube compensation (PC-CSVr) Spontaneous proportional assist (PC-CSVr) Spontaneous volume support (PC-CSVa)

Dräger Evita XL CMV (VC-CMVs) CMV with pressure-limited ventilation (VC-CMVd) SIMV (VC-IMVs, s) SIMV with automatic tube compensation (VC-IMVs, sr) SIMV with pressure-limited ventilation (VC-IMVd, s) SIMV with pressure-limited ventilation and automatic tube compensation (VC-IMVd, sr) Mandatory minute volume ventilation (VC-IMVa, s) Mandatory minute volume ventilation with automatic tube compensation (VC-IMVa, sr) Mandatory minute volume with pressure-limited ventilation (VC-IMVda, s) Mandatory minute volume with pressure-limited ventilation and automatic tube compensation (VCIMVda, sr) Pressure-control ventilation plus assisted (PC-CMVs) CMV with AutoFlow (PC-CMVa) CMV with AutoFlow and tube compensation (PCCMVar)

Pressure-control ventilation plus with pressure support (PC-IMVs, s) APRV (PC-IMVs, s) Mandatory minute volume with AutoFlow (PC-IMVa, s) SIMV with AutoFlow (PC-IMVa, s) Mandatory minute volume with AutoFlow and tube compensation (PC-IMVar, sr) SIMV with AutoFlow and tube compensation (PCIMVar, sr) Pressure-control ventilation plus with pressure support and tube compensation (PC-IMVsr, sr) APRV with tube compensation (PC-IMVsr, sr) CPAP with pressure support (PC-CSVs) SmartCare (PC-CSVi) CPAP with pressure support and tube compensation (PC-CSVsr)

Hamilton Medical G5 Synchronized controlled mandatory ventilation (VCCMVs) SIMV (VC-IMVs, s) SIMV with tube-resistance compensation (CV-IMVs, sr) Pressure control (CMV PC-CMVs) Pressure (SIMV PC-IMVs, s) NIV-spontaneous timed (PC-IMVs, s) Nasal CPAP with pressure support (PC-IMVs, s) APRV (PC-IMVs, s) DuoPAP (PC-IMVs, s) Adaptive pressure ventilation (SIMV PC-IMVa, s) Adaptive pressure ventilation SIMV with tuberesistance compensation (PC-IMVar, sr) ASV (PC-IMVoi, oi) IntelliVent-ASV (PC-IMVoi, oi) ASV with tube-resistance compensation (PC-IMVoir, oir) IntelliVent-ASV with tube-resistance compensation (PC-IMVoir, oir) Pressure SIMV with tube-resistance compensation (PC-IMVsr, sr) APRV with tube-resistance compensation (PC-IMVsr, sr) Spontaneous with tube-resistance compensation (PCCSVr) Spontaneous (PC-CSVs) NIV

Adaptive pressure ventilation (CMV PC-CMVa) Adaptive pressure ventilation CMV with tuberesistance compensation (PC-CMVar) Pressure control CMV with tube-resistance compensation (PC-CMVsr)

Getinge Servo-i Volume control (VC-IMVd, d) SIMV (volume control) (VC-IMVd, d) Automode (volume control to volume support) (VCIMVd, a) Pressure control (PC-CMVs) Pressure-regulated volume control (PC-CMVa) SIMV (pressure control) (PC-IMVs, s) BiVent (PC-IMVs, s) Automode (pressure control to pressure support) (PCIMVs, s) SIMV pressure-regulated volume control (PC-IMVa, s) Automode (pressure-regulated volume control to volume support) (PC-IMVa, a) Spontaneous with CPAP (PC-CSVs) Pressure support (PC-CSVs) Neurally adjusted ventilatory assist (PC-CSVr) Volume support (PC-CSVa) A/C, assist/control; APRV, airway pressure release ventilation; ASV, adaptive support ventilation; CMV, continuous mandatory ventilation; CPAP, continuous positive airway pressure; CSV, continuous spontaneous ventilation; IMV, intermittent mandatory ventilation; NIV, noninvasive ventilation; PC, pressure control; SIMV,

synchonized intermittent mechanical ventilation; VC, volume control. *Targeting schemes are represented by single lowercase letters: s = set-point, r = servo, a = adaptive, d = dual, i = intelligent, and o = optimal. Combinations include: sr = set-point with servo, da = dual with adaptive, as = adaptive with set-point, ar = adaptive with servo, oi = optimal with intelligent, and oir = optimal with intelligent and servo. Data from Chatburn RL, El-Khatib M, Mireles-Cabodevila E. A taxonomy for mechanical ventilation: 10 fundamental maxims. Respir Care. 2014;59(11):1747–1763. doi:10.4187/respcare.03057.

Ventilator Modes A ventilator mode may be described by its control variable, breath sequence, and targeting scheme employed. That said, there has been an extraordinary proliferation of ventilator modes available, along with an array of often-conflicting manufacturers’ terminology to describe these modes. We will focus our discussion on the five basic modes of ventilation described below.

Continuous Mandatory Ventilation The control variable with continuous mandatory ventilation [CMV] can be either pressure or volume, but there are no entirely spontaneous breaths. Put another way, with CMV, every breath is a mandatory breath. The patient may trigger inspiration, but every breath is machine cycled to expiration. Commonly referred to as assist/control ventilation, the patient can trigger or “assist” the ventilator-delivered primary breath. In the event of no spontaneous effort during the respiratory cycle time, the ventilator will deliver a “control” breath that is time triggered. For volume-control–continuous mandatory ventilation (VC-CMV), the control variable is volume and every breath is mandatory. While the patient can initiate inspiration, the clinician-defined tidal volume is delivered with each breath. Similarly, for pressure-control–continuous mandatory ventilation (PC-CMV), the control variable is pressure. The patient can initiate the breath, but each inspiration is provided at a clinician-defined inspiratory pressure. If no spontaneous breaths occur to initiate inspiration, both VC-CMV and PC-CMV will deliver a time-triggered inspiration, at a frequency normally determined by the set (mandatory) respiratory rate. Most modern critical care ventilators offer VC-CMV and PC-CMV, along with a host of other mode options. It should be noted that a few ventilators use set TI and TE to determine the mandatory, time-cycled rate and I:E ratio (e.g., pNeuton mini and Smiths Medical Pneupac babyPAC 100). With VC-CMV, if lung mechanics change (compliance or resistance), airway pressure will vary. A worsening lung condition in VC-CMV will result in higher peak and mean airway pressures and increased risk of pulmonary barotrauma. Improvements in lung mechanics during VC-CMV will result in lower ventilatory pressures.

With PC-CMV, tidal volume will vary with changes in lung mechanics. In this mode, as compliance is decreased or airway resistance increased, VT is reduced. Hypoventilation and respiratory acidosis with worsening hypoxemia may occur. Alternatively, with PC-CMV, if compliance and resistance improve, tidal volume will increase, possibly resulting in a respiratory alkalosis. With a form of PC-CMV known as pressure-control–inverse-ratio ventilation (PC-IRV) the control variable is pressure and the I:E ratio is greater than 1:1 (e.g., 1.5:1, 2:1). PC-IRV is sometimes used in patients with ARDS. In ARDS, there are variations in regional lung compliance and some areas have better and some have worse pulmonary mechanics. A prolonged TI may improve gas distribution and PaO2, although PC-IRV has not been shown to be effective in all cases of ARDS. Flow, pressure, and volume–time curves for time-triggered and patient-triggered volume ventilation (VCCMV) are illustrated in Figure 3-18.

FIGURE 3-18 Flow, Pressure, and Volume–Time Curves for Time-Triggered and Patient-Triggered Volume Ventilation (VC-CMV). (A) Time-triggered volume ventilation (VC-CMV), sometimes referred to as controlled

ventilation. (B) Patient-triggered volume ventilation (VC-CMV), sometimes referred to as assist/control ventilation. From Waugh JB, Deshpande VM, Brown MK, Harwood R. Rapid Interpretation of Ventilator Waveforms. 2nd ed. Upper Saddle River, NJ: Prentice Hall; 2006.

Description The National Institutes of Health Heart, Lung, and Blood Institute’s ARDS Clinical Network (ARDSNet) protocol for ventilation of patients with ARDS states that any ventilator mode may be used.19 Tidal volume is initiated at 8 mL/kg of PBW and then reduced by 1 mL/kg at intervals of 2 hours (or less) until reaching 6 mL/kg with Pplateau ≤ 30 cm H2O. Respiratory rate is adjusted to achieve an acceptable minute ventilation and pH. PEEP and FIO2 are titrated using PEEP tables to obtain a PaO2 of 55 to 80 mmHg or SpO2 of 88% to 95%. Many different ventilator modes and adjunctive techniques have been tried to improve outcomes in ARDS since the mid-1970s. Although equivocal results on mortality persist, the use of prone positioning to improve aeration of compromised lung fields in the ARDS patient may be helpful.20 In a 2006 study, Mancebo randomized 136 patients with severe ARDS to either supine or prone position and showed a modest reduction in mortality from 58% supine to 43% prone.21 Although the results were not statistically significant, the trend suggested a role for the prone positioning during mechanical ventilation of the ARDS patient. A more recent study, known as the PROSEVA (Proning Severe ARDS Patients) trial, used VT-matched (6 mL/kg) patients assigned to either prone or supine positions, and found a reduction in mortality from 32% supine to 16% while prone.22 Recall that the heart lies close to the sternum in the anterior portion of the thorax. With supine positioning, the dependent portions of the lung lie posterior to the heart, while nondependent portions of the lung lie close to the heart. With prone positioning, the dependent portions of the lung are adjacent to the heart and the nondependent portion of the lung lies away from the heart. When compared, there is somewhat better ventilation and oxygenation if the nondependent portion of the lung does not contain the heart (i.e., prone position). Schematic diagrams of the chest compartment while prone and supine (Figure 3-19) show decreased aeration in the gravity dependent regions.20

FIGURE 3-19 Graphic representation of anticipated aeration of lung units in ARDS patients in the supine (A, C) and prone (B, D) positions. From Henderson WR Griesdale DE Dominelli P, Ronco R Does prone positioning improve oxygenation and reduce mortality in patients with acute respiratory distress syndrome? Can Respir J. 2014;21(4):213–215.

Description

Intermittent Mandatory Ventilation

Intermittent mandatory ventilation (IMV) was introduced in the early 1970s and was advanced as a superior mode of ventilation for several reasons (e.g., reduced mean airway pressures, improved venous return, maintaining ventilatory muscle function, and rapid ventilator weaning). Early forms of IMV combined a time-triggered mandatory respiratory rate with a system to allow the patient to breath spontaneously in between mandatory breaths. Spontaneous breaths generally included a small amount of “physiologic PEEP” (e.g., 3 to 5 cm H2O) provided in the form of CPAP. Prior to being “synchronized” (SIMV), the patient could take a spontaneous inspiratory breath at any point in the cycle, although the ventilator was set by time to deliver its mechanical breath. That meant the patient could be inspiring or exhaling and the machine would still cycle into inspiration resulting in patient– ventilator asynchrony and increased WOB. Breath stacking could occur when a mandatory breath was stacked on top of a spontaneous breath. The patient could also be trying to exhale while the machine was forcing an inspiration. Synchronized intermittent mandatory ventilation (SIMV) was introduced to avoid these problems. This was achieved by allowing a window of time to open during which the patient could trigger a mandatory breath. If the patient did not trigger a breath during the time window provided, the ventilator would then provide a timetriggered mandatory breath. SIMV helped avoid breath stacking and patient– ventilator asynchrony. Today, most modern ventilators provide SIMV. While the term SIMV is common use, the recommended nomenclature is to use IMV for both timetriggered “traditional” IMV and for SIMV. Most modern critical care ventilators offer IMV/SIMV as a mode choice, which can be volume controlled or pressure controlled and used with (or without) CPAP and/or PSV. With volume-controlled IMV or V-SIMV, the clinician sets a tidal volume and rate. This guarantees a minimum minute volume to the patient. The patient can spontaneously breathe between the machine delivered breaths, and these spontaneous breaths may be pressure supported and provided with (or without) an elevated baseline (i.e., with or without PEEP/CPAP). If the patient begins to inspire spontaneously just prior to a time-cycled machine breath, the ventilator will treat that breath as an assisted, patient-triggered, machine-delivered mandatory breath with a preset tidal volume. With IMV, initial ventilator settings are usually set to provide full ventilatory support

(e.g., mandatory rate of 10 to 12 breaths/min with an adequate set tidal volume). Based on the patient’s response, the number of mandatory breaths can be then reduced, to provide partial ventilatory support, whereby the patient must contribute a sufficient level of his or her required ventilation in the form of spontaneous breathing. The mandatory rate could then be incrementally reduced to “wean” the patient from the ventilator. It must be noted, however, that weaning is not required for most patients and the preferred method for ventilator discontinuance is generally the spontaneous breathing trial (SBT). Care must be taken with V-SIMV to properly set the high-pressure alarm (and limits) to reduce the risk of pulmonary barotrauma and to set other alarms to detect hypoventilation, particularly when using low mandatory machine rates. Hypoventilation may occur if spontaneous minute volumes decrease for any reason (e.g., sedative or narcotic administration, ventilatory muscle fatigue, or CNS problems). With pressure-controlled IMV or P-SIMV, the clinician sets an inspiratory pressure and respiratory rate. Mandatory breath tidal volume is determined by the inspiratory pressure, inspiratory time (TI), and the patient’s lung mechanics (e.g., compliance and resistance). With P-SIMV the patient can breathe spontaneously between mandatory breaths and these spontaneous breaths may be pressure supported (e.g., PSV) with or without PEEP/CPAP. Properly adjusted alarm settings are important as the mandatory breath tidal volume and resultant minute ventilation may vary with changes in lung mechanics (Figure 3-20).

FIGURE 3-20 Graphic Display of the Differences Between VC-SIMV (A) and PC-SIMV (B). In A, the tidal volume is set by the respiratory therapist and does not change resulting in pressure variations with changes in lung mechanics (as noted in the second machine-delivered breath). In B, the pressure is set by the respiratory

therapist and VT will vary with changes in lung mechanics. From Tobin MJ. Principles and Practice of Mechanical Ventilation. 2nd ed. New York, NY: McGraw-Hill; 2006: 68−69.

Description

Positive End-Expiratory Pressure Positive end-expiratory pressure (PEEP) is intended to splint the airways open, improve the distribution of gas, and prevent alveolar collapse. PEEP increases functional residual capacity (FRC) and may improve oxygenation in patients with acute restrictive pulmonary disease (e.g., ARDS, pneumonia, and atelectasis). PEEP provides an elevated baseline pressure during expiration. Endotracheal intubation can result in a small reduction in patients’ FRC due to the loss of normal glottic function. A small amount (3 to 5 cm H2O) of “physiologic PEEP” has been suggested for most patients, to balance the loss of “natural PEEP” following endotracheal intubation. PEEP may reduce the incidence of ventilator-associated pneumonia and prevent the development of hypoxemia. PEEP applied intentionally for therapeutic purposes is known as extrinsic PEEP or applied PEEP. Unintentional PEEP due to incomplete airway emptying during expiration is known as intrinsic PEEP, “inadvertent PEEP,” “accidental PEEP,” “ghost PEEP,” or “autoPEEP.” Intrinsic PEEP causes pulmonary overinflation and can cause difficulty for the patient in triggering the ventilator. Steps to correct for autoPEEP should be taken, and may include using smaller tidal volumes, decreasing inspiratory time, increasing expiratory time, reducing mandatory respiratory rate, and the application of a small amount of extrinsic PEEP, usually less than the measured autoPEEP value (e.g., 50% of autoPEEP level). The use of extrinsic PEEP to balance autoPEEP probably should be limited to patients that have trouble triggering the ventilator. PEEP levels in the range of 5 to 20 cm H2O are often used to improve oxygenation and reduce the harmful effects of cyclic alveolar collapse and re-inflation that can occur with ARDS in the absence of PEEP. Improvement in patients’ PaO2/FIO2 ratio with PEEP is associated with decreased mortality in ARDS. Optimal PEEP levels have not been definitively identified, and many methods of applying PEEP have been advocated. These include using the least PEEP necessary to achieve an

acceptable FIO2 (aka minimal PEEP), titrating PEEP based on oxygen delivery, compliance-titrated PEEP, and use of pressure–volume curves to set the optimum PEEP level. The ARDS Clinical Network suggests use of an FIO2–PEEP table to adjust PEEP levels. Viewing the patient’s pressure–volume curves during mechanical ventilation can be helpful in the determination of an appropriate PEEP setting. When zero or subtherapeutic PEEP is applied in patients with ARDS, the small airways may collapse during expiration and re-inflate during inspiration. Each inspired breath may result in shearing forces or wall stress. This could lead to an increased inflammatory response and worsening of overall lung condition. With subtherapeutic PEEP, a slow flow (e.g., inspiratory flow < 10 L/min) pressure–volume curve may indicate low compliance at the initiation of the mandatory ventilator breath, followed by a shift in the curve as compliance improves. The point at which the curve shifts is known as the lower inflection point (LIP). Using this method, PEEP is set 2 cm H2O above the LIP. It must be noted that not all ARDS patients exhibit an LIP.

Lung Recruitment Maneuvers and PEEP Lung recruitment maneuvers are sometimes applied in patients with ARDS to improve V̇/Q̇ and reduce shunting. One method involves the use of pressure-control ventilation in which PEEP is set in the range of 20 to 25 cm H2O and the pressurecontrol level is set about 15 cm H2O above PEEP for a period of 2 to 3 minutes. This is followed by a decremental PEEP study to identify the PEEP level at which compliance is at its highest value. There are differences in mechanical ventilators when setting PEEP during pressure-control ventilation and the manuals for each ventilator should be consulted prior to initiation of a pressure-controlled mode. PEEP may contribute to pulmonary barotrauma and alveolar overdistention resulting in ventilator-associated lung injury. To avoid this, Pplateau should be kept ≤ 30 cm H2O. It should be noted that use of PEEP in severely hypoxemic patients with unilateral or focal lung disease (focal pneumonia) may be ineffective. PEEP should also be used very cautiously in patients with obstructive lung disease, hemodynamic instability, or increased ICP. Fick’s law applies to diffusion of gas across the alveolar capillary (AC) membrane, which is determined by PaO2 and the AC surface area; PEEP increases the surface

area for gas exchange. Respiratory care clinicians use combinations of FIO2 and PEEP to achieve target PaO2 and SaO2 values at a “safe” FIO2 (generally ≤ 0.50 to 0.60). PEEP contributes directly to the mean airway pressure, and when increases in PEEP are considered, the effects on venous return and cardiac output should be considered. When adjusting FIO2 and PEEP, there may be necessary tradeoffs between the hazards of O2 toxicity versus the possibility of ventilator-associated lung injury due to higher PEEP. Through research conducted and reported in the ARDSNet trials, it was noted that more severe ARDS patients may benefit from more aggressive PEEP levels (12 to 24 cm H2O) while mild cases of ARDS generally show improved oxygenation with lower PEEP levels. Protocols have reduced ventilator-induced lung injury and problems associated with pulmonary O2 toxicity. To summarize, PEEP can often be very useful in improving oxygenation in patients with acute, severe restrictive lung disease (e.g., ARDS). PEEP increases mean airway and intrathoracic pressure and may promote the development of barotrauma and ventilator-associated lung injury (VALI), and reduce venous return, cardiac output, and systemic blood pressure. PEEP can increase ICP, and this should be kept in mind when treating patients with increased ICP (e.g., head trauma).

Continuous Positive Airway Pressure Continuous positive airway pressure (CPAP) describes spontaneous breathing at an elevated baseline pressure. Like PEEP, CPAP increases mean airway pressure and mean intrathoracic pressure and FRC. In the ICU, CPAP may be provided through the ventilator, or independently using a high-flow, blended and humidified gas source and a PEEP valve. Acute care uses of CPAP include improving oxygenation in patients with respiratory failure, prevention of postoperative atelectasis, and treatment of cardiogenic pulmonary edema. A number of small, portable CPAP machines have also been developed for in-home use to treat obstructive sleep apnea (OSA); these units are sometimes employed in the acute care setting for patients with OSA. With CPAP, the patient both initiates and terminates an inspiration. Put another way, CPAP provides patient-triggered and patient-cycled breaths. CPAP can be provided as a standalone mode (i.e., continuous spontaneous ventilation [CSV]) or in

combination with pressure support. CPAP may also be used with IMV. CPAP may be provided by mask or via a cuffed endotracheal or tracheostomy tube. With CPAP, the breathing circuit pressure is elevated during inspiration and expiration. Thus, CPAP provides a form of inspiratory pressure augmentation that may reduce the inspiratory WOB during spontaneous breathing. This may be helpful in patients undergoing spontaneous breathing trials (SBTs) leading to extubation. Like PEEP, CPAP’s elevated expiratory pressure increases FRC and the lung surface area for gas exchange. Thus, CPAP may improve oxygenation and help prevent alveolar collapse and atelectasis. As noted, CPAP increases mean airway pressure and intrathoracic pressure; excessive levels may decrease venous return, decrease cardiac output, and decrease blood pressure. Figure 3-21 compares pressure–time curves for baseline spontaneous breathing and CPAP. As with PEEP, CPAP should be used cautiously in patients with obstructive lung disease and in those with hemodynamic instability or elevated ICP.

FIGURE 3-21 Comparison of the Pressure–Time Curves for Spontaneous Breathing and CPAP. Spontaneous breathing is measured at an atmospheric baseline pressure (0 cm H2O) and CPAP is measured at an elevated baseline pressure of +5 cm H2O.

CPAP and Obstructive Sleep Apnea Obstructive sleep apnea (OSA) is defined as the cessation of airflow for ≥ 10 seconds with evidence of sustained inspiratory effort. Noninvasive CPAP delivered by oral or nasal mask at pressures in the range of 4 to 20 cm H2O is the preferred

treatment for OSA. In this range, CPAP splints the soft tissue of the upper airway and prevents collapse, airway obstruction, and apnea. CPAP is also indicated for the treatment of clinically significant obstructive hypopneas. For OSA, the CPAP pressure should be titrated in the sleep laboratory for any patient with multiple comorbidities, significant cardiac history, or morbid obesity. Patients with high BMI may require very high levels of CPAP to control OSA. If CPAP of 20 cm H2O fails to adequately control OSA, BiPAP may be employed. BiPAP combines inspiratory positive airway and expiratory positive airway pressure (EPAP), which is titrated to a maximum setting of 30/25 cm H2O (IPAP/EPAP). Mask leak, patient intolerance of pressure, and aerophagia (air swallowing) are problems associated with high positive airway pressures. In addition to CPAP, other strategies for OSA management include sleeping with the head of the bed elevated, dental appliances, and weight loss (e.g., bariatric surgery). Other techniques that have been employed with varying degrees of success include autotitrating CPAP or autotitrating positive airway pressure (APAP) and adaptive servo-ventilation (ASV) with CPAP. Autotitrating CPAP varies the airway pressure during the night based on specific algorithms. ASV is a closed-loop form of ventilation that uses breath-to-breath analysis to target a desired minute volume and minimize WOB. ASV may be useful in patients with abnormal breathing patterns and complex sleep apnea. The major problem associated with CPAP and OSA treatment is patient compliance. Other complications associated with CPAP are highlighted in Box 3-8.

BOX 3-8 Complications of CPAP Therapy in OSA 1. Subtherapeutic pressures resulting in continued OSA, fatigue, and persistence of excessive daytime sleepiness (EDS) • Try: Sleep lab titration study or autoPAP trial (adjust range clinically). 2. Pressure intolerance • Try: CPAP desensitization, add Cflex, switch to BiPAP, in-lab titration, verify mask seal, or autoPAP trial (adjust range clinically). 3. Aerophagia (air swallowing) • Try: Decreasing CPAP pressure, abdominal gas relievers, or autoPAP trial (adjust range clinically).

4. Dry mouth after CPAP use • Try: Chin strap, full face mask, or consider weight loss, positional therapy, oral appliances or surgical alternatives. 5. Asynchrony • Verify pressure in BiPAP; check inspiratory rise time and inspiratory time. 6. Anxiety or vanity • Try: Education or sedatives or consider alternative forms of treatment. AutoPAP, automatic positive airway pressure; BiPAP, bilevel positive airway pressure; CPAP, continuous positive airway pressure; EDS, excessive daytime sleepiness; OSA, obstructive sleep apnea.

Recruitment Maneuvers with CPAP Very high levels of CPAP for brief periods of time (e.g., 40 cm H2O for 40 seconds) have been suggested as a part of recruitment maneuvers to open collapsed alveoli in patients with ARDS. Such recruitment maneuvers should not be routinely employed, although some patients may benefit.

Noninvasive Ventilation A commonly employed version of noninvasive ventilation (NIV) uses bilevel airway pressure (BiPAP) to provide ventilatory support. BiPAP combines IPAP with EPAP. With BiPAP, the patient typically initiates and terminates inspiration; however, inspiratory pressure augmentation is provided (i.e., IPAP) and expiratory pressure maintains an elevated baseline (i.e., EPAP). BiPAP is typically applied using an oral or nasal mask. EPAP is initially set in the range of 5 to 10 cm H2O and titrated to achieve acceptable oxygenation while minimizing patient discomfort. IPAP is set to achieve an inspiratory pressure of 5 to 15 cm H2O above EPAP and titrated to achieve adequate ventilation and reduced WOB. NIV may be especially useful in patients with acute respiratory failure due to COPD exacerbation to reduce the need for endotracheal intubation, decrease length of hospital stay, and decrease mortality. NIV is also indicated in patients at high risk for extubation failure, and extubation to NIV has been recommended in this group. NIV may be useful in other acute and chronic conditions, as further described in Chapter 10. NIV has not been shown to be helpful for patients with acute hypoxemic

respiratory failure (e.g., ARDS).

Pressure-Support Ventilation Pressure-support ventilation (PSV) provides for patient-triggered, pressure-limited, flow-cycled ventilation. PSV may be further described as spontaneous breathing with inspiratory pressure augmentation; expiration may include the addition of an elevated baseline (i.e., PEEP/CPAP). PSV allows the patient to achieve a given spontaneous tidal volume with less effort. PSV overcomes the resistance to ventilation caused by ventilator circuits and artificial airways. PSV may enhance weaning. PSV also allows the clinician to adjust the ventilatory workload of the patient. PSV may be used as a standalone mode or in conjunction with IMV/SIMV. Modest levels of pressure support (e.g., 5 to 15 cm H2O) can be used to overcome the imposed WOB due to endotracheal or tracheostomy tubes. Higher levels of PSV (e.g., 15 to 25 cm H2O) further reduce the patient’s WOB. Low levels of PSV (5 to 8 cm H2O) are often employed in conjunction with CPAP during spontaneous breathing trials (SBTs) to evaluate readiness for ventilator discontinuance and extubation. With PSV, patients can control their respiratory rate and inspiratory flows, times, and volumes. As a patient-triggered mode, pressure support should not be used in patients with unstable ventilatory drives or periods of apnea. High and low V̇E alarms should be set to help detect hypo- or hyperventilation. Choice of pressure-support pressure level depends on the specific goal. Common goals include: Reducing or eliminating the imposed work of breathing (WOBI) associated with spontaneous breaths in between mandatory breaths in the IMV/SIMV mode. PSV values needed to eliminate WOBI will vary depending on the patient’s ventilatory pattern and endotracheal or tracheostomy tube diameter but are generally the range of 5 to 15 cm H2O. Reducing or eliminating the imposed work of breathing (WOBI) associated with spontaneous breaths during a spontaneous breathing trial (SBT). Here, PSV values needed will also vary depending on the patient’s ventilatory pattern and endotracheal/tracheostomy tube diameter. Current guidelines suggest initiating PSV at 5 to 8 cm H2O during SBTs. Providing a relatively high level of ventilatory support that may improve patient–ventilator synchrony and comfort and reduce the WOB. PSV used in

this fashion is adjusted to achieve an adequate tidal volume (4 to 8 mL/kg IBW) usually at a reasonable spontaneous respiratory rate (f ≤ 25 breaths/min). To vary the tidal volume received by the patient, the respiratory care clinician simply increases or decreases the pressure-support level provided and monitors the resultant expired tidal volumes. Providing an alternative method for patient weaning from mechanical ventilatory support. PSV generally is initiated at a relatively high level for these patients. When the patient meets certain readiness criteria, PSV is reduced 2 to 4 cm H2O in a stepwise fashion. Each reduction in PSV level is followed by careful assessment for signs of distress to assess tolerance. PSV continues to be decreased, as tolerated. If signs of intolerance occur, PSV is returned to its previous level. Figure 3-15 illustrates flow, pressure, and volume waveforms typically seen with PSV.

Airway Pressure-Release Ventilation Airway pressure-release ventilation (APRV) is another mode used for spontaneously breathing patients (Figure 3-22). APRV provides two levels of CPAP that are time triggered and time cycled. Patients may breathe spontaneously at both levels. The high-pressure setting may last several seconds and is intended as an airway/alveolar recruitment technique like other modes of inverse-ratio ventilation (i.e., PC-IRV). As noted, the patient may spontaneously breathe while at the highpressure setting. The machine time cycles to the low-pressure setting to aid in CO2 elimination, lower mean airway pressures, and reduce the risk of cardiovascular compromise. The patient may also spontaneously breathe in the low-pressure setting.

FIGURE 3-22 Airway Pressure-Release Ventilation (APRV). Note that patients may breathe spontaneously at either CPAP level during APRV. From Pilbeam SP, Cairo JM, Barraza P. Special techniques in ventilatory support. In: Cairo JM (ed). Pilbeam’s Mechanical Ventilation. 5th ed. St. Louis, MO: Mosby; 2012: Figure 23-1. Available at https://thoracickey.com/special-techniques-in-ventilatory-support/.

The intent of this mode is ventilation and oxygenation in patients with regional lung compliance heterogeneity and severe oxygenation problems (e.g., ARDS). The ventilator controls and settings used to achieve APRV vary among different ventilators. Since there is a high-pressure set (Phigh) that is time based, the ventilator may call for a Thigh and Tlow to be set (Figure 3-23). The inspiratory phase may last 3 to 6 seconds and the expiratory phase (Tlow) may last 0.5 to 0.8 seconds. The high pressure (Pplateau or Phigh) should be ≤ 30 cm H2O. The pressure at Tlow may be zero (i.e., atmospheric) or elevated.

FIGURE 3-23 Airway Pressure-Release Ventilation. From Blosser S. Airway pressure release ventilation (APRV) management. APRV Final Exam. Available at https://www.pdffiller.com/101286566-aprvpdf-APRV-final-from-Sandy-Blosser-.

Description It is important in APRV to control exhalation to inspiration cycling to prevent derecruitment of alveoli during the expiratory phase. Tlow may be as short as 0.3 sec with restrictive lung disease or as long as 1.5 sec with obstructive lung disease.23 Weaning from APRV can be accomplished when Phigh is reduced to 10 cm H2O, Thigh at 12 to 15 seconds, and FIO2 < 50%. The clinician can switch to CPAP 10 cm H2O with PSV 5 to 10 cm H2O and wean as tolerated to extubation (Clinical Focus 3-4).

CLINICAL FOCUS 3-4 ARDS Your patient is a 72-year-old man 7 days post motor vehicle accident with chest wall trauma. He has been on mechanical ventilation with current settings: PC-

SIMV, FIO2 of 55%, PIP 32 cm H2O, RR 16 bpm, PEEP +8 cm H2O, and PS +8 cm H2O. His machine delivered VT has been 420 mL and he is breathing spontaneously with RRs of 14 bpm and spontaneous VT of 220 mL. He has a 90 pack-year history smoking and two right-side rib fractures (4th and 5th). The patient has a low-grade fever with an elevated white cell count, although the eosinophils are within normal limits (WNL). Auscultatory findings are bilateral inspiratory crackles (rales). The patient’s urine output has been dropping over the past 2 days and Lasix has been ordered. Blood urea nitrogen (BUN) and creatinine are becoming elevated. His weight has gone up 4 lbs since admission. His chest x-ray appears consolidated bilaterally with very little aeration noted. His BP is 90/58 and HR is 105 bpm. He can follow most oral commands. The most recent ABG findings are pH 7.29, PaCO2 64 mmHg, PaO2 47 mmHg, and HCO3− 30 mEq/L. A decision is made to switch to APRV. Questions: 1. What is this patient’s PaO2/FIO2 ratio? Is this consistent with a diagnosis of acute respiratory distress syndrome (ARDS)? 2. Is this scenario consistent with multiorgan dysfunction? 3. Why is this patient gaining weight while an inpatient? 4. What does the acronym APRV stand for? Answers: 1. The PaO2/FIO2 ratio is 82. Ratios of arterial O2 partial pressures to O2 concentrations < 300 but > 200, ≤ 200 but > 100, and ≤ 100 are consistent with mild, moderate, and severe ARDS respectively. 2. Yes: His lung, heart, kidney, and possibly CNS function appear to be affected. 3. He is retaining fluid as evidenced by the weight gain and decreasing urine output. 4. Airway pressure-release ventilation. APRV is initiated with the following settings: FIO2 55%, Phigh 28 cm H2O, Plow 4 cm H2O, Thigh 5 sec, and Tlow 1.0 sec. Following APRV initiation, ABGs were: pH 7.35, PaCO2 54 mmHg, PaO2 67 mmHg, and HCO3− 29 mEq/L. Questions: 1. Classify ABGs while on PC-SIMV and APRV. 2. What are the considerations for choosing the high and low APRV pressures? 3. When weaning from APRV, what mode can be used when Phigh ≤ 10 cm H2O? 4. Does the patient seem to be doing better with the change to APRV?

Answers: 1. PC-SIMV: Partially compensated respiratory acidosis with moderate hypoxemia. APRV: Compensated respiratory acidosis with mild hypoxemia. 2. A slow-flow pressure−volume curve may be obtained and the lower inflection point (LIP) pressure observed. Plow should then be adjusted to be 2 cm H2O above the LIP. The high inflection point should also be observed and Phigh should be below this point. As a general rule, Phigh should be ≤ 30 cm H2O and roughly equal to the Pplateau obtained during conventional mechanical ventilation. 3. CPAP 4. Yes

In a 2016 paper on the pros and cons of APRV, Mireles-Cabodevila and Kacmarek make the point that most of the positive aspects of APRV come from animal studies. Their summary suggests no clear advantage of APRV over conventional mechanical ventilation with lung protective strategies employed.24 In a recent study of 138 patients with ARDS, Zhou et al. found that compared to lung protective ventilation, APRV patients had a reduced mortality rate, reduced ventilator days, and reduced number of days in the ICU.25 A follow-up review of this work did note some of the potential limitations of their study including being unblinded, levels of sedation used, and increased comorbidity in the conventional mechanical ventilation/low VT control group.26 APRV is available on the Getinge Servo-i and Servo-u; Dräger Evita Infinity V500, Babylog VN500; Hamilton G5, C1, C3, MR1; T1, GE Carescape R 860; and Vyaire AVEA and VELA.

Automatic Tube Compensation Automatic tube compensation (ATC) is a variable form of pressure support used as an adjunct to other modes of ventilation and designed to reduce the WOB associated with endotracheal tube resistance. The difference is the within breath variability to adjust support in relation to the patient’s inspiratory flow rate. The improved control of WOB, when comparing ATC to PSV, is more evident in patients with high minute ventilation or increased respiratory drive. The advantage of ATC is inspiratory flow control using intratracheal pressure as the measured variable.

Support and flow are added during inspiration when spontaneous inspiratory activation alters the pressure difference across the endotracheal tube (Figure 3-24). When using ATC, variables are entered into the ventilator such as ET tube diameter and the percentage of support as determined by the clinical goals (e.g., resting the diaphragm or allowing some patient contribution to WOB) and clinician.27 Although intended to reduce the WOB in patients, one study comparing weaning using ATC vs. T-piece showed no significant difference in variables such as PETCO2, SaO2, RR, MAP, or HR. There was also no difference in the reintubation rates comparing ATC and T-piece trials.28 Automatic tube compensation is available on the Hamilton G5, Covidien PB 840 and PB 980, and Dräger Evita XL.

FIGURE 3-24 Automatic Tube Compensation (ATC) and Pressure-Support Ventilation (PSV) Compared. From Unoki T, Serita A, Grap, M. Automatic tube compensation during weaning from mechanical ventilation: Evidence and clinical implications. Crit Care Nurse. 2008; 28(4):34−42.

Description

Proportional Assist Ventilation Proportional assist ventilation (PAV) is an automated form of ventilatory support that adjusts the level of support provided based on the patient’s measured inspiratory flow, elastance, and resistance. The ventilator calculates the pressure required using an algorithm based on the equation of motion to achieve the clinicianset percentage of support (Box 3-9). Pressure varies depending on the amount of ventilatory flow and volume demanded by the patient and level of amplification selected by the clinician. The clinician may adjust the percentage of support from 5% to 95% to achieve a WOB in the range of about 0.3 to 0.7 joules/L. Simply put, PAV employs a servo-targeting scheme in which the support provided by the ventilator is proportional to the patient’s inspiratory effort.

BOX 3-9 Equation of Motion The equation of motion provides a mathematical model of patient–ventilator interaction, where: Pvent (t) = [E × V(t)] + [R × V̇(t)] The equation of motion describes the pressure required to overcome the elastic and resistive properties (or loads) of the lung. The elastic forces are proportional to tidal volume and the resistive forces are proportional to airflow. In the presence of both ventilatory work provided by the ventilator and work provided by the respiratory muscles, this becomes: Pvent + Pmusc = elastance × volume + resistance × flow From the equation, as volume and flow pressure assist from the ventilator approaches the elastic and resistive forces of the lung−thorax system, the pressure that must be generated by the respiratory muscles (interpreted as work) will be diminished. Put another way, the equation describes the elastic and resistive loads contributing to the WOB. The ventilator can perform some or all this work thus, “unloading” the ventilatory muscles.

Terms used are defined as follows: Pvent (t): the inspiratory pressure generated by the ventilator as a function of time Pmusc (t): the inspiratory pressure generated by the ventilatory muscles as a function of time. E: elastance of the respiratory system (lung and chest wall). Recall that elastance is the inverse of compliance. V(t): volume as a function of time R: respiratory system resistance V̇(t): gas flow as a function of time E × V(t): the elastic load of the system. R × V̇(t): the resistive load of the system

With PAV, the patient’s spontaneous inspiratory flow functions as an estimate of the neural output of the respiratory centers. PAV gained popularity as a mode using the patient’s inspiratory effort as the primary source of guided ventilatory support, while automatically adjusting to changing lung mechanics (compliance and resistance). The ventilator will deliver a pressure, flow, and volume based on the patient’s ventilatory demand and lung mechanics without clinician-determined tidal volumes or inspiratory pressures. This assumes intact patient neural control of respiration and a seal at the patient−ventilator interface (i.e., no leaks in the system). PAV is available on several ventilators (e.g., Covidien PB 840, PB 980). When using PAV, a leak in the system can be misinterpreted as increased patient effort and the inspiratory phase can continue into exhalation, like the “runaway” phenomenon as described by Younes,.29 This can be especially problematic if using the ventilator to deliver noninvasive ventilation (NIV) using a face mask, which may develop leaks. PAV incorporates almost continuous input of the patient’s lung mechanics and effort. Modern ventilators are capable of rapid elastance and resistance measures, allowing PAV to incorporate the equation of motion and function as a secondary source of ventilatory work (in addition to the diaphragm). With PAV, ventilation is determined by the patient and adequate alarm settings must be maintained. Proportional assist ventilation is available on the Covidien PB 840 and PB 980, Phillips Respironics V60, and Dräger Evita V500 (as “spontaneous proportional

pressure support.”)

Dual Modes and Adaptive Control Dual and adaptive targeting modes of ventilation have been developed to combine the best characteristics of both pressure-and volume-control ventilation. When using a single variable as the control, with pressure control, volume varied and with volume control, pressure varied. With pressure-control ventilation, the risks of underor overventilation occur as patients’ lung mechanics change. For example, as lung mechanics worsened with pressure-control ventilation, delivered tidal volume may decline. With volume-control ventilation, high airway pressures could occur with changes in lung mechanics (e.g., decreased compliance or increased resistance). When using volume- or pressure-control ventilation, ventilator alarms are set to monitor changes in delivered volumes and pressures. Patient safety may be compromised if alarms are silenced or ignored or set to values that do not detect important changes. Dual targeting allows the ventilator to switch between pressure control and volume control during a single inspiration (i.e. within breath adjustment), while adaptive targeting allows the ventilator to automatically adjust pressure to achieve the desired VT over several breaths (i.e. between breath adjustment).14

Pressure-Regulated Volume Control Pressure-regulated volume control (PRVC) is designed to deliver a volume-targeted, pressure-control breath. An adaptive targeting scheme is employed in which the ventilator automatically adjusts pressure between breaths to reach the targeted volume in response to varying patient conditions. Delivered tidal volume is measured and compared to the set tidal volume. The pressure-control value is then gradually increased or decreased until the target tidal volume is reached. Simply put, PRVC is a pressure-controlled mode of ventilation with a backup rate and set VT. PRVC allows for a patient trigger and the patient can control his or her respiratory rate. Delivered pressure (and the associated volume) will change based on the previous tidal breath. If the delivered tidal volume was less than the target, the pressure-control value will automatically increase; if the tidal volume was greater than the target, the pressure-control value will automatically decrease. Advantages of PRVC include maintaining a stable tidal volume delivery with pressure control in

the face of changing lung mechanics or changing patient inspiratory effort. Potential problems include inappropriate automatic pressure adjustments that may occur under certain conditions. When using PRVC, ventilators such as the Servo-i from Getinge will deliver a test tidal volume with a breath hold to measure the Pplateau. The Pplateau is then used to deliver the next breath and the exhaled VT is compared to the set VT. The tidal volume is delivered using a square pressure waveform and a decelerating flow waveform. The pressure is “regulated” to deliver the clinician set VT from breath to breath. If the volume falls short or exceeds the set VT, the pressure can increase or decrease incrementally +/– 3 cm H2O for the next breaths. The range of the auto-adjusting pressures are confined to within 5 cm H2O of the peak pressure alarm setting and minimum set PEEP; an alarm will sound at both extremes. Animal studies on PRVC vs. VC ventilation using a decelerating flow waveform have shown a significant reduction in the PIP using PRVC, although gas exchange, lung mechanics, and the distribution of ventilation did not appear to be affected. The reduced PIP associated with PRVC could lead to improved patient outcomes, although the clinical evidence has not been definitive.30 PRVC is currently available on the Getinge Servo-i and Servo-u, CareFusion AVEA, Vyaire VELA, Covidien PB 840 and PB 980, Hamilton G5, and Dräger Evita XL.

Volume Support Volume support (VS) can be used in spontaneously breathing patients not requiring time-cycled, machine-delivered breaths. Volume-support ventilation is like pressure support, in that it is patient triggered and flow cycled. However, with VS, the PSV level is automatically adjusted to achieve a volume target. Upon initiation, the ventilator sends a test pulse of 10 cm H2O pressure above PEEP and measures lung compliance and exhaled tidal volume. VS uses that information to adjust pressure support to deliver the set tidal volume on a breath-to-breath basis. In the absence of a patient trigger, VS does not have the option to set an adjustable time-triggered backup rate. Volume support is available on the Getinge Servo-i and Servo-u, Covidien PB 840 and PB 980, and Newport e360.

Automode

If a patient has a variable respiratory drive (fatigue, irritability, pain, changing lung mechanics, and intermittent apnea) a dual-control mode termed called automode is available on some ventilators such as the Getinge Servo-i and Servo-u. With automode, the ventilator can automatically titrate the level of support provided between control and support modes, dependent on the patient’s level of spontaneous ventilation. Automode can be set up to titrate the level of ventilation provided between the following modes: Volume control (VC)–volume support (VS) Pressure control (PC)–pressure support (PS) PRVC–VS For example, automode can be set to alternate between PRVC and VS. In this mode, target minute ventilation (V̇E) is based on the set tidal volume and set rate. PRVC mandatory breaths and VS spontaneous breaths are synchronized using IMV. An adaptive pressure targeting scheme is used in which VT is measured and inspiratory pressure adjusted between breaths to achieve an average exhaled tidal volume equal to the set VT target. If the spontaneous respiratory rate does not achieve the minimum minute ventilation (based on set tidal volume and rate), mandatory breaths are time triggered. A spontaneously breathing patient would receive patient-triggered, pressure-support ventilation with a VT target. If the patient becomes apneic, automode increases the number of time-triggered, volumetargeted, pressure-control breaths needed to achieve the set minimum V̇E (based on set VT and f). Automode can also be set up to use VC and VS or PC and PS to achieve the set minute ventilation. For example, a postoperative, apneic patient might be set up to receive time-triggered VC ventilation using automode. If the patient begins to breathe spontaneously, the ventilator will automatically switch to VS ventilation and titrate the level of VC breaths using IMV to achieve the minute volume goal (based on set VT and f). Simply put, automode is an interactive mode that switches between controlled and supported ventilation depending on the patient’s effort. With automode, the clinician should be aware that inappropriate ventilator sensitivity settings resulting in accidental ventilator triggering (autotriggering) may be sensed as patient effort. The ventilator may then inappropriately reduce the

frequency of machine-delivered, time-triggered breaths. Appropriate alarm settings, patient monitoring, assessment, and interprofessional teamwork are at the heart of good patient care.

Adaptive Support Ventilation Adaptive support ventilation (ASV) is another form of closed-loop, automated ventilation that combines aspects of pressure support and pressure control. With ASV, the ventilator adjusts the mandatory respiratory rate and inspiratory pressure based on measurements of respiratory mechanics to deliver a target V̇E and prescribed level of patient work (WOB); the ventilator will automatically adjust to changes in respiratory mechanics and patient inspiratory effort. With ASV, a set minimum V̇ E is maintained through self-adjusting pressure control and pressure-supported breaths; mandatory and spontaneous breaths are coordinated. Mandatory breaths are time triggered at a preset frequency and time cycled (i.e., pressure control). Mandatory breath pressure is set by the ventilator. Spontaneous breaths are patient triggered and flow cycled (i.e., pressure support) and may occur between and during mandatory breaths. The clinician sets the inspiratory pressure support level, rise time, and expiratory cycle sensitivity for spontaneous breaths. Specifically, the Hamilton G5 ventilator uses an algorithm to determine the optimal breathing frequency and tidal volume. The ventilator uses the patient’s ideal body weight (IBW) to determine a V̇E goal where the target V̇E is 100 mL/min/kg. This initial V̇E setting can be altered by the clinician from 20% to 200% of the machine– calculated V̇E. The VT goal is calculated based on the target minute volume (V̇E) where VT = V̇E/f. The ventilator uses a test breath to determine compliance, resistance, and autoPEEP. To setup ASV, the clinician enters the patient’s weight and percent predicted minute ventilation to support (20% to 200%). The ventilator automatically sets minimum and maximum values for tidal volume, mandatory breath frequency, inspiratory pressure, and inspiratory/expiratory time. Consistent with a lung protective strategy, tidal volume is automatically decreased as compliance decreases. ASV can also automatically adjust rate and I:E ratio to reduce the risk of autoPEEP (i.e., autoPEEP limitation). Specifically, the ventilator

automatically adjusts mandatory breath frequency to keep the expiratory time at least three time constants in length to minimize autoPEEP. ASV will add or reduce the amount of support provided to achieve the target V̇E. When the patient is breathing spontaneously, the mode shifts its focus to pressure support while monitoring lung mechanics and the target V̇E. With spontaneous breathing at a sufficient minute ventilation, no mandatory breaths will be delivered. ASV also incorporates unrestricted inspiratory flow. The ventilator automatically reduces the level of support in response to increased patient effort, providing a form of automatic ventilator weaning. ASV seems well suited to wean patients from mechanical ventilation, but unless properly monitored, problems associated with ventilatory muscle disuse atrophy from overly supported ventilation may result. ASV is available on the Hamilton G5, C3, C1, T1, and MR 1. It should be noted that ASV operates differently from Adaptive Servo Ventilation (ResMed) or Automatic Servo Ventilation (Respironics), two modes used in noninvasive treatment of complex or central sleep apnea.31

Pressure Augmentation and Volume-Assured Pressure Support Pressure augmentation, also known as known as volume-assured pressure support (VAPS), is another dual-control mode that monitors gas flow and volume during inspiration to ensure a preset VT is delivered. As originally introduced on the Bird 8400st (CareFusion, Viasys Corporation, San Diego, California) the mode delivered a patient-triggered, pressure-limited, flow-cycled breath (i.e., pressure support). With VAPS, inspiration begins with a patient-triggered, pressure-support breath. As originally designed, the ventilator then monitored inspiratory gas flow and volume during the pressure-supported breaths. If the VT target volume was achieved before the inspiratory flow termination criteria was reached, the ventilator would cycle to expiration by volume. If the target VT was not achieved before the inspiratory flow termination criteria was reached, the ventilator maintained gas flow until the volume was delivered. Thus, VAPS was similar to volume support (VS); however, tidal volume delivery was assured within a breath, while with VS, tidal volume is assured between breaths. Earlier critical care ventilators that offered pressure augmentation or VAPS are no longer available (e.g., Bear 1000, Bird 8400 ST,). Modes described as VAPS are

currently available with the Philips Respironics V6 and Respironics Trilogy 202 (as average volume-assured pressure support [AVAPS]) and the ResMed Lumis Tx and ResMed Astral 100/150 (as intelligent volume-assured pressure support [iVAPS]). With AVAPS, time- or patient-triggered mandatory pressure control breaths and pressure-supported spontaneous breaths are provided.17 If the patient does not trigger a breath within the interval determined by the rate control, the ventilator delivers a pressure-control breath with the set I-time. If the patient triggers a breath within the interval, the ventilator delivers a PSV breath. The pressure-control and pressure-support inspiratory pressure levels are continually adjusted over time to achieve the volume target. With iVAPS, the ventilator delivers a variable (from breath to breath) PSV level to reach a clinician-set target alveolar ventilation. Thus, the ventilator drops the level of support as patient activity increases and conversely increases the PSV level when patient activity is too low. iVAPS also has a backup rate, if needed.

High-Frequency Ventilation Various forms of high-frequency ventilation (HFV) have been in use since the 1960s. High-frequency ventilation employs very low tidal volumes, typically less than physiologic dead space volume and very rapid respiratory rates (> 60 to 3000 breaths/min). An advantage of HFV is the ability to ventilate patients in the face of large air leaks and indications include major airway disruption (e.g., tracheal esophageal fistula, bronchopleural fistula) that is unmanageable by conventional ventilation. HFV has also been advocated for use as a rescue technique in adult ARDS patients who are failing conventional support and in infants with respiratory failure unresponsive to conventional mechanical ventilation. HFV has been used extensively in neonates to support patients with respiratory distress syndrome (RDS), and those with pulmonary air leaks and bronchopulmonary dysplasia to reduce mean airway pressures. High-frequency ventilation reduces lung injury in animal models and had promise in preventing bronchopulmonary dysplasia and volutrauma in very low-birth-weight infants with RDS. It is important to note that no form of HFV has been shown to be consistently superior to conventional ventilation in reducing mortality and improving outcomes. The U.S. Food and Drug Administration (FDA) defines a high-frequency ventilator

as a device that can deliver a respiratory rate >150 breaths/min. There are four major types of HFV that differ based on breath delivery design. High-frequency positive pressure ventilation (HFPPV) generally uses tidal volumes in the range of 100 to 200 mL, with respiratory rates of 60 to 120 breaths/min, which can be accomplished using some conventional positive pressure ventilators; HFPPV is rarely used today. High-frequency jet ventilation (HFJV) was developed in 1956, but only became popular in the 1980s. HFJV tidal volumes can range from 3.5 to 4.5 mL/kg IBW with rates in the range of 100 to 200 breaths/min, although the Bunnell Life Pulse jet ventilator (Bunnell, Salt Lake City, Utah) can deliver frequencies in the range of 240 to 660 cycles per minute. HFJV employs a jet delivered through a special endotracheal tube adapter; tidal volume is dependent on the amplitude, jet driving pressure, size of the jet orifice, length of the pulsation, and the patient’s respiratory mechanics. HFJV is commonly used in infants with typical delivered tidal volumes in the range of 1 to 3 mL at a frequency of 420 cycles per minute. HFJV is usually operated in combination with conventional CMV with PEEP. High-frequency percussive ventilation (HFPV) was developed by Forrest Bird in the mid-1980s and incorporates a sliding Venturi he called a Phasitron. HFPV combines high-frequency oscillatory pulses (200 to 900 bpm) and small tidal volumes with pressure-control ventilation. HFPV may improve oxygenation and ventilation with reduced risk of barotrauma and hemodynamic compromise; HFPV can also be useful in promoting secretion clearance. HFPV, using the volumetric diffusive respirator (VDR), has been advocated for ventilation of burn patients with inhalational injury to maintain low peak airway pressures; facilitate clearance of soot, sloughed mucosa, and secretions; and to facilitate reinflation of collapsed alveoli. HFPV may also decrease ICP in patients with head injuries and reduce the incidence of pneumonia in patients with smoke inhalation. High-frequency oscillatory ventilation (HFOV) uses very small tidal volumes (50 to 250 mL) and very high frequencies in the range of 180 to 900 breaths/min (i.e., 3 to 15 Hz; 1 Hz = 60 breaths/min). HFOV is an active form of high-frequency ventilation as a vibrating diaphragm will create both a positive (inspiration) and negative (exhalation) wave. This wave is sent down the respiratory tract as the pulse is sent “through” a bias flow moving within the circuit. In ventilators employing a

passive form of high-frequency delivery, the exhalation cycle is a return to atmospheric or set PEEP. During high-frequency ventilation, the FIO2 and mean airway pressure affect changes in oxygenation, and frequency, amplitude, and TI influence ventilation (pH and PaCO2). Currently, HFOV is the most commonly used form of HFV in neonates and adults. HFOV is the only mode of ventilation available with the Vyaire 3100A (neonates, infants, and small children) and 3100B (adults and children > 35 kg) high-frequency oscillatory ventilators. In adults, the 3100B is primarily used as a rescue mode for ARDS patients with refractory hypoxemia that has failed to respond to conventional mechanical ventilation using a lung protective strategy. HFOV is not indicated for patients with less severe ARDS and is not recommended for routine use. When observing potential regions of the pressure–volume curve (Figure 3-25) that increase the risk of lung injury, one can see the value of ventilation within the two extremes of reduced compliance. HFOV allows for effective ventilation while maintaining lung inflation between the extremes of atelectasis and over distention.

FIGURE 3-25 The Pressure–Volume Curve. Areas in green show the oscillatory breaths and the region occupied within a pressure–volume curve. Conventional breaths that operate in cases of pathology at the extremes of the pressure–volume curve may result in atelectotrauma (low CL, bottom left region of the pressure–volume curve) or volutrauma (low CL, top right region of the PV curve).

Description HFOV uses a combination of mean airway pressure, frequency, and amplitude to inflate the lungs and promote O2 and CO2 exchange. Proximal airways and alveoli

are ventilated by bulk gas flow, but as the lung transitions to the more distal units, gas moves by diffusion. Possible mechanisms by which HFOV is thought to improve gas exchange include pendelluft, gas streaming, and Taylor-type dispersion. Pendelluft is the gas exchange between lung units with different time constants. Recall that time constants describe filling time and emptying time of lung units and are affected by compliance and resistance. Differences in compliance and resistance in different regions of the lung can affect oxygenation and ventilation during conventional positive pressure ventilation. Pendelluft may allow for collateral ventilation to enhance gas delivery during HFOV. Gas streaming during normal bulk gas flow causes gas in the center of the airway to move more rapidly than gas near the airway walls due to frictional effects (i.e., gas molecule to gas molecule in the center and gas molecule to airway wall in the outer part of the gas stream). While an oversimplification, pulsatile gas flow during HFOV may move through the center of the airways towards the gas exchange units, while gas flow near the walls of the airways may move away from the gas exchange units. This could result in simultaneous movement of “inspired” and “expired” gases during HFOV. Taylor-type dispersion is simply enhanced diffusion of gas caused by the rapidly oscillating gas stream reaching the small airways. Enhanced diffusion is thought to be the primary mechanism by which HFOV is effective in achieving gas exchange. In theory, HFOV may reduce the likelihood of ventilator-associated lung injury (VALI) by achieving ventilation within an optimal lung compliance curve, avoiding pulmonary overdistention and repetitive alveolar collapse and re-expansion due to decreased resting lung volumes (i.e., decreased FRC due to acute restrictive lung disease); see Figure 3-26. The HFOV volumes are usually close to the dead space volume and controlled by the amplitude of the pressure pulse.32 Figure 3-26 illustrates possible mechanisms for gas distribution during HFOV.

FIGURE 3-26 HFOV and Processes of Gas Distribution. Slutsky AS, Drazen JM. Ventilation with small tidal volumes. N Engl J Med. 2002; 347:631.

Description In summary, high-frequency ventilation combines very rapid respiratory rates with very small tidal volumes, at or below that of the physiologic dead space. HFV has been used in neonates, pediatric patients, and adults. Its primary use in adults is as a rescue mode for patients with severe ARDS. There are no universally agreed-upon indications for HFV, although it has been suggested for several disease states and conditions (e.g., bronchopleural fistula, severe ARDS, neonatal RDS, burns with inhalational injury, and head trauma with increased ICP). HFV may cause autoPEEP due to reduced expiratory times and probably should be avoided in patients with obstructive lung disease, as dynamic hyperinflation may occur.

Neurally Adjusted Ventilatory Assist

Neurally adjusted ventilatory assist (NAVA) uses the natural electrical discharge from the diaphragm (i.e., electrical activity of the diaphragm or EAdia) during inspiration to trigger a breath from the ventilator. The inspiratory signal trigger is the primary difference between NAVA and other modes of mechanical ventilation.33 The inspiratory signal is detected using diaphragmatic electromyography (EMGdia). While it is possible to pick up EAdia using EMG from regions of the chest wall, the best signals come from specifically designed esophageal catheters.

CLINICAL FOCUS 3-5 High-Frequency Ventilation in a Burn Patient Ms. Jones is a 27-year-old woman with second- and third-degree burns covering her face, chest, abdomen, upper back, and right arm. Using the rule of nines (11 sections of the body, each equaling 9% of the total body surface area + genitals 1%), it was estimated that 40.5% of her body was covered by burns that occurred due to an illicit drug operation explosion. Ms. Jones was a direct admit to the burn unit and was already intubated. She was taken to the shower for debridement, underwent bronchoscopy, and had vascular access lines placed. In the unit, she was placed on a volumetric diffusive respirator (VDR) for highfrequency percussive ventilation (HFPV) secondary to signs and symptoms of inhalation lung injury, including particulate matter, erythema, exudate, and swelling in the airways. After ensuring a minimal cuff leak of 10%, her initial VDR settings were: pulse frequency of 550 Hz, sinusoidal rate of 16, I:E ratio of 2:1 (TE = 2 sec), FIO2 100%, and PIP of 26 cm H2O. Sedation by protocol was maintained with combination drug therapy including propofol, ketamine, and dilaudid. Her initial ABG was: pH 7.27, PaCO2 60 mmHg, PaO2 65 mmHg, and HCO3– 27 mEq/L. The pulse frequency was decreased to 500 Hz and the PIP was increased to 28 cm H2O. A follow-up ABG was pH 7.33, PaCO2 54 mmHg, PaO2 70 mmHg, and HCO3– of 28 mEq/L. Five days after admission, the patient was taken to the operating room for debridement. She was taken off the VDR and placed on PC-AC ventilation at a PIP of 22 cm H2O, FIO2 100%, RR 16, and PEEP +5. After returning to the burn unit, an ABG was drawn: pH 7.17, PaCO2 87 mmHg, PaO2 40 mmHg, and HCO3– of 31 mEq/L. Her spontaneous RR and VT were 35 and 200 mL, respectively. Auscultatory findings were bilateral inspiratory crackles. She was placed back on the VDR at an FIO2 of 100%, pulse frequency 500 Hz, sinusoidal rate of 16, and I:E ratio of 2:1 (TE = 2 sec). The PIP was reduced to 25 cm H2O and a convective

pressure of 10 cm H2O was added to improve ventilation while maintaining a PAW < 35 cm H2O. A follow-up ABG was pH 7.36, PaCO2 58 mmHg, PaO2 148 mmHg, and HCO3– of 32 mEq/L. After 3 weeks of mechanical ventilation, operating room (OR) visits for debridement, multiple bronchoscopies, and trips to the shower, the VDR settings were weaned to oscillatory CPAP with a pulse frequency of 500 Hz/5 cm H2O and a FIO2 of 40%. The patient was disconnected from the VDR to obtain extubation criteria and the MIP/NIF was –44 cm H2O, VT 400 mL, RR 22, and rapid shallow breathing index (RSBI) of 55. Questions: 1. Classify the initial two ABGs. 2. What happened while ventilating the patient in the OR 5 days after admission? a. Classify the ABGs associated with the return from the OR. b. What do you think the strategy was when convective pressure was added? 3. Three weeks after admission, do you believe the patient is ready for extubation? Answers (pH/PaCO2/PaO2/HCO3–): 1. 7.27 / 60 / 65 / 27. Partially compensated respiratory acidosis with mild hypoxemia. 7.33/ 54 / 70 / 28. Partially compensated respiratory acidosis with mild hypoxemia. Somewhat better than the initial ABG. 2. Switching the patient from HFPV to PC-AC appeared to have resulted in derecruitment of lung alveolar units and an increase in atelectasis. a. 7.17 / 87 / 40 / 31. Partially compensated respiratory acidosis with severe hypoxemia. 7.36 / 58 / 148 / 32. Compensated respiratory acidosis with hyperoxemia. b. The apparent strategy was to recruit the previously closed lung units and improve the ventilation/perfusion (V̇/Q̇) ratio. 3. Yes. The RSBI is < 105 and the MIP/NIF is less than (more negative) –20 cm H2O. It appears that the patient’s ventilatory failure has resolved.

For normal inspiration to occur, a combination of cortical and medullary center outflow to the phrenic motoneurons is sent as a series of action potentials. The activated diaphragm contracts and the intensity and duration of inspiratory

contraction are related to lung mechanics and respiratory drive. The ability of the diaphragm to respond is dependent on the muscle’s inherent contractile properties from breath to breath. NAVA provides coordination of the patient’s central respiratory drive and the ventilator’s inspiratory trigger. The ventilator can be set to cycle to expiration when the diaphragmatic signal reaches 40% to 70% of its maximum signal strength. The idea is to cycle to expiration based on a diminished inspiratory EAdia. This is done to prevent continued inflation by the ventilator when the patient’s central respiratory control centers have switched to the expiratory phase. NAVA is intended to improve patient–ventilator synchrony. Disadvantages include esophageal catheter cost, catheter discomfort, catheter displacement, and apnea. In the case of apnea (or absence of an EMGdia signal), the ventilator will return to a pressure-controlled mode as a safety feature. The degree of NAVA support provided varies with the amplitude of the diaphragmatic signal and the assist level set by the clinician. The initial NAVA level applied should produce the same inspiratory pressure (or slightly lower) than the patient was receiving with conventional ventilation and then adjusted. As NAVA levels are increased, peak pressure and tidal volume will increase. If the support chosen is too low, the patient may exhibit signs of distress with increased respiratory rate and a fatiguing respiratory pattern. When the support is greater than necessary, large tidal breaths may occur with suppression of the EMGdia signal. Optimal NAVA support allows the patient to choose a respiratory rate and VT to maintain an appropriate PaCO2 while sufficiently unloading the respiratory muscles. As with any mode of mechanical ventilation, proper alarm settings are an important consideration when using NAVA. Figure 3-27 shows the Servo-u with NAVA capabilities. A graphic tracing display is used by the respiratory care clinician to adjust the position of the EMG catheter for optimal sensing of diaphragmatic activation/deactivation (Figure 328).

FIGURE 3-27 The NAVA Screen on the Getinge Servo-u. The yellow trace is actual pressure delivery and the gray trace is the estimated pressure delivery based on the diaphragm EMG signal and set NAVA level. From Getinge. The Basic Concept of NAVA and Edi NAVA modules 1 and 2. p. 17 (PPT slides: Training set from Servo-u sales rep).

Description

FIGURE 3-28 Placement of the NAVA Edi (Diaphragm EMG) Catheter. Correct placement is achieved when the second and third leads are highlighted in pink and the Edi signal is present. From Getinge. The Basic Concept of NAVA and Edi NAVA module 1 and 2, p. 38. PPT slides: Training set from Servo-u sales rep).

NAVA has been used in adults, children, and neonates. In one study of 160 randomly assigned (conventional mechanical ventilation vs. NAVA) pediatric patients, there was a significant difference in sedation (excluding opiates and postop patients) and length of pediatric ICU (PICU) stay indicating NAVA is a safe, effective form of ventilation that may improve patient–ventilator synchrony.34 NAVA is available on the Getinge Servo-i and Servo-u ventilators. Currently, there is no convincing evidence that NAVA improves clinically important patient outcomes.

Ventilator Parameters Ventilator parameters include pressures, flows, and volumes, as well as alarms and monitoring systems, as described below.

Flow Waveforms Modern critical care ventilators provide graphics packages that allow for observation and monitoring of pressures, flows, and volumes. Examination of pressure–time curves and flow–time curves can be very useful to identify the inspiratory trigger (e.g., patient-triggered or time-triggered breaths), the type of breath (e.g., mandatory or spontaneous), inspiratory gas flows and pressures, the cycle variable, and pressures and flows during expiration. The pressure–time waveform display, also known as the pressure–time scalar, can be very useful in identifying the mode of ventilation as well as PIP, Pplateau, and baseline pressure (e.g., PEEP or CPAP). Observation of the pressure–time scalar can also provide a visual representation of the inspiratory time, expiratory time, and I:E ratio. Volume–time curves provide visual confirmation of the patient’s actual inspired and expired tidal volumes. The flow–time curve or flow–time scalar provides a graphic display of the inspiratory and expiratory gas flow versus time. For mandatory breaths, the most common flow waveforms are the constant flow waveform (also known as the square wave, rectangular wave, or constant flow generator) and the decreasing flow waveform (also known as the down-ramp, decelerating flow, or descending ramp). During VC ventilation (VC-CMV and VC-IMV), several ventilators offer operator selectable inspiratory flow waveforms for mandatory breaths. Older ventilators (e.g., Hamilton Veolar) offered a choice of up to seven different inspiratory waveforms (e.g., square wave, full down-ramp, partial down-ramp, full up-ramp, partial up-ramp, sine wave, and accelerating flow). Most newer critical care ventilators offer a preset inspiratory flow waveform or only a few options: square or descending ramp (e.g., Covidien PB 840 and PB 960) or sine, square, and decelerating (e.g., Hamilton G5 and C3). Examples of flow, volume, and pressure waveforms are shown in Figure 329. Assuming a constant inspiratory time and tidal volume (VC mode), mean and peak airway pressure will vary in a predictable fashion with changes in the inspiratory flow waveform. Generally, a down-ramp will result in the lowest PIP but

highest mean airway pressure, while an up-ramp will tend to result in the highest PIP but lowest mean airway pressure. Put another way, flow waveforms that tend to increase mean airway pressure also decrease PIP and vice versa. Increasing mean airway pressure may be helpful to improve oxygenation and gas transfer, while reducing mean airway pressure may improve venous return and reduce the likelihood of cardiovascular compromise.

FIGURE 3-29 Pressure, Volume, and Flow Waveforms.35 (A) Descending (decelerating) flow waveform and square wave pressure waveform. (B) Square wave flow waveform with linearly increasing pressure waveform. (C) Up-ramp flow waveform with increasing pressure waveform. (D) Down-ramp flow waveform with curvilinear increasing pressure waveform. (E) Sine or sinusoidal flow waveform with increasing and then decreasing pressure waveform. Tobin MJ. Principles and Practice of Mechanical Ventilation. 2nd ed. New York, NY: McGraw-Hill; 2006: 41.

Description The square waveform is a common flow pattern offered on most mechanical ventilators during VC ventilation. With the square wave, volume and pressure increase in a linear fashion (Figure 3-29B). With a down-ramp type flow waveform, pressure and volume tend to increase in a curvilinear fashion (Figure 3-29D). A sine wave flow waveform results in a sinusoidal increase in volume and then an increase in pressure followed by a decrease in pressure at end-inspiration (Figure 3-29E). The sine flow waveform is thought to more closely resemble gas flow during normal, spontaneous breathing. The ascending, accelerating, or up-ramp flow waveforms

generally are not available on the current generation of critical care ventilators (Figure 3-29C). Flow waveforms during pressure-control ventilation (PCV) and pressure-support ventilation (PSV) generally are descending or decelerating, resulting in a squarewave–like pressure waveform (Figure 3-29A). With PCV and PSV, initial peak flow is rapidly achieved during the beginning of inspiration and then flow decreases until the breath terminates (Figure 3-29A). With PCV, inspiration cycles to expiration by time, with flow continuing to decrease until the set inspiratory time is reached. During PCV, if adequate inspiratory time is allowed, flow will reach zero at end inspiration followed by an inspiratory pause or hold (i.e., no flow). With PSV, inspiratory flow declines until the flow termination criterion is met, generally 5% to 25% of the peak flow or 5 L/min. Most modern ventilators allow for adjustment of inspiratory rise time and expiratory sensitivity during PSV and these adjustments will alter the inspiratory pressure and flow waveforms.

Inspiratory Pause Most modern mechanical ventilators allow the clinician to set an inspiratory pause or hold in the VC mode, which will result in an inspiratory pressure plateau (Pplateau). For example, with the Hamilton G5, an inspiratory pause may be set by the operator between 0% and 70% of cycle time, while the CareFusion AVEA and Covidien PB 840 allow the clinician to set an inspiratory hold from 0 to 3 seconds and 0 to 2 seconds, respectively. The inspiratory pause is designed to hold the inspired breath momentarily prior to the exhalation phase. Clinicians and automated monitoring systems incorporated within the ventilator routinely use this feature to make determinations of lung mechanics, compliance, and resistance. When inspiratory pause is activated, the airway pressure will decrease from PIP to a Pplateau, and the plateau will continue for the duration of the inspiratory pause. With a sufficient inspiratory plateau (0.5 to 2 sec), there should be complete equilibration between Pplateau and alveolar pressure. Under these circumstances, plateau pressure represents the force required to distend the lung within the thorax at a point of no gas flow. Total static compliance (CST) can then be easily calculated where: CST = VT ÷ (Pplateau – PEEP). CST is determined by the patient’s lung compliance and thoracic or chest wall compliance. Atelectasis, pneumonia, pulmonary edema, ARDS, and

pulmonary fibrosis will all decrease lung compliance. Thoracic cage deformities, ascites, obesity, and pregnancy will all decrease thoracic compliance. RC Insight In the volume-control mode, decreases in compliance will increase the PIP and Pplateau. In the pressurecontrol mode, decreases in compliance will decrease delivered VT; peak inspiratory pressure will remain the same.

The difference between PIP and Pplateau is due to airway resistance (RAW), which can also be easily calculated during VC ventilation where: RAW = (PIP – Pplateau) ÷ inspiratory flow rate. Normal CST is 60 to 100 mL/cm H2O while normal RAW in intubated patients is about 5 to 10 cm H2O/L/sec, depending on the diameter of the endotracheal tube and inspiratory gas flow rate. Bronchospasm, increased secretions, mucosal edema, mucus plugging, or endotracheal tube occlusion (secretions, kinking, or biting) may increase RAW. During volume ventilation, PIP will increase with decreases in compliance OR increases in resistance. With increased RAW, the PIP – Pplateau difference will increase. With decreased compliance, the Pplateau will increase (Figure 3-30).

FIGURE 3-30 Evaluation of the Peak and Plateau Pressures Using a Pressure–Time Curve.

Description

Inspiratory pause can also be applied to improve the distribution of inspired gases and may improve gas exchange. Devaquet et al. showed that inspiratory pause < 1 second over normal I times could increase CO2 removal by 6 mmHg in patients with ARDS ventilated with low lung volumes and keep measured autoPEEP < 0.5 cm H2O.36 RC Insight In the VC mode, increases in airway resistance (RAW) will increase PIP and increase the PIP – Pplateau difference.

FIO2 When initiating mechanical ventilation, the clinician must consider appropriate choice of fractional inspired oxygen (FIO2) concentration, based on the patient’s clinical condition and therapeutic goals. Modern critical care ventilators allow from 21% to 100% oxygen to be provided (FIO2 0.21 to 1.0). FIO2 and barometric pressure (PB) determine the partial pressure of inspired oxygen (PIO2) and PIO2 and alveolar ventilation determine the alveolar oxygen tension (PAO2) where: PIO2 (mmHg) = FIO2 (PB – PH2O) and the alveolar air equation:

PACO2 is the alveolar carbon dioxide tension (which approximately equals PaCO2) and R = the respiratory quotient (which is simply CO2 production divided by oxygen consumption; R = V̇CO2/V̇O2). Normal R is about 0.80. Clinically, alveolar oxygen tension (PAO2) can be approximated by the simplified alveolar air equation where: PAO2 = PIO2 – PaCO2/0.80

Thus, things that will increase PAO2 include increased FIO2, increased PB, and decreased PaCO2. As PAO2 increases, so does arterial oxygen tension (PaO2); however, the relationship between PAO2 and PaO2 is dependent on the matching of gas and blood in the lung (V̇/Q̇) and gas diffusion across the alveolar capillary membrane into the blood. Respiratory failure is a usual prelude to mechanical ventilation and as such, there are usually oxygenation problems that will need attention. As noted, FIO2 is an important contributor to alveolar and arterial oxygen partial pressures. PaO2, in turn is an important determinant of the oxygen saturation of the hemoglobin (SaO2) and arterial oxygen content (CaO2). Oxygen delivery to the tissues (ḊO2) requires an adequate CaO2 and cardiac output (Q̇T); recall that ḊO2 = CaO2 × Q̇T. When oxygen demand outstrips supply, the clinician will note an increasing lactate concentration as anaerobic metabolism replaces the Krebs cycle metabolism for ATP generation. O2 is well tolerated in the clinical setting, though excessive concentrations (FIO2 > 0.50 to 0.60) for prolonged periods may lead to adverse effects (e.g., oxygen toxicity, absorption atelectasis). Adequate oxygenation must be maintained to prevent tissue hypoxia and lactic acidosis. However, the lowest possible combination of FIO2 and PEEP should be used to keep the PaO2 between 60 and 80 mmHg and SaO2 between 90% and 96% for most patients.

PEEP/CPAP Positive end-expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) should be considered alongside FIO2 when addressing oxygenation issues in patients requiring mechanical ventilation. PEEP generally refers to positive endexpiratory pressure applied following a time-triggered or patient-triggered mandatory breath. CPAP generally refers to continuous positive airway pressure applied to spontaneously breathing patients. With IMV, mandatory breaths are interspersed with spontaneous breaths; some refer to this as PEEP/CPAP. PEEP and CPAP increase FRC, improve and maintain lung volumes, and help open and stabilize alveoli in patients with acute restrictive disease. As noted, small amounts (3 to 5 cm H2O) of PEEP or CPAP generally are used in most intubated

patients receiving mechanical ventilatory support to avoid end-expiratory alveolar collapse, which may be caused by the loss of normal glottic function; this is sometimes referred to as physiologic PEEP. Applied PEEP may also be helpful to offset the effects of autoPEEP and air trapping. Patients with obstructive lung disease often already have an elevated FRC, and PEEP should be used cautiously in these patients, except to offset autoPEEP. Higher PEEP levels are often used in patients with hypoxemic respiratory failure (e.g., ARDS, pneumonia, and pulmonary edema) to improve oxygenation and avoid VALI. PEEP or CPAP is indicated in patients with collapsed and unstable lung units, and arterial oxygenation is inadequate when using moderate to high concentrations of oxygen. PEEP/CPAP should be considered when PaO2 < 60 mmHg and FIO2 > 0.40. PEEP and CPAP increase mean airway pressure, which may impede venous return and compromise cardiac output in certain patients. Untreated tension pneumothorax is an absolute contraindication to the application of PEEP or CPAP. PEEP/CPAP should be used cautiously (if at all) in patients with hemodynamic instability, hypotension, shock, already elevated FRC (e.g., COPD, acute asthma), and elevated ICP. It is also important to note that not all ARDS patients respond to low-level PEEP and high levels of PEEP may improve outcomes in severe ARDS. There are also pulmonary and extrapulmonary causes of ARDS. Pulmonary causes include infectious pneumonia while extrapulmonary causes include sepsis, hemorrhagic shock, peritonitis, and multiple trauma. Extrapulmonary causes of ARDS may respond better to low levels of PEEP than pulmonary causes.

Alarms Industry has continually been making improvements in ventilator alarms. Alarm sensitivity can be set by the respiratory care clinician to provide high and low alarms for specific parameters such as volume, pressure, respiratory rate, minute ventilation, FIO2, and the development of apnea. Alarms systems often incorporate algorithms to assign importance from high to low with color and volume differentiation. Ventilator alarms should be adjusted to ensure clinicians are alerted when their attention is required, yet overly sensitive alarm settings should not result

in frequent nuisance alarms, which are then ignored. Put another way, the percentage of true positive alarms should be high, and the number of false positive alarms should be low to ensure patient safety while minimizing unnecessary environmental noise pollution in the ICU. To that end, The Joint Commission (which accredits health care organizations and programs) has issued National Patient Safety Goals (effective 1/2017) addressing all medical devices equipped with alarms.37 These goals reference a 2014 UCSF study that found an average of 187 audible alarms/bed/day; 45% were for arrhythmias and 88.8% were false alarms, resulting in alarm fatigue and desensitization.38 A sentinel event is defined by The Joint Commission as any unanticipated event in a healthcare setting resulting in death or serious physical or psychological injury (not related to the natural course of the patient’s illness). Alarms are at the heart of a Joint Commission statement on sentinel event alerts, suggesting a need for better alarm thresholds and improved routing of alarms to the appropriate responder. During mechanical ventilation, there are factory-set, priority alarms that signal power failure, high and low source machine pressures, and temperature. Clinicianset alarms are determined from patient to patient and dependent on institutional protocols and clinician experience. Examples of common clinician settings include: low tidal volume set 100 mL below set VT, low V̇E set 2 L/min below observed V̇E (total machine + spontaneous), high respiratory rate set 10 bpm above observed rate (total machine + spontaneous), PEEP set 2 to 5 cm H2O below set PEEP, and a peak pressure alarm set 5 to 10 cm H2O above observed PIP. Importantly, the alarms should be set to notify the clinician of problems that could jeopardize patient safety or lead to such sentinel events as injury or death. For instance, appropriate alarms for minute ventilation could signal a loss of the spontaneous contribution of ventilation post-analgesic administration. Ventilator alarms should notify nursing, medical, and respiratory care personnel of deterioration in the patient’s ventilatory support status before this deterioration manifests as cardiac arrhythmias or O2 desaturation. The priority of alarms for mechanical ventilation have been assigned three levels of importance as described in Box 3-10. Level 1 alarms require immediate attention, cannot be silenced, and are life threatening. In the event of a ventilator alarm signal,

the patient should be immediately disconnected from mechanical ventilation and ventilated manually (via resuscitation bag with 100% FIO2) until the problem can be identified and corrected. Replacing the ventilator with another unit should be immediately considered if the problem cannot be readily identified. Level 2 alarms may be life threatening, if left unattended. These alarms may be self-limiting with audible termination if normal function resumes. Level 3 alarms are generally associated with patient ventilatory parameter fluctuations including volume loss or lung mechanics alterations. In addition to these alarms, the clinician should consider supplementary systems that are routinely used for ventilatory monitoring such as SPO2 monitors and end-tidal CO2 monitors (i.e., PETCO2). Assessments of ventilation using PETCO2 can provide the clinician with real-time changes in gas exchange status; however, clinicians must understand the limitations of PETCO2 for patient monitoring. Oximetry and end-tidal CO2 monitoring should have appropriate alarm limits set and be managed by the responsible clinicians.39 Chapters 8 and 9 discuss patient assessment and monitoring in more detail.

BOX 3-10 Alarm Levels of Priority Level 1 1. 2. 3. 4.

Power failure Control circuit failure High or low primarily line pressure Exhalation valve failure

Level 2 1. Humidification failure 2. High or low PEEP 3. FIO2 blender control failure 4. Circuit leak 5. Circuit occlusion Level 3 1. AutoPEEP 2. High or low V̇E

3. High or low VT 4. High or low peak pressures *It should be noted that Level 1 alarms are noncancelling and must be corrected prior to reinitiation of mechanical ventilation. Level 3 alarms may also trigger a Level 2 alarm. **All alarms must be attended to in the interests of patient safety. Appropriate settings, alarm limits, and patient therapies (e.g., bronchodilators, suctioning, and sedation) must be considered.

Humidification Primary functions of the normal upper airway are to warm, filter, and humidify inspired gases. The isothermic saturation boundary (ISB) is the point at which inspired gases are 100% saturated at body temperature, which occurs two to three subdivisions below the trachea. By the time inspired gas reaches the ISB, the inspired air has been warned to 37ºC and humidified to 44 mg H2O/L with a water vapor pressure (PH2O) of 47 mmHg. During invasive mechanical ventilation, the normal anatomy of the upper airway is bypassed, and these primary functions of the upper airway are lost. Systems to provide humidification during mechanical ventilation include active humidification using a heated humidifier and passive humidification using a heat and moisture exchanger (HME). American Association for Respiratory Care Clinical Practice Guidelines for active humidification during invasive mechanical ventilation suggest humidification should be provided to achieve between 33 to 44 mg H2O/L at gas temperatures between of 34º to 41ºC (100% relative humidity) at the ventilator circuit connection to the artificial airway (i.e., Yconnector). This may be accomplished by several heated humidifiers designed to be used with mechanical ventilators (e.g., Fisher Paykel or Conchatherm heated humidifiers). When using a heat moisture exchanger (HME) to achieve passive humidification during invasive mechanical ventilation, the device should deliver 30 mg H2O/L. Passive humidification is not recommended for patients receiving NIV or for patients being ventilated with low tidal volumes (e.g., lung-protective ventilation) because the HME will add to dead-space volume.40 The International Organization for Standardization (ISO) suggests increased thermal injury risk at sustained inspired gas temperatures > 41ºC and active humidifiers and humidifier alarm limits should be set accordingly. The AARC Clinical Practice Guideline for active humidification recommends “high temperature be set no

higher than 41ºC (with a 43ºC over-temperature alarm) and the low-temperature alarm should be set no lower than 2ºC below the desired temperature at the circuit Y-piece.”39 Heating and humidification of the airways is an important component of body homeostasis and bronchial hygiene. Inadequate humidification can increase secretion viscosity and impair mucociliary transport. Proper management of heated humification systems during mechanical ventilation should aim to ensure adequate humidification while avoiding the potential for thermal injury or hyperthermia due to excessive temperatures. It is of interest to note that airway rewarming using a heated humidifier may provide a modest benefit for adult patients suffering from accidental hypothermia; however, airway rewarming is not a primary form of treatment in these patients.

Sigh Breaths Normal, spontaneously breathing individuals take an intermittent deep breath or sigh every 6 to 10 minutes to keep alveolar units inflated and prevent atelectasis. In the absence of PEEP, constant, shallow tidal breathing (< 7 mL/kg) without a sigh may result in progressive atelectasis. Therefore, postoperative abdominal or thoracic surgical patients are instructed to cough and deep breathe to prevent the development of postoperative atelectasis and respiratory failure. Volume ventilation became common in the ICU in the late 1960s and early 1970s when more sophisticated mechanical ventilators were introduced. These ventilators often included a sigh function. Tidal volumes were generally set in the normal range of 5 to 7 mL/kg IBW and intermittent sigh breaths of 1.5 to 2 × VT were provided every 6 to 10 minutes. Multiple sighs in a row could be set on some ventilators. Sigh breaths are known to prevent alveolar derecruitment and associated airway problems that lead to ventilation–perfusion mismatch and intrapulmonary shunt (Figure 3-31).

FIGURE 3-31 A Machine-Delivered Sigh Breath.42 From Patroniti N, Foti G, Cortinovis D, et al. Sigh improves gas exchange and lung volume in patients with acute respiratory distress syndrome undergoing pressure support ventilation. Anesthes. 2002;96(4):788–794.

Description Beginning in the mid-1970s, larger tidal volumes in the range of 10 to 15 mL/kg were often applied using intermittent mandatory ventilation (IMV). The use of larger tidal volumes made the use of sigh breaths unnecessary. However, it became apparent following the initiation of the ARDSNet, launched in 1994, that large tidal volumes of 12 mL/kg (predicted body weight) resulted in increased mortality as compared to small tidal volumes (6 mL/kg) with Pplateau ≤ 30 cm H2O. Today, it is recommended that most patients, including those with normal lungs, receive at least 5 cm H2O of PEEP to prevent atelectasis and that tidal volumes and pressures be limited (e.g., VT of 4 to 8 mL/kg; Pplateau < 28 to 30 cm H2O); sigh breaths are unnecessary. That said, it could be stated that recruitment maneuvers used in patients with ARDS represent a form of intermittent hyperinflation of the lung (i.e., a sigh). Sigh breaths may improve oxygenation and lung mechanics during PCV and PSV in patients with ARDS.41 The use of sigh breaths with PSV and PCV has been investigated in an animal model of mild lung injury, resulting in mixed

results.41

Effects of Mechanical Ventilation on Organ Systems Mechanical ventilation effects oxygenation, ventilation, airway pressures, ventilatory muscles, work of breathing, the cardiovascular system, and other organ systems, as described below.

Pulmonary System The primary function of a mechanical ventilator is to augment or replace normal ventilation and a primary indication for initiation of mechanical ventilation is absent or inadequate spontaneous breathing. The goal of mechanical ventilation is to support tissue oxygenation and removal of carbon dioxide. It is also important to note a patient’s baseline status when setting specific oxygenation and ventilation goals. For example, a patient who is apneic due to a drug overdose may otherwise have normal lungs. This patient may require ventilatory support to achieve a normal PaCO2, PaO2, and SaO2 using low to moderate concentrations of oxygen. Oxygenation and ventilation goals for an acute exacerbation of COPD in a patient who is a chronic CO2 retainer, however, would be different. This patient’s baseline condition might be described as chronic ventilatory failure and prior baseline arterial blood gases may indicate a compensated respiratory acidosis with mild hypoxemia. Ventilating this patient to achieve a normal PaCO2 may result in an unwanted alkalosis.

Oxygenation Although they are related processes, it is sometimes helpful to consider ventilation and oxygenation separately. FIO2 and PEEP are the primary tools used to achieve improvement in arterial oxygenation in ventilated patients. Modern ventilators allow the clinician to choose an FIO2 ranging from 0.21 to 1.0 and the effect of FIO2 on alveolar oxygen tension (PAO2) is highly predictable (see the earlier discussion on the alveolar air equation). Gas transfer across the alveolar capillary membrane, however, is dependent on many factors. There are four general mechanisms that may cause hypoxemia: hypoventilation, ventilation perfusion mismatch (i.e., V̇/Q̇ < 1 but > 0), shunt (V̇/Q̇ = 0), and diffusion impairment.

Hypoxemia due to hypoventilation can sometimes be partially or fully reversed with the restoration of normal ventilation and PaCO2. Such patients may have otherwise normal lung function (e.g., neuromuscular disease, postoperative patients who have been heavily sedated, and drug overdose without aspiration), and initiation of mechanical ventilatory support may correct their hypoxemia. Hypoxemia due to low V̇/Q̇ (e.g., V̇/Q̇ < 1 but > 0 due to asthma, emphysema, chronic bronchitis, and COPD) often responds well to administration of low to moderate concentrations of oxygen (FIO2 0.30 to 0.50). Hypoxemia due to intrapulmonary shunt (e.g., ARDS, pneumonia, significant atelectasis, and pulmonary edema) or diffusion defects may require much higher oxygen concentrations and the application of PEEP. RC Insights Hypoxemia due to V̇/Q̇ mismatch or hypoventilation is suggested by a PaO2 increase of 4 to 5 mmHg for each 1% increase in oxygen percentage; a < 5 mmHg increase in PaO2 for each 10% increase in oxygen percentage suggests the presence of significant shunt.

In general, the lowest necessary combinations of PEEP and FIO2 should be used to maintain adequate arterial oxygen partial pressures (PaO2) and O2 saturations (SpO2 and SaO2). Respiratory care clinicians must also keep in mind all the factors that affect tissue oxygenation, which include arterial blood oxygen content (CaO2 = 1.34 × Hb × SaO2 + 0.003 × PaO2), oxygen delivery (ḊO2 = CaO2 × Q̇T), and tissue oxygen uptake and utilization. Attention to cardiac output, blood pressure, and peripheral perfusion is important to ensure adequate tissue oxygenation. The use of high concentrations of oxygen for prolonged periods may cause oxygen toxicity. The toxic effects of oxygen on the nervous system (e.g., tremors, convulsions) are usually confined to patients receiving hyperbaric therapy. Breathing 100% oxygen at normal barometric pressure can damage the pulmonary capillary endothelium, resulting in interstitial edema and thickening of the alveolar capillary membrane. Continued breathing of very high concentrations of oxygen may then cause alveolar type I cell destruction and proliferation of alveolar type II cells. Alveolar fluid may continue to accumulate resulting in ventilation/perfusion mismatch, intrapulmonary shunt, and severe hypoxemia. Oxygen toxicity may then culminate in pulmonary fibrosis. To avoid the development of oxygen toxicity, most

clinicians try to limit the use of 100% oxygen to less than 24 hours. If an FIO2 of 1.0 is required, it has been suggested that the FIO2 be reduced to 0.70 within 2 days and 0.50 or less within 5 days. FIO2 < 0.60 is not likely to cause oxygen toxicity and FIO2 of 0.50 or less is generally considered safe for extended periods. It should be noted, however, that FIO2 should not be reduced arbitrarily in the face of continuing severe hypoxemia. Other detrimental effects of breathing higher concentrations of oxygen include the development of absorption atelectasis, depression of ventilation in some COPD patients with chronic hypercapnia (i.e. oxygen-associated hypercapnia), and retinopathy of prematurity in neonates. As discussed earlier, PEEP and CPAP are used to maximize alveolar recruitment and prevent cycles of recruitment and derecruitment in patients with acute restrictive pulmonary disease (e.g., ARDS). The goal of PEEP is to improve surface area for gas exchange, while avoiding alveolar overdistention. Alveolar overdistention may result in compression of pulmonary capillaries and redistribution of pulmonary blood flow resulting in increased shunt. PEEP also increases intrathoracic pressure, which may decrease venous return and has the potential to decrease cardiac output. The application of PEEP/CPAP for patients with acute restrictive pulmonary disease will often allow for a reduction in the FIO2 required to achieve adequate arterial oxygenation. Optimal PEEP should maximize oxygen delivery to the tissues. Other techniques that may help oxygenation in ventilated patients include prone positioning (for ARDS patients), increased mean airway pressures (e.g., prolonged inspiratory times, inverse ratio ventilation), alveolar recruitment maneuvers, secretion management (e.g., suctioning and airway care), and administration of bronchodilators. Conservative fluid management (to reduce pulmonary edema) and treatment of fever, anxiety, and pain (to reduce oxygen consumption) may also be helpful.

Ventilation Mechanical ventilation can increase tidal volume, increase minute ventilation (V̇E), and decrease the patient’s WOB. Mechanical ventilation with positive pressure will also increase mean airway pressure and may increase mean intrathoracic pressure, reduce venous return, and reduce cardiac output. Inspiratory mechanical bronchodilation occurs during positive pressure breathing, which may increase

pulmonary dead space. Mechanical ventilation also tends to increase ventilation to nondependent portions of the lung and may reduce blood flow to nondependent portions of the lung. Ventilatory failure, or acute hypercapnic respiratory failure, is a primary indication for mechanical ventilation. The goal of mechanical ventilation in this case is to improve the patient’s alveolar ventilation, which is inversely related to PaCO2 by the following equation: V̇A = (V̇CO2 × 0.863)/PaCO2, where V̇A is alveolar ventilation and V̇CO2 is CO2 production. As alveolar ventilation decreases, PaCO2 increases and vice versa. Thus, clinically speaking the single best index of alveolar ventilation is measurement of PaCO2. That said, CO2 production can affect ventilatory requirements. Normal V̇CO2 is about 200 mL/min; however, V̇CO2 varies directly with metabolic rate. For example, an increase in metabolic rate (e.g., fever, shivering, and agitation) will increase V̇CO2 and, in turn, ventilatory requirements. RC Insight The single best index of effective alveolar ventilation in the clinical setting is measurement of PaCO2.

With mechanical ventilation, V̇A and PaCO2 can be altered by adjusting tidal volume, inspiratory pressure, inspiratory time, and respiratory rate, depending on the mode employed. Normal adult spontaneous tidal volume is approximately 5 to 7 mL/kg. On mechanically ventilated patients, tidal volume may be initially set at 6 to 8 mL/kg PBW, calculated as follows: PBW (men) = [50 + 2.3 × height (in)] – 60 PBW (women) = [45.5 + 2.3 × height (in)] – 60 With volume ventilation, the tidal volume is set directly. With pressure ventilation, the pressure can be adjusted to achieve an initial VT of 6 to 8 mL/kg. A backup or mandatory respiratory rate is usually initiated in the range of 12 to 14 breaths/min if providing assist/control ventilation. A higher rate may be used in cases of acute

hypercapnia, metabolic acidosis, and ARDS. A lower rate may be used in exacerbations of obstructive lung disease (e.g., asthma and COPD) to minimize air trapping. Inspiratory time and I:E ratio are particularly important in patients with obstructive lung disease. For a given respiratory rate, a decrease in inspiratory time results in an increase in expiratory time, which may be needed in these patients to avoid gas trapping and autoPEEP. When considering alterations in ventilation to achieve a desired PaCO2, the clinician should always consider the relationship between PaCO2 and pH. For example, a patient may rapidly trigger the ventilator resulting in a lower PaCO2 in compensation for a metabolic acidosis (e.g., if pH = 7.20 expect PaCO2 = 20 for compensation). If the respiratory care clinician adjusts the level of ventilatory support to increase the patient’s PaCO2 to 40 mmHg, the patient’s pH will further decrease to about 7.04, a life-threatening value. In general, pH will decrease acutely about 0.08 units for each 10-mmHg increase in PaCO2. On the other hand, a patient with COPD and chronic CO2 retention (i.e., chronic ventilatory failure) may have a baseline PaCO2 of 55 mmHg resulting in a normal or near-normal pH. If the patient is sedated and the ventilator is adjusted to achieve a “normal” PaCO2 of 40 mmHg for this patient, an alkalosis will result. RC Insights For every acute change in PaCO2 of 10 mmHg, pH will vary by 0.08 units. Thus, an acute increase in PaCO2 of 10 mmHg will result in a decrease in pH of 0.08. An acute decrease in PaCO2 of 10 mmHg will result in an increase in pH of 0.08.

Airway Pressures Positive pressure ventilation increases peak and mean airway pressures, and these pressures are a function of the patient’s condition, ventilatory mode employed, and ventilator settings. Higher peak and plateau inspiratory pressures (PIP, Pplateau) are associated with increased risk of lung injury, while increased mean airway pressures (Paw) reduce venous return and may reduce cardiac output in hemodynamically unstable patients. Increased Paw, however, may also improve distribution of inspired gases and arterial oxygenation. Ventilator-induced lung injury (VILI) is an acute lung injury (ALI) caused or made

worse by mechanical ventilation. VILI is characterized by increased pulmonary capillary permeability, interstitial and alveolar edema, alveolar hemorrhage, surfactant loss, and alveolar collapse. VILI is most commonly seen in ARDS patients, although it may be seen with other conditions. Ventilator-associated lung injury (VALI) is a term used when it is not possible to determine if injury was due to the ventilator or other factors (e.g., worsening of the patient’s disease). VALI may be caused by volutrauma, atelectrauma, or biotrauma. Lung injury due to alveolar overdistention is referred to as volutrauma, although it is difficult to separate the effects of volume from the associated pressures during mechanical ventilation. Common causes of volutrauma are excessive tidal volumes, elevated Pplateau, and lung overdistention due to autoPEEP. Lung injury due to cyclic alveolar expansion and collapse is referred to as atelectrauma, as may be seen during mechanical ventilation of ARDS patients. Various open lung techniques and appropriate use of PEEP have been suggested to avoid atelectotrauma. Lung injury due to release of inflammatory mediators by injured lung tissue is sometimes referred to as biotrauma. Pulmonary barotrauma is caused by alveolar rupture due to elevated transalveolar pressures (the pressure difference between alveoli and the adjacent interstitial space). Types of barotrauma include pneumothorax, mediastinum, pneumoperitoneum, and subcutaneous emphysema. Barotrauma may be caused by excessive VT, elevated Pplateau, and PEEP. Other causes include chest trauma, thoracentesis, central line placement, biopsy, thoracic surgery, manual ventilation, and improper chest tube placement. In the VC mode, decreased compliance or increased airway resistance will increase PIP, and improvements in compliance or resistance will lower PIP. In general, PIP should be limited to not more than 40 cm H2O, and Pplateau should be limited to less than 28 to 30 cm H2O, to avoid ventilator-associated lung injury (VALI). Bronchospasm, mucosal edema, and secretions will increase airway resistance; suctioning, airway care, and administration of bronchodilators and antiinflammatory medications may be helpful. Lung compliance may decrease due to worsening pneumonia, ARDS, or pulmonary edema, while the development of abdominal distention (e.g., ascites) may worsen thoracic compliance. Attention to the specific cause of reduced compliance or increased resistance may result in lower

PIP. Specific ventilator adjustments can also reduce PIP during volume ventilation including lowering the set tidal volume, decreasing inspiratory peak flow, and change in the inspiratory flow waveform. For example, a down-ramp inspiratory flow waveform (aka decelerating flow) will tend to have a lower PIP then a square wave (although a down-ramp will also tend to have an increased Paw as compared to a square wave). With volume ventilation, mean airway pressure is affected by the tidal volume, inspiratory time, inspiratory flow waveform, respiratory rate, PIP, and PEEP. With volume ventilation, decreased compliance or increased resistance will also increase PIP and Paw. With flow-cycled pressure-support ventilation or time-cycled, pressurecontrol ventilation, increasing or decreasing inspiratory pressure will have a corresponding effect on mean airway pressure. The pressure pattern or pressure waveform will also affect Paw during pressure-control ventilation. For example, a square wave–like pressure waveform will produce a descending ramp flow waveform (aka decelerating flow) and increased Paw. A more linear or curvilinear increase in pressure (e.g., up-ramp pressure waveform) will produce a relatively lower Paw. With time-cycled pressure-control ventilation, increasing inspiratory time and reducing expiratory time will also increase mean airway pressure and vice versa. The addition of extrinsic PEEP or an increase in PEEP will also increase mean airway pressure, while a reduction in PEEP will reduce mean airway pressure. The effect of PEEP on Paw is direct; for each 1-cm H2O increase in PEEP, Paw will also increase by 1 cm H2O. AutoPEEP (aka intrinsic PEEP) is PEEP caused inadvertently, often due to inadequate expiratory times in patients with obstructive lung disease; autoPEEP also increases Paw, although autoPEEP measurement requires the use of an end-inspiratory pause.

Heterogeneous Ventilation Heterogeneous ventilation describes nonuniform distribution of inspired gas within the lung. This is related to regional lung compliance, airway resistance, and dependency (upper versus lower lung zones). These factors vary from region to region in the lung and thus ventilation is heterogeneous. For example, in the normal, upright lung, apical (nondependent) lung units tend to receive less perfusion, while lung units at the bases tend to receive more perfusion because of gravity. Better-

ventilated areas include those that are more compliant, nondependent, and have lower airway resistance. Conversely, poorly ventilated regions include those that are less compliant, dependent, and have higher airway resistance. While some degree of heterogeneity is always present, it is often more exaggerated in patients with airway and parenchymal lung disease.

Ventilation/Perfusion Mismatch Mechanical ventilation may produce three different forms of ventilation/perfusion (V̇/Q̇) mismatch: (1) -ventilation (V̇) > perfusion (Q̇): high V̇/Q̇ or dead space; (2) V̇< Q̇: V̇/Q̇ < 1 but > 0; and (3), V̇/Q̇ = 0 – shunt. During spontaneous ventilation, inspired gas is primarily distributed to the dependent and peripheral zones of the lungs. Conversely, when positive pressure is applied, the inspired gas tends to be distributed to the nondependent lung zones. These nondependent areas receive less perfusion resulting in ventilation of poorly perfused areas (V̇ > Q̇) or increased dead space ventilation. Positive pressure may also compress the pulmonary capillaries leading to increased pulmonary vascular resistance and decreased pulmonary blood flow to areas that are better ventilated. Perfusion is then redirected to the dependent areas of the lung that are less well ventilated (V̇/Q̇ mismatch). If there is no ventilation of perfused areas (V̇/Q̇ = 0), then intrapulmonary shunt is created. Positive pressure ventilation may reduce intrapulmonary shunt by improving alveolar ventilation and preventing or reversing atelectasis, especially when PEEP is applied. Positive pressure ventilation tends to increase dead space ventilation, in part due to inspiratory mechanical bronchodilation of the conducting airways. Normal dead space to tidal volume ratio (VD/VT) is 0.30 with a normal range of 0.20 to 0.40; VD/VT during mechanical ventilation may be 0.50 or higher.

Respiratory Muscles Generalized skeletal muscle weakness frequently occurs in critically ill ICU patients, and this may include the diaphragm. Acute restrictive lung disease (e.g., ARDS, pneumonia) stresses the ventilatory muscles and often leads to ventilatory muscle fatigue. Other causes of muscle weakness in ventilated patients include immobilization and the use of sedative, narcotic, and paralytic drugs; mechanical ventilation can be a contributing factor.

Controlled mechanical ventilation occurs when the patient is apneic due to his or her medical condition (e.g., coma, head trauma, and massive stroke) or the use of sedative or paralytic agents. With controlled ventilation, the WOB is eliminated allowing for complete ventilatory muscle rest. Controlled ventilation often requires the use of sedative and neuromuscular blocking agents, which may jeopardize patient safety in the event of a ventilator malfunction or disconnect. It should also be noted that while neuromuscular blocking agents paralyze the patient, they do not influence the patient’s consciousness or perception of pain and discomfort. Thus, neuromuscular blocking agents should not be used without the addition of appropriate sedation and pain control. Further, respiratory muscle weakness and atrophy may occur in patients receiving extended periods of controlled mechanical ventilation and the use of neuromuscular blocking agents. Neuromuscular weakness (e.g., critical illness myopathy and critical illness polyneuropathy) is often seen in critically ill patients, and is associated with sepsis, multiorgan failure, and systemic inflammatory response syndrome. Ventilatory muscle weakness and dysfunction may prolong the patient’s dependency on mechanical support and cause weaning difficulty. IMV allows for interspersing mandatory and spontaneous breathing and the provision of partial ventilatory support. It is of interest to note that early advocates of IMV suggested that an advantage of this mode was maintenance of ventilatory muscle function and avoidance of ventilatory muscle atrophy. Unfortunately, evidence has not shown IMV to be beneficial in this respect. Newer modes of ventilation that allow patients to continue to utilize their ventilatory muscles while receiving mechanical ventilatory support are available (see below).

Diaphragmatic Dysfunction Ventilator-induced diaphragmatic dysfunction can develop within hours and worsens with the duration of mechanical ventilation.43 This may be related to increased oxidative stress on the diaphragm. Direct measures of diaphragmatic function have been elusive. Maximal inspiratory pressure (MIP), respiratory frequency, tidal volume, and transdiaphragmatic pressures have all been used as surrogate measures of diaphragmatic function; however, these are all nonspecific and effort dependent. Nevertheless, diaphragmatic weakness occurs with mechanical ventilation and the optimal therapeutic strategy to avoid this development remains

unclear. It may be beneficial to allow ventilated patients to maintain some level of spontaneous diaphragmatic function as allowed by patient comfort and adequate gas exchange. Newer modes of mechanical ventilation, including neurally adjusted ventilatory assist (NAVA), adaptive support ventilation (ASV), and pressure-support ventilation (PSV) in which some level of spontaneous breathing continues may have advantages regarding maintenance of diaphragmatic function. Inspiratory muscle strength training has been explored in difficult to wean patients.44

Work of Breathing Properly applied, mechanical ventilation can reduce or eliminate the patient’s WOB. This is especially important in patients with respiratory muscle fatigue. The effects of mechanical ventilation on WOB are dependent on mode employed, ventilator settings, and the patient’s condition. Controlled ventilation eliminates the WOB, allowing for ventilatory muscle rest. As noted above, controlled ventilation may also promote the development of respiratory muscle weakness and atrophy. Assistcontrol ventilation allows the patient to trigger an inspiration and trigger work can be substantial with inappropriate trigger sensitivity settings or in the presence of autoPEEP. IMV allows the patient to spontaneously breathe between mandatory breaths; however, WOB can be substantial when the IMV rate is reduced to one-half of that required for full ventilatory support. For example, an IMV rate to achieve full ventilatory support may be 12 breaths/min; when the mandatory rate is reduced to 6 breaths/min, the patient’s WOB may approach that of unsupported spontaneous breathing. Mode of ventilation can have a direct impact on WOB. As noted, IMV can provide partial ventilatory support that increases the patient’s WOB. Patient-triggered modes (assist/control) can introduce significant trigger work. With pressure-support ventilation, increasing pressure will tend to decrease the WOB. With VC ventilation, inappropriate settings for inspiratory flow and inspiratory time may cause patient– ventilator asynchrony and increased WOB. With any mode that incorporates a patient trigger and/or spontaneous breathing (e.g., IMV or PSV), the patient’s spontaneous ventilatory pattern can be in opposition with the ventilator settings. For example, a patient with rapid shallow spontaneous breathing may poorly tolerate assist/control modes of ventilation by trying to exhale during the inspiratory phase of

the ventilator. Attention to avoiding patient–ventilator asynchrony is an important aspect of ventilator management to improve patient comfort and reduce the WOB.

Mucociliary Motility Mechanical ventilation appears to impair airway mucociliary motility, although the mechanism remains unclear. This dysfunction likely contributes to retention of secretions and development of ventilator-associated pneumonia. Adequate humidification, suctioning, and airway care should be routine in patients receiving mechanical ventilation.

Immune System Mechanical ventilation with positive pressure may influence the immune system. For example, ARDS patients receiving lung protective ventilation (small VT with higher PEEP) may have fewer circulating inflammatory mediators than those receiving large tidal volumes with no PEEP. Ventilator-associated pneumonia (VAP) is a form of hospital-acquired pneumonia that develops 48 hours or more after the initiation of mechanical ventilation. Clinical findings often include a new or progressive lung infiltrate on imaging, fever, purulent sputum, leukocytosis, and deteriorating oxygenation status.

Cardiovascular System Andre Cournand was among the first to publish data on the effects of positive intrathoracic pressures on cardiac output.45 During spontaneous ventilation, intrapleural and intrathoracic pressures decrease on inspiration, resulting in an increase in the venous return to the heart. Strong spontaneous inspiratory efforts can enhance this normal effect and increase the stroke volume and cardiac output. When intrathoracic pressures are positive during mechanical ventilation, the right ventricular (RV) preload may be reduced if high mean airway pressures reduce the cross-sectional area of the great vessels. The right ventricular afterload is affected by lung volume and its influence on pulmonary vascular resistance (PVR; Figure 3-32). As inspired volume approaches total lung capacity (TLC), PVR is increased along with an increase in RV afterload. The higher afterload will increase RV stroke work index but will reduce left ventricular (LV) preload. The degree of influence of

intrathoracic pressure on both right and left heart function are dependent on the transmural pressure gradient across the walls of the great vessels and myocardial walls. If the lungs are relatively compliant, the transmural wall pressure is directly influenced by alveolar pressure and the potential for a decrease in cardiac output, especially in hypovolemic patients, is more pronounced. On the other hand, if the lungs are relatively noncompliant, the transmural wall pressure may not be readily influenced, and higher pressures may not cause immediate reductions in venous return and cardiac output.

FIGURE 3-32 The Influence of Lung Volume on Pulmonary Vascular Resistance.

Description

RC Insight During positive pressure ventilation, alveolar, pleural, and intrathoracic pressures are increased and venous return to the right heart is reduced during inspiration and returns towards baseline during exhalation (in the absence of PEEP). Higher pressures and higher PEEP levels may further impede venous return, and this may reduce cardiac output in compromised patients.

In summary, positive pressure ventilation creates positive pleural and intrathoracic pressures that compress the intrathoracic veins resulting in decreased venous return and may result in decreased left ventricular output. Right ventricular output is also decreased as alveolar distention compresses the pulmonary capillaries resulting in increased pulmonary vascular resistance, or right ventricular afterload. The degree of decrease in right and left ventricular output correlates with increasing amounts of positive pressure and/or PEEP. As positive pressure increases, cardiac output may decrease. These effects are exaggerated in patients with low chest wall compliance (as in kyphoscoliosis) or high lung compliance (as in emphysema). In healthy patients, compensatory mechanisms, including increases in heart rate and systemic vascular resistance, maintain blood pressure. If compensatory mechanisms are inadequate, hypotension develops. It must be noted, however, that positive pressure ventilation may be beneficial in patients with left ventricular failure by reducing venous return and decreasing left ventricular afterload.

Renal System It may come as a surprise to some, but mechanical ventilation can impact renal function and is an independent risk factor for the development of acute renal failure. There are numerous hypotheses that have been proposed to explain this relationship, however the mechanisms remain poorly understood. It was once thought that the negative effects of mechanical ventilation on intrathoracic pressure, venous return, and cardiac output were to blame for reduced renal perfusion. There also may be a neurohumoral component to positive pressure ventilation’s effect on renal function. Mechanical ventilation has been shown to activate the reninangiotensin-aldosterone system and increase sympathetic tone, which may lead to decreased urine production. The effects of positive pressure on atrial natriuretic peptide (ANP) production is less than straightforward. There is also a link between lung injury and renal function.

Inflammatory cytokines resulting from or causing ARDS may contribute to renal dysfunction. In the ARDSNet trial, it was noted using lung protective strategies (including lower tidal volumes) resulted in a reduced incidence of renal failure.46 Lung injury may precede renal impairment as systemic inflammation leads to end organ failure. In summary, patients receiving mechanical ventilatory support may develop acute renal failure, and this may be due to multiple factors such as decreased renal blood flow due to decreased cardiac output, release of inflammatory mediators, humoral pathways, or increased sympathetic tone.

Gastrointestinal System Gastrointestinal tract stress ulcers associated with critical illness and mechanical ventilation can result in gastrointestinal bleeding. The incidence of esophagitis, diarrhea, gall bladder inflammation, and impaired gastrointestinal motility may also increase with positive pressure ventilation, although it remains unclear whether this is related to mechanical ventilation or critical illness in general. The splanchnic perfusion refers to the perfusion of the abdominal gastrointestinal organs (e.g., intestines, stomach, pancreas, liver, and spleen); positive pressure ventilation is associated with decreased splanchnic perfusion (Figure 3-33). There appears to be a dose-dependent decrease in splanchnic perfusion as the amount of positive pressure applied increases, especially with PEEP.47 This may be due to decreased cardiac output that may occur with increasing amounts of positive pressure. PaCO2 may also influence gut perfusion. Specifically, hypercapnia can cause reflex splanchnic vascular dilation that follows an initial vasoconstriction related to an increased sympathetic outflow associated with high PaCO2.48 Modes of ventilation that accommodate spontaneous breathing may improve splanchnic blood flow. In a 2003 animal model study on oleic acid induced lung injury, Hering et al. compared APRV ventilation with and without spontaneous breathing interspersed. In this animal study, there was an increase in gastrointestinal perfusion in the group with spontaneous breathing efforts.49 The utilization of lung protective strategies may also preserve gut function and reduce mortality associated with end-organ failure.

FIGURE 3-33 The Effects of Spontaneous Ventilation on Splanchnic Blood Flow. Data from Hering, R., Viehofer, A., Zinserling, J., Wrigge, H., Kreyer, S., Berg, A., Minor, T., Putensen, C. Effects of spontaneous breathing during airway pressure release ventilation on intestinal blood flow in experimental lung injury. Anesthesiology. 2003;99(5):1137-1144.

Description

Central Nervous System Mechanical ventilation can have both direct and indirect effects on the central nervous system. The most notable direct affect is increased ICP due to increased intrathoracic pressures and reduced venous return. The mere presence of an endotracheal tube can cause coughing and gagging and increased intrathoracic

pressures that may cause transient elevations in ICP. Impedance of venous return during positive pressure breathing can lead to increased ICP and decreased cerebral perfusion pressure. In healthy patients, cerebral autoregulation minimizes these effects by maintaining cerebral perfusion. However, in patients with underlying cerebrovascular compromise, such as head injuries or intracranial tumors, these autoregulatory mechanisms may be defective. This subset of patients may benefit from ICP monitoring while receiving mechanical ventilation. Ventilator settings and the resultant pH and PCO2 can also influence ICP. The influence of pH and PaCO2 on cerebral vasculature have been investigated since the works of Lambertson and colleagues in the 1960s. They concluded that rapid CO2 conversion to hydrogen ions and the CSF pH was the basis of vascular diameter alterations and control of cerebral blood flow. Low or high pH resulted in vasodilation and vasoconstriction, respectively.50-52 Harder & Madden showed PCO2’s effect on vascular constriction independent of pH, suggesting various potential mechanisms influencing cerebral blood flow (CBF) and ICP.53,54 Decreased PCO2 is a cerebral vasoconstrictor while increased PCO2 is a cerebral vasodilator. Thus, hyperventilation can be used to lower ICP, and this has been suggested in the past to treat patients with severe head trauma and/or cerebral edema. Unfortunately, hyperventilation may also cause cerebral ischemia and contribute to secondary brain injury and is currently not recommended in the initial treatment of severe traumatic brain injury. Optimal ICP management requires a multimodal approach combining symptoms, imaging, and other physiological parameters to an individualized treatment plan.55,56 Anxiety, agitation, and pain are common in patients receiving mechanical ventilatory support. There is a component of discomfort associated with the endotracheal tube and a common patient response is to attempt to remove the source of that discomfort (i.e., self extubation). Many ICU procedures and activities may increase patients’ discomfort. These include blood sampling, suctioning and airway care, wound care, bathing, linen changes, and other diagnostic and therapeutic procedures. Patients may experience anger, fear, pain, and frustration; explaining procedures and providing reassurance may be helpful. Oversedation, however, may delay ventilator weaning and is associated with reduced spontaneous ventilatory drive, increased ventilator days, and higher costs.57 The appropriate use

of sedatives and analgesics continues to be a mainstay of pain management.58 Development of ICU delirium is a common problem and steps to reduce delirium, and minimize hemodynamic and respiratory effects of sedative drugs, should be implemented.59

Sleep ICU patients often suffer from poor sleep quality and disordered sleep. This is due to disease-related factors, patient care activities causing arousal and awakening and environmental noise. Maintaining normal circadian rhythms, limiting environmental noise, reducing administration of sedatives and hypnotics, and taking steps to treat or avoid the development of delirium may be helpful. Sleep disruption in the ICU and sleep fragmentation related to mechanical ventilation are difficult to differentiate. Sleep disruption refers to a disrupted sleepwake cycle. Sleep fragmentation refers to repetitive, short interruptions in sleep. Pain is a common cause of sleep fragmentation. Bright lights, noise, movement, and anything that distracts from a dark, quiet environment can lead to sleep fragmentation and daytime fatigue. Secretions, bronchospasm, and patient– ventilator asynchrony can also awaken the patient. Inappropriate alarm settings can result in further sleep fragmentation. When sleep fragmentation is displaced by sleep loss, daytime sleepiness is the result, which may delay weaning from mechanical ventilation. Historically, ICU staff have been aware of sleep disruption and measures have been employed to improve sleep in mechanically ventilated patients.

Complications of Mechanical Ventilation The complications related to mechanical ventilation are numerous and include both pulmonary and extrapulmonary organ systems.

Pulmonary The pulmonary complications attributed to mechanical ventilation are comprehensively called “ventilator-associated lung injury” or VALI. These complications include airway complications, pneumothorax, equipment failure, lung injury related to the application of pressure, development of ventilator associated pneumonia (VAP), and oxygen toxicity.

Airway Complications Most airway complications are associated with the endotracheal tube (ETT) itself. Laryngeal and tracheal injuries (including laryngeal edema, vocal cord injury, and tracheal stenosis) are the most common complications described. These are secondary to the direct pressure and inflammation induced by the ETT and inflated cuff. The purpose of the ETT cuff is two-fold: (1) to seal the airway for optimal delivery of mechanical ventilation and (2) to prevent aspiration and reduce incidence of VAP. This must be balanced with the potential for tracheal mucosal ischemia and resultant granulation, fibrosis, and stenosis. These changes are often seen with cuff pressures exceeding 30 cm H2O, thus it is recommended that cuff pressures be monitored and maintained at 20 to 30 cm H2O.

Equipment Failure Present-day mechanical ventilators are equipped with numerous alarms to alert health care providers to changes in pressures, volumes, and respiratory rate. These alarms allow for early troubleshooting and avoidance of adverse events. However, these safeguards may be rendered ineffective by ventilator malfunction or power failure, which may contribute to the morbidity and mortality of mechanically ventilated patients. For this reason, a manual resuscitator (often referred to as an “ambu-bag”) with PEEP valve should be readily available at the bedside to assure continued ventilation and oxygenation of the patient while the ventilator malfunction is assessed and rectified.

Lung Injury Due to Pressure Ventilator-induced lung injury (VILI) refers to the damage to the lung induced by the application of positive pressure. Alveolar overdistention, the primary driver of VILI, is thought to induce biophysical and biochemical changes that result in increased permeability of the alveolar-capillary membrane, pulmonary edema, cell injury and necrosis, impaired oxygen delivery, and diffuse alveolar damage.60 The transpulmonary pressure, which is the difference between the plateau pressure and pleural pressure, determines the degree of alveolar distention. As plateau pressure rises, so does the transpulmonary pressure, which can result in “volutrauma,” or lung injury related to high lung volumes. Barotrauma refers to injuries caused by high ventilation pressure, resulting in alveolar rupture and release of gas. Clinically, this includes pneumothorax, pneumomediastinum, pneumopericardium, and subcutaneous emphysema. Pneumothorax can be life threatening, especially in patients on ongoing mechanical ventilation, due to the development of tension pneumothorax. Tension pneumothorax is a medical emergency that requires prompt recognition and management including needle decompression followed by tube thoracostomy. Pneumomediastinum, pneumopericardium, and subcutaneous emphysema typically have less clinical consequence; however, close monitoring for development of pneumothorax in patients with pneumomediastinum is prudent. Additionally, airway pressures should be minimized (if possible) to prevent further lung injury. Conversely, ventilation at low tidal volumes can induce “atelectrauma,” the repeated collapse and opening of the alveoli with each breath. Unfortunately, due to the heterogeneity of lung disease, particularly prevalent in ARDS, a given pressure can induce atelectrauma in regions with decreased compliance while causing volutrauma in regions with normal compliance. Because of this, it is recommended that patients receive low tidal volumes (typically 6 to 8 mL/kg IBW) to limit volutrauma, with an appropriate level of PEEP to minimize atelectrauma.

Ventilator-Associated Pneumonia As noted above, ventilator-associated pneumonia (VAP) is pneumonia that develops after 48 hours on mechanical ventilation. Intubated patients are particularly susceptible to the development of pneumonia because the protective mechanisms of the upper airway are bypassed. Most cases of VAP are thought to be caused by

microaspiration of secretions from the oropharynx or upper gastrointestinal tract. The ventilator circuit itself provides an environment for bacterial growth and biofilm production. Notably, exchanging the ventilator circuit does not appear to decrease the incidence of VAP. Most cases are polymicrobial, especially by gram-negative organisms, although the frequency of isolation of methicillin-resistant strains of Staphylococcus aureus are rising. Due to associated morbidity and mortality, high cost, and changes in reimbursement strategies, prevention of VAP has become an area of extensive research. Many different interventions have been studied to reduce VAP including a variety of cuff designs, subglottic suctioning, chlorhexidine oral rinses, and gastric decontamination to name a few; however, no clear prevention strategy has been established. Nevertheless, VAP prevention strategies include avoiding invasive mechanical ventilation when possible, minimizing time on mechanical ventilation by minimizing sedation and implementing weaning protocols early, elevating the head of bed to 30 to 45 degrees, and removal of subglottic secretions. Formation of VAP bundle protocols implementing these strategies has been associated with a significant reduction in the development of VAP.

Oxygen Toxicity High concentrations of inspired oxygen can contribute to a wide range of lung injury, from mild tracheobronchitis to diffuse alveolar damage that is histologically indistinguishable from ARDS. Hyperoxia produces reactive oxygen species that deplete the cell’s antioxidants and induces cellular injury. Since the airway lining and alveoli are most exposed to inspired oxygen, they are also most at risk for cellular injury. Clinical consequences include absorption atelectasis, worsening hypercapnia, and airway and parenchymal damage. High levels of inspired oxygen result in alveolar nitrogen washout and ultimately alveolar closure, or atelectasis. Hyperoxic hypercarbia results from the Haldane effect and increased dead space ventilation. The Haldane effect describes the affinity of hemoglobin for oxygen or carbon dioxide. Increases in inspired oxygen leads to rightward displacement of the CO2-hemoglobin dissociation curve given that oxyhemoglobin binds CO2 less avidly than deoxyhemoglobin. There is an increase in oxyhemoglobin with increased FIO2 resulting in increased dissociation of CO2 from hemoglobin leading to increased serum CO2 levels. Airway erythema and edema can be seen in the large airways

bronchoscopically within 6 hours on oxygen therapy, even without positive pressure.60 Parenchymal injury can also be seen, although it remains unclear whether this is from oxygen therapy alone or secondary to VILI. Certain drugs, such as bleomycin (Blenoxane), may increase the sensitivity of the lungs to oxygen therapy. The general goal should be to minimize FIO2 (particularly to < 0.60 if possible) and administer PEEP to minimize alveolar derecruitment. The role of antioxidants remains unclear.

Extrapulmonary Organ Systems Extrapulmonary complications of mechanical ventilation may be cardiac, cardiovascular, renal, neurologic, neuromuscular, psychologic, or gastrointestinal. Mechanical ventilation may also have an input on the patient’s immune system and nutritional status.

Cardiac/Cardiovascular As discussed previously, the application of positive pressure increases pleural and intrathoracic pressures, which compresses intrathoracic veins leading to decreased venous return. This results in the pooling of venous blood in the extrathoracic vasculature, particularly within the abdominal viscera. Increased intrathoracic pressure is also transmitted to adjacent structures, which can falsely elevate hemodynamic measurements, including central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). The magnitude of elevation is dependent upon the compliance of the lung and the amount of PEEP applied.

Renal As mentioned above, positive pressure ventilation is an independent risk factor for the development of acute renal failure in critically ill patients.62 The mechanism is poorly understood, but thought to be related to hemodynamic, neurohormonal, and biotrauma factors. The systemic hemodynamic effects of positive pressure ventilation, as previously discussed, decrease renal blood flow thereby reducing glomerular filtration rate and urine output.63 Positive pressure ventilation affects numerous neurohormonal pathways including the renin-angiotensin axis, nonosmotic

vasopressin release, and atrial natriuretic peptide (ANP) production. This series of complex interactions culminates in a decrease in renal blood flow and GFR, and fluid retention with resulting oliguria.64 Finally, positive pressure ventilation activates the inflammatory cascade with the release of multiple pro-inflammatory cytokines including IL-6, IL-8, and TNFα. These mediators contribute to the development of oxidative stress and cellular apoptosis, which leads to further decline in renal blood flow and GFR.

CNS/Psychological Cerebral blood flow (CBF) is proportional to cerebral perfusion pressure (CPP), which is the difference between mean arterial pressure (MAP) and ICP. Thus, CPP (and CBF) decreases as MAP decreases and ICP increases. Critically ill patients may have decreases in MAP due to shock, high PEEP, and high mean airway pressures. Elevations in ICP may be seen in traumatic brain injury, cerebrovascular accident, intracerebral hemorrhage, and intracranial tumors. Cerebral autoregulation is the ability of the cerebral circulation to maintain CBF with wide changes in CPP by adjusting the cerebral vascular resistance. Cerebral autoregulation is limited by the ability of the cerebral arterioles to constrict and dilate. In the normal healthy individual, cerebral autoregulation can maintain CBF with CPP of 60 to 150 mmHg. In chronically hypertensive or critically ill patients, this adaptation is often compromised.

Neuromuscular ICU acquired weakness is widely prevalent in patients following ICU hospitalizations and can manifest in three ways: polyneuropathy, myopathy, and/or muscle atrophy. Definitive diagnosis is made by electrophysiology testing. Motor and sensory nerves are stimulated, and the resultant action potentials analyzed for nerve injury, muscle injury, or a combination of both. Critical illness polyneuropathy (CIP) is a symmetric, distal sensory-motor axonal polyneuropathy that affects motor (especially extremity and respiratory muscles), sensory, and autonomic nerves. Critical illness myopathy (CIM) results in extremity and respiratory muscle weakness; however, sensory function is preserved (unlike in CIP). Both may result in extremity and respiratory muscle weakness and difficulty weaning from the ventilator.

Nutritional Critical illness results in increased catabolism by means of the inflammatory cascade. Providing adequate nutritional support is often challenging in the ICU. Excessive nutritional support increases metabolic rate and increases ventilation requirement. Insufficient nutritional support can contribute to respiratory muscle catabolism and atrophy, resulting in increased risk of nosocomial pneumonia. Nutritional support is essential. A retrospective analysis of over 4000 patients showed that early enteral feeding (within 48 hours) resulted in a decrease in ICU and hospital mortality.65 The EDEN study showed no significant difference in outcomes (ventilator days, 60-day mortality, and infectious complications) between patients who received trophic feeds and those receiving full feeds.66 Thus, the general consensus of nutritional guidelines is that enteral nutrition should be instituted within 24 to 48 hours of ICU admission.

Gastrointestinal The effects of positive pressure ventilation on the gastrointestinal system are primarily secondary to changes in cardiac output and the resulting splanchnic hypoperfusion. This hypoperfusion leads to increases in splanchnic resistance that can culminate in gastric mucosal ischemia and stress ulcer formation. For this reason, mechanical ventilation for more than 48 hours is considered an indication for stress ulcer prophylaxis. Agents used for stress ulcer prophylaxis include cytoprotective agents (i.e., sucralfate) or acid suppression agents (i.e., histamine receptor 2 antagonists or proton pump inhibitors). Mucosal breakdown may also increase risk of bacterial translocation from the gastrointestinal tract to the blood and result in nosocomial infection. Gastrointestinal motility is often impaired in patients on positive pressure ventilation for unclear reasons. This may manifest as an intolerance to enteral feeding.

Immune System Positive pressure ventilation triggers activation of the inflammatory cascade. Patients who receive large tidal volume ventilation and low PEEP have higher concentrations of inflammatory mediators than patients who receive smaller tidal volumes and higher PEEP.46, 60 This potent activation of the inflammatory cascade is implicated in

the pathogenesis of VILI and is thought to be the basis for improved outcomes in low tidal volume ventilation.

Key Points The iron lung and chest cuirass are examples of negative pressure ventilators; the iron lung saved many lives during the polio epidemics. Patient-triggered, pressure-cycled ventilators (e.g., Bird Mark 7) and flowsensitive breathing valves (e.g., Bennett PR-2) were based on technology developed during World War II. Patient- or time-triggered volume ventilators were introduced in the late 1960s and allowed for precise control of the patient’s tidal volume, respiratory rate, and minute ventilation. V̇O2 is defined as the volume of oxygen taken up by the body per minute; normal resting V̇O2 is about 250 mL O2/min. V̇CO2 is defined as the volume of carbon dioxide produced by the body per minute; normal resting V̇CO2 is about 200 mL CO2/min. Inspiratory time (TI) is defined as the time from the beginning to the end of inspiration, including any breath hold time. Expiratory time (TE) is the time from the end of inspiration until the end of expiration and the beginning of the next breath. The total cycle time (Ttot) = TI + TE; Ttot = 60 ÷ respiratory rate (f). Normal tidal volume (VT) is about 7 mL/kg of PBW; VT varies with size, gender, age, activity, and disease. The dead space volume (VD) is the volume of inspired gas that fills the conducting zone of the lung and any unperfused alveoli. Alveolar ventilation per minute (V̇A) is tidal volume (VT) minus dead space (VD) times rate (f): V̇A = (VT – VD) × f. During invasive positive pressure ventilation, the airway must be sealed to deliver pressure, flow, and volume; a cuffed endotracheal or tracheostomy tube is commonly used to accomplish the seal (hence the term invasive ventilation). During noninvasive positive pressure ventilation, the airway must also be sealed to deliver pressure, flow, and volume. An oro or nasal mask interface is commonly used to accomplish the seal (hence the term noninvasive ventilation). Peak inspiratory pressure (PIP) is the highest proximal airway pressure attained during the inspiratory phase of mechanical ventilation. Plateau pressure (Pplateau) is the pressure measured during an inspiratory hold maneuver, typically 1 second or less in duration. Extrinsic PEEP is intentionally applied to the airway at end expiration for therapeutic purposes. AutoPEEP (aka intrinsic PEEP, occult PEEP) is unintended PEEP, usually caused by airflow obstruction and/or inadequate TE. It is also known as air trapping or dynamic hyperinflation and is more common in patients with

obstructive lung disease. Continuous positive airway pressure (CPAP) describes spontaneous breathing at an elevated baseline pressure. PEEP and CPAP increase mean airway pressure, increase functional residual capacity (FRC), and increase the surface area for gas exchange. Physiologic PEEP is a small amount of PEEP (3 to 5 cm H2O) used for most patients to prevent expiratory alveolar collapse. One approach to optimal PEEP adjusts the PEEP level for the best tissue oxygen delivery (ḊO2). Mean airway pressure (Paw) is affected by tidal volume, PIP, PEEP, autoPEEP, rate, inspiratory time, inspiratory flow and pressure waveforms, expiratory time, I:E ratio, and the patient’s respiratory mechanics (compliance [C] and resistance [RAW]). Input power refers to the power source used by the ventilator to perform the required work; input power may be electric or pneumatic. Most modern critical care ventilators are microprocessor controlled and control systems may be open loop or closed loop. For most ventilator patients, VT is initiated at 6 to 8 mL/kg of predicted or ideal body weight (PBW or IBW; the terms are often used interchangeably). Clinically, the best index of effective ventilation is measurement of PaCO2. VT and respiratory rate (f) are adjusted to alter PaCO2 and pH. FIO2 and PEEP are adjusted to alter oxygenation (PaO2, SaO2). Pressure control (PC) and volume control (VC) are the two primary control variables for invasive mechanical ventilation. Mandatory breaths occur when the ventilator delivers the same breath type with every breath. Spontaneous breaths occur when the start and end of inspiration are determined by the patient, independent of other ventilator settings. With CMV, all breaths are mandatory; with IMV mandatory breaths are interspersed with spontaneous breaths. VC and PC may be combined with continuous mandatory ventilation (CMV) or intermittent mandatory ventilation (IMV); thus, the primary modes of mechanical ventilation are VC-CMV, VC-IMV, PC-CMV, and PC-IMV. The trigger variable is the method by which inspiration begins; triggers include time or patient effort (as sensed by a pressure or flow change or a neural signal with NAVA). The cycle variable is the method by which inspiration stops; cycle variables include volume, time, pressure, and flow. In the volume-control mode, VT is set, and PIP will vary with changes in compliance and resistance; in the pressure-control mode, inspiratory pressure is

set and VT will vary with changes in compliance and resistance. Spontaneous VT can be pressure supported to reduce work of breathing (WOB) and compensate for the imposed WOB due to the artificial airway. Assist-control ventilation (AC) is an older term used to refer to time- or patienttriggered CMV. AC may be volume controlled (VC-CMV) or pressure controlled (PC-CMV). Synchronized intermittent mandatory ventilation (SIMV) refers to IMV in which mandatory breaths may be patient or time triggered. Mandatory minute ventilation (MMV) is a mode of ventilation in which the ventilator automatically makes adjustments to assure a minimum set V̇E. Pressure-support ventilation (PSV) is a patient-triggered, flow-cycled form of pressure ventilation. PSV can be used as a standalone, spontaneous form of breathing or in conjunction with IMV. Airway pressure-release ventilation (APRV) is a dual CPAP mode of ventilation. Automatic tube compensation (ATC) is an automated form of pressure support designed to reduce the work of breathing associated with endotracheal tube resistance. Volume-assured pressure support (VAPS) or pressure augmentation refers to a “within breath” form of volume-targeted pressure support. Proportional assist ventilation (PAV) is an automated form of ventilatory support that adjusts the level of support provided based on the patient’s measured inspiratory flow, elastance, and resistance. Pressure-regulated volume control (PRVC) automatically varies pressure breath to breath to achieve a set VT. Automode automatically titrates the level of support provided between control and support modes, depending on the patient’s level of spontaneous ventilation. Adaptive support ventilation (ASV) is another form of closed-loop, automated ventilation that combines aspects of pressure support and pressure control. Types of high-frequency ventilation (HFV) include high-frequency positive pressure ventilation (HFPPV), high-frequency jet ventilation (HFJV), highfrequency percussive ventilation (HFPV), and high-frequency oscillatory ventilation (HFOV). High-frequency oscillatory ventilation (HFOV) uses much lower than normal VT and very high ventilatory rates to maintain ventilation while lowering the risk of ventilator-induced lung injury (VILI). Neurally adjusted ventilatory assist (NAVA) uses the diaphragm’s electrical (EMG) signal to initiate and cycle the breath from I to E. A specially designed nasogastric catheter must be correctly positioned for NAVA to function. The inspiratory flow waveforms include square, ascending, descending, and sinusoidal. Mechanical ventilation alarms must be properly adjusted to assure proper

monitoring and patient safety. Active humidification during invasive mechanical ventilation should be targeted at 33 to 44 mg/L at inspired temperatures of 34º to 41ºC; risk of thermal injury is increased at > 41ºC. Increases in mean airway pressure (Paw) decrease venous return and may reduce cardiac output. Respiratory muscle atrophy and ventilator-induced diaphragmatic dysfunction can develop in patients receiving mechanical ventilatory support. Hazards and complications associated with mechanical ventilation include increased ICP, acute renal failure, and gastrointestinal bleeding. Other hazards of mechanical ventilation include ventilator-associated pneumonia (VAP), VILI, airway complications, and the risk of ventilator failure or accidental disconnect. Reduced PCO2 is a cerebral vasoconstrictor while increased PCO2 is a cerebral vasodilator; this should be considered when caring for with patients with head trauma or traumatic brain injury. Sleep fragmentation can impact patient outcomes and care should be taken to reduce sleep disruption.

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1992;145:114–120. 30. Porra L, Bayat S, Malaspinas I, et al. Pressure-regulated volume control vs. volume control ventilation in healthy and injured rabbit lung: An experimental study. Eur J Anaesthesiol. 2016;33(10):767–775. 31. Johnson KG, Johnson DC. Treatment of sleep-disordered breathing with positive airway pressure devices: Technology update. Med Devices (Auckl). 2015;8:425–437. 32. Cheri, NK. HFOV - High frequency oscillatory ventilation. [Slideshow]. 2015. Available at https://www.slideshare.net/cherinaveen/hfov20-20-high20frequency20oscillatory20ventilation. Accessed May 13, 2018. 33. Maquet Getinge Group. Neurally adjusted ventilatory assist (NAVA®): Personalized ventilation. Available at https:\\www.maquet.com/int/products/nava/. Updated 2016. 34. Kallio M, Peltoniemi O, Anttila E, et al. Neurally adjusted ventilatory assist (NAVA) in pediatric intensive care: A randomized controlled trial. Pediatr Pulmonol. 2014;50(1):55–62. 35. Tobin, MJ. Principles and Practice of Mechanical Ventilation. 2nd ed. New York, NY: McGraw-Hill; 2006. 36. Devaquet J, Jonson B, Niklason L, et al. Effects of inspiratory pause on CO2 elimination and arterial PCO2 in acute lung injury. J Appl Physiol. 1985;105(6):1944–1949. 37. The Joint Commission. R3 Report: Alarm system safety. December 11, 2013. Available at https://www.jointcommission.org/assets/1/18/R3_Report_Issue_5_12_2_13_Final.pdf. 38. Drew B, Harris P, Zègre-Hemsey J, et al. Insights into the problem of alarm fatigue with physiologic monitor devices: A comprehensive observational study of consecutive intensive care unit patients. PLOS. 2014;9(10):1–23. 39. Restrepo R, Hirst K, Wittnebel L, Wettstein R. Clinical practice guideline: Transcutaneous monitoring of carbon dioxide and oxygen. Respir Care. 2012;57(11):1955–1962. 40. Restrepo R, Walsh B. Humidification during invasive and noninvasive mechanical ventilation: 2012. Respir Care. 2012;57(5):782–788. 41. Moraes L, Santos CL, Santos RS, et al. Effects of sigh during pressure control and pressure support ventilation in pulmonary and extrapulmonary mild acute lung injury. Crit Care. 2014;18:474(4):1–13. 42. Patroniti N, Foti G, Cortinovis B, et al. Sigh improves gas exchange and lung volume in patients with acute respiratory distress syndrome undergoing pressure support ventilation. Anesthesiology. 2002;96(4):788– 794. 43. Levine S, Nguyen T, Taylor N, et al. Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans. N Engl J Med. 2008;358:1327–1335. 44. Martin D, Smith B, Gabrielli A. Mechanical ventilation, diaphragm weakness and weaning: A rehabilitation perspective. Respir Physiol Neurobiol. 2013;189(2):377–383. 45. Cournand A, Motley H, Werko L, Richards D Jr. Physiological studies on the effects of intermittent positive pressure breathing on cardiac output in man. Am J Physiol. 1948;152:162–174. 46. ARDSNet, Brower R, Matthay M, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–1308. 47. Beyer J, Conzen P, Schosser R, Messmer K. The effect of PEEP ventilation on hemodynamics and regional blood flow with special regard to coronary blood flow. Thorac Cardiovasc Surg. 1980;28(2):128–132. 48. Fujita Y, Sakai T, Ohsumi A, Takaori M. Effects of hypocapnia and hypercapnia on splanchnic circulation and hepatic function in the beagle. Anesth Analg. 1989;69(2):152–157. 49. Hering R, Viehofer A, Zinserling J, et al. Effects of spontaneous breathing during airway pressure release ventilation on intestinal blood flow in experimental lung injury. Anesthesiology. 2003;99(5):1137–1144. 50. Lambertsen CJ, Semple SJ, Smyth MG, Gelfand R. H+ and pCO2 as chemical factors in respiratory and cerebral circulatory control. J Appl Physiol. 1961;16:473–484. 51. Harper AM, Bell RA. The effect of metabolic acidosis and alkalosis on the blood flow through the cerebral cortex. J Neurol Neurosurg Psychiatr. 1963;26:341–344. 52. Severinghaus JW, Lassen N. Step hypocapnia to separate arterial from tissue PCO2 in the regulation of cerebral blood flow. Circ Res. 1967;20:272–278. 53. Harder D, Madden A. Cellular mechanism of force development in cat middle cerebralartery by reduced PCO2. Pflugers Arch. 1985;403:402–404. 54. Yoon S, Zuccarello M, Rapoport R. pCO2 and pH regulation of cerebral blood flow. Front Physiol. 2012;3:1– 8.

55. LeRoux P. Intracranial pressure monitoring and management. In: Laskowitz D, Grant G, eds. Translational Research in Traumatic Brain Injury. Boca Raton, FL: CRC Press/Taylor and Francis Group; 2016. 56. Schirmer-Mikalsen K, Vik A, Skogvoll E, et al. Intracranial pressure during pressure control and pressureregulated volume control ventilation in patients with traumatic brain injury: A randomized crossover trial. Neurocrit Care. 2016;24(3):332–341. 57. Liu L, Wu A, Yang Y, et al. Effects of propofol on respiratory drive and patient-ventilator synchrony during pressure support ventilation in postoperative patients: A prospective study. Chin Med J. 2017;130(10):1155–1160. 58. Tate J, Dabbs A, Hoffman L, et al. Anxiety and agitation in mechanically ventilated patients. Qual Health Res. 2012;22(2):157–173. 59. Chlan L, Skaar D, Tracy M, et al. Safety and acceptability of patient-administered sedatives during mechanical ventilation. Am J Crit Care. 2017;26(4):288–296. 60. Slutsky AS. Ventilator-induced lung injury. N Engl J Med. 2014:979–980. doi: 10.1056/NEJMc1400293. 61. Sackner MA, Landa J, Hirsch J, Zapata A. Pulmonary effects of oxygen breathing. Ann Intern Med. 1975;82:40–43. 62. Vivino G, Antonelli M, Moro ML, et al. Risk factors for acute renal failure in trauma patients. Intens Care Med. 1998;24(8):808–814. 63. Jarnberg PO, de Vilotta ED, Eklund J, Granberg PO. Effects of positive end-expiratory pressure on renal function. Acta Anaesthesiol Scand. 1978;22:508–514. 64. Koyner JL, Murray PT. Mechanical ventilation and lung–kidney interactions. J Am Soc Nephrol. 2008;3:562–570. doi:10.2215/CJN.03090707. 65. Artinian V, Krayem H, DiGiovine B. Effects of early enteral feeding on the outcome of critically ill mechanically ventilated medical patients. Chest. 2006;129(4):960–967. doi:129.96007.10.1378/chest.129.4.960. 66. Rice TW, Wheeler AP, Thompson BT, et al. Initial trophic vs full enteral feeding in patients with acute lung injury: the EDEN randomized trial. JAMA. 2012;307(8):795-803. doi:10.1001/jama.2012.137.

CHAPTER

4 Mechanical Ventilators John Davies

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Critical Care Ventilators HAMILTON-G5 HAMILTON-C3 HAMILTON-C1 Getinge Servo-i Getinge Servo-u Covidien Puritan Bennett 840 Ventilator Covidien Puritan Bennett 980 Ventilator Newport e360 Ventilator Vyaire AVEA Vyaire VELA Dräger Evita Infinity V500 Dräger Evita XL GE Healthcare CARESCAPE R860 Philips Respironics V60 Ventilator High-Frequency Ventilators Vyaire 3100B High-Frequency Oscillator Percussionaire VDR-4 Bunnell Life Pulse Portable Ventilators HAMILTON-T1 HAMILTON-MR1 Airon pNeuton pNeuton mini pNeuton A and S Bio-Med Devices Crossvent 4+

Vyaire ReVel Vyaire LTV 1200 Dräger Carina Dräger Oxylog 3000 Plus Medtronic Newport HT70 Plus ZOLL Eagle II Philips Respironics Trilogy Ventilator DeVilbiss IntelliPAP Bilevel S DeVilbiss IntelliPAP AutoBilevel ResMed Lumis Tx ResMed Astral 100/150 Neonatal Ventilators Dräger Babylog VN500 Smiths Medical Pneupac babyPAC 100 Vyaire Infant Flow SiPAP

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Define key terms related to mechanical ventilation. Describe the five “basic” modes of mechanical ventilation possible. Summarize each critical care ventilator in terms of a brief description, manufacturer’s specifications, and controls. List the monitored parameters and alarms for each critical care ventilator. Describe each of the critical care ventilators to include modes of ventilation available and the main operator controls for each mode. Explain the special features and accessories available on each critical care ventilator. List the monitored parameters, manufacturer’s specifications, and alarms for each critical care ventilator. Describe the clinical application of each of the critical care ventilators. Explain the uses and application of the high-frequency ventilators. Describe the function and operation of the portable ventilators. Overview the use and operation of the neonatal ventilators.

KEY TERMS adaptive pressure ventilation apnea backup breath continuous positive airway pressure (CPAP) cycle flow inspiratory flow inspiratory pressure inspiratory time mechanical ventilator nebulizer parameters positive end-expiratory pressure (PEEP) pressure assist pressure assist/control pressure support respiratory mechanics respiratory rate sensitivity synchronized intermittent mandatory ventilation (SIMV) spontaneous ventilation

tidal volume trigger volume assist volume assist/control

Introduction Mechanical ventilators incorporate sophisticated life support technology designed to provide flow and pressure to the patient to support oxygen (O2) and carbon dioxide (CO2) transport between the environment and the pulmonary capillary bed. The clinical goals are to sustain adequate oxygenation and ventilation while, at the same time, reducing the load on the respiratory muscles (work of breathing) without harming the lungs. Modern-day ventilators are technologically advanced with enhanced graphics and a variety of modes from which to choose. Unfortunately for the clinician, in many cases the available modes are given slightly different names depending on the manufacturer. For the purposes of this chapter, the following basic terminology will be used to refer to the different modes: volume assist/control (VAC), volumesynchronized intermittent mandatory ventilation (V-SIMV), pressure assist/control (PAC), pressure-synchronized intermittent mandatory ventilation (P-SIMV), and pressure support (PS). These modes are depicted in Table 4-1 and Table 4-2. For completeness, a more detailed taxonomy will be included in the tables throughout the chapter.1 TABLE 4-1 Trigger, Target, and Cycle Variables in the Different Breath Types

Description Abbreviations: PA, pressure assist; PC, pressure control; PEEP, positive end-expiratory pressure; PS, pressure support; SV, spontaneous ventilation; VA, volume assist; VC, volume control.

TABLE 4-2 Different Breath Types That Make Up the Different Modes

Description Abbreviations: Breath types: PA, pressure assist; PC, pressure control; PS, pressure support; VA, volume assist; VC, volume control. Modes: PAC, pressure assist/control; P-SIMV, pressure-synchronized intermittent mandatory ventilation; PSV, pressure-support ventilation; VAC, volume assist/control; V-SIMV, volumesynchronized intermittent mandatory ventilation.

The ventilators discussed in this chapter will be classified into five categories: critical care ventilators, portable ventilators, high-frequency ventilators, neonatal ventilators, and noninvasive ventilators. Modes of ventilation available will be described, including newer modes that incorporate closed-loop control.2,3 While a comprehensive survey of current ventilators is provided, it is beyond the scope of this chapter to discuss every single ventilator on the market; thus, only the more commonly used ventilators will be discussed.

Critical Care Ventilators There are currently a number of critical care ventilators in common use. Specific ventilators differ on features and modes available, monitoring and graphic displays provided, and cost. Ventilator choice should be driven by consideration of the patient's needs, specific clinical goals, and the clinician’s familiarity with the ventilator to be employed. When choosing a specific ventilator, the ventilator’s features, modes, pressure and flow capabilities, and integrated alarms and monitoring systems should be considered. The ventilator chosen should adequately and safely ventilate patients under changing conditions and provide the features and modes required. Most manufacturers offer several ventilators with different capabilities and features. In this chapter we will consider some of the major critical care ventilators in current clinical use.

HAMILTON-G5 The HAMILTON-G5 ventilator (see Figure 4-1)is a critical care ventilator designed for hospital use by healthcare professionals trained in optimizing mechanical ventilation.4 It has the ability to ventilate adult and pediatric patients with an option for infant and neonatal patients. The G5 is electrically powered from an alternating current (AC) outlet and has an internal battery backup. The electrical power controls a pneumatic ventilation system that delivers the gas. It employs a disposable proximal flow sensor, which is a requirement, and it works in conjunction with other internal sensors to adjust gas delivery to the patient. The HAMILTON-G5 operator interface is displayed in Figure 4-2. It consists of a touch screen, some keys, and a turn-and-press knob. Turning the knob changes the values of the parameter chosen, and pressing the knob confirms the selection.

FIGURE 4-1 The HAMILTON-G5 Ventilator. Courtesy of Hamilton Medical.

FIGURE 4-2 The HAMILTON-G5 Operator Interface. Courtesy of Hamilton Medical.

Modes The different modes available on the HAMILTON-G5 are classified and depicted in Table 4-3. TABLE 4-3 HAMILTON-G5 Modes of Ventilation

Description Abbreviations: APVcmv, adaptive pressure ventilation with controlled mandatory ventilation; ASV, adaptive support ventilation; CPAP, continuous positive airway pressure; I:E, inspiration-to-expiration ratio; nCPAP-PS, nasal continuous positive airway pressure; NIV, noninvasive ventilation; NIV-ST, spontaneous/timed noninvasive ventilation; PA, pressure assist; PAC, pressure assist/control; PC, pressure control; PC-IMV, pressure-control-intermittent mandatory ventilation; P-CMV, pressure-controlled mandatory ventilation; PS, pressure support; P-SIMV, pressure-synchronized intermittent mandatory ventilation; PSV, pressure-support ventilation; (S)CMV, synchronized controlled mandatory ventilation; VA, volume assist; VAC, volume assist/control; VC, volume control; V-SIMV, volume-synchronized intermittent mandatory ventilation.

Synchronized Controlled Mandatory Ventilation Synchronized controlled mandatory ventilation [(S)CMV] is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patientassisted breaths.4 Spontaneous breaths are not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: Fraction of inspired oxygen (FIO2) Positive end-expiratory pressure (PEEP) VT Flow

Respiratory rate (RR) Inspiratory time Inspiration-to-expiration ratio (I:E) The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.4

Synchronized Intermittent Mandatory Ventilation Synchronized intermittent mandatory ventilation (SIMV) combines two breath types, VAC and either PS or spontaneous breathing, while on continuous positive airway pressure (CPAP).4 Thus, the ventilator permits mandatory, time-triggered breaths, patient-assisted breaths, or spontaneous breaths. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a patient-assisted VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow RR I:E Inspiratory time Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.4 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.4

Pressure-Controlled Mandatory Ventilation Pressure-controlled mandatory ventilation (P-CMV) is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.4 Spontaneous breaths are not allowed. The breath cycles to exhalation

once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR I:E The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.4

Pressure-Synchronized Intermittent Mandatory Ventilation Pressure-synchronized intermittent mandatory ventilation (P-SIMV) is similar to SIMV described earlier, except that the target is now pressure instead of volume. PSIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP.4 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time I:E RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on

inspiratory pressure level, patient effort, and patient respiratory system mechanics.4 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.4

Spontaneous Ventilation In the spontaneous ventilation mode, the patient triggers all of the breaths and will receive either PS or CPAP (if the PS is set at 0).4 If the PS is set at 0, then the patient must contribute all of the work of breathing. This is sometimes used for a spontaneous breathing trial to assess the potential for liberation from the ventilator. During PS, the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.4 Clinical Focus 4-1 describes ventilator adjustments in a COPD patient receiving pressure support ventilation in the spontaneous ventilation mode.

CLINICAL FOCUS 4-1 Ventilator Adjustments: COPD Patient The nurse calls you in to the room of a patient with chronic obstructive pulmonary disease (COPD), who appears uncomfortable and is on the following settings: PS of 8 cm H2O, PEEP 5 cm H2O, and FIO2 0.30. His respiratory rate is 18 and his tidal volume is 600 mL (approximately 8 mL/kg ideal body weight). You also note that his inspiratory time is about 1.6 seconds. Question 1: Why is this issue a problem to be addressed? Answer: This COPD patient’s inspiratory time is much too long, and his expiratory time is reduced. This is leading to patient–ventilator asynchrony.

The patient may also develop autoPEEP due to inadequate expiratory time. The patient’s inspiratory time is 1.6 seconds and respiratory rate is 16, resulting in a respiratory cycle time of 3.75 seconds. This leaves only about 2 seconds for expiratory time in a patient with obstructive lung disease, which may lead to the development of pulmonary overinflation due to autoPEEP. This overinflation may lead to a delayed or missed trigger on the ensuing breath. Question 2: What can you do with the ventilator that could make this patient more comfortable? Answer: Option 1: You could adjust his expiratory sensitivity to shorten the inspiratory time. The default value on most ventilators is 25%. If this was the case here, you could increase the expiratory sensitivity to 50% or higher (depending on the maximum value allowed by that particular ventilator). Option 2: You could switch him to PAC with a low set rate (most ventilators allow you to go as low as 1 breaths per minute [bpm]). The inspiratory time could then be set directly to a more reasonable time (0.8–1.0 seconds). Since the patient seems to have a stable respiratory drive, all of the breaths would then be patient triggered as they were in PS. The only difference here is a clinician-set inspiratory time. As noted, due to the excessively long inspiratory time this patient may also not be completely emptying his lungs before he tries and triggers the ensuing breath leading to trigger delays. The shortened inspiratory time will also help resolve this issue.

Volume Support In volume-support (VS) mode, the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.4 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator has the potential to drop the level of support as patient effort increases and conversely may increase the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity

The VT may not match the operator setting because the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.4 Any change in patient effort from the previous breath may result in a deviation from the VT setting.4

Adaptive Pressure Ventilation with Controlled Mandatory Ventilation Adaptive pressure ventilation with controlled mandatory ventilation (APVcmv) is a VT-targeted pressure-regulated mode. In other words, the clinician sets the desired VT and the ventilator uses varying levels of inspiratory pressure to achieve the target.4 Similar to VS, the ventilator relies on calculations from previous breaths to deliver what it calculates the inspiratory pressure level needs to be to achieve the VT. It is different from VS in that the ventilator now uses PAC breaths as opposed to PS breaths. However, the same principle applies: the ventilator may reduce the inspiratory pressure level as patient effort increases and conversely may increase the inspiratory pressure level when patient effort is too low. The breaths may be either time triggered or patient triggered. Main operator controls include: FIO2 PEEP VT target RR Inspiratory time I:E The VT may not match the operator setting due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.4 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Adaptive Pressure Ventilation with Synchronized Intermittent Mandatory Ventilation Adaptive pressure ventilation with synchronized intermittent mandatory ventilation (APVsimv) combines a VT-targeted PAC breath with spontaneous PS breaths in

between.4 The type of breaths delivered are the same as P-SIMV; what is different is that the inspiratory pressure level is controlled by the ventilator (variable) in APVsimv as opposed to being clinician set (P-SIMV). Main operator controls include: FIO2 PEEP VT target Inspiratory time I:E RR Pressure-support level The VT may not match the operator setting for the PAC breaths due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.4 Any change in patient effort from the previous breath may result in a deviation from the VT setting. During the PS breaths, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics

Duo Positive-Pressure Ventilation Duo positive-pressure ventilation (DuoPAP) is a pressure-targeted mode of ventilation that allows for spontaneous breathing at two different pressure levels.4 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the positive end-expiratory pressure (PEEP) level (termed Plow in this mode). This is important, because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP

Phigh Plow Thigh Tlow Pressure support Expiratory sensitivity DuoPAP generally is used in “normal” I:E ratios (not inversed).4 The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (if set > 0), patient effort, and patient respiratory system mechanics.

Airway Pressure-Release Ventilation Airway pressure-release ventilation (APRV) is a mode of ventilation that is similar to DuoPAP in that it allows for spontaneous breathing at two different pressure levels.4 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. Unlike DuoPAP, APRV generally is used in an inverse ratio fashion. Most of the time is spent at Phigh with brief, periodic releases to Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level (which is termed Plow in this mode). This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow Pressure support Cycle sensitivity The VT will be variable and depend on the inspiratory pressure level (Phigh), PS

level (if set > 0), patient effort, and patient respiratory system mechanics.4 There is no respiratory rate control and cycling is determined by the Thigh and Tlow settings.

Adaptive Support Ventilation Adaptive support ventilation (ASV) is a “feedback” mode that adjusts the inspiratory pressure and RR to meet a minimum-minute volume set by the clinician.4 This results in a variable form of P-SIMV. The machine-timed breaths are PAC, while the spontaneously generated breaths are PS. The amount of breathing that the patient does determines how many machine-generated breaths will be delivered. Main operator controls include: FIO2 PEEP %MinVol Cycle sensitivity Maximum inspiratory pressure Patient height and sex Endotracheal (ET) tube information The VT will be variable and depend on inspiratory pressure level for the PAC breaths, PS level for the spontaneous breaths, patient effort, and patient respiratory system mechanics.4

Noninvasive Ventilation In the noninvasive ventilation (NIV) mode, the patient triggers all of the breaths and will receive PS breaths. As the name would suggest, NIV is designed for use with a mask or other noninvasive patient interface.4 Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.4

Spontaneous/Timed Noninvasive Ventilation Spontaneous/timed noninvasive ventilation (NIV-ST) is also designed for use with a mask or other noninvasive patient interface.4 It is essentially P-SIMV without an endotracheal tube. NIV-ST combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, timetriggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.4 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.4

Nasal Continuous Positive Airway Pressure Nasal continuous positive airway pressure (nCPAP-PS) is available only in the neonatal mode and is designed for use with a noninvasive interface.4 It also is essentially a P-SIMV without an endotracheal tube. Slightly different from P-SIMV, if the patient triggers regularly, all breaths are patient-triggered spontaneous breaths, i.e., there are no time-triggered mandatory breaths. Only when the patient trigger is not detected during the defined breath cycle time (or total breath time) does the ventilator deliver time-triggered mandatory breaths. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous

breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.4 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.4

Special Features Special features available with the HAMILTON G5 include a pressure/volume tool, apnea backup ventilation, Intellicuff(R), a dynamic heart/lung panel and INTELLiVENT-ASV.

Pressure/Volume Tool The pressure/volume (P/V) tool is a respiratory mechanics maneuver that performs a quasistatic P/V curve on the ventilator (Figure 4-3).4 During the maneuver, the G5 slowly increases the pressure to a clinician-set upper level and then slowly decreases the pressure either back to baseline or to an elevated PEEP level, ultimately producing an inflation and deflation limb. It will only work on passive patients because any effort by the patient will terminate the maneuver. It allows for a breath hold at the top of the curve (recruitment maneuver, in essence) and can be set to terminate at a higher-than-baseline PEEP level to maintain any gained recruitment.

FIGURE 4-3 P/V Tool on the HAMILTON-G5. Courtesy of Hamilton Medical

Apnea Backup Ventilation The ventilator will go into apnea backup ventilation if no breaths are detected in the clinician-set interval.4 The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-3). The G5’s apnea backup is bidirectional, i.e., if no patient triggering is detected within a defined apnea time, the ventilator switches to the defined backup mode; if the patient breaths resume, the device switches back to the previous support mode. The back-and-forth switching is fully automatic.

Intellicuff® Intellicuff® is an integrated, automated endotracheal tube cuff pressure controller that is used to both monitor and maintain the cuff pressure.4

Dynamic Heart/Lung Panel The dynamic heart/lung panel is a pictorial representation of the heart and lungs.4 It also displays VT, interaction with the heart, patient triggering, and resistance in real time.

INTELLiVENT-ASV INTELLiVENT-ASV (not available in the United States at this time) is an entirely closed-loop mode of ventilation.4 It uses ASV (see above) to adjust the inspiratory pressure and RR to achieve a minute ventilation target. In passive patients, the target minute volume is adjusted according to exhaled partial pressure of end-tidal CO2. INTELLiVENT also controls the oxygenation. PEEP and FIO2 are adjusted according to blood oxygen saturation level (SpO2) (finger or ear probe) and are based on a table derived from ARDSNet publications.2,3 Clinicians can also opt for INTELLiVENT to wean the patient (if tolerated) and do spontaneous breathing trials.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the HAMILTON-G5 are listed in Table 4-4.4 TABLE 4-4 Manufacturer’s Specifications for the HAMILTON-G5 Setting

Range

Pressure Inspiratory pressure

5 to 100 cm H2O

Pressure support

0 to 100 cm H2O

PEEP

0 to 50 cm H2O

Volume Tidal volume

0.02 to 2.0 L

Flow Inspiratory flow Time

1 to 180 L/min

Inspiratory time

0.1 to 10 seconds

Mandatory breath rate

5 to 120/min

Sensitivity Trigger

0.5 to 10 cm H2O (pressure) 0.5 to 15 L/min (flow)

Cycle

5% to 70% of peak flow

Alarms

Range

Pressure High pressure

10 to 120 cm H2O

Low pressure

2 to 119 cm H2O

Volume High tidal volume

0.1 to 3.0 L

Low tidal volume

0 to 2.95 L

High exhaled minute volume

2 to 50 L/min

Low exhaled minute volume

0.1 to 49 L/min

Time High respiratory rate

2 to 130 breaths/min

Low respiratory rate

0 to 128 breaths/min

Apnea time

15 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Peak pressure

fSpont

Mean pressure

TI

Pause pressure

TE

PEEP/CPAP

Cstat

AutoPEEP

P0.1

Inspiratory flow

PTP

Expiratory flow

PCexp

Inspired tidal volume

RCinsp

Expired tidal volume

Rexp

Expired minute volume

Rinsp

Leak volume

RSB

I:E

WOBimp

fTotal

Oxygen

Accessories The HAMILTON-G5 has the following accessories available: end-tidal CO2 (ETCO2) measurement, pulse oximetry, an integrated vibrating mesh Aerogen® nebulizer for aerosolized medication delivery, and esophageal manometry.4 ETCO2 can be either mainstream or sidestream and it can be used for volumetric capnography and airway deadspace calculations. Pulse oximetry is another parameter that can be displayed on the ventilator. The G5 is compatible with Masimo and Nihon Kohden cables. Both ETCO2 and pulse oximetry measurements require special modules that attach to the ventilator. The integrated Aerogen® system consists of the Aerogen nebulizer and the Aerogen module of the HAMILTON-G5.

HAMILTON-C3 The HAMILTON-C3 ventilator is intended to provide positive-pressure ventilatory support to adults, pediatrics, and optionally infants and neonates.5 It is pictured in Figure 4-4. The ventilator is electrically powered and pneumatically driven. The C3 incorporates an air compressor and internal battery backup, which can facilitate intrahospital transport. The C3 also incorporates a proximal flow sensor that facilitates measurement at the patient wye. The C3 operator interface is depicted in Figure 4-5. It consists of a touch screen, some keys, and a turn-and-press knob. Turning the knob changes the values of the parameter chosen and pressing the knob confirms the selection.

FIGURE 4-4 The HAMILTON-C3 Ventilator. Courtesy of Hamilton Medical.

FIGURE 4-5 The HAMILTON-C3 Operator Interface. Courtesy of Hamilton Medical.

Modes The different modes available on the HAMILTON-C3 are classified and depicted on Table 4-5. TABLE 4-5 HAMILTON-C3 Ventilation Modes

Description

Synchronized Controlled Mandatory Ventilation Synchronized controlled mandatory ventilation [(S)CMV] is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patientassisted breaths.5 Spontaneous breaths are not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Flow RR I:E The resulting pressure created is variable and depends on VT, flow, and patient

respiratory system mechanics.5

Synchronized Intermittent Mandatory Ventilation Synchronized intermittent mandatory ventilation (SIMV) combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.5 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow RR Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.5 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.5

Pressure-Controlled Ventilation+ Pressure-controlled ventilation+ (PCV+) is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted PAC breaths.5 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time

I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.5

Pressure Synchronized Intermittent Mandatory Ventilation+ Pressure synchronized intermittent mandatory ventilation+ (P-SIMV+) is similar to SIMV described above except that the target is now pressure instead of volume.5 PSIMV+ also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner, as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.5 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.5

Spontaneous Mode In the spontaneous mode, the patient triggers all of the breaths and will receive either PS or CPAP (if the PS is set at 0).5 If the PS is set at 0, then the patient must

contribute all of the work of breathing. This is sometimes used for a spontaneous breathing trial to assess the potential for liberation from the ventilator. During PS, the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.5

Adaptive Pressure Ventilation with Controlled Mandatory Ventilation Adaptive pressure ventilation with controlled mandatory ventilation (APVcmv) is also referred to as (S)CMV+.5 It is a VT-targeted, pressure-regulated mode. In other words, the clinician sets the VT that is wanted, and the ventilator uses varying levels of PAC to achieve the target. Similar to VS, the ventilator relies on calculations from previous breaths to deliver what it calculates the inspiratory pressure level needs to be to achieve the VT. It differs from volume support in that the ventilator now uses PAC breaths as opposed to PS breaths. However, the same principle applies; the ventilator drops the inspiratory pressure level as patient effort increases and conversely increases the inspiratory pressure level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target I:E The VT may not match the operator setting due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.5 Any change in patient effort from the

previous breath may result in a deviation from the VT setting.

Adaptive Pressure Ventilation with Synchronized Intermittent Mandatory Ventilation Adaptive pressure ventilation with synchronized intermittent mandatory ventilation (APVsimv) is also referred to as SIMV+.5 It combines a VT-targeted PAC breath with spontaneous PS breaths in between. The type of breaths delivered are the same as P-SIMV; what is different is that the inspiratory pressure level is controlled by the ventilator (variable) in APVsimv as opposed to clinician set (P-SIMV). Main operator controls include: FIO2 PEEP VT target Inspiratory time Pressure-support level Cycle sensitivity The VT may not match the operator setting for the PAC breaths due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.5 Any change in patient effort from the previous breath may result in a deviation from the VT setting. During the PS breaths, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics

Duo Positive-Pressure Airway Pressure Duo positive-pressure airway pressure (DuoPAP) is a pressure-targeted mode of ventilation that allows for spontaneous breathing at two different pressure levels.5 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level (which is termed Plow in this mode). This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form

of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow Pressure support Cycle sensitivity DuoPAP generally is used with “normal” I:E ratios (not inversed).5 The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (if set > 0), patient effort, and patient respiratory system mechanics.

Airway Pressure-Release Ventilation Airway pressure-release ventilation (APRV) is a mode of ventilation that is similar to DuoPAP in that it allows for spontaneous breathing at two different pressure levels.5 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. Unlike DuoPAP, APRV generally is used in an inverse ratio fashion. Most of the time is spent at Phigh with brief, periodic releases to Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level (which is termed Plow in this mode). This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh

Tlow The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (if set > 0), patient effort, and patient respiratory system mechanics.5

Adaptive Support Ventilation Adaptive support ventilation (ASV) is a “feedback” mode that adjusts the inspiratory pressure and RR to meet a minimum minute volume set by the clinician.5 This results in a variable form of P-SIMV. The machine-timed breaths are PAC while the spontaneously generated breaths are PS. The amount of breathing that the patient does determines how many machine-generated breaths will be delivered. The algorithm for ASV is centered around lung protection. Main operator controls include: FIO2 PEEP %MinVol Cycle sensitivity Patient height Endotracheal tube information The VT will be variable and depend on: inspiratory pressure level for the PAC breaths, PS level for the spontaneous breaths, patient effort, and patient respiratory system mechanics.5

Noninvasive Ventilation In the NIV mode, the patient triggers all of the breaths and may receive PS with or without CPAP or CPAP alone.5 As the name would suggest, NIV is designed for use with a mask or other noninvasive patient interface. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient

respiratory system mechanics.5

Spontaneous/Timed Noninvasive Ventilation Spontaneous/timed NIV (NIV-ST) is also designed for use with a mask or other noninvasive patient interface.5 It is essentially P-SIMV without an endotracheal tube. NIV-ST combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths. If the patient triggers regularly, all breaths are patient-triggered spontaneous breaths, i.e., no time-triggered mandatory breath. Only when the patient trigger is not detected during the defined breath cycle time (or total breath time), the ventilator delivers time-triggered mandatory breath. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.5 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.5

Nasal Continuous Positive Airway Pressure Nasal CPAP (nCPAP-PS) is available only in the neonatal mode and is designed for use with a noninvasive interface.5 It also is essentially P-SIMV without an endotracheal tube. Slightly different from P-SIMV, if the patient triggers regularly, all

breaths are patient-triggered spontaneous breaths, i.e., no time-triggered mandatory breath. Only when the patient trigger is not detected during the defined breath cycle time (or total breath time) does the ventilator deliver time-triggered mandatory breaths at a clinician selected backup rate. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.5 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.5

Special Features Similar to the HAMILTON G5, the C3 has a number of special features.

Pressure/Volume Tool The pressure/volume (P/V) tool is a respiratory mechanics maneuver that generates a quasistatic P/V curve (Figure 4-3).5 During the maneuver, the C3 slowly increases the pressure to a clinician-set upper level and then slowly decreases the pressure either back to baseline or an elevated PEEP level ultimately producing an inflation and deflation limb. It will only work on passive patients because any effort will terminate the maneuver. It allows for a breath hold at the top of the curve (recruitment maneuver, in essence) and can be set to terminate at a higher-thanbaseline PEEP level to maintain any gained recruitment.

Apnea Backup Ventilation The ventilator will go into apnea backup ventilation if no breaths are detected in the

clinician-set interval.5 The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-5).

Nebulizer A pneumatic nebulization function powers a standard inline nebulizer for delivery of prescribed medications in the ventilator circuit.5 When nebulization is active, the nebulizer flow is synchronized with the inspiratory phase of each breath for 30 minutes. Nebulization can be activated in all modes of ventilation.

High-Flow Oxygen Therapy High-flow oxygen therapy is a therapy in which a continuous flow of heated and humidified air and oxygen is delivered to the patient.5 The level of oxygen and flow are preset by the operator. High-flow oxygen therapy can be delivered using singleor double-limb breathing circuits.

Dynamic Heart/Lung Panel The dynamic heart/lung panel is a pictorial representation of the heart and lungs.5 It also displays VT, interaction with the heart, patient triggering, and resistance in real time.

INTELLiVENT-ASV INTELLiVENT-ASV (not available in the United States at this time) is an entirely closed-loop mode of ventilation.5 It uses ASV (see above) to adjust the inspiratory pressure and RR to achieve a minute ventilation target. In passive patients, the target minute volume is adjusted according to exhaled partial pressure of end-tidal CO2. INTELLiVENT also controls the oxygenation. PEEP and FIO2 are adjusted according to SpO2 (finger or ear probe) based on table derived from ARDSNet recommendations. Clinicians can also opt for INTELLiVENT to wean the patient (if tolerated) and do spontaneous breathing trials.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the HAMILTON-C3 are listed in Table 4-6.

TABLE 4-6 Manufacturer’s Specifications for the HAMILTON-C3 Setting

Range

Pressure Inspiratory pressure

0 to 60 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.02 to 2.0 L

Flow Inspiratory flow

1 to 80 L/min

Time Inspiratory time

0.1 to 12 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 to 15 cm H2O (pressure) 1 to 20 L/min (flow)

Cycle

5% to 80% of peak flow

Alarms

Range

Pressure High pressure

15 to 70 cm H2O

Low pressure

4 to 60 cm H2O

Volume High tidal volume

0.1 to 3.0 L

Low tidal volume

0 to 3.0 L

High exhaled minute volume

0.1 to 50 L/min

Low exhaled minute volume

0.1 to 50 L/min

Time High respiratory rate

0 to 99 breaths/min

Low respiratory rate

0 to 99 breaths/min

Apnea time

15 to 60 seconds

Other O2 high

18% to 105%

O2 low

18% to 97%

ETco2 high

1 to 100 mm Hg

ETco2 low

0 to 100 mm Hg

Monitored Parameters Peak pressure

fTotal

Mean pressure

fSpont

Plateau pressure

fControl

Pause pressure

TI

PEEP/CPAP

TE

AutoPEEP

Cstat

Inspiratory flow

IBW

Expiratory flow

P0.1

Inspired tidal volume

PTP

Expired tidal volume

RCexp

Expired minute volume

Rinsp

Spontaneous minute volume

VTEspont

Vleak (%)

Oxygen %

MV leak

FETco2

I:E

PETco2

Accessories The HAMILTON-C3 has the following accessories available: end-tidal CO2 (ETCO2) measurement, pulse oximetry, and an integrated vibrating mesh Aerogen® nebulizer for aerosolized medication delivery.5 ETCO2 can be either mainstream or sidestream and it can be used for volumetric capnography and airway deadspace calculations.

Pulse oximetry is another parameter that can be displayed on the ventilator. The C3 is compatible with Masimo and Nihon Kohden cables. Both ETCO2 and pulse oximetry measurements require special modules that attach to the ventilator. The integrated Aerogen® system consists of the Aerogen nebulizer and the Aerogen module of the HAMILTON-G5.

HAMILTON–C1 The HAMILTON-C1 ventilator is intended to provide positive-pressure ventilatory support to adults, pediatrics, and optionally infants and neonates.6 It is pictured in Figure 4-6. It is intended to be used in the intensive care ward, intermediate care ward, emergency ward, long-term acute care hospital, or in the recovery room. The HAMILTON-C1 is an electronically controlled pneumatic system with an integrated air compressor. It runs on AC power with battery backup to protect to facilitate intrahospital transport. The HAMILTON-C1’s pneumatics deliver gas, and its electrical systems control pneumatics, monitor alarms, and distribute power. The C1 also incorporates a proximal flow sensor that facilitates measurement at the patient wye. The C1 operator interface is depicted in Figure 4-7. It consists of a touch screen, some keys, and a turn-and-press knob. Turning the knob changes the values of the parameter chosen and pressing the knob confirms the selection.

FIGURE 4-6 The HAMILTON-C1 Ventilator. Courtesy of Hamilton Medical.

FIGURE 4-7 The Operator Interface for the HAMILTON-C1. Courtesy of Hamilton Medical.

Modes The different modes available on the HAMILTON-C1 are classified and depicted on Table 4-7. TABLE 4-7 HAMILTON-C1 Ventilation Modes

Description

Synchronized Controlled Mandatory Ventilation Plus Synchronized controlled mandatory ventilation plus [(S)CMV+] is a VT-targeted, pressure-regulated mode.6 In other words, the clinician sets the VT that is wanted and the ventilator uses varying levels of PAC to achieve the target. The ventilator relies on calculations from previous breaths to deliver what it calculates the inspiratory pressure level needs to be to achieve the VT. In this mode the ventilator has the potential to drop the inspiratory pressure level as patient effort increases and conversely may increase the inspiratory pressure level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target I:E RR The VT may not match the operator setting due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.6 Any change in patient effort from the

previous breath may result in a deviation from the VT setting.

Synchronized Intermittent Mandatory Ventilation Plus Synchronized intermittent mandatory ventilation plus (SIMV+) combines a VTtargeted PAC breath with spontaneous PS breaths in between.6 The type of breaths delivered are the same as P-SIMV; what is different is that the inspiratory pressure level is controlled by the ventilator (variable) in SIMV+. Main operator controls include: FIO2 PEEP VT target Inspiratory time RR Pressure-support level Cycle sensitivity The VT may not match the operator setting for the PAC breaths due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.6 Any change in patient effort from the previous breath may result in a deviation from the VT setting. During the PS breaths, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics

Pressure-Controlled Ventilation+ Pressure-controlled ventilation+ (PCV+) is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.6 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level I:E RR

The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.6

Pressure Synchronized Intermittent Mandatory Ventilation+ Pressure synchronized intermittent mandatory ventilation+ (P-SIMV+) is similar to SIMV described above except that the target is now pressure instead of volume.6 PSIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.6 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.6

Spontaneous/CPAP During spontaneous/CPAP, the patient regulates the respiratory rate and the VT.6 The patient triggers all of the breaths and will receive either no additional support (CPAP) or the clinician-set PS level. With a pressure support, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the

inspiratory peak flow. The CPAP is sometimes used for spontaneous breathing trials. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.6

Duo Positive-Pressure Airway Pressure Duo positive-pressure airway pressure (DuoPAP) is a pressure-targeted mode of ventilation that allows for spontaneous breathing at two different pressure levels.6 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level (which is termed Plow in this mode). This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Thigh RR Pressure support Cycle sensitivity DuoPAP generally is used with “normal” I:E ratios (not inversed).6 The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (If set > 0), patient effort, and patient respiratory system mechanics.

Airway Pressure-Release Ventilation

APRV is a mode of ventilation that is similar to DuoPAP in that it allows for spontaneous breathing at two different pressure levels.6 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. It differs from DuoPAP-APRV in that it is used in an inverse ratio fashion. Most of the time is spent at Phigh with brief, periodic releases to Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level (which is termed Plow in this mode). This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (if set > 0), patient effort, and patient respiratory system mechanics.6

Adaptive Support Ventilation ASV is a “feedback” mode that adjusts the inspiratory pressure and RR to meet a minimum minute volume set by the clinician.6 This results in a variable form of PSIMV. The machine-timed breaths are PAC while the spontaneously generated breaths are PS. The amount of breathing that the patient does determines how many machine-generated breaths will be delivered. The algorithm for ASV is centered around lung protection. Main operator controls include: FIO2 PEEP %MinVol

Cycle sensitivity Patient height Endotracheal tube information The VT will be variable and depend on inspiratory pressure level for the PAC breaths, PS level for the spontaneous breaths, patient effort, and patient respiratory system mechanics.6

Noninvasive Ventilation In the NIV mode, the patient triggers all of the breaths and will receive either PS or CPAP (if the pressure is set to 0). As the name would suggest, NIV is designed for use with a mask or other noninvasive patient interface. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.6

Spontaneous/Timed Noninvasive Ventilation NIV-ST is also designed for use with a mask or other noninvasive patient interface. It is essentially P-SIMV without an endotracheal tube.6 NIV-ST combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. If the patient triggers regularly, all breaths are patient-triggered spontaneous breaths, i.e., no time-triggered mandatory breath. Only when the patient trigger is not detected during the defined breath cycle time (or total breath time), the ventilator delivers time-triggered mandatory breath. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur.

Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.6 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.6

Nasal Continuous Positive Airway Pressure Nasal continuous positive airway pressure (nCPAP) is available only in the neonatal mode and is designed for use with a noninvasive interface.6 As the name would suggest, this is a purely spontaneous mode with CPAP as the baseline pressure with no additional pressure added on inspiration. Main operator controls include: FIO2 CPAP RR The VT created will be variable and depend on patient effort and patient respiratory system mechanics.6

Nasal Continuous Positive Airway Pressure-Pressure Control Nasal CPAP-pressure control (nCPAP-PC) is a noninvasive, pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.6 The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP

Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.6

Special Features The HAMILTON C1’s special features include apnea ventilation, a standard nebulizer and a dynamic lung model.

Apnea Backup Ventilation The ventilator will go into apnea backup ventilation if no breaths are detected in the clinician-set interval.6 The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-7).

Nebulizer A pneumatic nebulization function powers a standard inline nebulizer for delivery of prescribed medications in the ventilator circuit.6 When nebulization is active, the nebulizer flow is synchronized with the inspiratory phase of each breath for 30 minutes. Nebulization can be activated in all modes of ventilation.

Dynamic Lung Panel The dynamic lung panel visualizes tidal volume, lung compliance, patient triggering, and resistance in real time.6 The lungs expand and contract in synchrony with actual breaths. Numeric values for resistance (Rinsp) and compliance (Cstat) are displayed. In addition, the shape of the lungs and the bronchial tree are also related to the compliance and resistance values. If all values are in a normal range, the panel is framed in green.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the HAMILTON-C1 are listed in Table 4-8.

TABLE 4-8 The Manufacturer’s Specifications for the HAMILTON-C1 Setting

Range

Pressure Inspiratory pressure

3 to 60 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.02 to 2.0 L

Time Inspiratory time

0.1 to 12 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 to 20 L/min (flow)

Cycle

5% to 80% of peak flow

Alarms

Range

Pressure High pressure

15 to 70 cm H2O

Low pressure

4 to 60 cm H2O

Volume High tidal volume

0.1 to 3.0 L

Low tidal volume

0 to 3.0 L

High exhaled minute volume

0.03 to 50 L/min

Low exhaled minute volume

0.01 to 50 L/min

Time High respiratory rate

0 to 210 breaths/min

Low respiratory rate

0 to 200 breaths/min

Apnea time

5 to 60 seconds

Other 18% to 105%

O2 high O2 low

18% to 97%

ETco2 high

1 to 100 mm Hg

ETco2 low

0 to 100 mm Hg

Monitored Parameters Inspiratory pressure

fTotal

Peak pressure

fSpont

Mean pressure

fControl

Plateau pressure

TI

Pause pressure

TE

PEEP/CPAP

Cstat

AutoPEEP

IBW

Inspiratory flow

P0.1

Expiratory flow

PTP

Inspired tidal volume

RCexp

Expired tidal volume

Rinsp

Expired minute volume

VTEspont

Spontaneous minute volume

Oxygen %

Vleak (%)

FETco2

MV leak

PETco2

I:E

Accessories The HAMILTON-C1 has the following accessories available: end-tidal CO2 (ETCO2) measurement, pulse oximetry, and an integrated vibrating mesh Aerogen® nebulizer for aerosolized medication delivery.6

Getinge Servo-i The Getinge Servo-i is a critical care ventilator intended for treatment and monitoring of neonates, infants, and adults with respiratory failure or respiratory insufficiency.7 It

is pictured in Figure 4-8. The Servo-i is electrically powered from an AC outlet with an internal battery backup and is designed to be used by healthcare providers in hospitals or healthcare facilities and for inhospital transport. The Getinge Servo-i operator interface is displayed in Figure 4-9. Its controls consist of a touch screen, buttons, and knobs. The largest knob is the main control knob (Figure 4-9A). The touch screen is used to select the variable to be changed; the main control knob adjusts the settings by turning and is pressed to confirm the settings. The supplemental control knobs allow the clinician to make quick, direct setting adjustments of FIO2, tidal volume, inspiratory pressure, depending on the mode, respiratory rate, and PEEP (Figure 4-9A). The buttons on the bottom provide for manual breath trigger, O2 breaths (100% O2 for 1 min), and inspiratory and expiratory holds. The buttons up the right side of the operator interface are related to alarm settings, system information, and navigation (Figure 4-9A).

FIGURE 4-8 The Getinge Servo-i Ventilator. Courtesy of Getinge.

FIGURE 4-9 The Operator Interface of the Getinge Servo-i. Courtesy of Getinge.

Modes The different modes available on the Getinge Servo-i are classified and depicted on Table 4-9. TABLE 4-9 Getinge Servo-i Modes

Description

Volume Control Volume control is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.7 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT)

has been delivered. Volume control also incorporates flow adaptation so that, if the patient’s inspiratory effort is large enough, inspiration will switch from volume control to pressure support with flow cycling. The breaths can be delivered by a decelerating or fixed flow. Main operator controls include: FIO2 PEEP VT or mechanical ventilation (MV) RR Inspiratory time or I:E The resulting pressure created is variable and depends on VT, flow, patient effort, and patient respiratory system mechanics.7

SIMV (Volume Control) SIMV (volume control) combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.7 Thus, the ventilator provides mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. The volume-control breaths also incorporate flow adaptation so that if the patient’s inspiratory effort is large enough, inspiration will switch from volume control to pressure support with flow cycling. Main operator controls include: FIO2 PEEP VT or MV SIMV rate Inspiratory time or I:E Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on

VT, flow, patient effort, and patient mechanics.7 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.7

Pressure Control Pressure control is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.7 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time or I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.7

SIMV (Pressure Control) SIMV (pressure control) is similar to SIMV (volume control) described above except that the target is now pressure instead of volume.7 SIMV (pressure control) also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level

Inspiratory time or I:E SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.7 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.7

Pressure Support During pressure support (PS), the patient regulates the respiratory rate and the VT with support from the ventilator.7 The patient triggers all of the breaths and will receive the clinician-set PS level. The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.7

Spontaneous/CPAP Spontaneous breathing on CPAP occurs when the inspiratory pressure level is set to zero in pressure support.7 The patient triggers all the breaths and does all the work of breathing. This is sometimes used for a spontaneous breathing trial to assess the potential for liberation from the ventilator. Main operator controls include: FIO2 PEEP Pressure support – 0 The VT will be variable and depend on the patient effort and respiratory system

mechanics.7

Pressure-Regulated Volume Control Pressure-regulated volume control (PRVC) is a pressure-targeted (either PC or PA breaths) mode that uses the pressure breaths to achieve a clinician-set VT.7 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. The pressure change between breaths is up to 3 cm H2O. The maximum pressure used depends on the set upper pressure limit alarm, always staying 5 cm H2O below this limit. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target or MV Inspiratory time or I:E The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.7

SIMV (PRVC) SIMV (PRVC) combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.7 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate

VT or MV Inspiratory time or I:E Pressure-support level Cycle sensitivity RC Insight 4-1 When using PRVC, the inspiratory pressure must be closely watched because it has potential to reach dangerous levels. The high-pressure alarm should also be set to a limit that keeps the patient in the “safe” zone.

During the control breaths, the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.7 During the PS breaths the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Volume Support In VS the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.7 The ventilator changes the PS level as needed to reach the set VT. Thus, the ventilator may drop the level of support as patient effort increases and conversely may increase the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.7 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Automode Automode is a feedback mechanism whereby the ventilator switches between an

assist/control (A/C) mode and a supported mode depending on the patient’s spontaneous breathing activity.7 If the number of spontaneous efforts is low, the majority of the breaths will be controlled. If the number of spontaneous efforts is high, the ventilator will stay in the supported mode and allow for longer pauses in effort before switching back to the controlled mode. There are three mode combinations that the clinician can set up using automode: 1. Volume Control–Volume Support 2. PRVC–Volume Support 3. Pressure Control–Pressure Support All of these modes have been described in detail above. Main operator controls include: Volume Control/Volume Support FIO2 PEEP VT or MV RR Inspiratory time or I:E VT target for volume-support breaths Cycle sensitivity PRVC/Volume Support: FIO2 PEEP RR VT target Inspiratory time or I:E VT target for volume-support breaths Cycle sensitivity Pressure Control/Pressure Support FIO2 PEEP RR Inspiratory pressure level–pressure control Inspiratory pressure level –pressure support Inspiratory time or I:E ratio Cycle sensitivity Automode is not available in the noninvasive mode.

Bi-Vent Bi-Vent is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels and can be used for APRV.7 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and PEEP. Thigh is the length of time at Phigh and TPEEP is the length of time spent at PEEP. Bi-Vent is mainly used in an inverse I:E fashion. An important difference from the previously described pressuretargeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level. This is important because increases in PEEP will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Thigh Tpeep PS above Phigh PS above PEEP Cycle sensitivity The VT will be variable and depend on the Phigh, PEEP, PS level (if set > 0), patient effort, and patient respiratory system mechanics.7

Neurally Adjusted Ventilatory Assist Neurally adjusted ventilatory assist (NAVA) is a spontaneous mode of ventilation that delivers ventilatory assist in proportion to the electrical activity of the patient’s diaphragm (Edi); i.e., the ventilator will deliver assistance synchronized with the timing and effort of the patient’s own diaphragmatic breathing.7 It requires a separate module on the ventilator and a special catheter. The Edi signal is obtained through use of a specialized nasogastric catheter that has a series of transducers designed to detect the electrical activity of the diaphragm. The breath trigger is also based on the Edi. If the Edi signal is lost, the ventilator switches over to traditional pressure support. NAVA is available both for invasive and noninvasive ventilation and can be

used with any patient population (adult, pediatrics, and neonates). Monitoring of the Edi is available in all ventilation modes as well as in standby. Main operator controls include: FIO2 PEEP NAVA level Edi trigger threshold Pressure support Cycle sensitivity VT, flow, and pressure are all variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.7

Noninvasive Ventilation Modes available during noninvasive ventilation are pressure control, pressure support, and NAVA.7 Noninvasive ventilation is designed to be used with a variety of masks and infant nasal prongs. The Servo-i automatically adapts to the variation of leakage in order to maintain the required pressure and PEEP level. If leakage is excessive, the ventilator will issue a high-priority alarm and deliver a flow according to settings.

Nasal CPAP As the name would suggest, nasal CPAP involves delivering CPAP through a nasal cannula; it is only available for infants.7 During NIV, the ventilator automatically adapts to the variation of leakage in order to maintain the required pressure. If the leakage is excessive, the ventilator will issue a high-priority alarm, deliver a continuous flow and pause breath cycling.

Special Features The Servo-i has a number of special features including an open lung tool, apnea backup ventilation, leak compensation, stress index calculation, and heliox.

Open Lung Tool The open lung tool is a special display that allows the clinician to examine endinspiratory pressure, PEEP, VT, dynamic compliance, and this should be end tidal

CO2 (with CO2 analyzer option; see below) on a breath-to-breath basis.7 There is an adjustable cursor that allows the clinician to see the values at specific points in time.

Apnea Backup Ventilation The ventilator will go into apnea backup ventilation if no breaths are detected in the clinician-set interval. The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-5).7

Leak Compensation Leak compensation comes into play with noninvasive ventilation as it automatically adapts to any inherent leaks in the system and maintains the pressure level and trigger and cycle sensitivity.7

Stress Index Stress index is designed to assist the clinician in identifying potentially harmful ventilatory patterns by analyzing changes in the inspiratory pressure waveform during the constant flow of volume-control breaths.7 It is continually calculated while ventilating in volume- control mode or SIMV(VC) + PS. It is intended for adults only. Stress index is measured within a range of 0.5 to 1.5. A smaller range of 0.8 to 1.2 is displayed in the graph in the stress index window.

Helium/Oxygen (Heliox) Heliox (HeO2)delivery is possible through a Heliox-enabled Servo-i ventilator system.7 This specialized system compensates monitoring and flow delivery when HeO2 is used. HeO2 gas is connected to the Servo-i ventilator system via a Heliox adapter, which is connected to the air/HeO2 inlet. The Servo-i automatically detects if air or HeO2 is connected and compensates accordingly.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Getinge Servo-i are listed in Table 4-10. TABLE 4-10

Manufacturer’s Specifications for the Getinge Servo-i Setting

Range

Pressure Inspiratory pressure

0 to 120 cm H2O

PEEP

0 to 50 cm H2O

Volume Tidal volume

2 to 4.0 L

Minute ventilation

0.3 to 60 L/min

Flow Inspiratory flow

0 to 3.3 L/s

Time Inspiratory time

0.1 to 5 seconds

Mandatory breath rate

4 to 150/min

Sensitivity Trigger

–20 to 0 cm H2O (pressure) 0% to 100% fraction of bias flow (flow) 0.1 to 2.0 µV (NAVA)

Cycle

1% to 70% of peak flow

Alarms

Range

Pressure High pressure

16 to 120 cm H2O

High end-expiratory pressure

0 to 55 cm H2O

Low end-expiratory pressure

0 to 47 cm H2O

Volume High exhaled minute volume

0.01 to 60 L/min

Low exhaled minute volume

0.01 to 40 L/min

Time Respiratory rate

1 to 160 breaths/min

Apnea time

2 to 45 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Breathing frequency

TI/TTOT

Spontaneous breaths per minute

I:E ratio

Peak airway pressure

Total PEEP

Mean airway pressure

Edi peak

Pause airway pressure

Edi min

End-expiratory pressure

O2 concentration (measured)

CPAP pressure

CO2 end-tidal concentration (ETco2)

Inspired VT

CO2 minute elimination (CO2)

Expired VT

Tidal CO2 elimination (VTCO2)

Inspired minute volume

MVe sp/MVe

Expired minute ventilation

Spontaneous exp. minute ventilation (MVe sp)

Leakage fraction in NIV (%)

Accessories The Servo-i has available an optional CO2 analyzer that provides continuous monitoring of: CO2 concentration vs. time (waveform), end-tidal CO2 concentration (ETCO2), CO2 minute elimination, CO2 tidal elimination, and alarm limits for high and low ETCO2.7 For aerosolized medications, the Aerogen Micropump vibrating mesh nebulizer can be integrated. It has the advantage of not adding any flow to the circuit.

Getinge Servo-u The Getinge Servo-u is a critical care ventilator intended for treatment and monitoring of neonates, infants, and adults with respiratory failure or respiratory insufficiency.8 It is pictured in Figure 4-10. The Servo-u is electrically powered from an AC outlet with an internal battery backup and is designed to be used by healthcare providers in hospitals or healthcare facilities and for inhospital transport. The Getinge Servo-u operator interface is displayed in Figure 4-11. It operates

through the use of a touch screen. The touch screen is used to make changes to ventilation parameters, navigate through the different screen display, and manage alarm settings.

FIGURE 4-10 The Getinge Servo-u Ventilator. Courtesy of Getinge.

FIGURE 4-11 THE Servo-u Operator Interface. Courtesy of Getinge.

Modes The different modes available on the Getinge Servo-u are classified and depicted in Table 4-11. TABLE 4-11 Getinge Servo-u Modes

Description

Volume Control Volume control is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.8 Spontaneous breathing is not allowed. The breath cycles to exhalation once the VT has been delivered. Volume control also incorporates flow adaptation so that, if the patient’s inspiratory effort is large enough, inspiration will switch from volume control to pressure support with flow cycling. Main operator controls include: FIO2 PEEP VT or MV RR Inspiratory time or I:E

The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.8

SIMV (Volume Control) SIMV (volume control) combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.8 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. The volumecontrol breaths also use dual targeting so that, if the patient’s inspiratory effort is large enough, inspiration will switch from volume control to pressure control with flow cycling. Main operator controls include: FIO2 PEEP VT or MV SIMV rate Inspiratory time or I:E Pressure-support level Cycle sensitivity for the PS breaths During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.8 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.8

Pressure Control Pressure control is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.8 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Operator controls include:

FIO2 PEEP Inspiratory pressure level Inspiratory time or I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.8

SIMV (Pressure Control) SIMV (pressure control) is similar to SIMV (volume control) described above except that the target is now pressure instead of volume.8 SIMV (pressure control) also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time or I:E SIMV rate Pressure-support level Cycle sensitivity for the PS breaths During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.8 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.8

Pressure Support/CPAP During pressure support/CPAP, the patient regulates the respiratory rate and the VT.8

The patient triggers all of the breaths and will receive either no additional support (CPAP) or the clinician-set PS level. With a pressure support, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. The CPAP is sometimes used for spontaneous breathing trials. Main operator controls include: FIO2 PEEP/CPAP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level (if any), patient effort, and patient respiratory system mechanics.8

Pressure-Regulated Volume Control Pressure-regulated volume control (PRVC) is a pressure-targeted (either PC or PA breaths) mode that uses the pressure breaths to achieve a clinician-set VT during the set inspiratory time.8 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. The pressure change between breaths is up to 3 cm H2O. The maximum pressure used depends on the set upper pressure limit alarm, always staying 5 cm H2O below this limit. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target or MV Inspiratory time or I:E The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.8

SIMV (PRVC)

SIMV (PRVC) combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.8 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT or MV Inspiratory time or I:E Pressure-support level Cycle sensitivity for the PS breaths During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.8 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Volume Support In VS, the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.8 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity

The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.8 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Automode Automode is a feedback mechanism whereby the ventilator switches between an A/C mode and a supported mode depending on the patient’s spontaneous breathing activity.8 If the number of spontaneous efforts is low, the majority of the breaths will be controlled. If the number of spontaneous efforts is high, the ventilator will stay in the supported mode and allow for longer pauses in effort before switching back to the controlled mode. There are three automode combinations that the clinician can set up: 1. Volume Control–Volume Support 2. PRVC–Volume Support 3. Pressure Control–Pressure Support All of these modes have been described in detail above. Main operator controls include: Volume Control/Volume Support PEEP FIO2 VT RR Inspiratory time/I:E ratio Cycle sensitivity VT target for volume-support breaths PRVC/Volume Support PEEP FIO2 RR VT target Inspiratory time/I:E ratio Cycle sensitivity VT target for volume-support breaths Pressure Control/Pressure Support

PEEP FIO2 RR Inspiratory pressure level–pressure control Inspiratory pressure level–pressure support Inspiratory time/I:E ratio Cycle sensitivity Automode is not available in noninvasive ventilation.

Bi-Vent/APRV Bi-Vent/APRV is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.8 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and PPEEP. Thigh is the length of time at Phigh and Tlow is the length of time spent at Tpeep. Bi-Vent is mainly used with inverse I:E ratios. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level. This is important because increases in PPEEP will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh PPEEP Thigh TPEEP PS above Phigh PS above PPEEP Cycle sensitivity The VT will be variable and depend on the Phigh, Plow, PS level (if set > 0), patient effort, and patient respiratory system mechanics.8

Neurally Adjusted Ventilatory Assist

NAVA is a spontaneous mode of ventilation that delivers ventilatory assist in proportion to the patient’s Edi (the electrical activity of the diaphragm); i.e., the ventilator will deliver assistance synchronized with the timing and effort of the patient’s own diaphragmatic breathing.8 It requires a separate module on the ventilator and a special catheter. The Edi signal is obtained through use of a specialized nasogastric catheter that has a series of transducers designed to detect the electrical activity of the diaphragm. The breath trigger is also based on the Edi. If the Edi signal is lost the ventilator switches over to traditional pressure support. NAVA is available both for invasive and noninvasive ventilation and can be used with any patient population (adult, pediatrics, and neonates). Monitoring of the Edi is available in all ventilation modes as well as in standby. Main operator controls include: FIO2 PEEP NAVA level Edi trigger threshold PS and PC backup Cycle sensitivity VT, flow, and pressure are all variable and will depend on the NAVA support level, patient effort, and patient respiratory system mechanics.8

Noninvasive Ventilation Modes available during noninvasive ventilation are PC, PS, and NAVA.8 Noninvasive ventilation is designed to be used with a variety of masks, infant nasal prongs, and neonatal uncuffed endotracheal tubes. The Servo-u automatically adapts to the variation of leakage in order to maintain the required pressure and PEEP level. If leakage is excessive, the ventilator will issue a high-priority alarm and deliver a flow according to settings.

Nasal CPAP As the name would suggest, nasal CPAP involves delivering CPAP through a nasal cannula; it is only available for infants.8 During NIV, the ventilator automatically adapts to the variation of leakage in order to maintain the required pressure. If the

leakage is excessive, the ventilator will issue a high-priority alarm, deliver a continuous flow, and pause breath cycling.

Special Features Special features available with the Servo-u include apnea backup ventilation and leak compensation.

Apnea Backup Ventilation The ventilator will go into apnea backup ventilation if no breaths are detected in the clinician-set interval.8 The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-11).

Leak Compensation Leak compensation comes into play in neonatal patient category in invasive ventilation, and for all patient categories with noninvasive ventilation.8 It automatically adapts to any inherent leaks in the system and maintains the pressure level.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Getinge Servo-u are listed in Table 4-12. TABLE 4-12 Manufacturer’s Specifications for the Getinge Servo-u Setting

Range

Pressure Inspiratory pressure

0 to 120 cm H2O

PEEP

1 to 50 cm H2O

Volume Tidal volume

0.1 to 4.0 L

Minute volume

0.1 to 60 L/min

Flow

Inspiratory flow

Not specified

Time Inspiratory time

0.1 to 5 seconds

Mandatory breath rate

4 to 150/min

Sensitivity Trigger

–20 to 0 cm H2O (pressure) 0 to 2 L/min (flow) 0.1 to 2.0 µV (NAVA)

Cycle

1% to 70% of peak flow

Alarms

Range

Pressure High pressure

16 to 120 cm H2O

High end-expiratory pressure

0 to 55 cm H2O

Low end-expiratory pressure

0 to 47 cm H2O

Volume High exhaled minute volume

1 to 60 L/min

Low exhaled minute volume

0.01 to 40 L/min

Time Respiratory rate high

2 to 160 breaths/min

Respiratory rate low

1 to 59 breaths/min

Apnea time

2 to 45 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Inspiratory tidal volume

Expiratory tidal volume

Expiratory minute volume

Respiratory rate

O2 concentration

System response time O2

Barometric pressure compensation

Edi peak

Airway pressure

Edi min

End-expiratory pressure

CO2 end-tidal concentration (ETco2)

CPAP pressure

CO2 minute elimination (CO2)

Leakage fraction in NIV (%)

Tidal CO2 elimination (VTco2)

Spontaneous expiratory minute ventilation (MVe sp)

MVe sp/MVe

Accessories The Servo-u has available an optional CO2 analyzer that provides continuous monitoring of: CO2 concentration vs. time (waveform), end-tidal CO2 concentration (ETCO2), CO2 minute elimination, CO2 tidal elimination, and alarm limits for high and low ETCO2.8 For aerosolized medication delivery, the Aerogen Micropump vibrating mesh nebulizer can be employed. It has the advantage of not adding any flow to the circuit. There is an optional Y sensor that provides proximal flow and pressure measurement as well as triggering in invasive ventilation. This is recommended for VT < 10 mL.

Covidien Puritan Bennett 840 Ventilator The Covidien Puritan Bennett 840 ventilator is a critical care ventilator designed for use in adult, pediatric, and neonatal patients in both acute and subacute clinical locations. It is pictured in Figure 4-12.9 It is electrically controlled and pneumatically powered. If there is no piped compressed air, an external compressor would be required. The operator interface on the PB 840 employs a combination of a touch screen, buttons (real and virtual), and a control knob (Figure 4-13). It is a three-step process to make a change to a setting. The clinician first touches a virtual button on the touch screen. Second, the control knob is used to change the value of the setting. Last, the “accept” button must be pressed to confirm. The screen displays change depending on the operation being carried out. For instance, the alarm screen looks different than the monitoring screen and so forth. There are a number of different screens.

FIGURE 4-12 The Covidien PB 840 Ventilator.

© 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

FIGURE 4-13 The Covidien PB 840 Operator Interface. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

Modes The ventilation modes available on the Covidien PB 840 are classified and depicted in Table 4-13. TABLE 4-13 Modes Available on the Covidien PB 840

Description

Assist/Control (Volume Control) Assist/control (volume control) [A/C (VC)] is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.9 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.9

RC Insight 4-2 If a patient with a very strong inspiratory demand flow is starved in VAC, options to meet this increased demand include simply increasing the set flow (however, this will reduce the TI), switching to PAC, or perhaps switching to PS (in both PAC and PS, the VT will be variable).

SIMV Volume Control SIMV (volume control) combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.9 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory flow SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.9 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.9

Assist/Control Pressure Control Assist/control pressure control (A/C/PC) is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.9 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2

PEEP Inspiratory pressure level Inspiratory time or I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.9

SIMV Pressure Control SIMV (pressure control) is similar to SIMV (volume control) described above except that the target is now pressure instead of volume.9 SIMV (pressure control) also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.9 During the PS breaths, the volume will be variable and depends on the PS level, patient effort, and patient respiratory system mechanics.9

Spontaneous Pressure Support During spontaneous pressure support, the patient regulates the respiratory rate and the VT with support from the ventilator.9 The patient triggers all of the breaths and will

receive the clinician-set PS level. If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.9 If the PS level is set to 0, all breaths will be unsupported.

Volume Control+ VC+ is a pressure-targeted (either PC or PAC breaths) mode that uses the pressure breaths to achieve a clinician-set VT.9 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.9

SIMV Volume Control+ SIMV-VC+ combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.9 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and

spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level Cycle sensitivity During the control breath, the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.9 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on the patient effort and patient respiratory system mechanics.

Spontaneous Volume Support In spontaneous volume support, the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.9 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity The VT may not match the operator setting due to the fact that the ventilator is

using PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.9 Any change in patient effort from the previous breath may result in a deviation from the VT setting. The inspiratory pressure will be variable and depends on the target VT, patient effort, and patient respiratory system mechanics.9

Bilevel Bilevel is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.9 The ventilator switches between two different clinicianset pressure levels (the lower of which can be CPAP). These pressure levels are referred to as PEEPH and PEEPL. TH is the length of time at PEEPH and TL is the length of time spent at PEEPL. Bilevel is used mainly with an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the PEEPH level is now referenced to atmosphere as opposed to the PEEPL. This is important because increases in PEEPL will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEPH PEEPL TH TL Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity The VT will be variable and depend on the PEEPH, PEEPL, PS level (if set > 0), patient effort, and patient respiratory system mechanics.9

Proportional Assist Ventilation Proportional assist ventilation (PAV) is an optional mode on the PB 840.9 It is a spontaneous mode that delivers variable flow, pressure, and volume to the patient. The PB 840 calculates the work of breathing on an intrabreath basis and responds with the clinician-set variable support. Instead of setting a pressure or volume target,

the target is work of breathing (WOB). The clinician sets as a percentage (a direct setting) how much of the WOB that the ventilator will contribute. The balance is picked up by the patient. For example, if the clinician sets the ventilator to do 60%, then the patient does the other 40%. Main operator controls include: FIO2 PEEP Work of breathing (WOB) Cycle sensitivity The VT and inspiratory pressure will be variable and depend on the WOB setting, patient effort, and patient respiratory system mechanics.9

Noninvasive Ventilation Most modes are available for use in NIV with the exception of bilevel, VC+, PAV, and VS.9 Noninvasive ventilation is designed to be used with a variety of masks, infant nasal prongs, and neonatal uncuffed endotracheal tubes. The PB 840 automatically adapts to the variation of leakage in order to maintain the required pressure and PEEP level.

Special Features Special features of the PB 840 include apnea backup ventilation, tube compensation, neomode, and leak compensation.

Apnea Backup Ventilation The ventilator engages apnea backup ventilation when no breath has been delivered by the time the clinician selected apnea interval elapses.9 It can be set in either A/C/VC or A/C/PC.

Tube Compensation The PB 840 increases pressure during inspiration to overcome the extra resistance created by the artificial airway.9 The clinician must set the following parameters: percentage of the resistive load, artificial airway tube type, artificial airway tube diameter, and type of humidification.

Neomode Neomode is optional on the PB 840 and it allows clinicians to set smaller VT and flow parameters in order to ventilate neonates.9

Leak Compensation The leak compensation option is designed to compensate for leaks in the circuit.9 It maintains the PEEP level and optimizes synchrony between the patient and the ventilator by preventing autotriggering. It works in both invasive and noninvasive ventilation modes. It works in all three patient populations and is available for A/C/PC, pressure support, bilevel, and CPAP.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Medtronic Covidien PB 840 are listed in Table 4-14. TABLE 4-14 Manufacturer’s Specifications for the Covidien PB 840 Setting

Range

Pressure Inspiratory pressure

5 to 90 cm H2O

Pressure support

0 to 70 cm H2O

PEEP

0 to 45 cm H2O

Volume Tidal volume

0.25 to 2.5 L

Flow Inspiratory flow

1 to 150 L/min

Time Inspiratory time

0.2 to 8 seconds

Mandatory breath rate

1 to 150/min

Sensitivity

Trigger

0.1 to 20 cm H2O below PEEP (pressure) 0.2 L/min to ≤20 L/min (flow)

Cycle

1% to 80% of peak flow

Alarms

Range

Pressure High pressure

7 to 100 cm H2O

Low pressure

PEEP-peak pressure

Volume High VT

0.005 to 3 L

Low VT

0.3 to 2.5 L

Low spontaneous VT

0 to 2.5 L

Time Respiratory rate

10 to 170 breaths/min

Apnea time

10 to 60 seconds

Other O2 sensor

Enabled/disabled

Leak

10% to 65%

Monitored Parameters Breath type

Intrinsic PEEP

Peak pressure (Ppeak)

Plateau pressure

Mean airway pressure (Pmean)

Rapid shallow breathing index (RSBI)

Positive end-expiratory pressure (PEEP)

Spontaneous inspiratory time

I:E ratio (I:E)

Spontaneous minute volume

Respiratory rate (ftot)

Spontaneous percent inspiratory time

Exhaled tidal volume (Vte)

Compliance

Exhaled minute ventilation (Ve tot)

Resistance

% O2

Total PEEP

Accessories An optional Aerogen Aeroneb vibrating mesh nebulizer, can be used with the PB

840.9 Unlike the many available jet nebulizers, the Aerogen nebulizer does not add any flow to the circuit (which ultimately would increase the delivered volume).

Covidien Puritan Bennett 980 Ventilator The Covidien Puritan Bennett 980 ventilator is a critical care ventilator designed for use in adult, pediatric, and neonatal patients in both acute and subacute clinical locations.10 It is pictured in Figure 4-14. It is electrically controlled and pneumatically powered. If there is no piped compressed air, an external compressor would be required. The operator interface on the PB 980 employs a combination of a touch screen, buttons (real and virtual), and a control knob (Figure 4-15). It is a three-step process to make a change to a setting. The clinician first touches a virtual button on the touch screen. Second, the control knob is used to change the value of the setting. Last, the “accept” button must be pressed to confirm. The screen displays change depending on the operation being carried out. For instance, the alarm screen looks different than the monitoring screen and so forth. There are a number of different screens.

FIGURE 4-14 The ovidien PB 980 Ventilator. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

FIGURE 4-15 The Covidien PB 980 Operator Interface. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

Modes The ventilation modes available on the Medtronic PB 980 are classified and depicted in Table 4-15. TABLE 4-15

Modes Available on the Covidien PB 980

Description

Assist/Control (Volume Control) A/C (VC) is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.10 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.10

SIMV Volume Control SIMV (volume control) combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.10 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory flow SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.10 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.10

Assist/Control Pressure Control A/C/PC is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.10 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time or I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are

variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.10

SIMV Pressure Control SIMV pressure control (SIMV-PC) is similar to SIMV volume control described above except that the target is now pressure instead of volume.10 SIMV PC also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.10 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.10

Spontaneous Pressure Support During spontaneous pressure support, the patient regulates the respiratory rate and the VT with support from the ventilator.10 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include:

FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.10 If the PS level is set to 0, all breaths will be unsupported.

Volume Control+ Volume control+ (VC+) is a pressure-targeted mode that uses the pressure breaths (either PC or PA breaths) to achieve a clinician-set VT.10 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.10

SIMV Volume Control+ SIMV-VC+ combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.10 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur.

Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level Cycle sensitivity During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.10 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Spontaneous Volume Support In spontaneous volume support the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.10 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity RC Insight 4-3 Volume support and PRVC both use a pressure-targeted mode to achieve the clinician-set VT. PRVC uses PAC, while volume support uses PS.

The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breaths to

make the calculation.10 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Bilevel Bilevel is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.10 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as PEEPH and PEEPL. TH is the length of time at PEEPH and TL is the length of time spent at PEEPL. BPRV/ACMV is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the PEEPH level is now referenced to atmosphere as opposed to the PEEPL. This is important because increases in PEEPL will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEPH PEEPL TH TL Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity The VT will be variable and depend on the PEEPH, PEEPL, PS level (if set > 0), patient effort, and patient respiratory system mechanics.10

Proportional Assist Ventilation PAV is an optional mode on the PB 980.10 It is a spontaneous mode that delivers variable flow, pressure, and volume to the patient. The PB 980 calculates the work of breathing on an intrabreath basis and responds with the clinician-set variable support. Instead of setting a pressure or volume target, the target is work of breathing. The clinician sets how much of the work of breathing as a percentage (a direct setting) that the ventilator will contribute. The balance is picked up by the patient. For example, if the clinician sets the ventilator to do 60% then the patient

does the other 40%. Main operator controls include: FIO2 PEEP Work of breathing (WOB) Cycle sensitivity The VT and inspiratory pressure will be variable and depend on the WOB setting, patient effort, and patient respiratory system mechanics.10

Noninvasive Ventilation Most modes are available for use in NIV except for bilevel, VC+, PAV+, and VS.10 Noninvasive ventilation is designed to be used with a variety of masks, infant nasal prongs, and neonatal uncuffed endotracheal tubes. The PB 980 automatically adapts to the variation of leakage in order to maintain the required pressure and PEEP level.

Special Features Special features of available with the PB 980 include apnea backup ventilation, tube compensation, neomode, and leak sync.

Apnea Backup Ventilation The ventilator engages apnea backup ventilation when no breath has been delivered by the time the clinician-selected apnea interval elapses.10 It can be set in either A/C/VC or A/C/PC.

Tube Compensation (TC) The PB 980 increases pressure during inspiration to overcome the extra resistance created by the artificial airway.10 It is available in SIMV, spontaneous, and bilevel modes. The clinician must set the following parameters: percentage of the resistive load, artificial airway tube type, artificial airway tube diameter, and type of humidification.

Neomode 2.0

NeoMode 2.0 is intended to provide respiratory support to neonatal patients with predicted body weights down to 0.3 kg.10 It supports delivered tidal volumes as low as 2 mL.

Leak Sync The Leak Sync option is designed to compensate for leaks in the circuit.10 It maintains the PEEP level and optimizes synchrony between the patient and the ventilator by preventing autotriggering. It works in both invasive and noninvasive ventilation modes. Leak Sync allows the ventilator to determine the leak level and allows the operator to set the flow trigger and peak flow sensitivities to a selected threshold

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Medtronic Covidien PB 980 are listed in Table 4-16. TABLE 4-16 Manufacturer’s Specifications for the Covidien PB 980 Setting

Range

Pressure Inspiratory pressure

5 to 90 cm H2O

Pressure support

0 to 70 cm H2O

PEEP

0 to 45 cm H2O

Volume Tidal volume

0.25 to 2.5 L

Flow Inspiratory flow

3 to 150 L/min

Time Inspiratory time

0.2 to 8 seconds

Mandatory breath rate

1 to 150/min

Sensitivity

Trigger

0.1 to 20 cm H2O below PEEP (pressure) 0.2 L/min to –20 L/min (flow)

Cycle

1% to 80% of peak flow

Alarms

Range

Pressure High pressure

7 to 100 cm H2O

Low pressure

PEEP-peak pressure

Volume High VT

0.005 to 6 L

Low VT

1 to 2.5 L

Low spontaneous VT

1 to 2.5 L

High exhaled minute volume

1 to 100 L/min

Low exhaled minute volume

0.05 to 60 L/min

Time High respiratory rate

10 to 110 breaths/min

Apnea time

10 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Breath type

Intrinsic PEEP

Peak pressure (Ppeak)

Plateau pressure

Mean airway pressure (Pmean)

RSBI

Positive end-expiratory pressure (PEEP)

Spontaneous inspiratory time

I:E ratio (I:E)

Spontaneous minute volume

Respiratory rate (ftot)

Spontaneous percent inspiratory time

Inspired tidal volum (Vti)

Compliance

Exhaled tidal volume (Vte)

Resistance

Exhaled minute ventilation (Ve tot)

Total PEEP

% O2

Accessories An optional Aerogen Aeroneb vibrating mesh nebulizer can be used with the PB 980.10 Unlike the many available jet nebulizers, the Aerogen nebulizer does not add any flow to the circuit (which ultimately would increase the delivered volume). An optional proximal flow sensor is available to measure flow, volumes, and pressures at the patient wye. ETCO2 measurement is an additional option.

Newport e360 Ventilator The Newport e360 features a dual servo gas delivery system, a servo-controlled active exhalation valve, a user interface, and a touch screen graphics monitor.11 It is designed for use in adult, pediatric, and neonatal patients in both acute and subacute clinical locations and is depicted in Figure 4-16. The operator interface on the e360 employs a combination of a touch screen, buttons (real and virtual), and a control knob (Figure 4-17). It is a three-step process to make a change to a setting. The clinician first touches a panel button or virtual button on the touch screen. Second, the control knob is used to change the value of the setting. Last, the “accept” button must be pressed to confirm. The screen displays change depending on the operation being carried out. For instance, the alarm screen looks different than the monitoring screen and so forth. There are a number of different screens available for viewing.

FIGURE 4-16 The Newport e360 Ventilator. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

FIGURE 4-17 The Newport e360 Operator Interface. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

Modes The ventilation modes available on the Medtronic Newport e360 are classified and depicted in Table 4-17. TABLE 4-17 Modes Available on the Newport e360 Ventilator

Description

Volume-Control/Assist/Control Mandatory Ventilation VC/ACMV is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.11 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow Inspiratory time (t Insp) RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.11

Volume-Control SIMV VC/SIMV combines two breath types, VAC and either PS or spontaneous breathing,

while on CPAP.11 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory flow Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.11 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.11

Pressure-Control Assist/Control Mandatory Ventilation (PC/ACMV) PC/ACMV is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.11 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level (pressure limit) Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.11

Pressure-Control SIMV (PC/SIMV) PC/SIMV is similar to VC/SIMV described above except that the target is now pressure instead of volume.11 PC/SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.11 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.11

Volume Control/Spontaneous During VC/SPONT the patient regulates the respiratory rate and the VT with support from the ventilator.11 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level

Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.11 If the PS level is set to 0, all breaths will be unsupported. Volume control is only active with manual breaths.

Pressure Control/Spontaneous During PC/SPONT the patient regulates the respiratory rate and the VT with support from the ventilator.11 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If the PS level is set to 0, all breaths will be unsupported.11 Pressure control is only active with manual breaths.

Volume-Target Pressure-Control/Assist/Control Mandatory Ventilation VTPC/ACMV is a pressure-targeted (either PC or PA breaths) mode that uses the pressure breaths to achieve a clinician-set VT.11 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time

The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.11

Volume-Target Pressure-Control/Synchronized Intermittent Mandatory Ventilation (VTPC/SIMV) VTPC/SIMV combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.11 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level Cycle sensitivity During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.11 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.11 If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Volume-Target Pressure Control/Spontaneous In volume-target pressure control/spontaneous (VTPC/SPONT), the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.11 The ventilator changes the PS level as needed to reach the VT. Thus, the

ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.11 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Biphasic Pressure-Release Ventilation/Assist/Control Mandatory Ventilation Biphasic pressure-release ventilation/assist/control mandatory ventilation (BPRV/ACMV) is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.11 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as PEEPH and PEEPL. TH is the length of time at PEEPH and TL is the length of time spent at PEEPL. BPRV/ACMV is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the PEEPH level is now referenced to atmosphere as opposed to the PEEPL. This is important because increases in PEEPL will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Inspiratory pressure Inspiratory time Respiratory rate The VT will be variable and depend on the inspiratory pressure, PEEP, patient

effort, and patient respiratory system mechanics.11

Biphasic Pressure-Release Ventilation/Synchronized Intermittent Mandatory Ventilation Biphasic pressure-release ventilation/synchronized intermittent mandatory ventilation (BPRV/SIMV) is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.11 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as PEEPH and PEEPL. TH is the length of time at PEEPH and TL is the length of time spent at PEEPL. BPRV/SMIV is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the PEEPH level is now referenced to atmosphere as opposed to the PEEPL. This is important because increases in PEEPL will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Inspiratory pressure Inspiratory time Respiratory rate Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity The VT will be variable and depend on the inspiratory pressure, PEEP, PS level (if set > 0), patient effort, and patient respiratory system mechanics.11

Noninvasive Ventilation All modes are available for use in NIV. NIV is activated by pressing a button on the front panel.

Special Features Newport e360 special features include backup ventilation, leak compensation, and flex cycle.

Backup Ventilation Backup ventilation is activated when the low expired minute volume (MVE) alarm is violated.11 If the current mode is A/CMV or SIMV, the current settings are used with a respiratory rate of 1.5 times the current setting. If the current mode is SPONT, the ventilator delivers pressure-control mandatory breaths (TI 0.6 sec for pediatrics and infants and 1.0 sec for adults, RR 20 for pediatrics and infants and 12 for adults, pressure limit of 15 above PEEP).

Leak Compensation The e360 provides 3 L/min of bias flow through the circuit during exhalation to facilitate both flow triggering and the stabilization of baseline pressure and flow in order to minimize autotriggering of breaths.11 When the The Leak Compensation button is pressed, the ventilator automatically adjusts the bias flow 3 to 8 L/min for pediatrics and infants and 3 to 15 L/min for adults in order to maintain an endexpiratory base flow of 3 L/min. Leak Comp automatically comes on when NIV is selected.

Flex Cycle When the Flex Cycle option is selected the ventilator automatically adjusts the expiratory threshold setting on a breath-by-breath basis in pressure support.11 In other words, the ventilator now controls when the breaths cycle to exhalation as opposed to a clinician-set percent flow in pressure support.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Newport e360 are listed in Table 4-18. TABLE 4-18 Manufacturer’s Specifications for the Newport e360 Setting

Range

Pressure Inspiratory pressure

0 to 80 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 45 cm H2O

Volume Tidal volume

0.02 to 3.0 L

Flow Inspiratory flow

1 to 180 L/min

Time Inspiratory time

0.1 to 5 seconds

Mandatory breath rate

1 to 120/min

Sensitivity Trigger

0.0 to –5 cm H2O below PEEP (pressure) 0.1 L/min to 2 L/min (flow)

Cycle

5% to 55% of peak flow

Alarms

Range

Pressure High pressure

5 to 120 cm H2O

Low pressure

3 to 95 cm H2O

Volume High exhaled minute volume

0.02 to 60 L/min

Low exhaled minute volume

0.01 to 50 L/min

Time High respiratory rate

Off or 10 to 120 breaths/min

Apnea time

5 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Breath type

Cdyn effective

Cstat

FIO2

I:E

MVe

MVi

P0.1

PEEP

Baseline pressure

Pmean

Ppeak

Pplateau

Expiratory resistance

Inspiratory resistance

Respiratory rate

RSBI

NIF

Total PEEP

Inspiratory time

Tidal volume

Time constant

Inspiratory tidal volume

Expiratory tidal volume

VTE % Var

WOBimp

Inspiratory flow

Expiratory flow

Vyaire AVEA The Vyaire AVEA ventilator is a critical care ventilator designed for use in adult, pediatric, and neonatal patients in both acute and subacute clinical locations.12 It is pictured in Figure 4-18. The AVEA is a fourth-generation, servo-controlled, softwaredriven ventilator. The Vyaire AVEA operator interface consists of a flat-panel color LCD screen with real-time graphic displays and digital monitoring capabilities, a touch screen, membrane keys, and a dial for changing settings and operating parameters. It is pictured in Figure 4-19. Settings are entered by pressing a virtual button to select the parameter to be changed, then the control dial is turned to select the new value, and finally the “ACCEPT” button is pressed. Alternatively the virtual button can be pressed again to confirm the setting. The real buttons provide various features related to menu navigation, access to alarm settings, and alarm silence among other things.

FIGURE 4-18 The Vyaire AVEA Ventilator. © 2018 Vyaire Medical, Inc. Used with permission.

FIGURE 4-19 The Vyaire AVEA Operator Interface. © 2018 Vyaire Medical, Inc. Used with permission.

Modes The ventilation modes available on the Vyaire AVEA are classified and depicted in Table 4-19. TABLE 4-19 Modes Available on the Vyaire AVEA

Description *Neonatal ventilation

Volume A/C Volume A/C is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.12 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.12

Volume SIMV

Volume SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.12 Thus, mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.12 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.12

Pressure A/C Pressure A/C is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.12 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.12

Pressure SIMV Pressure SIMV is similar to SIMV (volume A/C) described above except that the target is now pressure instead of volume.12 SIMV (pressure control) also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.12 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.

CPAP/Pressure Support (CPAP/PSV) During CPAP/PSV the patient regulates the respiratory rate and the VT with support from the ventilator.12 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level

Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.12 If the PS level is set to 0, all breaths will be unsupported.

Pressure-Regulated Volume Control (Assist/Control) PRVC A/C is a pressure-targeted (either PC or PA breaths) mode that uses its pressure breaths to achieve a clinician-set VT.12 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.12 Clinical Focus 42 describes ventilator adjustments during PRVC.

CLINICAL FOCUS 4-2 Ventilator Adjustments: PRVC You go into a patient’s room to monitor the ventilator and note that the patient appears agitated and uncomfortable. She is on PRVC with the following settings: VT 450 mL, FIO2 0.35, PEEP 5, and inspiratory time 0.80 seconds. You note that the inspiratory pressure has dropped from 20 to about 6 cm H2O while the tidal volume has remained close to 450 mL. Question 1: What is the primary problem or issue to be addressed? Answer: The patient is experiencing difficulty due to the fact that the ventilator cannot distinguish between what it perceives as an increase in compliance and the

increase in patient effort (due to things like anxiety or inadequate pain management). Because of the excessive patient effort, the tidal volume may temporarily rise, causing the ventilator to drop the inspiratory pressure to get back to the target tidal volume. This, in turn, may cause the patient further agitation and tidal volume fluctuations and has been termed “runaway.” Question 2: What can you do with the ventilator to help calm the patient and improve patient–ventilator synchrony? Answer: Option 1: Switch the mode to PAC or PS with a set inspiratory pressure. This may result in an increased tidal volume initially, but since the patient is now receiving the support she was trying to get on PRVC, she should eventually calm down and the tidal volume should reset to a safer value. Careful assessment and minor adjustments may still be needed until the patient is completely comfortable. Option 2: Switch to VAC with a set tidal volume. This may not be the optimal solution, since the flow is also set; given that the patient has such an active respiratory drive, it likely will not satisfy the patient’s flow requirements.

PRVC SIMV PRVC SIMV combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.12 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level Cycle sensitivity

During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.12 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.12 If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Airway Pressure-Release Ventilation/Biphasic APRV/biphasic is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.12 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. APRV/biphasic is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the Plow. This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity The VT will be variable and depend on the Phigh, Plow, PS level (if set > 0), patient effort, and patient respiratory system mechanics.12

Time Cycled Pressure Limited A/C (TCPL A/C) TCPL A/C is only available for neonates.12 It is a pressure-targeted mode of

ventilation similar to pressure A/C in adults. The pressure is held in the lungs for a clinician-specified period of time (inspiratory time). The main difference is that the clinician sets the inspiratory flow, which is variable in pressure A/C (there is no setting for flow). The inspiratory flow is used to achieve a set inspiratory pressure. Spontaneous breathing is not allowed. Main operator controls include: FIO2 PEEP RR Inspiratory time Inspiratory flow The pressure and flow will be consistently delivered from breath to breath; VT will be variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.12

Time Cycled Pressure Limited SIMV (TCPL SIMV) TCPL SIMV is only available for neonates.12 It combines two breath types, the TCPL breath and PS. There is a combination of mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a TCPL breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a TCPL breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP RR Inspiratory time Inspiratory flow During the TCPL breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.12 During the PS breaths, the volume will be variable and depend on the PS level,

patient effort, and patient respiratory system mechanics.12

Pressure A/C with Volume Guarantee (Pressure A/C + VG) Pressure A/C + VG is a pressure-targeted (either PC or PA breaths) mode that uses pressure breaths to achieve a clinician-set VT.12 The inspiratory pressure level is now adjusted by the ventilator instead of the clinician. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.12

Pressure SIMV with Volume Guarantee (Pressure SIMV + VG) Pressure SIMV + VG is only available for neonates.12 It combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level Cycle sensitivity During the control breath the amount of pressure and flow delivered will be

variable and depend on the VT setting, patient effort, and patient respiratory system.12 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Time Cycled Pressure Limited with Volume Guarantee (TCPL + VG) TCPL + VG is only available for neonates.12 It is a pressure-targeted (either PC or PA breaths) mode that uses its pressure breaths to achieve a clinician-set VT. The inspiratory pressure level is now adjusted by the ventilator instead of the clinician. The inspiratory flow stops when the pressure target is reached. Spontaneous breathing is not allowed. Main operator controls include: FIO2 PEEP RR VT Inspiratory time Inspiratory flow Inspiratory pressure will be variable and will depend on the VT, patient effort, and patient respiratory system mechanics.12

Nasal Continuous Positive Airway Pressure/Intermittent Mandatory Ventilation Continuous positive airway pressure (purely spontaneous) is provided with or without intermittent mandatory ventilation (mix of control and spontaneous breaths).

Special Features Special features of the Vyaire AVEA include apnea backup ventilation, artificial airway compensation, and leak compensation. A number of advanced settings and special maneuvers are also provided.

Apnea Backup Ventilation

The ventilator engages apnea backup ventilation when no breath has been delivered by the time the clinician-selected apnea interval elapses.12 It can be adjusted in either volume A/C, pressure A/C, or TCPL A/C (Table 4-20). Apnea backup ventilation is available in CPAP/PS and APRV/biphasic. When in A/C or SIMV modes, the apnea backup rate is determined by the operator-set mandatory breath rate or the apnea interval setting (whichever provides the highest respiratory rate). When the apnea interval setting (found in the alarm limits window) determines the backup rate, the ventilator will continue to ventilate at this rate until the apnea has been resolved. All other controls for apnea ventilation in A/C and SIMV are set when the primary control values for these modes are selected. TABLE 4-20 Advanced Settings on the Vyaire AVEA

Description

Artificial Airway Compensation When artificial airway compensation is activated, the ventilator calculates the pressure drop from the proximal to the distal end of the ETT and applies sufficient pressure to counter balance this drop.12 The clinician has to input ETT diameter and length.

Advanced Settings The advanced settings and the modes in which they are available are depicted in Table 4-20.12 These advanced settings serve to give the clinician mode options and possibly more control of the delivered breaths. Volume limit: sets the volume limit for a pressure-targeted breath. Machine volume (Mach Vol): sets the minimum tidal volume delivered from the ventilator. Inspiratory rise (Insp Rise): controls the slope of the pressure rise during a mandatory breath. Flow Cycle: sets the percentage of the peak inspiratory flow (Peak Flow), at which the inspiratory phase of a breath is terminated. Waveform: square or decelerating flow pattern. Demand Flow: offers additional flow in volume-controlled ventilation when the set flow is not enough for the patient. Sigh: when activated the ventilator delivers a sigh volume breath (1.5 times the VT) every 100th breath. Bias Flow: sets the background flow available between breaths as well as establishing the base flow that is used for flow triggering. Pressure trigger (Pres Trig): sets the level below PEEP at which the inspiratory trigger mechanism is activated Vsync: changes the target from volume to pressure with a set VT. Vsync Rise: sets the slope of the pressure rise during the volume breath. PSV Rise: sets the slope of the pressure rise during a pressure-support breath. PSV Cycle: sets the percentage of peak inspiratory flow at which a pressure support breath will cycle to exhalation. PSV Tmax: sets the maximum inspiratory time for a pressure-support breath. Thigh Sync: establishes the length of trigger (Sync) window while in Thigh. Thigh PSV: makes pressure-support breaths available during Thigh in APRV/biPhasic. Tlow Sync: establishes the length of trigger (Sync) window while in Tlow.

Leak Compensation Leak compensation option is designed to compensate for leaks in the circuit.12 PEEP is maintained through a cooperation between the flow control valve and the exhalation valve. If the circuit pressure drops, the flow control valve supplies flow up to a maximum flow rate for the patient’s size. It is not active during breath delivery.

Maneuvers

The Vyaire AVEA has a number of maneuvers available including: esophageal manometry, maximum inspiratory pressure (MIP), P100, Pflex, AutoPEEP detection, and capnometry (optional).12

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Vyaire AVEA are listed in Table 4-21. TABLE 4-21 Manufacturer’s Specifications for the Vyaire AVEA Setting

Range

Pressure Inspiratory pressure

0 to 90 cm H2O

Pressure support

0 to 90 cm H2O

PEEP

0 to 50 cm H2O

Volume Tidal volume

0.1 to 2.5 L

Flow Inspiratory flow

0.4 to 150 L/min

Time Inspiratory time

0.15 to 5 seconds

Mandatory breath rate

1 to 150/min

Sensitivity Trigger

0.1 to 20 cm H2O below PEEP (pressure) 0.1 L/min to 20 L/min (flow)

Cycle

5% to 45% of peak flow

Alarms

Range

Pressure High peak pressure

10 to 105 cm H2O

Low peak pressure

3 to 99 cm H2O

Low PEEP

0 to 60 cm H2O

Volume High VT

0.1 to 3 L

Low VT

0.0 to 3 L

High Ve

0 to 75 L/min

Low Ve

0 to 50 L/min

Time Respiratory rate

1 to 200 breaths/min

Apnea time

6 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Expired VT (Vte)

% O2

Inspired VT (Vti)

Breath type

Spont VT

Inspiratory time

Mandatory VT

Expiratory time

% Leak

Peak pressure

Minute volume (Ve)

PEEP

Spontaneous minute volume (Spont Ve)

Plateau pressure

RR

Mean airway pressure

Spont RR

I:E ratio

Peak expiratory flow rate

Peak inspiratory flow rate

AutoPEEP

RSBI

Accessories The AVEA supplies blended gas to power a jet nebulizer (not provided), which is synchronized with inspiration.12 The ventilator has a port that can facilitate independent lung ventilation.12 Accessories include the following: Volumetric capnometry (optional).12

Esophageal manometry.12 The AVEA can deliver Heliox through the use of a special adaptor.12

Vyaire VELA The Vyaire VELA ventilator is a critical care ventilator designed for use in adult and pediatric patients in both acute and subacute clinical locations.13 It is pictured in Figure 4-20. It can ventilate critically ill patients and can be used for intrahospital transports. The Vyaire VELAoperator interface consists of a flat-panel color LCD screen with real-time graphic displays and digital monitoring capabilities, a touch screen, membrane keys, and a dial for changing settings and operating parameters. It is pictured in Figure 4-21. Settings are entered by pressing a virtual button to select the parameter to be changed, then the control dial is turned to select the new value, and finally the “ACCEPT” button is pressed. Alternatively, the virtual button can be pressed again to confirm the setting. The real buttons provide various features related to menu navigation, access to alarm settings, and alarm silence among other things.

FIGURE 4-20 The Vyaire VELA Ventilator. © 2018 Vyaire Medical, Inc. Used with permission.

FIGURE 4-21 The Vyaire VELA Operator Interface. © 2018 Vyaire Medical, Inc. Used with permission.

Modes The ventilation modes available on the Vyaire VELA are classified and depicted in Table 4-22. TABLE 4-22

Ventilation Modes Available on the Vyaire VELA

Description

Volume A/C Volume A/C is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.13 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.13

Volume SIMV Volume SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.13 Thus, mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths are all provided. The ventilator prevents

“breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.13 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.13

Pressure A/C Pressure A/C is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.13 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.13

Pressure SIMV Pressure SIMV is similar to SIMV (volume A/C) described above except that the

target is now pressure instead of volume.13 Pressure SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.13 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.13

CPAP/Pressure Support (CPAP/PSV) During CPAP/PSV the patient regulates the respiratory rate and the VT with support from the ventilator.13 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient

respiratory system mechanics.13 If the PS level is set to 0, all breaths will be unsupported.

Pressure-Regulated Volume Control (A/C) PRVC A/C is a pressure-targeted (either PC or PA breaths) mode that uses its pressure breaths to achieve a clinician-set VT.13 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.13

PRVC SIMV PRVC SIMV combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.13 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT

Inspiratory time Pressure-support level Cycle sensitivity During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.13 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.13 If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Airway Pressure-Release Ventilation/Biphasic APRV/biphasic is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.13 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. APRV/biphasic is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the Plow. This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity The VT will be variable and depend on the Phigh, Plow, PS level (if set > 0), patient effort, and patient respiratory system mechanics.13

Noninvasive Positive-Pressure Ventilation A/C (NPPV A/C) NPPV A/C is pressure A/C delivered through a mask instead of an endotracheal tube.13 It is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths. Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.13

Noninvasive Positive-Pressure Ventilation/SIMV (NPPV/SIMV) NPPV/SIMV is pressure SIMV (see above) delivered through a mask instead of an endotracheal tube.13 NPPV/SIMV combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, timetriggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity

During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.13 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.13

Noninvasive Positive-Pressure Ventilation/CPAP/Pressure Support (NPPV/CPAP/PS) NPPV/CPAP/PS is CPAP/PS (see above) delivered through a mask instead of an endotracheal tube.13 During NPPV/CPAP/PSV the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.13 If the PS level is set to 0, all breaths will be unsupported.

Special Features Special features available with the Vyaire VELA include apnea backup ventilation, NPPV leak compensation, and a number of advanced settings and maneuvers.

Apnea Backup Ventilation The ventilator engages apnea backup ventilation when no breath has been delivered by the time the clinician-selected apnea interval elapses.13 It can be adjusted in either volume A/C or pressure A/C. Apnea backup ventilation is available in CPAP/PS and APRV/biphasic. When in A/C or SIMV modes, the apnea backup rate is determined by the operator-set mandatory breath rate or the Apnea Interval setting (whichever provides the highest respiratory rate). When the Apnea Interval

setting (found in the Alarm Limits window) determines the backup rate, the ventilator will continue to ventilate at this rate until the apnea has been resolved. All other controls for apnea ventilation in A/C and SIMV are set when the primary control values for these modes are selected.

Advanced Settings The advanced settings and the modes that are available are depicted in Table 423.13 These advanced settings serve to give the clinician mode options and possibly more control of the delivered breaths. TABLE 4-23 Advanced Settings on the Vyaire VELA

Description Assured volume: sets the minimum tidal volume in pressure-control breaths. Volume limit: sets the volume limit for a pressure-targeted breath. Insp Rise: controls the slope of the pressure rise during a mandatory breath. Waveform: square or decelerating flow pattern. Sigh: when activated the ventilator delivers a sigh volume breath (1.5 times the VT) every 100th breath. Bias flow: sets the background flow available between breaths as well as establishing the base flow that is used for flow triggering. PC Flow Cycle: sets the percentage of peak inspiratory flow at which the inspiratory phase of a PC breath is terminated. Vsync: changes the target from volume to pressure with a set VT.

PSV Cycle: sets the percentage of peak inspiratory flow at which a pressuresupport breath will cycle to exhalation. PSVTmax: sets the maximum inspiratory time for a pressure-support breath. % Thigh Sync: sets the trigger (sync) window to transition from Pressure high to Pressure low. Thigh PSV: makes pressure-support breaths available during Thigh in APRV/biPhasic. % Tlow Sync: sets the trigger (sync) window to transition from Plow to Phigh.

NPPV Leak Compensation NPPV leak compensation adjusts bias flow to maintain the set PEEP level if there is a leak present in the system. It can compensate up to 40 L/min.13

Maneuvers The Vyaire VELA has a number of maneuvers available including: maximum inspiratory pressure/negative inspiratory force (MIP/NIF), AutoPEEP detection, static compliance, circuit resistance, and capnometry (optional).13

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Vyaire VELA are listed in Table 4-24.13 TABLE 4-24 Manufacturer’s Specifications for the Vyaire VELA Setting

Range

Pressure Inspiratory pressure

0 to 100 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.05 to 2.0 L

Flow Inspiratory flow

10 to 140 L/min

Time Inspiratory time

0.3 to 10 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 L/min to 20 L/min (flow)

Cycle

5% to 70% of peak flow

Alarms

Range

Pressure High pressure

5 to 120 cm H2O

Low pressure

0 to 60 cm H2O

Volume Low minute volume

0 to 99.9 L/min

Time Respiratory rate

0 to 150 breaths/min

Apnea time

10 to 60 seconds

Other O2 sensor

Enabled/disabled

High ETco2

0 to 150 mm Hg

Low ETco2

0 to 150 mm Hg

Monitored Parameters Total breath rate (ƒ)

Spontaneous breath rate (ƒ)

I:E ratio

Exhaled minute volume (Ve)

Spontaneous exhaled minute volume (Spont Ve)

Mandatory exhaled minute volume (Mand Ve)

Peak inspiratory pressure (Ppeak)

Mean airway pressure (Pmean)

Inspiratory time (TI)

Expiratory time (TE)

Positive end-expiratory pressure (PEEP)

Mandatory exhaled tidal volume (Mand VT)

Spontaneous exhaled tidal volume (Spont VT)

Inspired tidal volume (Vti)

Oxygen regulated pressure

Oxygen%

f/VT

ETco2

Accessories The VELA supplies blended gas to power a jet nebulizer (not provided), which is synchronized with inspiration.13 Volumetric capnometry is optional.13

Dräger Evita Infinity V500 The Dräger Evita Infinity V500 ventilator is a critical care ventilator designed for use in adult, pediatric, and neonatal patients in both acute and subacute clinical locations.14 It is pictured in Figure 4-22. The Evita Infinity is electrically powered and controlled. It is designed to be used in acute and subacute clinical settings. It requires an external compressor if piped air is not available. The Infinity V500 operator interface is depicted in Figure 4-23. It consists of a flat panel touch screen, buttons, and a control dial to change and confirm settings. Settings are entered by pressing a button on the touch screen to select the parameter to be changed, then the control dial is turned to select the new value, and then the control dial is pressed to confirm.

FIGURE 4-22 The Dräger Evita Infinity V500 Ventilator. Courtesy of Dräger.

FIGURE 4-23 The Dräger Evita Infinity V500 Operator Interface. Courtesy of Dräger.

Modes The ventilation modes available on the Dräger Evita Infinity V500 are classified and depicted in Table 4-25. TABLE 4-25 Modes Available on the Dräger Evita Infinity V500

Description

Volume-Control–Continuous Mandatory Ventilation Volume-control–continuous mandatory ventilation (VC-CMV) is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths only.14 Patient-assisted breaths and spontaneous breathing are not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.14

Volume Control–A/C

Volume control (VC)–A/C is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.14 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.14

Volume-Control–Synchronized Intermittent Mandatory Ventilation VC-SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.14 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory flow SIMV rate Inspiratory time Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.14

During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.14

Volume-Control-Mandatory Minute Volume Ventilation (VC-MMV) VC-MMV guarantees that the patient always receives at least the set minute volume MV.14 The patient can always breathe spontaneously at PEEP level (with or without pressure support). If the spontaneous breathing of the patient is insufficient to achieve the set minute ventilation, VAC breaths are applied. These mandatory breaths are synchronized with the patient’s own breathing attempts. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR Inspiratory time Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.14 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system.14

Pressure-Control-Continuous Mandatory Ventilation (PC-CMV) PC-CMV is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths only (patient-assisted breaths are not allowed).14 Spontaneous breathing is, however, permitted during the entire breathing cycle. The mandatory breaths cycle to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP I:E or inspiratory pressure level Inspiratory time RR

The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.14 For PC-CMV, pressure-control settings are not automatically adjusted for PEEP but are referenced to atmospheric pressure; an increase in PEEP will decrease delta P (ΔP) and tidal volume, if pressure control is not also adjusted.

Pressure Control-A/C (PC-A/C) Pressure control A/C is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.14 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level I:E or inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.14 For PC-A/C, pressure-control settings are not automatically adjusted for PEEP but are referenced to atmospheric pressure; an increase in PEEP will decrease delta P (ΔP) and tidal volume, if pressure control is not also adjusted. Clinical Focus 4-3 describes ventilator adjustments during PAC.

CLINICAL FOCUS 4-3 Ventilator Adjustments: Asynchrony with PAC You go in to monitor a patient and note that the patient is slightly uncomfortable. She is on PAC with the following settings: inspiratory pressure of 15 cm H2O, PEEP 5 cm H2O, FIO2 0.35, and an inspiratory time of 1.2 seconds. Upon careful examination you note that there is diaphragmatic activity prior to exhalation near the end of the breath. Question 1: What is the primary problem or issue to be addressed?

Answer: It’s likely that the set inspiratory time is too long and the patient is trying to exhale before the inspiratory time has elapsed. Question 2: What can you do with the ventilator to make this patient more comfortable? Answer: Option 1: Since the patient is clearly interacting with the ventilator during the breath, PS might be a more optimal mode. The patient will have more control over when the breath terminates (assuming the expiratory sensitivity is set properly). Option 2: Merely shorten the set inspiratory time in PAC. This may resolve the issue unless the patient’s innate inspiratory time is variable. Option 3: Switch to VAC. The set tidal volume and set flow will then determine the inspiratory time. This would most likely be the least optimal solution since you would taking more control of the breath away from the patient and giving it to the ventilator.

Pressure-Control-Synchronized Intermittent Mandatory Ventilation (PCSIMV) Pressure-control SIMV is similar to VC-SIMV described above except that the target is now pressure instead of volume.14 PC-SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Spontaneous breathing is allowed throughout the entire breath cycle. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate

Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.14 For PC-SIMV, pressure-control settings are not automatically adjusted for PEEP and an increase in PEEP will decrease delta P (ΔP) and tidal volume, if pressure control is not also adjusted. During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.14

Pressure-Control-Synchronized Intermittent Mandatory Ventilation+ (PCSIMV+) PC-SIMV+ is essentially PC-SIMV with an added synchronization feature.14 Synchronization of mandatory breaths reduces the expiratory time. Evita V500 therefore extends the subsequent expiratory time or spontaneous breathing time by the missing time.

Pressure-Control-Pressure-Support Ventilation (PC-PSV) PC-PSV is similar to PC-SIMV in that it combines two breath types, PAC and PS.14 The inspiratory pressure level is referenced to atmosphere as opposed to the PEEP level. Therefore, changes in PEEP will affect the distending pressure. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Spontaneous breathing is allowed throughout the entire breath cycle. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate

Pressure-support level Cycle sensitivity The resulting VT is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.14 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.14

Pressure-Control-Airway Pressure-Release Ventilation (PC-APRV) PC-APRV is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.14 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. PC-APRV is mainly used with an inverse I:E ratio. Phigh level is referenced to atmosphere as opposed to the Plow. This is important because increases in Plow will decrease ΔP. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow The VT will be variable and depend on the Phigh, Plow, patient effort, and patient respiratory system mechanics.14 Pressure levels (Phigh and Plow) are time triggered and time cycled, independent of patient effort.

Spontaneous-Continuous Positive Pressure/Pressure Support (SPNCPAP/PS) During SPN-CPAP/PS the patient regulates the respiratory rate and the VT with support from the ventilator.14 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow.

Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.14 If the PS level is set to 0, all breaths will be unsupported.

Spontaneous-Continuous Positive Airway Pressure/Volume Support (SPN-CPAP/VS) In SPN-CPAP/VS the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.14 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.14 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Spontaneous-Continuous Positive Airway Pressure (SPN-CPAP) SPN-CPAP is only available in noninvasive ventilation and is designed only for the neonatal population.14 During SPN-CPAP the patient regulates the respiratory rate and the VT with support from the ventilator. Main operator controls include: FIO2 PEEP

Tmaninsp (manual inspiration time) Pmaninsp (manual inspiration pressure) The VT will be variable and depend on patient effort and patient respiratory system mechanics.

Spontaneous-Proportional Pressure Support (SPN-PPS) In ventilation mode SPN-PPS, the Evita V500 supports the patient's spontaneous breathing in proportion to the inspiratory effort.14 If the patient breathes strongly, the ventilator will support this effort with high-pressure support. If the patient has shallow breathing, the ventilator responds with low-pressure support. Mechanical support is omitted altogether if there is no spontaneous breathing. Main operator controls include: FIO2 PEEP Volume assist Flow assist VT and pressure are variable and will depend on: volume assist setting, flow assist setting, patient effort, and patient respiratory system mechanics.14 The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.14

Special Features Evita Infinity V500 special features include apnea backup ventilation, autoflow, automatic tube compensation, low flow PV loop, variable pressure support, nebulizer, and NIV.

Apnea Backup Ventilation The ventilator engages apnea backup ventilation when no breath has been delivered by the time the apnea interval elapses.14 If the patient is in a volume-control mode without AutoFlow (see description of AutoFlow below) they will receive apnea backup ventilation in VC-SIMV without AutoFlow with the preset apnea respiratory rate and tidal volume. In all other cases apnea backup ventilation will be VC-SIMV with AutoFlow.

AutoFlow When AutoFlow is activated the ensuing breaths become pressure-targeted with a volume guarantee.14 The ventilator determines what pressure to use in order to achieve the set tidal volume. AutoFlow is only available in the volume-targeted modes. RC Insight 4-4 On the Dräger ventilators when “AutoFlow” is enabled the inspiratory pressure now becomes referenced to atmosphere as opposed to the PEEP level. So switching on AutoFlow will reduce the distending pressure. Regardless of the mode, patients need to be assessed for patient ventilator synchrony, even (or perhaps especially) in the “closed loop modes.”

Automatic Tube Compensation When automatic tube compensation is activated, the ventilator calculates the pressure drop from the proximal to the distal end of the ETT and ventilation pressure in the breathing circuit is increased during inspiration or decreased during expiration.14 The airway pressure is adjusted to the tracheal level if 100% compensation of the tube resistance has been selected. The clinician has to input ETT diameter and length.

Low-Flow Pressure-Volume (PV) Loop The low-flow PV loop measuring procedure records a static pressure-volume curve, which can be used to assess the mechanical properties of the lungs.14

Variable Pressure-Support (PS) Ventilation Variable pressure-support ventilation is optional on the V500.14 It functions by generating random variation values in pressure-support levels and then applies those values to the pressure support delivered to the patient. Regardless of the patient’s spontaneous breathing effort, variable PS increases and decreases the tidal volume.

Nebulizer The Evita V500 incorporates an internal pneumatic nebulizer.14 In adults, the nebulizer synchronizes with the inspiratory phase and adds no additional flow and the FIO2 is constant. For pediatrics and neonates, the nebulizer operates

continuously.

Noninvasive Ventilation NIV is available for adults in all ventilator modes.14 For neonates the ventilator supplies NIV in SPN-CPAP and PC-CMV.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Dräger Evita Infinity V500 are listed in Table 4-26. TABLE 4-26 Manufacturer’s Specifications for the Dräger Evita V500 Setting

Range

Pressure Inspiratory pressure

0 to 95 cm H2O

Pressure support

0 to 95 cm H2O

PEEP

0 to 50 cm H2O

Volume Tidal volume

0.002 to 3.0 L

Flow Inspiratory flow

2 to 120 L/min

Time Inspiratory time

0.1 to 10 seconds

Mandatory breath rate

0.5 to 150/min

Sensitivity Trigger

0.2 L/min to 15 L/min (flow)

Cycle

1% to 80% of peak flow

Alarms

Range

Pressure Airway pressure

7 to 105 cm H2O

Volume High VT

0.003 to 3.1 L

Low VT

0.001 to 2.9 L

High Ve

0.3 to 60 L/min

Low Ve

0.2 to 400 L/min

Time Respiratory rate

5 to 200 breaths/min

Apnea time

5 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Airway pressure

Maximum airway pressure

O2 concentration

Expired minute volume

RR

VT

End-expiratory CO2 concentration

P0.1

Intrinsic PEEP

NIF

C20/C

Accessories Accessories include optional CO2 monitoring with the CapnoPlus.14 In the neonatal mode, a neonatal sensor provides flow measurement at the wye.14 SmartCare is an optional weaning mode that gradually reduces the PS level based on inputs from ETCO2, RR, and VT.14

Dräger Evita XL The Dräger Evita XL ventilator is a critical care ventilator designed for use in adult, pediatric, and neonatal patients in both acute and subacute clinical locations.15 It is pictured in Figure 4-24. The Evita XL is electrically powered and controlled. It is designed to use in acute and subacute clinical settings. It requires an external compressor if piped air is not available. The Evita XL operator interface is depicted in Figure 4-25. It consists of a flat-panel touch screen, buttons, and a control dial to

change and confirm settings. Settings are entered by pressing a button on the touch screen to select the parameter to be changed, then the control dial is turned to select the new value, and the control dial is pressed to confirm.

FIGURE 4-24 The Dräger Evita XL Ventilator.

Courtesy of Dräger.

FIGURE 4-25 The Dräger Evita XL Ventilator Operator Interface. Courtesy of Dräger.

Modes The ventilation modes available on the Dräger Evita XL are classified and depicted in Table 4-27. TABLE 4-27 Modes on the Dräger Evita XL

Description

Continuous Mandatory Ventilation (CMV)

CMV is a volume-targeted mode of ventilation (VAC) that allows for mandatory, timetriggered breaths and patient-assisted breaths.15 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.15

Synchronized Intermittent Mandatory Ventilation SIMV combines two breath types, VAC and spontaneous breathing, while on CPAP.15 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow SIMV rate Inspiratory time During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.15 During the CPAP spontaneous breaths, the volume will be variable and depend on patient effort and patient respiratory system mechanics.15

Synchronized Intermittent Mandatory Ventilation/Pressure Support SIMV/PSupp combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.15 Thus, mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow SIMV rate Inspiratory time Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.15 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.15

Mandatory Minute Volume Ventilation (MMV) MMV guarantees that the patient always receives at least the set minute volume MV.15 The patient can always breathe spontaneously at PEEP level (with or without pressure support). If the spontaneous breathing of the patient is insufficient to achieve the set minute ventilation, VAC breaths are applied. These mandatory breaths are synchronized with the patient’s own breathing attempts. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR

Inspiratory time Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.15 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system.15

Pressure-Control Ventilation+ (PCV+) PCV+ is a pressure-targeted mode of ventilation that delivers mandatory, timetriggered breaths only.15 However, spontaneous breathing is permitted during the whole breathing cycle. The mandatory breaths cycle to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.15 Pressure-control settings are not automatically adjusted for PEEP and an increase in PEEP will decrease delta P (ΔP) and tidal volume, if pressure control is not also adjusted.

Pressure-Controlled Ventilation+/Pressure-Supported Spontaneous Breathing PCV+/PSupp is a pressure-targeted mode of ventilation that delivers mandatory, time-triggered breaths and pressure support breaths.15 Spontaneous breathing is permitted during the whole breathing cycle. The mandatory breaths cycle to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2

PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.15 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.15 Inspiratory pressure level is not automatically adjusted for PEEP and an increase in PEEP will decrease delta P (ΔP) and tidal volume, if pressure control is not also adjusted.

Pressure-Controlled Ventilation+ (PCV+ Assist) PCV+ Assist is a pressure-targeted mode of ventilation that delivers mandatory, time-triggered patient-assisted breaths.15 However, spontaneous breathing is permitted during the whole breathing cycle. The mandatory breaths cycle to exhalation once the inspiratory time has been reached. The inspiratory breaths are equivalent to those of PCV+, however, the switch from Pinsp to PEEP is not synchronized with patient expiration. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.15 Inspiratory pressure level is not automatically adjusted for PEEP and an increase in PEEP will decrease delta P (ΔP) and tidal volume, if pressure control is not also adjusted.

Airway Pressure-Release Ventilation APRV is a mode of ventilation that allows for spontaneous breathing at two different

clinician-set pressure levels.15 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. APRV is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the Plow. This is important because increases in Plow will decrease the distending pressure. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow The VT will be variable and depend on the Phigh, Plow, patient effort, and patient respiratory system mechanics.15

Special Features Similar to the Evita Infinity V500, the Evita XL has a number of special features as described below.

Apnea Ventilation The ventilator engages apnea ventilation when no breath has been delivered by the time the apnea interval elapses.15 When apnea ventilation has been triggered, the ventilator switches over to CMV and ventilates with the set respiratory rate and VT. As in SIMV, the patient can breathe spontaneously during apnea ventilation and mandatory breaths will be synchronized with the patient's spontaneous breathing. The apnea respiratory rate remains constant.

AutoFlow AutoFlow is a supplemental function that controls inspiratory flow during mandatory breaths in the volume-controlled ventilation modes CMV, SIMV, and MMV.15 In essence, breaths become pressure targeted with a volume guarantee. The ventilator

determines what pressure to use in order to achieve the set tidal volume. In the neonatal population, AutoFlow is automatically activated in all volume-controlled modes. A neonatal flow sensor is required.

Automatic Tube Compensation When automatic tube compensation is activated, the ventilator calculates the pressure drop from the proximal to the distal end of the ETT and ventilation pressure in the breathing circuit is increased during inspiration or decreased during expiration.15 The airway pressure is adjusted to the tracheal level if 100% compensation of the tube resistance has been selected. The clinician has to input ETT diameter and length.

Low-Flow PV Loop The low-flow PV loop measuring procedure records a static pressure-volume curve, which can be used to assess the mechanical properties of the lungs.15

Nebulizer The Evita XL employs a pneumatic nebulizer for the delivery of medication.15 In the adult patient category nebulization is available in all modes. The nebulizer synchronizes with the inspiratory phase and adds no additional flow while keeping the FIO2 is constant. In the neonatal and pediatric patient categories, medication nebulization is only possible in volume-controlled ventilation modes.

Noninvasive Ventilation NIV is activated when the mask ventilation application mode is selected.15 All ventilation modes can be used. Patients with spontaneous breathing are supported with noninvasive ventilation therapies via a nasal or facial mask.

Neonatal Ventilation Ventilation of neonates is accomplished through the use of the NeoFlow option, which offers flow measurement at wye.15

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms

The manufacturer’s specifications, controls, monitored parameters, and alarms for the Dräger Evita XL are listed in Table 4-28. TABLE 4-28 Manufacturer’s Specifications for the Dräger Evita XL Setting

Range

Pressure Inspiratory pressure

0 to 95 cm H2O

Pressure support

0 to 95 cm H2O

PEEP

0 to 50 cm H2O

Volume Tidal volume

0.02 to 2.0 L

Flow Inspiratory flow

6 to 120 L/min

Time Inspiratory time

0.1 to 10 seconds

Mandatory breath rate

0 to 100/min

Sensitivity Trigger

0.2 L/min to 15 L/min (flow)

Cycle

25% of peak flow

Alarms

Range

Pressure Airway pressure

10 to 100 cm H2O

Volume VT

0.021 to 4.0 L

Ve

0.01 to 40 L/min

Time Respiratory rate

5 to 120 breaths/min

Apnea time

5 to 60 seconds

Other

O2 sensor

Enabled/disabled

Monitored Parameters Maximum airway pressure (Ppeak)

Plateau pressure (Pplateau)

PEEP

Mean airway pressure (Pmean)

Minimum airway pressure (Pmin)

FIO2

End-expiratory CO2 concentration

Minute volume (MV)

Spontaneously breathed minute volume (MVspn)

Tidal volume (VTe)

Spontaneously breathed tidal volume

Inspiratory tidal volume during a PSupp breath (VT PSupp)

Respiratory rate (Ftot)

Spontaneous respiratory rate (Ftotal)

Mechanical respiratory rate (Fmand)

Breathing gas temperature

CO2 measurement

End-expiratory CO2 concentration (ETco2)

Serial dead space (Vds)

Dead space ventilation (Vds/VT)

Leakage minute volume (MVleak)

Compliance

Resistance

Rapid shallow breathing

Negative inspiratory force (NIF)

Accessories Accessories include optional CO2 monitoring with the CapnoPlus.15 In the neonatal mode, a neonatal sensor provides flow measurement at the wye.15 SmartCare offers an optional weaning mode that gradually reduces the PS level based on inputs from ETCO2, RR, and VT.15

GE Healthcare CARESCAPE R860 The CARESCAPE R860 ventilator (pictured in Figure 4-26) is a critical care ventilator designed to provide mechanical ventilation or support to neonatal, pediatric, and adult patients weighing 0.25 kg and above.16 It is microprocessor based, electronically controlled, and pneumatically driven, and can be used for intrahospital transport as well. The operator interface on the GE CARESCAPE R860 employs a combination of a touch screen, buttons (real and virtual), and a trim knob (Figure 4-27). It is a three-step process to make a change to a setting. The clinician

first touches a virtual button on the touch screen. Second, the trim knob is used to change the value of the setting. Last, the trim knob must be pressed to confirm. The screen displays change depending on the operation being carried out. For instance, the alarm screen looks different than the monitoring screen and so forth. There are a number of different screens.

FIGURE 4-26 The GE CARESCAPE R860 Ventilator. Courtesy of GE Healthcare.

FIGURE 4-27 The GE CARESCAPE R860 Operator Interface. Courtesy of GE Healthcare.

Modes The ventilation modes available on the CARESCAPE R860 are classified and depicted in Table 4-29. TABLE 4-29 GE CARESCAPE R860 Modes of Ventilation

Description

A/C Volume Control A/C VC is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.16 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR Inspiratory time (Tinsp) or I:E The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.16

Synchronized Intermittent Mandatory Ventilation Volume Control SIMV VC combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.16 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking”

(a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory flow SIMV rate Inspiratory time (Tinsp) Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.16 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.16

A/C Pressure Control A/C PC is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.16 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure (Pinsp) Tinsp or I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.16

Synchronized Intermittent Mandatory Ventilation Pressure Control SIMV PC is similar to SIMV VC described above except that the target is now pressure instead of volume.16 SIMV (pressure control) also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Pinsp Tinsp SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.16 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.16

Continuous Positive Airway Pressure/Pressure Support During CPAP/PS the patient regulates the respiratory rate and the VT with support from the ventilator.16 The patient triggers all of the breaths and will receive the clinician-set PS level (if PS is set to 0 the patient breathes spontaneously on CPAP). If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP

Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.16 If the PS level is set to 0, all breaths will be unsupported.

A/C Pressure-Regulated Volume Control A/C PRVC is a pressure-targeted (either PC or PA breaths) mode that uses the pressure breaths to achieve a clinician-set VT.16 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include: FIO2 PEEP RR VT target Tinsp or I:E The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.16

Synchronized Intermittent Mandatory Ventilation Pressure-Regulated Volume Control SIMV PRVC combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.16 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include:

FIO2 PEEP SIMV rate VT Tinsp Pressure-support level Cycle sensitivity During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.16 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Volume Support (VS) In VS, the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.16 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.16 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

BiLevel Airway Pressure Ventilation During Bilevel mode, the ventilator alternates between the set PEEP level and the set inspiratory pressure level (Pinsp) based on the set rate and inspiratory time (Tinsp).16 The patient can breathe spontaneously at either level. An important

difference from the previously described pressure-targeted modes is that the Pinsp level is now referenced to atmosphere as opposed to the PEEP. This is important because increases in PEEP will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Pinsp Tinsp RR Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity The VT will be variable and depend on the Pinsp, PEEP, PS level (if set > 0), patient effort, and patient respiratory system mechanics.16

BiLevel Airway Pressure Ventilation Volume Guaranteed In Bilevel VG the ventilator alternates between a set PEEP and the minimum pressure to deliver the set tidal volume (VT) based on the set rate and inspiratory time (Tinsp).16 The patient can breathe spontaneously at either level. Again the Pinsp level is referenced to atmosphere as opposed to the PEEP. This is important because increases in PEEP will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP VT Tinsp RR Pressure support (can be left at 0 if no additional pressure is needed) Cycle sensitivity RC Insight 4-5

Some ventilators allow the clinician to set PS during the inspiratory phase in APRV. The resulting transpulmonary pressure then is a total of the AutoPEEP, inspiratory pressure, PS level, and inspiratory effort. It is important to keep in mind that the total of these four variables may be in the unsafe range.

Noninvasive Ventilation During NIV mode, the patient draws spontaneous breaths as the ventilator maintains the set PEEP level and provides PS breaths.16 Patients should have a reliable respiratory drive since all breaths are spontaneous. Both flow and pressure triggers are applied simultaneously in NIV mode to help counterbalance the leak in the system.

Special Features CARESCAPE R860 special features include apnea backup ventilation, tube compensation, leak compensation, spontaneous breathing trial, FRC procedure, metabolics, and spirodynamics as described below.

Apnea Backup Ventilation Backup mode is available upon activation of the apnea alarm or the patient’s expired minute volume (MVexp) dropped below 50% of the set low MVexp alarm.16 All of the CARESCAPE R860’s modes with mandatory breaths can be used as the backup mode.

Tube Compensation Tube compensation is designed to add additional pressure to compensate for the difference between the lung pressure and breathing circuit pressure during the inspiratory phase of pressure-controlled and pressure-supported breaths.16 It can be used to offset all or part of the resistance caused by the endotracheal or tracheal tube

Leak Compensation Leak compensation is used to compensate for leaks in the circuit.16 The CARESCAPE R860 uses increases in tidal volume to compensate in volumetargeted modes (A/C VC, A/C PRVC, SIMV VC, SIMV PRVC, Bilevel VG, and VS). The maximum tidal volume increase for adults is 25% of the set VT. For pediatric and

neonates the maximum increase is 100%.

Spontaneous Breathing Trial The spontaneous breathing trial (SBT) mode can be used to evaluate readiness for liberation from the ventilator.16 The clinician sets the FIO2, PEEP, PS level, and SBT duration. There is an “SBT view” screen that allows the clinician to examine the trial in more detail.

Functional Residual Capacity (FRC) Procedure The FRC procedure measures the patient's FRC using a nitrogen washout process.16 The nitrogen washout uses the changes in FIO2 delivered to the patient to measure FRC.

Metabolics (Indirect Calorimetry) Indirect calorimetry calculates the energy expenditure (EE) and respiratory quotient (RQ) by measuring respiratory gas exchange, the consumption of oxygen, and the production of carbon dioxide.16

SpiroDynamics SpiroDynamics uses the intratracheal pressure catheter connected to the Paux port to measure tracheal pressures and intrinsic PEEP.16 The idea is that the catheter bypasses the resistance created by the endotracheal tube to theoretically provide more accurate alveolar pressures.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the GE CARESCAPE R860 are listed in Table 4-30. TABLE 4-30 Manufacturer’s Specifications for the GE CARESCAPE R860 Setting Pressure

Range

Inspiratory pressure

1 to 98 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 50 cm H2O

Volume Tidal volume

0.1 to 2.0 L

Flow Inspiratory flow

2 to 160 L/min

Time Inspiratory time

0.25 to 15 seconds

Mandatory breath rate

3 to 120/min

Sensitivity Trigger

1 L/min to 9 L/min (flow) –10 to –0.25 cm H2O (pressure)

Cycle

5% to 80% of peak flow

Alarms

Range

Pressure Ppeak High

7 to 100 cm H2O

Ppeak Low

1 to 97 cm H2O

PEEPi High

1 to 20 cm H2O

PEEPe High

5 to 50 cm H2O

PEEPe Low

1 to 20 cm H2O

Paux

12 to 100 cm H2O

Volume VTexp High

0.003 to 2 L

VTexp Low

0.001 to 1.95 L

MVexp High

0.02 to 99 L/min

MVexp Low

0.01 to 40 L/min

Time RR High

2 to 150 breaths/min

RR Low

1 to 99 breaths/min

Apnea time

5 to 60 seconds

Other O2 sensor

Enabled/disabled

ETco2 High

0.2% to 15%

ETco2 Low

0.1% to 14.9%

ETo2 High

11% to 100%

ETo2 Low

10% to 99%

Monitored Parameters Peak pressure (Ppeak)

Plateau pressure (Pplateau)

Mean airway pressure (Pmean)

PEEPe

PEEPi

VTinsp

VTexp

MVinsp

MVexp

I:E

Tinsp

Texp

RR

Cycle time

Leak (%)

MVexp spont

RR spont

VTexp spont

MVexp mech

RRmech

VTexp mech

RSBI

FIO2

ETo2

ETco2

Accessories Bilevel, APRV, and NIV are all optional modes on the CARESCAPE R860.16 Neonatal ventilation is an option as well and neonates that weigh a minimum of 0.25 kg can be ventilated with the use of a proximal flow sensor. All modes are available in neonatal ventilation as well as nasal CPAP (nCPAP). The CARESCAPE R860 has the ability to deliver aerosolized medications through the use of an Aerogen Solo

vibrating mesh nebulizer. The nebulizer does not add flow to the circuit, so it does not interfere with ventilation.

Philips Respironics V60 Ventilator The Philips Respironics V60 is a microprocessor-controlled ventilator designed for use in adult and pediatric patients > 20 kg.17 It delivers bilevel positive airway pressure (BiPAP) during both invasive and noninvasive ventilation. It is pictured in Figure 4-28. The operator interface on the V60 employs a combination of a touch screen, buttons, and a control knob (Figure 4-29). It is a three-step process to make a change to a setting. The clinician first touches a virtual button on the touch screen. Second, the control knob is used to change the value of the setting. Last, the control button must be pressed to confirm.

FIGURE 4-28 The Philips Respironics V60 Ventilator. Courtesy of Philips Healthcare.

FIGURE 4-29 The Philips Respironics V60 Operator Interface. Courtesy of Philips Healthcare.

Modes The ventilation modes available on the V60 are classified and depicted in Table 431. TABLE 4-31 Philips Respironics V60 Modes of Ventilation

Description

Pressure-Control Ventilation Pressure-control ventilation (PCV) is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.17 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. The triggering and cycling sensitivities are not set by the clinician, so the ventilator uses its Auto-Trak Sensitivity algorithms (discussed in more detail in the “Special Features” section). Main operator controls include: FIO2 EPAP (expiratory positive airway pressure) IPAP (inspiratory positive airway pressure) Inspiratory time RR

The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.17

Spontaneous/Timed Mode The spontaneous/timed (S/T) mode delivers pressure-controlled, time-cycled mandatory and pressure supported spontaneous breaths.17 If the patient fails to trigger a breath within the interval determined by the rate setting, the ventilator triggers a mandatory breath with the set inspiratory time. The triggering and cycling sensitivities are not set by the clinician; the ventilator uses its Auto-Trak Sensitivity algorithms (discussed in more detail in the “Special Features” section). Main operator controls include: FIO2 EPAP IPAP Inspiratory time RR The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.17

Continuous Positive Airway Pressure Mode (CPAP mode) In CPAP mode, the ventilator functions as a demand flow system, with the patient triggering all breaths and determining their timing, pressure, and size.17 The triggering and cycling sensitivities are not set by the clinician; the ventilator uses its Auto-Trak Sensitivity algorithms (discussed in more detail in the “Special Features” section). Main operator controls include: FIO2 CPAP The VT will be variable and depend on patient effort and patient respiratory system mechanics.17

Average Volume-Assured Pressure Support (AVAPS) The AVAPS mode delivers PAC mandatory breaths and pressure-supported spontaneous breaths.17 If the patient does not trigger a breath within the interval determined by the rate control, the ventilator delivers a PAC breath with the set inspiratory time. If the patient triggers a breath within the interval, the ventilator delivers a PS breath. The PAC and PS inspiratory pressure levels are continually adjusted over a period of time to achieve the volume target. The triggering and cycling sensitivities are not set by the clinician; the ventilator uses its Auto-Trak Sensitivity algorithms (discussed in more detail in the “Special Features” section). Main operator controls include: FIO2 EPAP VT target Inspiratory time RR Max P Min P The VT may not match the operator setting due to the fact that the ventilator is using PAC PS to target the VT as opposed to VAC and relies on the previous breath sequence to make the calculation.17 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Proportional Pressure Ventilation (PPV) PPV is an optional mode that provides patient-triggered breaths that deliver pressure in proportion to patient effort.17 This is accomplished by setting a percentage of the maximum elastance (Max E) and the maximal resistance (Max R). The patient effort determines the pressure, flow, and tidal volume delivered by the ventilator as well as when to start and end a breath. There is a user-settable backup rate that activates PAC breaths if the patient becomes apneic. Main operator controls include: FIO2 EPAP Max V

Max P RR IPAP Inspiratory time The VT and inspiratory pressure will be variable and depend on the Max E, Max R, patient effort, and patient respiratory system mechanics.17

Special Features Special features available with the V60 include noninvasive ventilation, apnea backup ventilation, leak adaptation, and auto-track sensitivity.

Noninvasive Ventilation The V60 is primarily designed for noninvasive ventilation and all modes can be set up for this purpose.17

Apnea Backup Ventilation There is no backup mode if apnea occurs except in PPV where backup PAC breaths are delivered in the event of apnea.17

Leak Adaptation To maintain prescribed pressures in the presence of leakage, the ventilator adjusts its baseline flow.17 The V60 uses two main mechanisms to update its baseline flow, expiratory flow adjustment and tidal volume adjustment.

Auto-Trak Sensitivity With Auto-Trak Sensitivity the V60 automatically adjusts its triggering and cycling algorithms to maintain optimum performance in the presence of leaks.17 The V60 does this by using an algorithm called the shape signal method. The shape signal or “shadow trigger” method uses a mathematical model derived from the flow signal to achieve optimal triggering and cycling.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for

the Philips Respironics V60 are listed in Table 4-32. TABLE 4-32 Manufacturer’s Specifications for the Philips Respironics V60 Setting

Range

Pressure Inspiratory pressure (IPAP)

4 to 40 cm H2O

Pressure support

6 to 40 cm H2O

PEEP (EPAP)

4 to 25 cm H2O

Volume Tidal volume

0.2 to 3.5 L

Time Inspiratory time

0.3 to 3 seconds

Mandatory breath rate

4 to 60/min

Sensitivity Trigger

Auto-Trak

Cycle

Auto-Trak

Alarms

Range

Pressure High inspiratory pressure

5 to 50 cm H2O

Low inspiratory pressure

1 to 40 cm H2O

Volume High tidal volume

0.2 to 3.5 L

Low tidal volume

0.005 to 1.5 L

Low exhaled minute volume

0.1 to 99 L/min

Time High respiratory rate

5 to 90 breaths/min

Low respiratory rate

1 to 89 breaths/min

Low inspiratory pressure delay

5 to 60 seconds

Other

O2 sensor

Enabled/disabled

Monitored Parameters Peak inspiratory pressure (PIP)

Pt. Leak

Pt. Trig

Rate

TI/TTOT

Tot. Leak

Ve

VT

High-Frequency Ventilators High frequency ventilators include the Vyaire 3100B, Percussionaire VDR-4 and Bunnell Life Pulse.

Vyaire 3100B High-Frequency Oscillator As the name would suggest, the Vyaire 3100B delivers oscillations to patients (35 kg or larger) at a high frequency or rate.18 It is depicted in Figure 4-30. The 3100B operator interface consists of various knobs and LED readouts; see Figure 4-31.

FIGURE 4-30 The Vyaire 3100B High-Frequency Oscillator. © 2018 Vyaire Medical, Inc. Used with permission.

FIGURE 4-31 The Operator Interface for the Vyaire 3100B. © 2018 Vyaire Medical, Inc. Used with permission.

Mode The 3100B is a high-flow CPAP system with oscillations being superimposed on the gas in the patient circuit using an electrically driven diaphragm.18 Essentially, the CPAP (called mean airway pressure, or MAP), along with the FIO2, provide oxygenation while the oscillations provide CO2 removal. The frequency of the oscillations can be set between 3 and 15 Hz (each Hz comprises 60 oscillations). Oscillatory pressure amplitude is controlled by a thumb wheel knob that controls the power driving the piston forward. The frequency of the oscillations is set by the frequency-Hz control. It is displayed in Hz and each Hz corresponds to 60 cycles per minute. Contrary to conventional ventilation, decreasing the Hz tends to increase CO2 removal. The % inspiratory time represents the percentage of each respiratory cycle (oscillation) that the piston is moving forward and helps facilitate CO2 removal. The mean airway pressure is adjusted with a control that varies the resistance at the exhalation valve and can be set from approximately 5 to 55 cm H2O. Since it is not feedback controlled, the MAP can vary depending on the other settings. There is a

sweep gas (called bias flow) that runs continuously through the circuit and it can be set from 0 to 60 L/min. The maximum pressure swing is approximately 140 cm H2O measured at the patient wye but the actual pressure swings in the trachea would be in the range of 10% of this value because of attenuation in the tracheal tube. Tidal volumes tend to be small and often close to anatomic dead space. The maximum tidal volume will be approximately 250 mL depending on the ventilator settings, tracheal tube size, and the patient's pulmonary compliance.

Special Features The 3100B has a special circuit designed specifically for delivery of high frequency oscillatory ventilation (HFOV), described further in Chapter 11.

Circuit The Vyaire 3100B has to be used with the circuit and humidifier provided.18

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Vyaire 3100B are listed in Table 4-33. TABLE 4-33 Manufacturer’s Specifications for the Vyaire 3100B Setting

Range

Pressure Mean airway pressure (MAP)

3 to 55 cm H2O (bias flow dependent)

Flow Bias flow

0 to 60 L/min

Time Inspiratory time

30% to 50%

Respiratory rate

3 to 15 Hz or 180 to 900 bpm

Alarms

Range

Pressure

Maximum mean airway pressure

0 to 59 cm H2O

Minimum mean airway pressure

0 to 59 cm H2O

Monitored Parameters Bias flow

Inspiratory time %

Mean airway pressure

Amplitude (oscillatory peak to trough airway pressure)

Frequency-Hz

Percussionaire VDR-4 VDR-4 stands for Volumetric Diffusive Respirator-4.19 It is depicted in Figure 4-32. It is the latest in the line of percussionators with previous versions shown in Figure 433. It is a pneumatically powered, pressure-limited, time-cycled, high-frequency flow interrupter that delivers high-frequency percussive ventilation (HFPV). The VDR-4 operates in conjunction with the Monitron II Waveform Analyzer, which provides airway pressure waveforms and alarm monitoring. The VDR-4 operator interface consists of various knobs for adjusting pressures relating to the high-frequency ventilation; see Figure 4-34.

FIGURE 4-32 The Percussionaire VDR-4 Ventilator. Courtesy of Percussionaire.

FIGURE 4-33 Percussionaire IPV-1C and IPV-2C. Courtesy of Percussionaire.

FIGURE 4-34 The Operator Interface for the Percussionaire VDR-4. Courtesy of Percussionaire.

Mode High-frequency percussive ventilation (HFPV) produced by the VDR-4 provides subtidal volumes in conjunction with time-cycled, pressure-limited controlled mechanical ventilation (i.e., pressure-control ventilation, PCV).19 It can be conceptualized as HFOV oscillating around two different pressure levels, the inspiratory and expiratory airway pressures. HFPV is possible because of a device called a Phasitron. The Phasitron is an inspiratory and expiratory valve located at the end of the endotracheal tube. High-pressure gas drives the Phasitron to deliver small tidal volumes at a high frequency (200 to 900 beats per minute), superimposed on the inspiratory and expiratory airway pressures of PCV. The PCV is typically delivered at a respiratory rate of 10 to 15 breaths per minute. The resulting waveform can be seen on the monitor in Figure 4-32.

Bunnell Life Pulse The Bunnell Life Pulse high-frequency ventilator (Figure 4-35) is a microprocessor-

controlled infant ventilator capable of delivering and monitoring between 240 and 660 heated, humidified breaths per minute.20 The Life Pulse is composed of five subsystems (Figure 4-36): the monitor (displays patient and machine pressures), the alarms (indicate various conditions that may require attention), the controls (regulate the on-time, peak inspiratory pressure, and rate of the HFV breaths), the humidifier (monitors and controls the temperature and humidification of gas flowing through the disposable humidifier circuit to the patient), and the patient box (contains the pinch valve that breaks the flow of pressurized gas into tiny jet pulses and sends pressure information back to the ventilator’s microprocessor).

FIGURE 4-35 The Bunnell Life Pulse High-Frequency Ventilator. Courtesy of Bunnell.

FIGURE 4-36 The Operator Interface and Subsystems for the Bunnell Life Pulse. Courtesy of Bunnell.

Mode The Life Pulse itself provides high-frequency breaths, airway pressure monitoring, humidification, and alarms.20 The Life Pulse is used in conjunction with a conventional infant ventilator. The conventional ventilator has four functions: to

provide fresh gas for spontaneous breathing, to provide and regulate PEEP, to provide supplementary IMV if needed, and to provide periodic dilation of airways when needed. The link between the Life Pulse and the conventional ventilator is the LifePort Adapter (Figure 4-37). It consists of a 15-mm port to provide the standard connection for the conventional ventilator, the jet port to provide the entrance for the high-frequency pulses provided by the Life Pulse, and the pressure monitoring tube that allows the Life Pulse to display approximations of distal tip airway pressures.

FIGURE 4-37 The LifePort Adaptor. Courtesy of Bunnell.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Bunnell Life Pulse high-frequency ventilator are listed in Table 4-34. TABLE 4-34

Manufacturer’s Specifications for the Bunnell Life Pulse Setting

Range

Pressure Inspiratory pressure

8 to 50 cm H2O

Time Inspiratory time

0.020 to 0.034 seconds

Frequency

240 to 660/min

Alarms

Range

Pressure Peak pressure

Automatic adjustment

Mean airway pressure

Automatic adjustment

Servo

Automatic adjustment

Monitored Parameters Peak airway pressure

Mean airway pressure

PEEP

Delta pressure

Servo pressure

I:E

Portable Ventilators Currently, there are very large number of ventilators specifically designed for patient transport, subacute care, in-home applications, and for the treatment of patients with sleep apnea. Features available on these ventilators range from sophisticated mode options to basic CPAP units for treatment of OSA.

HAMILTON-T1 The HAMILTON-T1 ventilator is intended to provide positive-pressure ventilatory support to adults and pediatrics, and optionally infants and neonates.21 It is pictured in Figure 4-38. It is meant to be used in the ICU, intermediate care, emergency room, long-term acute care hospital, or during transport. The HAMILTON-T1 is an electronically controlled pneumatic ventilator with an integrated air compressing system. It runs on AC or direct current (DC) power with battery backup. The HAMILTON-T1’s pneumatics deliver gas, and its electrical systems control pneumatics, monitor alarms, and distribute power. It employs a proximal flow sensor to monitor and deliver gas. The T1 operator interface utilizes a combination of numerics and real-time waveforms and is depicted in Figure 4-39. It consists of a touch screen, some keys, and a turn-and-press knob. Turning the knob changes the values of the parameter chosen and pressing the knob confirms the selection.

FIGURE 4-38 The HAMILTON-T1 Ventilator. Courtesy of Hamilton Medical.

FIGURE 4-39 The Operator Interface for the HAMILTON-T1. Courtesy of Hamilton Medical.

Modes The different modes available on the HAMILTON-T1 are classified and depicted on Table 4-35. TABLE 4-35 HAMILTON-T1 Ventilation Modes

Description

Synchronized Controlled Mandatory Ventilation + [(S)CMV+] (S)CMV+ is a VT-targeted, pressure-regulated mode.21 In other words, the clinician sets the VT and the ventilator uses varying levels of pressure to achieve the target. The ventilator relies on calculations from previous breath sequences to deliver what it calculates the inspiratory pressure level needs to be to achieve the desired VT. Main operator controls include: VT target PEEP FIO2 I:E The VT may not match the operator setting due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.21 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Synchronized Intermittent Mandatory Ventilation + (SIMV+) SIMV+ combines a VT-targeted PAC breath (see SCMV+ above) with spontaneous PS breaths in between.21 Thus, there exists mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. The ventilator prevents “breath stacking” (a SCMV+ breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a SCMV+ breath. If the patient attempts to trigger a breath outside the window, then a spontaneous PS breath will occur. Main operator controls include: VT target PEEP FIO2 Inspiratory time Pressure-support level The VT may not match the operator setting for the SCMV+ breaths due to the fact

that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breath sequences to make the calculation.21 Any change in patient effort from the previous breath may result in a deviation from the VT setting. During the SCMV+ breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics. During the PS breaths, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.

Pressure-Controlled Ventilation + (PCV+) PCV+ is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.21 The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Free breathing is allowed at both the PEEP and the inspiratory pressure levels. Main operator controls include: Inspiratory pressure level I:E ratio RR PEEP FIO2 The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.21

Pressure Synchronized Intermittent Mandatory Ventilation+ (P-SIMV+) P-SIMV+ is similar to SIMV+ described above except that the target is now pressure instead of volume and that inspiratory pressure is now set by the clinician. P-SIMV+ also combines two breath types, PAC (PCV+) and either PS or spontaneous breathing, while on CPAP.21 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a

spontaneous breath will occur. Main operator controls include: Inspiratory pressure level Inspiratory time RR PEEP FIO2 Pressure-support level Cycle sensitivity for the PS breaths During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.21 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.21

Spontaneous (SPONT) In the spontaneous mode, the patient triggers all of the breaths and will receive either PS or CPAP (if the PS is set at 0).21 If the PS is set at 0, then the patient must contribute all of the work of breathing. This is sometimes used for a spontaneous breathing trial to assess the potential for liberation from the ventilator. During PS, the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: PEEP FIO2 Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.21

Duo Positive-Pressure Ventilation (DuoPAP) DuoPAP is a pressure-targeted mode of ventilation that allows for spontaneous

breathing at two different pressure levels.21 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and PEEP. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level. This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Thigh RR PS DuoPAP generally is used in “normal” I:E ratios (not inversed).21 The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (If set > 0), patient effort, and patient respiratory system mechanics.

Airway Pressure-Release Ventilation Airway pressure-release ventilation (APRV) is a mode of ventilation that is similar to DuoPAP in that it allows for spontaneous breathing at two different pressure levels.21 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. Unlike DuoPAP, APRV generally is used in an inverse ratio fashion. Most of the time is spent at Phigh with brief, periodic releases to Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level. This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort.

Main operator controls include: FIO2 Phigh Plow Thigh Tlow PEEP The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (if set > 0), patient effort, and patient respiratory system mechanics.21

Adaptive Support Ventilation ASV is a “feedback” mode that adjusts the inspiratory pressure and RR to meet a minimum minute volume set by the clinician.21 This results in a variable form of PSIMV. The machine-timed breaths are PAC while the spontaneously generated breaths are PS. The amount of breathing that the patient does determines how many machine-generated breaths will be delivered. The algorithm for ASV is centered around lung protection. Main operator controls include: %MinVol PasvLimit PEEP FIO2 Patient height Endotracheal tube information The VT will be variable and depend on: inspiratory pressure level for the PAC breaths, PS level for the spontaneous breaths, patient effort, and patient respiratory system mechanics.21

Noninvasive Ventilation In the NIV mode the patient triggers all of the breaths and will receive PS.21 As the name would suggest, NIV is designed for use with a mask or other noninvasive patient interface. Main operator controls include:

PEEP FIO2 Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.21

Spontaneous/Timed Noninvasive Ventilation (NIV-ST) NIV-ST is also designed for use with a mask or other noninvasive patient interface.21 It is essentially P-SIMV without an endotracheal tube. NIV-ST combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. If the patient triggers regularly, all breaths are patient-triggered spontaneous breaths, i.e., no time-triggered mandatory breaths. Only when the patient trigger is not detected during the defined breath cycle time (or total breath time), the ventilator delivers time-triggered mandatory breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: Inspiratory pressure level Inspiratory time RR PEEP FIO2 Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.21 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.21

Special Features Special features of the HAMILTON T1 include the oxygen system, apnea backup ventilation, nebulizer, and optional CO2 monitoring.

Oxygen High-pressure oxygen can be provided by a central gas supply or a gas cylinder (41 to 87 psi).21 Low-pressure oxygen can be provided by a concentrator or liquid cylinder (flow ≤ 15 L/min, ≤ 87 psi).

Apnea Backup Ventilation The ventilator will go into apnea backup ventilation if no breaths are detected in the clinician-set interval.21 The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-35).

Nebulizer A pneumatic nebulization function powers a standard inline nebulizer for delivery of prescribed medications in the ventilator circuit.21 When nebulization is active, the nebulizer flow is synchronized with the inspiratory phase of each breath for 30 minutes. Nebulization can be activated in all modes of ventilation.

CO2 Monitoring An optional CO2 sensor is available to allow monitoring of end-tidal and volumetric expired CO2.21

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the HAMILTON-T1 are listed in Table 4-36. TABLE 4-36 Manufacturer’s Specifications for the HAMILTON-T1 Setting Pressure

Range

Inspiratory pressure

0 to 60 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.02 to 2.0 L

Flow Inspiratory flow

0 to 260 L/min (0 to 120 on 100% oxygen)

Time Inspiratory time

0.1 to 12 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 to 20 L/min (flow)

Cycle

5% to 80% of peak flow

Alarms

Range

Pressure High pressure

15 to 70 cm H2O

Low pressure

4 to 60 cm H2O

Volume High tidal volume

0.01 to 3.0 L

Low tidal volume

0.01 to 3.0 L

High exhaled minute volume

0.1 to 50 L/min

Low exhaled minute volume

0.1 to 50 L/min

Time High respiratory rate

0 to 99 breaths/min

Low respiratory rate

0 to 99 breaths/min

Apnea time

15 to 60 seconds

Other O2 high

18% to 105%

O2 low

18% to 97%

ETco2 high

1 to 100 mm Hg

ETco2 low

0 to 100 mm Hg

Monitored Parameters Inspriatory pressure

PEEP/CPAP

Mean pressure

Peak pressure

Plateau pressure

AutoPEEP

Inspiratory flow

Expiratory flow

Expired minute volume

Spontaneous minute volume

Inspired VT

Expired VT

Leak

I:E ratio

Mandatory RR

Spontaneous RR

Total RR

Inspiratory time

Expiratory time

Static compliance

IBW

P0.1

Pressure time product

Expiratory time constant

Inspiratory resistance

FIO2

Expired spontaneous VT

FETco2

Alveolar VT

PETco2

Alveolar minute volume

Alveolar dead space

Inspired CO2 volume

Expired CO2 volume

HAMILTON–MR1 The HAMILTON-MR1 ventilator is intended to provide positive-pressure ventilatory support to adults and pediatrics, and optionally infants and neonates.22 It is pictured in Figure 4-40. It is intended for use in the magnetic resonance imaging (MRI) department, intensive care ward, intermediate care ward, emergency ward, longterm acute-care hospital, or in the recovery room. The MR1 can also be used as a transport ventilator. The HAMILTON-MR1 ventilator is classified as MR Conditional with the use of 1.5 Tesla and 3.0 Tesla static magnetic field scanners. The HAMILTON-MR1 is an electronically controlled pneumatic ventilation system with an integrated air compressing system. It uses an external power supply connected to

AC mains with battery backup. The ventilator’s pneumatics deliver gas, and its electrical systems control pneumatics, monitor alarms, and distribute power. The operator interface of the MR1 is pictured in Figure 4-41. The user provides inputs to the microprocessor system through a touch screen, keys, and a press-and-turn knob. The ventilator receives inputs from the proximal flow sensor and other sensors within the ventilator.

FIGURE 4-40 The HAMILTON-MR1 Ventilator.

Courtesy of Hamilton Medical.

FIGURE 4-41 The Operator Interface of the HAMILTON-MR1 Ventilator. Courtesy of Hamilton Medical.

Modes The different modes available on the HAMILTON-MR1 are classified and depicted on Table 4-37. TABLE 4-37 HAMILTON-MR1 Ventilation Modes

Description

Synchronized Controlled Mandatory Ventilation + ((S)CMV+) (S)CMV+ is a VT-targeted, pressure-regulated mode.22 In other words, the clinician sets the VT that is wanted and the ventilator uses varying levels of PAC to achieve the target. The ventilator relies on calculations from previous breaths to deliver what it calculates the inspiratory pressure level needs to be to achieve the VT. In this mode the ventilator has the potential to drop the inspiratory pressure level as patient effort increases and conversely may increase the inspiratory pressure level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target I:E RR The VT may not match the operator setting due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breath sequences to make the calculation.22 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Synchronized Intermittent Mandatory Ventilation +(SIMV+) SIMV+ combines a VT-targeted PAC breath with spontaneous PS breaths in between.22 The type of breaths delivered are the same as P-SIMV; what is different is that the inspiratory pressure level is controlled by the ventilator (variable) in SIMV+. Main operator controls include: FIO2 PEEP VT target Inspiratory time RR Pressure-support level

Cycle sensitivity The VT may not match the operator setting for the PAC breaths due to the fact that the ventilator is using inspiratory pressure to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.22 Any change in patient effort from the previous breath may result in a deviation from the VT setting. During the PS breaths, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics

Pressure-Controlled Ventilation+ PCV+ is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.22 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.22

Pressure Synchronized Intermittent Mandatory Ventilation+ (P-SIMV+) P-SIMV is similar to SIMV described above except that the target is now pressure instead of volume.22 P-SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, timetriggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur.

Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.22 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.22

Spontaneous Mode In the spontaneous mode the patient triggers all of the breaths and will receive either PS or CPAP (if the PS is set at 0).22 If the PS is set at 0 then the patient must contribute all of the work of breathing. This is sometimes used for a spontaneous breathing trial to assess the potential for liberation from the ventilator. During pressure support the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.2

Duo Positive-Pressure Airway Pressure DuoPAP is a pressure-targeted mode of ventilation that allows for spontaneous breathing at two different pressure levels.2 The ventilator switches between two

different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level. This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow PEEP Thigh Tlow RR Pressure support Cycle sensitivity DuoPAP generally is used in “normal” I:E ratios (not inversed).2 The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (If set > 0), patient effort, and patient respiratory system mechanics.

Airway Pressure-Release Ventilation APRV is a mode of ventilation that is similar to DuoPAP in that it allows for spontaneous breathing at two different pressure levels.22 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the length of time spent at Plow. Different from DuoPAP, APRV generally is used in an inverse ratio fashion. Most of the time is spent at Phigh with brief, periodic releases to Plow. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the PEEP level. This is important because increases in Plow will decrease the distending pressure. Additional ventilator support can also be added in the form

of PS at both pressure levels to augment the patient effort. Main operator controls include: FIO2 PEEP Phigh Plow Thigh Tlow The VT will be variable and depend on the inspiratory pressure level (Phigh), PS level (if set > 0), patient effort, and patient respiratory system mechanics.22

Adaptive Support Ventilation ASV is a “feedback” mode that adjusts the inspiratory pressure and RR to meet a minimum minute volume set by the clinician.22 This results in a variable form of PSIMV. The machine-timed breaths are PAC while the spontaneously generated breaths are PS. The amount of breathing that the patient does determines how many machine-generated breaths will be delivered. The algorithm for ASV is centered around lung protection. Main operator controls include: FIO2 PEEP %MinVol Cycle sensitivity Patient height Endotracheal tube information The VT will be variable and depend on: inspiratory pressure level for the PAC breaths, PS level for the spontaneous breaths, patient effort, and patient respiratory system mechanics.22

Noninvasive Ventilation In the NIV mode the patient triggers all of the breaths and will receive PS.22 As the name would suggest, NIV is designed for use with a mask or other noninvasive patient interface.

Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.22

Spontaneous/Timed Noninvasive Ventilation NIV-ST is also designed for use with a mask or other noninvasive patient interface.22 It is essentially P-SIMV without an endotracheal tube. NIV-ST combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. If the patient triggers regularly, all breaths are patient-triggered spontaneous breaths, i.e., no time-triggered mandatory breath. Only when the patient trigger is not detected during the defined breath cycle time (or total breath time), the ventilator delivers time-triggered mandatory breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.22 During the PS breaths, the volume will be variable and depend on the PS level,

patient effort, and patient respiratory system mechanics.22

Nasal Continuous Positive Airway Pressure nCPAP is available only in the neonatal mode and is designed for use with a noninvasive interface.22 As the name would suggest this is a purely spontaneous mode with CPAP as the baseline pressure with no additional pressure added on inspiration. Main operator controls include: FIO2 CPAP RR The VT created will be variable and depend on patient effort and patient respiratory system mechanics.22

Nasal Continuous Positive Airway Pressure-Pressure Control nCPAP-PC is a noninvasive pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.22 The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.22

Special Features Special features of the HAMILTON MR1 include apnea backup ventilation, nebulizer, and its dynamic lung panel.

Apnea Backup Ventilation

The ventilator will go into apnea backup ventilation if no breaths are detected in the clinician-set interval.22 The mode of apnea backup ventilation depends on the mode that the patient is in (Table 4-37).

Nebulizer A pneumatic nebulization function powers a standard inline nebulizer for delivery of prescribed medications in the ventilator circuit.22 When nebulization is active, the nebulizer flow is synchronized with the inspiratory phase of each breath for 30 minutes. Nebulization can be activated in all modes of ventilation.

Dynamic Lung Panel The dynamic lung panel visualizes tidal volume, lung compliance, patient triggering, and resistance in real time.22 The lungs expand and contract in synchrony with actual breaths. Numeric values for resistance (Rinsp) and compliance (Cstat) are displayed. In addition, the shape of the lungs and the bronchial tree are also related to the compliance and resistance values. If all values are in a normal range, the panel is framed in green.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the HAMILTON-MR1 are listed in Table 4-38. TABLE 4-38 Manufacturer’s Specifications for the HAMILTON-MR1 Setting

Range

Pressure Inspiratory pressure

3 to 60 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.02 to 2.0 L

Time Inspiratory time

0.1 to 12 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 to 20 L/min (flow)

Cycle

5% to 80% of peak flow

Alarms

Range

Pressure High pressure

15 to 70 cm H2O

Low pressure

4 to 60 cm H2O

Volume High tidal volume

0.1 to 3.0 L

Low tidal volume

0 to 3.0 L

High exhaled minute volume

0.01 to 50 L/min

Low exhaled minute volume

0.01 to 50 L/min

Time High respiratory rate

0 to 99 breaths/min

Low respiratory rate

0 to 99 breaths/min

Apnea time

15 to 60 seconds

Other O2 high

18% to 105%

O2 low

18% to 97%

Monitored Parameters Inspiratory pressure

fTotal

Peak pressure

fSpont

Mean pressure

fControl

Plateau pressure

TI

Pause pressure

TE

PEEP/CPAP

Cstat

AutoPEEP

IBW

Inspiratory flow

P0.1

Expiratory flow

PTP

Inspired tidal volume

RCexp

Expired tidal volume

Rinsp

Expired minute volume

VTEspont

Spontaneous minute volume

Oxygen %

Vleak (%) MV leak I:E

Accessories The HAMILTON-MR1 has an integrated vibrating mesh Aerogen nebulizer for aerosolized medication delivery.22

Airon pNeuton The family of pNeuton ventilators is depicted in Figure 4-42.23–25 The ventilators are small (< 15 pounds), pneumatically powered, pneumatically controlled, and MRI compatible. The operator interfaces consist of a series of control knobs and a pressure gauge. Being pneumatically driven, they can provide ventilation while on transport or in the MRI suite. The pNeuton Mini is designed to ventilate neonatal, infant, and pediatric patients. The pNeuton A and S models are designed to ventilate pediatric and adult patients.

FIGURE 4-42 Family of Airon pNeuton Ventilators. A. pNeuton Mini (neonatal/infant/pediatric). B. pNeuton S (pediatric/adult). C. pNeuton A (pediatric/adult). Courtesy of Airon Corporation.

Modes The ventilation modes available on the pNeuton ventilators are classified and depicted in Table 4-39. TABLE 4-39 Modes of Ventilation for the pNeuton Ventilators

Description

pNeuton mini The pNeuton mini provides CPAP and IMV modes as described below.

Continuous Positive Airway Pressure CPAP is a purely spontaneous mode of ventilation.23 No mandatory breaths are delivered. Throughout the breath cycle the clinician-set pressure is provided. The breaths are supported only with demand flow. Main operator controls include: FIO2 CPAP The VT will be variable and depend on patient effort and patient respiratory system mechanics.23

Intermittent Mandatory Ventilation (IMV) + CPAP IMV delivers a set number of pressure-targeted (Pinsp) breaths in which the inspiratory time is directly controlled by the clinician while the respiratory rate is controlled by the expiratory time setting.23 In between these IMV breaths, the patient

can breathe spontaneously from the baseline pressure setting (CPAP spontaneous). Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time Expiratory time Flow (Vinsp)

pNeuton Models A and S The pNeuton A and S also provide CPAP and IMV modes, as well as certain special features.

Continuous Positive Airway Pressure CPAP is a purely spontaneous mode of ventilation.24,25 No mandatory breaths are delivered. Throughout the breath cycle the clinician-set pressure is provided. The breaths are supported only with demand flow. Main operator controls include: FIO2 CPAP The VT will be variable and depend on patient effort and patient respiratory system mechanics.24,25

Intermittent Mandatory Ventilation (IMV) + CPAP with Pressure Limit IMV delivers a set number of volume-targeted breaths in which the pressure limit is clinician set.24,25 The inspiratory time and respiratory rate are directly controlled by the clinician. The breath terminates either when the set tidal volume is delivered (volume target) or the pressure limit is met (pressure target). In between these IMV breaths, the patient can breathe spontaneously from the baseline pressure setting (CPAP spontaneous). Main operator controls include: FIO2

PEEP Tidal volume Peak pressure Inspiratory time Respiratory rate

Special Features FIO2 is reset at either 65% or 100%.24,25 All three ventilators can provide noninvasive ventilation.23–25 All three models are MRI compatible.23–25

Other The ventilators are designed for patient transport.23–25 Leak compensation and backup ventilation are not available.23–25

Manufacturer’s Specifications, Controls, and Alarms The manufacturer’s specifications, controls, and alarms for the pNeuton ventilators are listed in Table 4-40. TABLE 4-40 Specifications for the pNeuton Ventilators Setting

Range

Pressure Inspiratory pressure

10 to 75 cm H2O 15 to 60 cm H2O (mini)

PEEP

0 to 20 cm H2O

Volume Tidal volume

0.36 to 1.5 L (S and A models only)

Flow Flow

36 L/min 6 to 20 L/min (mini)

Time Inspiratory time

0.6 to 2.5 seconds

0.25 to 2 seconds (mini) Expiratory time

0.6 to 30 seconds 0.25 to 20 seconds (mini)

RR

2 to 50 bpm 3 to 120 bpm (mini)

Alarms

Range

Pressure Low inlet pressure

< 30 psi < 40 psi or pressure differential 15 psi (mini) Disconnect

Bio-Med Devices Crossvent 4+ The Bio-Med Crossvent 4+ ventilator is depicted in Figure 4-43.26 Bio-Med Devices actually provides a series of Crossvent ventilators: the CV 4+, CV 3+, CV 2+, and CV2i+. The CV 4+ is the most recent of the models and can ventilate all patient populations both invasively and noninvasively. The ventilator is compact small (< 10 pounds), pneumatically powered, and microprocessor controlled. The operator interface consists three adjustment dials and a liquid crystal display (see Figure 443).

FIGURE 4-43 The Bio-Med Crossvent 4+ Ventilator. Courtesy Bio-Med Devices

Modes The ventilation modes available on the Crossvent ventilators are classified and depicted in Table 4-41. TABLE 4-41 Bio-Med Devices Crossvent Modes of Ventilation

Description

Assist/Control A/C is a volume-targeted mode of ventilation (VAC) that allows for mandatory, timetriggered breaths or patient-assisted breaths.26 Spontaneous breathing is not available. The breath cycles to exhalation once the tidal volume (VT) has been delivered or when the maximum inspiratory pressure has been reached. Main operator controls include: PEEP VT Inspiratory flow RR Max press The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.26

Synchronized Intermittent Mandatory Ventilation SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.26 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths will occur.

Main operator controls include: PEEP VT Inspiratory flow SIMV rate Pressure-support level During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.26 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.26

Continuous Positive Airway Pressure CPAP is a purely spontaneous mode of ventilation.26 No mandatory breaths are delivered. Throughout the breath cycle the clinician-set pressure is provided. Pressure support can be added. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: PEEP (CPAP) Pressure-support level The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.26 If the PS level is set to 0, all breaths will be unsupported.

Special Features FIO2 can be set at 50% or 100% with optional air entrainment feature. An external blender can also be added.26 NIV is available but the mode(s) is (are) not specified.26 A backup rate can be set in CPAP in the event that apnea occurs.26

Other The ventilators are designed for patient transport.26 Leak compensation and nebulizer are not available.26

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Crossvent ventilators are listed in Table 4-42. TABLE 4-42 Specifications for the Bio-Med Crossvent Ventilator Setting

Range

Pressure Peak pressure

0 to 120 cm H2O

Pressure support

0 to 50 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.005 to 2.5 L

Flow Flow

1 to 120 L/min

Time Inspiratory time

0.1 to 3 seconds 0.25 to 2 seconds (mini)

RR

0.6 to 150 bpm

Sensitivity Trigger

–0.2 to 10 cm H2O

Alarms

Range

Pressure Peak pressure

0 to 125 cm H2O

PEEP

0 to 99 cm H2O

Mean pressure

0 to 125 cm H2O

Volume Tidal volume

0.05 to 4 L

Minute volume

0 to 200 L

Time Respiratory rate

0 to 199 bpm

Monitored Parameters Peak pressure

Respiratory rate

Oxygen

PEEP/CPAP

Mean pressure

Low supply pressure

Exhaled VT

Exhaled minute volume

Vyaire ReVel The Vyaire ReVel ventilator is designed for pediatric (> 5 kg) and adult patients during transport or in subacute care situations.27 It is pneumatically driven and electronically controlled. It is pictured in Figure 4-44. The operator interface consists of a series of knobs and LED readouts and is depicted in Figure 4-45. The ventilator comes with a docking station that can interface with a graphics monitor and nurse call system.

FIGURE 4-44 The Vyaire ReVel Ventilator.

© 2018 Vyaire Medical, Inc. Used with permission.

FIGURE 4-45 The Operator Interface of the Vyaire ReVel Ventilator. © 2018 Vyaire Medical, Inc. Used with permission.

Description

Modes The ventilation modes available on the Vyaire ReVel are classified and depicted in Table 4-43. TABLE 4-43 Ventilation Modes Available on the Vyaire ReVel

Description

A/C + Volume A/C + volume is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.27 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.27

Synchronized Intermittent Mandatory Ventilation + Volume SIMV + volume combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.27 Thus, mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on

VT, flow, and patient mechanics.27 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.27

A/C + Pressure A/C + pressure is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.27 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.27

SIMV + Pressure SIMV + pressure is similar to SIMV + volume described above except that the target is now pressure instead of volume.27 SIMV + pressure also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level

Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.27 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.27

CPAP + Pressure-Support Ventilation During CPAP + PSV, the patient regulates the respiratory rate and the VT with support from the ventilator.27 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.27 If the PS level is set to 0, all breaths will be unsupported.

A/C + Pressure-Regulated Volume Control (A/C) A/C + PRVC is a pressure-targeted (either PC or PA breaths) mode that uses its pressure breaths to achieve a clinician-set VT.27 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths. Main operator controls include:

FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.27

SIMV + PRVC SIMV + PRVC combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.27 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level Cycle sensitivity During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.27 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Pressure-Regulated Volume Support (VS)

In pressure-regulated VS the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.27 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target Cycle sensitivity The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breaths to make the calculation.27 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Noninvasive Positive-Pressure Ventilation A/C NPPV A/C is A/C + pressure (see above) delivered through a mask instead of an endotracheal tube.27 It is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths. Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.27

Noninvasive Positive-Pressure Ventilation/CPAP/Pressure Support (NPPV/CPAP/PS)

NPPV/CPAP/PS is CPAP + PSV (see above) delivered through a mask instead of an endotracheal tube.27 During NPPV/CPAP/PS the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.27 If the PS level is set to 0, all breaths will be unsupported.

Special Features Special features of the Vyaire Revel include apnea backup ventilation, oxygen system, spontaneous breathing trial, nebulizer, and optional pulse oximetry and graphics monitor.

Apnea Backup Ventilation The ventilator engages apnea backup ventilation when no breath has been delivered by the time the clinician-selected apnea interval elapses.27 When in A/C or SIMV modes, the apnea backup rate is determined by the operator-set mandatory breath rate or the apnea interval setting (whichever provides the highest respiratory rate). In CPAP + PS, apnea backup ventilation is provided in the PAC. When the apnea interval setting (found in the alarm limits window) determines the backup rate, the ventilator will continue to ventilate at this rate until the apnea has been resolved. All other controls for apnea ventilation in A/C and SIMV are set when the primary control values for these modes are selected.

Oxygen When the ventilator is attached to a high-pressure oxygen source of 40 psi to 88 psi

the percentage of oxygen to be delivered through the ventilator’s oxygen blending system can be set directly.27 When the O2% control is set to low-pressure source (LPS), oxygen can be supplied from a low-pressure, low-flow oxygen source of < 10 psi such as a flow meter. Oxygen from the low-pressure source is mixed with air inside the ventilator. When connected to a low-pressure source, the estimated O2 percent delivered to the patient is determined by the O2 inlet flow and the minute volume and is not regulated by the ventilator. A separate chart is provide to help estimate the delivered FIO2.

Spontaneous Breathing Trial During a spontaneous breathing trial, various parameters can be displayed.27 These include SBT f/VT, SBT respiratory rate, SBT VT, and SBT time remaining.

Nebulizer Nebulization is only available during volume breaths in assist/control mode only.27 When the nebulizer is activated, a 6 L/min nominal flow is delivered to the nebulizer drive port. This drives an aerosol nebulizer that doses medication into the patient circuit.

Other Optional pulse oximetry is available along with a separate graphics monitor.27

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Vyaire ReVel are listed in Table 4-44. TABLE 4-44 Manufacturer’s Specifications for the Vyaire ReVel Setting

Range

Pressure Inspiratory pressure

1 to 99 cm H2O

Pressure support

1 to 60 cm H2O

PEEP

0 to 20 cm H2O

Volume Tidal volume

0.05 to 2.0 L

Flow Inspiratory flow

0 to 120 L/min

Time Inspiratory time

0.3 to 9.9 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 to 9 L/min (flow) 1 to 20 cm H2O (pressure)

Cycle

10% to 40% of peak flow

Alarms

Range

Pressure High pressure

5 to 100 cm H2O

High PEEP

5 to 40 cm H2O

Low peak pressure

1 to 60 cm H2O

Low PEEP

1 to 20 cm H2O

Volume Low minute volume

0.1 to 99.9 L/min

Time Respiratory rate

1 to 120 breaths/min

Apnea time

10 to 60 seconds

Other SBT > f

15 to 80 bpm

SBT > f/VT

70 to 900 bpm/L

SBT < f

1 to 40 bpm

SBT < f/VT

5 to 90 bpm/L

SBThigh PEEP

3 to 40 cm H2O

SBTlow PEEP

1 to 20 cm H2O

Monitored Parameters Airway pressure (Paw)

Exhaled minute ventilation (VE)

I:E ratio

Exhaled tidal volume (Vte)

FIO2

Inspiratory tidal volume (Vti)

Peak inspiratory flow

Mean airway pressure (MAP)

Peak inspiratory pressure

SBT f/VT

Positive end-expiratory pressure (PEEP)

SBT time remaining

Spontaneous tidal volume (Sp Vte)

Spo2

Total breath rate

Spontaneous breath rate (Sp f)

Measured leak

O2 source pressure

Peak expiratory flow

Vyaire LTV 1200 The Vyaire LTV 1200 ventilator is designed for pediatric (> 11 lbs) and adult patients in institutional, home, and transport settings.28 It is blower driven and electronically controlled and can ventilate either invasively of noninvasively. It is pictured in Figure 4-46. The operator interface consists of a series of buttons, LED readouts, and an adjustable control knob (Figure 4-47).

FIGURE 4-46 The Vyaire LTV 1200 Ventilator. © 2018 Vyaire Medical, Inc. Used with permission.

FIGURE 4-47 The Operator Interface for the Vyaire LTV 1200. © 2018 Vyaire Medical, Inc. Used with permission.

Modes The ventilation modes available on the Vyaire LTV 1200 are classified and depicted in Table 4-45. TABLE 4-45 Ventilation Modes Available on the Vyaire LTV 1200

Description

Volume A/C Volume A/C is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.28 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT)

has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.28

Volume SIMV Volume SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.28 Thus, mandatory, time-triggered breaths, patientassisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Flow SIMV rate Pressure-support level Cycle sensitivity for the PS breaths During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.28 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.28

Pressure A/C Pressure A/C is a pressure-targeted mode of ventilation that allows for mandatory,

time-triggered breaths or patient-assisted breaths.28 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.28

Pressure SIMV Pressure SIMV is similar to volume SIMV described above except that the target is now pressure instead of volume.28 Pressure SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity for the PS breaths During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.28

During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.28

CPAP/Pressure Support During CPAP/pressure support the patient regulates the respiratory rate and the VT with support from the ventilator.28 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.28 If the PS level is set to 0, all breaths will be unsupported.

Noninvasive Positive Pressure Ventilation NPPV is PS (see above) delivered through a mask instead of an endotracheal tube.28 During NPPV the patient regulates the respiratory rate and the VT with support from the ventilator. The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.28 If the PS level is set to 0, all breaths will be

unsupported

Special Features Special features of the LTV1200 includes its oxygen system, apnea backup ventilation, and ability to allow for spontaneous breathing trials.

Apnea Backup Ventilation The ventilator engages apnea backup ventilation when no breath has been delivered by the time the clinician-selected apnea interval elapses.28 Backup ventilation will occur in the assist/control mode related to the current settings (Table 4-45).

Oxygen When the ventilator is attached to a high-pressure oxygen source of 40 psi to 80 psi, the percentage of oxygen to be delivered through the ventilator’s oxygen blending system can be set directly.28 When the O2% control is set to low-pressure source (LPS), oxygen can be supplied from a low-pressure, low-flow oxygen source of < 35 psi such as a flow meter. Oxygen from the low-pressure source is mixed with air inside the ventilator. When connected to a low-pressure source, the estimated O2 percent delivered to the patient is determined by the O2 inlet flow and the minute volume and is not regulated by the ventilator. A separate chart is provide to help estimate the delivered FIO2.

Spontaneous Breathing Trial During a spontaneous breathing trial various parameters can be displayed.28 These include SBT f/VT, SBT respiratory rate, SBT VT, and SBT time remaining.

Other Leak compensation is not available in the LTV 1200.28

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Vyaire LTV 1200 are listed in Table 4-46.

TABLE 4-46 Manufacturer’s Specifications for the Vyaire LTV 1200 Setting

Range

Pressure Inspiratory pressure

1 to 99 cm H2O

Pressure support

1 to 60 cm H2O

PEEP

0 to 20 cm H2O

Volume Tidal volume

0.05 to 2.0 L

Flow Inspiratory flow

Not specified

Time Inspiratory time

0.3 to 9.9 seconds

Mandatory breath rate

1 to 80/min

Sensitivity Trigger

1 to 9 L/min (flow) – 3 cm H2O (backup pressure trigger)

Cycle

10% to 40% of peak flow

Alarms

Range

Pressure High pressure limit

5 to 100 cm H2O

High PEEP

3 to 20 cm H2O above set PEEP

Low peak pressure

1 to 60 cm H2O

Low PEEP

–3 to –20 cm H2O below set PEEP

Volume Low minute volume

0.1 to 99.9 L/min

Time High breath rate

5 to 80 breaths/min

Apnea time

10 to 60 seconds

Other SBT > f

15 to 80 bpm

SBT > f/VT

70 to 900 bpm/L

SBT < f

1 to 40 bpm

SBT < f/VT

5 to 90 bpm/L

SBThigh PEEP

3 to 40 cm H2O

SBTlow PEEP

1 to 20 cm H2O

Monitored Parameters Peak flow

Exhaled tidal volume

I:E ratio

Mean airway pressure

O2 cylinder duration

Peak inspiratory pressure

Peak inspiratory flow

Mean airway pressure (MAP)

PEEP

f/VT

Frequency (f)

SBT minutes

Total breath rate

Total minute ventilation

Dräger Carina The Dräger Carina ventilator is designed for treatment of subacute care patients in hospitals or medical rooms and can be used for transport and in the hospital setting.29 It is a lightweight ventilator (5.5 kg) that is pneumatically powered through blender technology and electrically driven. The Carina can deliver invasive or noninvasive ventilation and is pictured in Figure 4-48. The operator interface consists of an LCD screen with an array of buttons and a control knob.

FIGURE 4-48 The Dräger Carina Ventilator. Courtesy of Dräger.

Modes The ventilation modes available on the Dräger Carina are classified and depicted in Table 4-47. TABLE 4-47 Modes on the Dräger Carina

Description

Volume-Control Synchronized Intermittent Mandatory Ventilation with AutoFlow VC-SIMV with AutoFlow combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.29 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the

ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time or I:E Pressure-support level During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.29 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Pressure Control-A/C PC-A/C is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.29 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time or I:E RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.29

Pressure Control-Biphasic Positive Airway Pressure (PC-BiPAP) PC-BiPAP is a form of pressure SIMV that combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP.29 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. Spontaneous breathing is allowed throughout the entire breath cycle. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time or I:E SIMV rate Pressure-support level During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.29 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.

Spontaneous-Continuous Positive Airway Pressure/Pressure Support During SPN-CPAP/PS the patient regulates the respiratory rate and the VT with support from the ventilator.29 The patient triggers all of the breaths and will receive the clinician-set PS level. The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: PEEP FIO2 Pressure-support level The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.29

Spontaneous-Continuous Positive Airway Pressure In SPN-CPAP, the ventilator maintains a baseline pressure level (CPAP) and the patient breaths spontaneously.29 The patient receives no additional support from the

ventilator. Main operator controls include: FIO2 CPAP The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequences to make the calculation.29 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Spontaneous-Continuous Positive Airway Pressure/Pressure Support with Volume Guarantee In SPN-CPAP/PS with volume guarantee the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.29 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. Main operator controls include: FIO2 PEEP VT target The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequences to make the calculation.29 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Special Features Special features of the Dräger Carina include backup ventilation, noninvasive ventilation, and its oxygen system.

Backup Ventilation Available in SPN-CPAP, SPN-CPAP/PS, and SPN-CPAP/PS with volume guarantee.29 The ventilator will deliver VC-SIMV with AutoFlow breaths.

Oxygen Oxygen levels of 21% to 100% are delivered when supplied with a high pressure of 40 to 87 psi.29 Low-pressure (> 7 psi) oxygen delivery is also available. The delivered FIO2 will vary depending on the O2 inlet flow and the minute volume.

Noninvasive Ventilation NIV is available in all available modes.29 The ventilator will adjust the trigger level based on the leak when NIV is selected.

Other Nebulizer and neonatal ventilation are not available.29

Manufacturer’s Specifications, Controls, and Alarms The manufacturer’s specifications, controls, and alarms for the Dräger Carina are listed in Table 4-48. TABLE 4-48 Manufacturer’s Specifications for the Dräger Carina Setting

Range

Pressure Inspiratory pressure

5 to 50 cm H2O

Pressure support

0 to 47 cm H2O

PEEP

3 to 20 cm H2O

Volume Tidal volume

0.1 to 2.0 L

Flow Inspiratory flow

Not specified

Time Inspiratory time

0.3 to 8 seconds

Mandatory breath rate

5 to 50/min

Sensitivity Trigger

Multisense trigger: off, normal, or sensitive

Alarms

Range

Pressure High airway pressure

10 to 55 cm H2O

Volume Inspiratory minute volume high

2 to 60 L/min

Inspiratory minute volume low

0.1 to 39 L/min

Time Tachypnea monitoring (RRhigh)

10 to 74 breaths/min

Apnea alarm time

5 to 60 seconds

Dräger Oxylog 3000 Plus The Dräger Oxylog 3000 plus is a time-cycled, volume-controlled, and pressurecontrolled emergency and transport ventilator for patients requiring mandatory or assisted ventilation with a tidal volume from 50 mL upwards.30 The Oxylog 3000 plus can deliver invasive or noninvasive ventilation and is pictured in Figure 4-49. The operator interface consists of an LCD screen with an array of buttons and a control knob. The operator interface is pictured in Figure 4-50.

FIGURE 4-49 The Dräger Oxylog 3000 Plus Ventilator. Courtesy of Dräger.

FIGURE 4-50 The Dräger Oxylog 3000 Plus Operator Interface. Courtesy of Dräger.

Modes The ventilation modes available on the Dräger Oxylog 3000 plus are classified and depicted in Table 4-49. TABLE 4-49 Modes Available on the Dräger Oxylog 3000 Plus

Description

Volume Control–Continuous Mandatory Ventilation VC-CMV is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths only.30 Patient-assisted breaths and spontaneous breathing are not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: PEEP FIO2 VT Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.30

Volume Control-A/C VC-A/C is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.30 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: PEEP FIO2 VT Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.30

Volume Control-Synchronized Intermittent Mandatory Ventilation

VC-SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.30 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: PEEP FIO2 VT Flow SIMV rate Inspiratory time Pressure-support level Cycle sensitivity for the PS breaths During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.30 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.30

Volume Control-Continuous Mandatory Ventilation with AutoFlow VC-CMV with AutoFlow is a pressure-targeted (PC breaths) mode that uses the pressure breaths to achieve a clinician-set VT.30 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. This mode delivers mandatory, time-triggered breaths only. There are no spontaneous breaths allowed. VC-CMV is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths only. Patient-assisted breaths and spontaneous breathing are not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered.

Main operator controls include: PEEP FIO2 VT target Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.30

Volume Control-A/C with AutoFlow VC-A/C with AutoFlow is a pressure-targeted (either PC or PA breaths) mode that uses the pressure breaths to achieve a clinician-set VT.30 The inspiratory pressure level, however, is now adjusted by the ventilator instead of the clinician. Since the ventilator relies on a previous breath sequence to deliver the ensuing breath, the VT tends to be somewhat variable, especially in patients with inconsistent efforts. There are no spontaneous breaths allowed. Main operator controls include: FIO2 PEEP RR VT target Inspiratory time The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.30

Volume Control-Synchronized Intermittent Mandatory Ventilation with AutoFlow VC-SIMV with AutoFlow combines two breath types, PAC (ventilator-controlled inspiratory pressure) and either PS or spontaneous breathing, while on CPAP.30 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath)

through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP SIMV rate VT Inspiratory time Pressure-support level During the control breath the amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system mechanics.30 During the PS breath flow, the VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics. If CPAP is used, the spontaneous breath VT will be variable and depend on patient effort and patient respiratory system mechanics.

Pressure Control-Biphasic Positive Airway Pressure (PC-BiPAP) PC-BiPAP is a form of pressure SIMV that combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP.30 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. Spontaneous breathing is allowed throughout the entire breath cycle. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.30 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.30

Spontaneous-Continuous Positive Pressure (SPN-CPAP) During SPN-CPAP the patient regulates the respiratory rate and the VT with support from the ventilator.30 The patient triggers all of the breaths and will receive the clinician-set PS level or no additional support (CPAP). If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: PEEP FIO2 Pressure-support level The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.30 If the PS level is set to 0, all breaths will be unsupported.

Special Features Special features of the Oxylog 3000plus include noninvasive ventilation, backup ventilation, its oxygen system, and optional CO2 sensor.

Backup Ventilation Backup ventilation is available in SPN-CPAP only.30 The ventilator will deliver VCCMV breaths.

Oxygen 40% to 100% is supplied with a high pressure of 39 to 87 psi through either a medical pipeline system or portable oxygen tank.30 The actual FIO2 may vary somewhat depending on the inspiratory flow rate and mean airway pressure.

Noninvasive Ventilation NIV is available in SPN-CPAP (PS), PC-BiPAP VC-CMV/AF, VC-A/C/AF, and VCSIMV/AF.30 The ventilator will compensate for inherent leaks and the leakage alarm will be deactivated.

Other

An optional CO2 sensor is available to allow for the measurement of exhaled CO2.30 Nebulizer and neonatal ventilation are not available.30 Previous versions of this ventilator include the Oxylog 3000, Oxylog 2000 plus, and the Oxylog 1000.30 An Internal battery will operate for approximately 7.5 to 9.5 hours (depending on the parameter settings) on full charge.30

Manufacturer’s Specifications, Controls, and Alarms The manufacturer’s specifications, controls, and alarms for the Dräger Oxylog 3000 plus are listed in Table 4-50. TABLE 4-50 Manufacturer’s Specifications for the Dräger Oxylog 3000 Plus Setting

Range

Pressure Inspiratory pressure

PEEP +3 to 55 cm H2O

Pressure support

0 to 35 cm H2O

PEEP

0 to 20 cm H2O

Volume Tidal volume

0.05 to 2.0 L

Flow Maximal inspiratory flow

100 L/min @ supply pressures > 51 psi 80 L/min @ supply pressures < 51 psi 39 L/min @ supply pressures < 39 psi

Time Inspiratory time

0.2 to 10 seconds

Mandatory breath rate

2 to 60 bpm

Sensitivity Trigger

1 to 15 L/min (flow)

Alarms

Range

Pressure High airway pressure

20 to 60 cm H2O

Low airway pressure

When pressure difference between inspiration and expiration < 5

cm H2O or when the set pressure level is not reached Volume Inspiratory minute volume high

2 to 41 L/min

Inspiratory minute volume low

0.5 to 40 L/min

Time High respiratory rate

10 to 100 breaths/min

Apnea alarm time

15 to 60 seconds

Medtronic Newport HT70 Plus The Medtronic Newport HT70 plus ventilator is designed to provide ventilatory support for infant, pediatric, and adult patients in emergency care, transport, critical care, subacute care, home care, and emergency preparedness applications.31 It is electronically controlled and functions with a twin micro-piston pump to power the pneumatic system and has servo-controlled, leak-compensated PEEP. The HT70 may be used with an endotracheal tube, tracheal tube, facemask, nasal mask or prongs, or a mouthpiece. The HT70 plus is pictured in Figure 4-51. The operator interface uses a color-coded LCD touch screen featuring an array of buttons along with a display screen. Settings are entered by selecting a parameter and then adjusting the value using the up/down arrow buttons. The interface is pictured in Figure 4-52.

FIGURE 4-51 The Medtronic Newport HT70 Plus Ventilator. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

FIGURE 4-52 Medtronic Newport HT70 Plus Operator Interface. © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

Modes The ventilation modes available on the Medtronic Newport HT70 plus are classified

and depicted in Table 4-51. TABLE 4-51 Modes Available on the Medtronic Newport HT70 Plus Ventilator

Description

Assist/Control Mandatory Ventilation Volume Control A/C MV VC is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.31 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory flow Inspiratory time (Tinsp) RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.31

Synchronized Intermittent Mandatory Ventilation/ Volume Control SIMV/VC combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.31 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory flow Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on

VT, flow, and patient mechanics.31 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.31

Assist/Control Mandatory Ventilation Pressure Control A/C MV PC is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.31 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.31

Synchronized Intermittent Mandatory Ventilation/Pressure Control SIMV PC is similar to SIMVVC described above except that the target is now pressure instead of volume.31 SIMV PC also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level

Inspiratory time SIMV rate Pressure-support level Cycle sensitivity for the PS breaths During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.31 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.31

Spontaneous Ventilation (SPONT Mode) During SPONT mode the patient regulates the respiratory rate and the VT.31 The patient triggers all of the breaths and will receive either CPAP or a clinician-set PS level. If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.31 If the PS level is set to 0, all breaths will be unsupported.

Special Features Special features of the Newton HT 70 include noninvasive ventilation, backup ventilation, battery backup, and its oxygen system.

Backup Ventilation Backup ventilation occurs when either the low minute volume (MVI/MVE), the apnea alarm, or both are activated.31 It is available in all of the ventilator modes. If the current mode is A/C MV or SIMV, the current settings are used with a respiratory rate of 1.5 times the current setting. If the current mode is SPONT mode, the ventilator

delivers SIMV/PC breaths at a RR of 15, inspiratory pressure 15 cm H2O above set PEEP, and a 1.0 second inspiratory time.

Oxygen The HT70 plus can use a 35 to 65 psig source and can deliver an FIO2 from 0.21 to 1.0.31

Battery Backup The internal dual battery system consists of two internal independent but coordinated lithium ion batteries, one located on the back of the ventilator and the secondary backup battery inside the ventilator.31 The internal dual battery system can provide up to 10 hours of operation at standard settings when new and fully charged.

NIV The HT70 plus can be used for noninvasive ventilation in all modes.31 It is activated switching the NIV toggle switch to on. When NIV is activated the bias flow is increased to 10 L/min (and can be adjusted from 3-30 L/min), the low minute volume alarm can be turned off, the low-pressure alarm can be set closer to the base pressure (1 cm H2O above baseline), and the high minute volume alarm range is expanded to 80 L/min.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Medtronic Newport HT70 plus are listed in Table 4-52. TABLE 4-52 Manufacturer’s Specifications for the Medtronic Newport HT70 Plus Setting

Range

Pressure Inspiratory pressure

5 to 60 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 30 cm H2O

Volume Tidal volume

0.05 to 2.2 L

Flow Inspiratory flow

6 to 100 L/min

Time Inspiratory time

0.1 to 3 seconds

Respiratory rate

1 to 99/min

Sensitivity Trigger

–9.9 to 0 cm H2O below PEEP (pressure) 0.1 L/min to 10 L/min (flow)

Cycle

5% to 85% of peak flow

Alarms

Range

Pressure High pressure

4 to 99 cm H2O

Low pressure

3 to 98 cm H2O

Volume High exhaled minute volume

1.1 to 50 L/min

Low exhaled minute volume

0.01 to 49 L/min

Time High respiratory rate

Off or 30 to 100 breaths/min

Apnea time

5 to 60 seconds

Other O2 sensor

Enabled/disabled

Cylinder usage time Battery life Monitored Parameters Minute volume

Insp/exp VT

RR total

PPeak

PMean

PBase (PEEP)

(Peak) flow

O2 cylinder time

Battery time

O2 percent (optional)

I:E ratio

ZOLL Eagle II The ZOLL Eagle II ventilator is a full-feature, portable, mechanical ventilator designed to operate in hospitals, during transport, and in severe environments, where it may be exposed to rain, dust, rough handling, and extremes in temperature and humidity (Figure 4-53).32 With an appropriate third-party filter in place, the ventilator may be operated in environments where chemical and/or biological toxins are present. When marked with an “MRI conditional” label, they are suitable for use in an MRI environment with appropriate precautions. The Eagle II is a volume and pressure-targeted, time- or flow-cycled ventilator designed to use either oxygen from a 55 psig source or fresh air using its internal compressor to deliver a positivepressure breath. When the FIO2 is set to 21%, clinicians can connect a low-flow oxygen source at the Fresh Gas/Emergency Air Intake using a reservoir. The operator interface (Figure 4-54) consists of a liquid crystal display (LCD), which provides continuous display of control settings, operating conditions, power, and alarm status information. Most unit functions are controlled by pressing the parameter button associated with the parameter you wish to change. Pressing the parameter button highlights the primary parameter; additional presses highlight secondary parameters moving in a clockwise direction. When the parameter you wish to change is highlighted, a knob called the rotary encoder is used to adjust the parameter to the desired setting, and then it is confirmed by pressing the confirm/select button.

FIGURE 4-53 The ZOLL Eagle II Ventilator. Courtesy of ZOLL.

FIGURE 4-54 The Operator Interface for the ZOLL Eagle II. Courtesy of ZOLL.

Modes The different modes available on the ZOLL Eagle II are classified and depicted on Table 4-53.

TABLE 4-53 Ventilation Modes Available on the ZOLL Eagle II

Assist/Control Volume Target A/C volume target is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.32 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Inspiratory flow is preset to be a square waveform. Main operator controls include: FIO2 PEEP VT

I:E or inspiratory time RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.32

Synchronized Intermittent Mandatory Ventilation Volume Target SIMV volume target combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.32 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Inspiratory flow is preset to be a square waveform. Main operator controls include: FIO2 PEEP VT I:E or inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.32 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.32

Assist/Control Pressure Target A/C pressure target is a pressure-targeted mode of ventilation that allows for mandatory, time-triggered breaths or patient-assisted breaths.32 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include:

FIO2 PEEP Inspiratory pressure level I:E or inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.32

Synchronized Intermittent Mandatory Ventilation Pressure Target SIMV pressure target is similar to SIMV volume target described above except that the target is now pressure instead of volume.32 SIMV pressure target also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level I:E or inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.32 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.32

Continuous Positive Airway Pressure During CPAP the patient regulates the respiratory rate and the VT with support from

the ventilator.32 The patient triggers all of the breaths and will receive either a purely spontaneous breath (demand flow only available) or the clinician-set PS. If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: FIO2 PEEP Pressure-support level Cycle sensitivity

Noninvasive Positive-Pressure Ventilation (NPPV) NPPV provides flow during the expiratory phase to maintain the baseline pressure (CPAP) in spontaneously breathing patients with a leaking airway or facemask.32 The amount of leak compensation depends on the leak flow rate during the expiratory period and ranges from 0 to 15 L/min and is automatically adjusted by the ventilator in order to maintain the CPAP target. NPPV/CPAP/PS is CPAP/PS (see above) delivered through a mask instead of an endotracheal tube. During NPPV, the patient regulates the respiratory rate and the VT. Main operator controls include: FIO2 CPAP The VT will be variable and depend on patient effort and patient respiratory system mechanics.32

Special Features Special features of the ZOLL Eagle II include its oxygen system, backup ventilation, and optional pulse oximeter.

Oxygen The unit can use oxygen from low-flow sources, oxygen flow meters, and oxygen concentrators to provide supplemental oxygen to patients.32 To do this, oxygen is delivered through the Fresh Gas/Emergency Air Intake when the unit’s internal compressor cycles to deliver a breath.

Backup Ventilation Depending upon the preexisting conditions at the time of failure, the backup ventilator will begin operation in one of two ways: (1) if no preexisting alarm condition(s) exists, backup operation will continue using the current settings; (2) if a preexisting alarm condition(s) exists, backup operation will revert to the startup default settings (Mode A/C [P], volume target, BPM 12, PIP 20 cm H2O, FIO2 21%, PEEP 5 cm H2O, I:E 1:2.5, and PIP high limit 35 cm H2O).32

Other An optional pulse oximeter can be used.32

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the ZOLL Eagle II are listed in Table 4-54. TABLE 4-54 Manufacturer’s Specifications for the ZOLL Eagle II Setting

Range

Pressure Peak inspiratory pressure

10 to 80 cm H2O

Pressure support

0 to 60 cm H2O

PEEP

0 to 25 cm H2O

Volume Tidal volume

0.05 to 1.5 L

Flow Inspiratory flow

0 to 100 L/min

Time Inspiratory time

0.3 to 3 seconds

Breath rate

1 to 60/min

Sensitivity

Trigger

–6 to –0.5 cm H2O (pressure)

Cycle

10% to 70% of peak flow

Alarms

Range

Pressure High pressure

20 to 100 cm H2O

Low pressure

0 to 35 cm H2O

Monitored Parameters Peak inspiratory pressure

Tidal volume (VT del)

Respiratory rate (BPM)

FIO2

Spo2

Inspiratory time (TI)

Mean airway pressure (MAP)

Minute volume (Vmin)

Philips Respironics Trilogy Ventilator The Respironics Trilogy 202 system provides continuous or intermittent ventilatory support for the care of individuals who require mechanical ventilation with or without FIO2 blending.33 It is pictured in Figure 4-55 and intended for pediatric through adult patients weighing at least 5 kg. The ventilator is meant to be used in hospitals and institutions, and for portable applications such as wheelchairs and gurneys only when in an institutional setting. It may be used for both invasive and noninvasive ventilation. It is not intended to be used as a transport ventilator. The Trilogy 202 can be used with either a single-limb or double-limb circuit. The operator interface consists of a central screen with some buttons to make parameter and setting adjustments and is depicted in Figure 4-56.

FIGURE 4-55 The Philips Respironics Trilogy Ventilator. Courtesy of Philips Respironics.

FIGURE 4-56 The Philips Respironics Trilogy Operator Interface. Courtesy of Philips Respironics.

Modes The ventilation modes available on the Trilogy 202 are classified and depicted in Table 4-55. TABLE 4-55 Philips Respironics Trilogy Modes of Ventilation

Description

Control Ventilation (CV)

CV is a volume-targeted mode of ventilation (VAC) that allows for mandatory, timetriggered breaths only.33 Patient-triggered breaths and spontaneous breathing are not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory time RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.33

Assist/Control Assist/control (A/C) is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths only or patient-assisted breaths.33 The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: FIO2 PEEP VT Inspiratory time RR The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.33

Synchronized Intermittent Mandatory Ventilation SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.33 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window,

then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP VT Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.33 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.33

Pressure Control PC is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.33 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: FIO2 EPAP (expiratory positive airway pressure) IPAP (inspiratory positive airway pressure) Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.33

Pressure Control-Synchronized Intermittent Mandatory Ventilation PC-SIMV is similar to SIMV described above except that the target is now pressure instead of volume.33 PC-SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. In the

same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time RR Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.33 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.33

Continuous Positive Airway Pressure In CPAP mode, the ventilator functions as a demand flow system, with the patient triggering all breaths and determining their timing, pressure, and size.33 Main operator controls include: FIO2 CPAP level The VT will be variable and depend on patient effort, and patient respiratory system mechanics.33

Spontaneous Mode Spontaneous mode delivers pressure-targeted breaths that are patient triggered and flow cycled.33 Main operator controls include: FIO2

IPAP EPAP Flow (expiratory) sensitivity The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.33

Spontaneous/Timed The S/T mode delivers pressure-controlled, time-cycled mandatory and pressuresupported spontaneous breaths.33 If the patient fails to trigger a breath within the interval determined by the rate setting, the ventilator triggers a mandatory breath with the set inspiratory time. Main operator controls include: FIO2 EPAP IPAP Inspiratory time RR The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.33

Timed (T Mode) The T mode delivers pressure-controlled, time-cycled mandatory breaths only.33 Patient-triggered and spontaneous breaths are not allowed. Main operator controls include: FIO2 EPAP IPAP Inspiratory time RR The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.33

Average Volume-Assured Pressure Support (AVAPS)

The AVAPS mode delivers PAC mandatory breaths (S/T, PC, and T modes) and pressure-supported spontaneous breaths (S/T, S modes).33 If the patient does not trigger a breath within the interval determined by the rate control, the ventilator delivers a PAC breath with the set inspiratory time. If the patient triggers a breath within the interval the ventilator delivers a PS breath. The PAC and PS inspiratory pressure levels are continually adjusted over a period of time to achieve the volume target. It is only available in the S, S/T, PC, and T modes and can be manually turned on and off. Main operator controls include: FIO2 EPAP VT target Inspiratory time RR Max P Min P The VT may not match the operator setting due to the fact that the ventilator is using PAC PS to target the VT as opposed to VAC and relies on the previous breath sequences to make the calculation.33 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Special Features Philips Respironics Trilogy special features include backup ventilation, leak compensation, and Auto-Trak sensitivity.

Apnea Backup Ventilation Apnea ventilation can be turned on or off with a time frame of 10 to 60 seconds and a breath rate of 4 to 60.33

Leak Compensation Leak compensation is available in the “passive” configuration in the following modes: CPAP, S, S/T, PC, PC-SIMV, A/C, and SIMV.33 When using the “active flow,” the circuit flow trigger with leak compensation can be enabled (default setting). The

clinician has the option of disabling the leak compensation; however, unintentional leaks will then not be compensated for.

Neonatal Ventilation Neonatal ventilation is not available.33

Auto-Trak Sensitivity With Auto-Trak sensitivity, the Trilogy 202 automatically adjust its triggering and cycling algorithms to maintain optimum performance in the presence of leaks.33 It is only available with the “passive” circuit configuration.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Philips Trilogy 202 are listed in Table 4-56. TABLE 4-56 Manufacturer’s Specifications for the Philips Respironics Trilogy Setting

Range

Pressure Inspiratory pressure (IPAP)

4 to 50 cm H2O

Pressure support

0 to 30 cm H2O

PEEP (EPAP)

0 to 25 cm H2O

Volume Tidal volume

0.05 to 2.0 L

Time Inspiratory time

0.3 to 5 seconds

Mandatory breath rate

0 to 60/min

Sensitivity Trigger

1 to 9 L/min

Cycle

10% to 90%

Alarms

Range

Volume High tidal volume

0.05 to 2.0 L

Low tidal volume

0.05 to 2.0 L

High minute volume

1 to 99 L/m

Low exhaled minute volume

1 to 99 L/min

Time High respiratory rate

4 to 80 breaths/min

Low respiratory rate

4 to 80 breaths/min

Circuit disconnect

10 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters VT

Minute ventilation

Estimated leak rate

RR

Peak inspiratory flow

Peak inspiratory pressure

Mean airway pressure

% patient triggered breaths

I:E ratio

DeVilbiss IntelliPAP Bilevel S The DeVilbiss IntelliPAP Bilevel S is intended for use in treating obstructive sleep apnea (OSA) in spontaneously breathing patients 30 kg (66 lbs) and above by means of application of positive air pressure.34 The device has automatic leak compensation and is intended to be used in home and clinical environments. It is pictured in Figure 4-57.

FIGURE 4-57 DeVilbiss IntelliPAP Bilevel S. Medical Depot, Inc. Courtesy of Medical Depot, Inc.

Modes The ventilation modes available on the DeVilbiss IntelliPAP Bilevel S are classified and depicted in Table 4-57. TABLE 4-57 Modes Available on the DeVilbiss IntelliPAP Bilevel S

Description

Continuous Positive Airway Pressure CPAP is a pressure-targeted mode of ventilation that allows for spontaneous breathing from a fixed pressure baseline.34 No additional support is provided during inspiration. Main operator controls include: CPAP The ventilator provides a baseline pressure and the patient breaths spontaneously from that baseline; VT and flow are variable and will depend on patient effort and patient respiratory system mechanics.34

Bilevel The bilevel mode is a pressure-targeted mode that delivers patient-triggered pressure-assist breaths.34 Main operator controls include: IPAP EPAP VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.34

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms

The manufacturer’s specifications, controls, monitored parameters, and alarms for the DeVilbiss IntelliPAP Bilevel S are listed in Table 4-58. TABLE 4-58 Manufacturer’s Specifications for the DeVilBiss IntelliPAP Bilevel S Setting

Range

Pressure Inspiratory pressure

3 to 25 cm H2O

Expiratory pressure

3 to 25 cm H2O

Time Inspiratory time

N/A

RR

N/A

Sensitivity Inspiratory

1 to 10, increments of 1

Expiratory

1 to 10, increments of 1

Monitored Parameters Inspiratory pressure

Expiratory pressure

DeVilbiss IntelliPAP AutoBilevel The DeVilbiss IntelliPAP AutoBilevel is intended for use in treating OSA in spontaneously breathing patients 30 kg (66 lbs) and above by means of application of positive air pressure.35 The device has automatic leak compensation and is intended to be used in home and clinical environments. It is pictured in Figure 4-58. AutoBilevel is typically used for OSA patients with higher prescribed pressures. During AutoBilevel mode, the ventilator automatically increases IPAP in response to clinical events such as hypopnea, apnea, and snoring. The EPAP level stays below the IPAP level by a constant amount.

FIGURE 4-58 The DeVilbiss IntelliPAP AutoBilevel Ventilator. Medical Depot, Inc.

Modes The ventilation modes available on the DeVilbiss IntelliPAP Bilevel S are classified and depicted in Table 4-59. TABLE 4-59 Modes Available on the DeVilbiss IntelliPAP AutoBilevel

Description

Continuous Positive Airway Pressure CPAP is a pressure-targeted mode of ventilation that allows for spontaneous breathing from a fixed pressure baseline.35 No additional support is provided during inspiration. Main operator controls include: CPAP The ventilator provides a baseline pressure and the patient breaths spontaneously from that baseline; VT and flow are variable and will depend on patient effort and patient respiratory system mechanics.35

Bilevel The bilevel mode is a pressure-targeted mode that delivers patient-triggered pressure-assist breaths.35 Main operator controls include: IPAP EPAP VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.35

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms

The manufacturer’s specifications, controls, monitored parameters, and alarms for the DeVilbiss IntelliPAP AutoBilevel are listed in Table 4-60. TABLE 4-60 Manufacturer’s Specifications for the DeVilBiss IntelliPAP AutoBilevel Setting

Range

Pressure Inspiratory pressure

3 to 25 cm H2O

Expiratory pressure

3 to 25 cm H2O

Time Inspiratory time

N/A

RR

N/A

Sensitivity Inspiratory

1 to 10, increments of 1

Expiratory

1 to 10, increments of 1

Monitored Parameters Inspiratory pressure

Expiratory pressure

ResMed Lumis Tx The Lumis Tx (Figure 4-59) is a hospital ventilator designed for patients with sleepdisordered breathing, central breathing disorders, and respiratory insufficiency.36 It is suitable for a variety of hospital environments.

FIGURE 4-59 The ResMed Lumis Tx Ventilator. © ResMed Limited. All rights reserved.

Modes The ventilation modes available on the ResMed Lumis Tx are classified and depicted in Table 4-61. TABLE 4-61 Ventilation Modes Available on the ResMed Lumis Tx

Description

CPAP Mode In CPAP mode, the Lumis delivers a constant baseline level of pressure during inspiration and expiration.36 The patient receives no additional inspiratory pressure during inspiration. Main operator controls include: Set pressure (CPAP) The VT will be variable and depend on patient effort and patient respiratory system mechanics.36

Adaptive Support Ventilation ASV is a pressure-targeted mode in which the ventilator automatically adjusts the pressure-support level to meet a target minute ventilation.36 This mode is designed to consist of solely patient-initiated breaths, but a timed backup mandatory rate does exist that automatically calculates the required breath rate to meet the target minute ventilation. Main operator controls include: EPAP Max PS Min PS VT and flow are variable and will depend on the delivered inspiratory pressure level, patient effort, and patient respiratory system mechanics.36

ASVAuto Mode In addition to the functionality of the ASV mode, the ASVAuto mode automatically adjusts the expiratory pressure in order to provide only the amount of EPAP required to maintain upper airway patency.36 This mode is designed to consist of solely patient-initiated breaths but there does exist a timed backup mandatory rate that automatically calculates the required breath rate to meet the target minute ventilation. Main operator controls include: Max EPAP Min EPAP Max PS Min PS VT and flow are variable and will depend on the delivered inspiratory pressure level, patient effort, and patient respiratory system mechanics.36

Pressure A/C (PAC) PAC is a pressure-targeted mode of ventilation mode that delivers pressurecontrolled breaths.36 Inspiration is initiated either by the ventilator at a set rate (timetriggered breath) or by the patient (spontaneous-triggered breath). The ventilator

cycles to expiration when the inspiratory time has been reached. Main operator controls include: IPAP EPAP Inspiratory time RR The VT will be variable and depend on the IPAP, patient effort, and patient respiratory system mechanics.36

Spontaneous Mode Spontaneous mode is a bilevel pressure ventilation mode delivering pressuresupported spontaneous breaths.36 Inspiration is initiated only by the patient (spontaneous-triggered breath). The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: EPAP IPAP Cycle sensitivity The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.36

Spontaneous/Timed (S/T) Mode S/T mode is a bilevel pressure ventilation mode delivering pressure-supported spontaneous breaths.36 Inspiration is initiated either by the ventilator at a set rate (time-triggered breath) or by the patient (spontaneous-triggered breath). The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: EPAP IPAP RR Cycle sensitivity

The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.36

Timed (T) Mode T mode is a bilevel pressure ventilation mode delivering pressure-targeted breaths.36 Inspiration is initiated only by the ventilator at a set rate (time-triggered breath). Spontaneous breathing is not allowed. The breath cycles to expiration when the inspiratory time has been reached. Main operator controls include: EPAP IPAP RR Inspiratory time The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.36

Intelligent Volume-Assured Pressure Support (iVAPS) In iVAPS, the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set target alveolar ventilation. Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. iVAPS also has a backup rate, if needed. Main operator controls include: Target VA (L/min) Target patient rate Patient height EPAP Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for

the ResMed Lumis Tx are listed in Table 4-62. TABLE 4-62 Manufacturer’s Specifications for the ResMed Lumis Tx Setting

Range

Pressure Set pressure

4 to 20 cm H2O

IPAP

4 to 30 cm H2O

EPAP

3 to 25 cm H2O

Pressure support

0 to 10 cm H2O

Volume Target alveolar ventilation

1 to 30 L/min

Time Inspiratory time

0.3 to 4 seconds

Respiratory rate

5 to 50 breaths/min

Sensitivity Trigger

Very low to very high (flow)

Alarms

Range

Volume Low minute volume

1 to 10 L/min

Leak High leak

On/off

Time Apnea alarm

10 to 60 seconds

Monitored Parameters Leak

Minute ventilation

Target minute ventilation

Respiratory rate

Tidal volume

Pressure support

Alveolar minute ventilation

Target alveolar minute ventilation

Inspiratory time

I:E

% spontaneous triggering/cycling

ResMed Astral 100/150 The ResMed Astral 100/150 (Figure 4-60) provides continuous or intermittent ventilatory support for patients weighing more than 11 lb (5 kg) who require mechanical ventilation.37 The Astral is intended to be used in home, institution/hospital, and portable applications for both invasive and noninvasive ventilation. It is suitable for a variety of hospital environments.

FIGURE 4-60 The ResMed Astral 100/150 Ventilator. © ResMed Limited. All rights reserved.

Modes The ventilation modes available on the ResMed Astral are classified and depicted in Table 4-63.

TABLE 4-63 Ventilation Modes Available on the ResMed Astral

Description

(Assisted) Volume-Controlled Ventilation

(A)CV is a volume-targeted mode of ventilation (VAC) that allows for mandatory, time-triggered breaths or patient-assisted breaths.37 Spontaneous breathing is not allowed. The breath cycles to exhalation once the tidal volume (VT) has been delivered. Main operator controls include: PEEP VT Inspiratory flow RR Inspiratory time The resulting pressure created is variable and depends on VT, flow, and patient respiratory system mechanics.37

Volume-Synchronized Intermittent Mandatory Ventilation V-SIMV combines two breath types, VAC and either PS or spontaneous breathing, while on CPAP.37 Thus, mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths are all provided. The ventilator prevents “breath stacking” (a VAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a VAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: PEEP VT Flow SIMV rate Inspiratory time Pressure-support level Cycle sensitivity During the VAC breaths, the resulting pressure created is variable and depends on VT, flow, and patient mechanics.37 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.37

(Assisted) Pressure-Controlled Ventilation P(A)CV is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.37 Spontaneous breaths are not allowed. The breath cycles to exhalation once the inspiratory time has been reached. Main operator controls include: PEEP Inspiratory pressure level Inspiratory time RR The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.37

Pressure-Synchronized Intermittent Mandatory Ventilation P-SIMV is similar to V-SIMV described above except that the target is now pressure instead of volume.37 P-SIMV also combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP. There is a combination of mandatory, timetriggered breaths, patient-assisted breaths, and spontaneous breaths. In the same manner as discussed above, the ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Main operator controls include: PEEP Inspiratory pressure level Inspiratory time SIMV rate Pressure-support level Cycle sensitivity During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.37 During the PS breaths, the volume will be variable and depend on the PS level,

patient effort, and patient respiratory system mechanics.37

Pressure Support PS is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.37 The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: PEEP RR Pressure-support level Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.37

Continuous Positive Airway Pressure In CPAP, a baseline pressure is maintained by the ventilator and then receives no additional support during the spontaneous breaths.37 Other than the baseline pressure, the patient controls all other aspects of the breath. Main operator controls include: CPAP The VT will be variable and depend on patient effort and patient respiratory system mechanics.37

(Spontaneous) Timed (S/T) Mode (S)T is a bilevel pressure ventilation mode delivering pressure-supported spontaneous breaths.37 Inspiration is initiated either by the ventilator at a set rate (time-triggered breath) or by the patient (spontaneous-triggered breath). The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: EPAP

IPAP RR Cycle sensitivity The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.37

Pressure (Assist) Control P(A)C is a bilevel pressure ventilation mode delivering pressure-targeted breaths.37 Inspiration is initiated either by the ventilator at a set rate (time-triggered breath) or the patient. The breath cycles to expiration when the inspiratory time has been reached. Main operator controls include: EPAP IPAP RR Inspiratory time The VT will be variable and depend on the IPAP, EPAP, patient effort, and patient respiratory system mechanics.37

Intelligent Volume-Assured Pressure Support (iVAPS) In iVAPS, the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set target alveolar ventilation.37 Thus, the ventilator drops the level of support as patient effort increases and conversely increases the PS level when patient effort is too low. iVAPS also has a backup rate, if needed. Main operator controls include: Target VA (L/min) Target patient rate Patient height EPAP Cycle sensitivity The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.37

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the ResMed Astral are listed in Table 4-64. TABLE 4-64 Manufacturer’s Specifications for the ResMed Astral Setting

Range

Pressure Inspiratory pressure

2 to 50 cm H2O

Pressure support

2 to 50 cm H2O

PEEP

3 to 20 cm H2O

IPAP

4 to 50 cm H2O

EPAP

2 to 25 cm H2O

Volume Tidal volume

0.1 to 2.5 L

Flow Inspiratory flow

5 to 120 L/min

Time Inspiratory time

0.3 to 3 seconds

Mandatory breath rate

2 to 80/min

Sensitivity Trigger

0.5 L/min to 5 L/min (flow) Very low to very high (pressure)

Cycle

5% to 90%

Alarms

Range

Pressure High pressure

10 to 55 cm H2O

Low pressure

2 to 54 cm H2O

Low PEEP

Off/on

Volume High VT

0.06 to 3L

Low VT

0.05 to 2.99 L

High minute ventilation

0.6 to 60 L/min

Low minute ventilation

0.5 to 59.9 L/min

Time High respiratory rate

3 to 80 breaths/min

Low respiratory rate

2 to 79 breaths/min

Apnea time

5 to 60 seconds

Other Leak

5 to 80 L/min

High FIO2

19% to 100%

Low FIO2

18% to 99%

High Spo2

51% to 100%

Low Spo2

50% to 99%

Monitored Parameters FIO2

I:E

Leak

Minute volume

Exhaled minute volume

Inhaled minute volume

Pressure

PEEP

Mean pressure

% spont cycle

% spont trigger

Peak inspiratory flow

Peak inspiratory pressure

RR

RSBI

O2 saturation

Inspiratory time

Expiratory time

Alveolar minute ventilation

Exhaled VT

Inhaled VT

Average VT

Average VT/kg

Neonatal Ventilators Many modern critical care ventilators have neonatal ventilation capabilities. In addition, ventilators designed solely for neonatal applications are available, including the Dräger Babylog VN500, Smith’s Medical Pneupac babyPAC 100 and Vyaire Infant Flow SiPAP.

Dräger Babylog VN500 The Babylog VN500 ventilator (Figure 4-61) is intended for the ventilation of neonatal patients from 0.4 kg (0.88 lbs) up to 10 kg (22 lbs) and pediatric patients from 5 kg (11 lbs) up to 20 kg (44 lbs) bodyweight.38 The Babylog VN500 operator interface is depicted in Figure 4-62. It consists of a flat-panel touch screen, buttons, and a control dial to change and confirm settings. Settings are entered by pressing a button on the touch screen to select the parameter to be changed, then the control dial is turned to select the new value, and then the control dial is pressed to confirm.

FIGURE 4-61 The Dräger Babylog VN500 Ventilator.

Courtesy of Dräger.

FIGURE 4-62 Operator Interface for the Dräger Babylog VN500. Courtesy of Dräger.

Modes The ventilation modes available on the Dräger Babylog VN500 are classified and depicted in Table 4-65. TABLE 4-65 Modes Available on the Dräger Babylog VN500

Description

Pressure Control-Continuous Mandatory Ventilation (PC-CMV) PC-CMV is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths only (patient-assisted breaths are not allowed).38 Spontaneous breathing is, however, permitted during the entire respiratory cycle through an “open” system. The mandatory breaths cycle to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: FIO2 PEEP Inspiratory pressure level (Pinsp) Inspiratory time RR VT – if volume guarantee is switched on The pressure will be consistently delivered from breath to breath if the volume guarantee is switched off.38 VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics. If the volume guarantee is turned on, the VT will be consistent while Pinsp will vary to meet the VT target.

Pressure Control-A/C (PC-A/C) PC-A/C is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths or patient-assisted breaths.38 Spontaneous breathing can occur during the mandatory breaths. The breath cycles to exhalation once the inspiratory time has been reached or when the high-pressure alarm is tripped. Main operator controls include: PEEP Inspiratory pressure level (Pinsp) Inspiratory time RR VT – if volume guarantee is switched on The pressure will be consistently delivered from breath to breath if the volume

guarantee is switched off.38 VT and flow are variable, and that will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics. If the volume guarantee is turned on, the VT will be consistent while Pinsp will vary to meet the VT target.

Pressure Control-Synchronized Intermittent Mandatory Ventilation (PCSIMV) PC-SIMV is a pressure-targeted mode that combines two breath types, PAC and either PS or spontaneous breathing, while on CPAP.38 There is a combination of mandatory, time-triggered breaths, patient-assisted breaths, and spontaneous breaths. The ventilator prevents “breath stacking” (a PAC breath compounded by a PS breath) through the use of a “timing window.” If the patient attempts to trigger a breath in this timing window, then the ventilator will deliver a PAC breath. If the patient attempts to trigger a breath outside the window, then a spontaneous breath will occur. Spontaneous breathing is allowed throughout the entire respiratory cycle. Main operator controls include: FIO2 PEEP Inspiratory pressure level (Pinsp) Inspiratory time SIMV rate VT – if the volume guarantee is switched on Pressure-support level During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.38 If the volume guarantee is turned on, the VT will be consistent while Pinsp will vary to meet the VT target. During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.

Pressure Control-Pressure Support Ventilation (PC-PSV) PC-PSV is a pressure-targeted mode in which the patient triggers all the breaths and receives the set pressure.38 The breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow.

Main operator controls include: FIO2 PEEP Maximum inspiratory time Pressure-support level VT – if the volume guarantee is switched on The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.38 If the volume guarantee is turned on, the VT will be consistent while Pinsp will vary to meet the VT target.

Pressure Control-Mandatory Minute Volume Ventilation (PC-MMV) PC-MMV is a pressure-targeted mode that guarantees that the patient receives a set VT during the mandatory breaths and at least the set minute volume MV.38 The patient can always breathe spontaneously at PEEP level (with or without pressure support). If the spontaneous breathing of the patient is insufficient to achieve the set minute ventilation, mandatory breaths are applied. These mandatory breaths are synchronized with the patient’s own breathing attempts. Main operator controls include: FIO2 PEEP VT RR Inspiratory time Pressure-support level The mandatory breaths should produce a consistent VT while Pinsp varies.38 During the PS breaths, the volume will be variable and depend on the PS level, patient effort, and patient respiratory system.

Pressure Control-Airway Pressure-Release Ventilation PC-APRV is a mode of ventilation that allows for spontaneous breathing at two different clinician-set pressure levels.38 The ventilator switches between two different clinician-set pressure levels (the lower of which can be CPAP). These pressure levels are referred to as Phigh and Plow. Thigh is the length of time at Phigh and Tlow is the

length of time spent at Plow. PC-APRV is mainly used in an inverse I:E ratio. An important difference from the previously described pressure-targeted modes is that the Phigh level is now referenced to atmosphere as opposed to the Plow. This is important because increases in Plow will decrease the distending pressure. Main operator controls include: PEEP FIO2 Phigh Plow Thigh Tlow The VT will be variable and depend on the Phigh, Plow, patient effort, and patient respiratory system mechanics.38

Spontaneous-Continuous Positive Pressure/Pressure Support During SPN-CPAP/PS the patient regulates the respiratory rate and the VT with support from the ventilator.38 The patient triggers all of the breaths and will receive the clinician-set PS level. If a pressure-support level > 0 cm H2O is set, the breath cycles to expiration when the inspiratory flow decreases below a preset percentage of the inspiratory peak flow. Main operator controls include: PEEP FIO2 Pressure-support level The VT will be variable and depend on the PS level, patient effort, and patient respiratory system mechanics.38 If the PS level is set to 0, all breaths will be unsupported.

Spontaneous-Continuous Positive Airway Pressure/Volume Support In SPN-CPAP/VS the ventilator delivers a variable (from breath to breath) PS level in order to reach a clinician-set VT.38 The ventilator changes the PS level as needed to reach the VT. Thus, the ventilator drops the level of support as patient effort

increases and conversely increases the PS level when patient effort is too low. Main operator controls include: PEEP FIO2 VT target The VT may not match the operator setting due to the fact that the ventilator is using PS to target the VT as opposed to VAC and relies on the previous breath sequences to make the calculation.38 Any change in patient effort from the previous breath may result in a deviation from the VT setting.

Spontaneous-Continuous Positive Airway Pressure SPN-CPAP is only available in NIV and is designed only for the neonatal population.38 During SPN-CPAP the patient regulates the respiratory rate and the VT with support from the ventilator. Main operator controls include: PEEP FIO2 FIO2 Tmaninsp (manual inspiration time) Pmaninsp (manual inspiration pressure) The VT will be variable and depend on patient effort and patient respiratory system mechanics.38

Spontaneous-Proportional Pressure Support In SPN-PPS mode, the Babylog VN500 supports the patient's spontaneous breathing in proportion to the inspiratory effort.38 If the patient breathes strongly, the ventilator will support this effort with high-pressure support. If the patient has shallow breathing, the ventilator responds with low-pressure support. Mechanical support is omitted altogether if there is no spontaneous breathing. Main operator controls include: PEEP Volume assist

Flow assist VT and pressure are variable and will depend on volume-assist setting, flow-assist setting, patient effort, and patient respiratory system mechanics.38 The amount of pressure and flow delivered will be variable and depend on the VT setting, patient effort, and patient respiratory system.38

Special Features Babylog VN500 special features include noninvasive ventilation, apnea ventilation, automatic tube compensation and its nebulizer function.

Apnea Ventilation Babylog VN500 detects apnea when no expiratory flow is measured or insufficient inspiratory gas is delivered during the set apnea alarm time (Tapn).38 If apnea ventilation is activated, the device starts volume-guaranteed SIMV with the RR and VT set by the clinician. The inspiratory time for apnea ventilation is determined from the set apnea respiratory rate and a fixed I:E ratio of 1:2. Apnea ventilation is available in the following modes: PC-SIMV, PC-APRV, SPN-CPAP/PS, SPNCPAP/VS, and SPN-PPS.

Automatic Tube Compensation When automatic tube compensation is activated, the ventilator calculates the pressure drop from the proximal to the distal end of the ETT and ventilation pressure in the breathing circuit is increased during inspiration or decreased during expiration.38 The airway pressure is adjusted to the tracheal level if 100% compensation of the tube resistance has been selected. The clinician has to input ETT diameter and length.

Nebulizer The Babylog VN500 uses a gas mixture to drive the medication nebulizer that is designed to minimize deviations from the set FIO2.38 The medication nebulizer nebulizes continuously.

Noninvasive Ventilation

For pediatric patients, NIV is available in every mode except SPN-CPAP.38 For neonates, NIV is only available in SPN-CPAP and PC-CMV.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Dräger Babylog VN500 are listed in Table 4-66. TABLE 4-66 Manufacturer’s Specifications for the Dräger Babylog VN500 Setting

Range

Pressure Inspiratory pressure

0 to 80 cm H2O

Pressure support

0 to 80 cm H2O

PEEP

0 to 35 cm H2O

Volume Tidal volume

0.002 to 0.3 L

Flow Inspiratory flow

2 to 300 L/min

Time Inspiratory time

0.1 to 3 seconds

Mandatory breath rate

0.5 to 150/min

Sensitivity Trigger

0.2 to 5 L/min (flow)

Alarms

Range

Pressure Upper airway pressure

7 to 105 cm H2O

Upper ETco2

1 to 98 mm Hg

Lower ETco2

0 to 97 mm Hg

Volume

High Ve

0.03 to 60 L/min

Low Ve

0.02 to 40 L/min

Time Respiratory rate

5 to 200 breaths/min

Apnea time

5 to 60 seconds

Other O2 sensor

Enabled/disabled

Monitored Parameters Airway pressure

Maximum airway pressure

O2 concentration

Expired minute volume

RR

VT

End-expiratory CO2 concentration

Apnea alarm time

Smiths Medical Pneupac babyPAC 100 The babyPAC 100 ventilator is a gas- and battery-powered, time-cycled pressure generator that depends solely on the pressure of the supply gas for its operation (Figure 4-63).39 It consists of a control module with a conventional Y patient circuit and the ventilator has been rated MRI compatible up to 3 Tesla. The babyPAC 100 portable ventilator is designed for use in and outside hospitals. It is for ventilation during transportation and for resuscitation of neonates and infants up to a bodyweight of 20 kg. The operator interface (Figure 4-64) consists of a series of knobs and a pressure gauge.

FIGURE 4-63 Smiths Medical Pneupac babyPAC 100 Ventilator. Courtesy of Smiths Medical.

FIGURE 4-64 Smiths Medical Pneupac babyPAC 100 Ventilator Operator Interface. Courtesy of Smiths Medical.

Modes The ventilation modes available on the Smiths Medical Pneupac babyPAC 100 are classified and depicted in Table 4-67. TABLE 4-67 Modes Available on the Smiths Medical Pneupac babyPAC 100

Description

Controlled Mandatory Ventilation CMV is a pressure-targeted mode of ventilation that allows for mandatory, timetriggered breaths only (patient-assisted breaths are not allowed).39 The mandatory breaths cycle to exhalation once the inspiratory time has elapsed. Main operator controls include: FIO2 PEEP Inspiratory pressure level Inspiratory time (Tinsp) Expiratory time (Texp) The pressure will be consistently delivered from breath to breath; VT and flow are variable and will depend on the inspiratory pressure level, patient effort, and patient respiratory system mechanics.39 If the CMV + active PEEP is selected a continuous flow is generated through the circuit during exhalation and the patient can draw a spontaneous breath from this flow.39

Intermittent Mandatory Ventilation and Continuous Positive Airway Pressure IMV + CPAP is a pressure-targeted mode that combines two breath types, PAC and CPAP.39 There is a continuous flow of 10 L/min in the circuit, and the patients can draw spontaneous breaths from this flow in between mandatory breaths. Main operator controls include: FIO2 CPAP Inspiratory pressure level Inspiratory time Expiratory time During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.39 During the CPAP period, the VT is also variable and depends on patient effort and respiratory system mechanics.

Continuous Positive Airway Pressure During CPAP a constant baseline pressure is maintained by the ventilator through a 10 L/min continuous flow through the circuit and the patient regulates his or her respiratory rate and VT.39 Main operator controls include: CPAP FIO2 The VT will be variable and depend on patient effort and respiratory system mechanics.39

Special Features The babyPAC 100 has limited special features, as described below.

Apnea Ventilation There is no backup ventilation.39

Oxygen A gas mixing system enables the selection of the oxygen concentration by means of the calibrated rotary control.39 There is a double calibration in order to be able to select the concentration with the two different gas supply possibilities. If oxygen alone is available as a compressed supply gas, then a concentration range of 45% to 100% oxygen concentration is possible. If both oxygen and air are connected as gas sources, then the yellow scale becomes operative, and it is possible to select from 21% to 70% oxygen. The clinician has to input ETT diameter and length.

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Smiths Medical Pneupac babyPAC 100 are listed in Table 4-68. TABLE 4-68 Manufacturer’s Specifications for the Smiths Medical Pneupac babyPAC 100 Setting

Range

Pressure Inspiratory pressure

12 to 70 cm H2O

PEEP/CPAP

0 to 20 cm H2O

Time Inspiratory time

0.25 to 2 seconds

Expiratory time

0.25 to 4 seconds

Alarms

Range

Pressure Airway pressure

12 to 80 cm H2O

PEEP

> 10 cm H2O

Low pressure/disconnect Monitored Parameters Airway pressure

Vyaire Infant Flow SiPAP Vyaire Infant Flow SiPAP (shown in Figure 4-65) is designed to provide noninvasive ventilation for infants in hospital environments through either nasal prongs or a nasal mask.40 It has a backup battery for patient transport. The ventilator is available in two configurations: Plus or Comprehensive. The main difference between the two configurations is that Comprehensive provides an additional mode (BiPhasic tr, discussed in the Special Features section) and apnea backup breaths. Infant Flow SiPAP operator interface (Figure 4-66) consists of an LCD touch screen display with keypad, pressure time waveform graphics, separate flowmeter controls for adjustment of NCPAP /Plow and Phigh, and a %O2 blender control.

FIGURE 4-65 The Vyaire Infant Flow SiPAP Ventilator.

© 2018 Vyaire Medical, Inc. Used with permission.

FIGURE 4-66 The Vyaire Infant Flow SiPAP Operator Interface. Courtesy of Vyaire. © 2018 Vyaire Medical, Inc.Used with permission.

Modes The ventilation modes available on the Vyaire Infant Flow SiPAP are classified and depicted in Table 4-69. TABLE 4-69 Modes Available on the Vyaire Infant Flow SiPAP

Description

Nasal Continuous Positive Airway Pressure NCPAP is a pressure-targeted mode of ventilation that allows for spontaneous breathing from a fixed pressure baseline.40 No additional support is provided during inspiration. Main operator controls include: FIO2 CPAP The ventilator provides a baseline pressure and the patient breathes spontaneously from that baseline; VT and flow are variable and will depend on patient effort and patient respiratory system mechanics.40

BiPhasic The BiPhasic mode is a pressure-targeted mode that delivers time-triggered pressure-assist breaths.40 The patient can breathe spontaneously both between and during the pressure breaths. Main operator controls include: FIO2 PEEP (Plow flowmeter) Inspiratory pressure level (Phigh flowmeter) Inspiratory time (Thigh)

RR During the PAC breaths, the resulting VT created is variable and depends on inspiratory pressure level, patient effort, and patient respiratory system mechanics.40 During the CPAP period, the VT is also variable and depends on patient effort and respiratory system mechanics.40

Special Features The Vyaire Infant Flow SiPAP features include BiPhasic tr and apnea backup ventilation.

Apnea Ventilation There an apnea backup rate that can be set from 1 to 120 breaths per minute.40 This becomes active after the adjustable apnea timeout period has elapsed. The breaths are pressure targeted.

BiPhasic tr BiPhasic tr requires the use of a special abdominal sensor for the trigger signal.40 The breaths delivered during BiPhasic tr are the same as the BiPhasic mode. BiPhasic tr is not presently available in the United States.

Nebulizer There is no nebulizer available.40

Manufacturer’s Specifications, Controls, Monitored Parameters, and Alarms The manufacturer’s specifications, controls, monitored parameters, and alarms for the Vyaire Infant Flow SiPAP are listed in Table 4-70. TABLE 4-70 Manufacturer’s Specifications for the Vyaire Infant Flow SiPAP Setting

Range

Pressure Inspiratory pressure

Phigh flowmeter, 0 to 15 L/min

PEEP/CPAP

Plow flowmeter, 0 to 5 L/min

Time Inspiratory time

0.1 to 3 seconds

RR

1 to 120 bpm

Alarms

Range

Pressure High airway pressure

Automatic to 3 cm H2O above measured airway pressure

Low airway pressure

Automatic to 2 cm H2O below measured airway pressure

Time Apnea interval

10 to 30 seconds

Monitored Parameters CPAP

PEEP

Mean airway pressure

Inspiratory pressure

% O2

I:E

Spontaneous rate (Rspont)

Key Points It is important to understand what triggers a breath (trigger setting or time mandate), what the set point is (pressure or volume), and what ends the breath (VT delivery, time, or cycle sensitivity). The breath sequence can be (1) continuous mandatory ventilation (CMV), in which all breaths are controlled by the machine but can be triggered by the patient in most cases; (2) intermittent mandatory ventilation (IMV), in which the patient can take spontaneous breaths between mandatory breaths; and (3) continuous spontaneous ventilation (CSV), in which all breaths are spontaneous. In volume ventilation, the VT and inspiratory flow are set (and indirectly the inspiratory time) while the resultant pressure varies. Worsening lung mechanics in volume assist/control will manifest as increases in ventilatory pressure. In pressure-targeted ventilation, the inspiratory pressure and inspiratory time are set, while the VT and inspiratory flow vary. Worsening lung mechanics in pressure A/C will manifest as decreases in VT Volume support (VS) is a feedback mode in which the ventilator delivers a variable (from breath to breath) PSV level in order to reach a clinician-set VT. The ventilator drops the level of support as patient effort increases and conversely increases the PSV level when patient activity is too low. PRVC (also referred to as VC+, AutoFlow, A/C PRVC, or VTPC) is pressure control but the clinician sets a target VT and the ventilator adjusts the inspiratory pressure level to achieve the desired VT ASV (available on the Hamilton ventilators) is an automatic mode in which the ventilator targets a selected MV using a combination of inspiratory pressure (to achieve a specific VT) and RR. In a passive patient, most, if not all, breaths are PAC. In a spontaneously breathing patient, there may be a combination of PS and PAC, or most of the breaths may be PS if the patient generates enough MV him- or herself. SmartCare (available on the Dräger ventilators) is designed to be an automated weaning tool where by the ventilator automatically adjusts the PS level based on certain monitored parameters (RR, ETCO2, and VT). Automode (available on the Servo ventilators) is a feedback feature that switches between a control mode of ventilation (either PC, PRVC, or VC) and a supported mode (either volume support or pressure support) depending on the patients spontaneous breathing activity. MMV is designed to assure that the patient receives a clinician-set MV. If the patient’s spontaneous efforts are not sufficient the ventilator will provide support

to maintain the target MV. PAV (available on Covidien PB ventilators) is a purely spontaneous mode that delivers variable flow, pressure, and volume to the patient. The clinician sets the WOB that the ventilator will do on an intrabreath basis and the remainder of the total WOB is assumed by the patient. NAVA (available on the Servo ventilators) is a purely spontaneous mode of ventilation that delivers ventilatory assistance in proportion to the electrical activity of the patient’s diaphragm. With this mode the clinician sets the inspiratory pressure (cm H2O) per diaphragm microvolt activity. It is important to realize that the newer models and other feedback modes are unproven in terms of a mortality benefit. They also can be difficult to optimize for the patient if the clinician is unfamiliar with the mode.

References 1. Chatburn RL, El-Khatib M, Mireles-Cabodevila E. A taxonomy for mechanical ventilation: 10 fundamental maxims. Respir Care. 2014;59(11):1747–1763. 2. Arnal JM. Feasibility study with full closed-loop control ventilation in ICU patients with acute respiratory failure. Crit Care. 2013;17(5):R196. 3. Beijers AJR. Fully automated closed-loop ventilation is safe and effective in post-cardiac surgery patients. Intens Care Med. 2014;40(5):752–753. 4. Hamilton Medical AG. HAMILTON-G5 operator manual PN 9616187. Bonaduz, Switzerland: Hamilton Medical AG; 2016. 5. Hamilton Medical AG. HAMILTON-C3 operator manual PN 9616187. Bonaduz, Switzerland: Hamilton Medical AG; 2015. 6. Hamilton Medical AG. HAMILTON-C1 operator manual. Bonaduz, Switzerland: Hamilton Medical AG; 2015. 7. Maquet. Servo-i operator manual. Solna, Sweden: Maquet Critical Care AB; 2015. 8. Maquet. Servo-u operator manual. Solna, Sweden: Maquet Critical Care; 2015. 9. Medtronic. Covidien Puritan Bennett 840 operator manual. Mansfield, MA: Medtronic; 2016. 10. Medtronic. Covidien Puritan Bennett 980 operator manual PN 7,117,438. Mansfield, MA: Medtronic; 2017. 11. Medtronic. Newport e360 operator manual PN 6,439,229. Mansfield, MA: Medtronic; 2011. 12. Vyaire. AVEA operator manual. Yorba Linda, CA: Vyaire; 2017. 13. Vyaire. VELA operator manual. Yorba Linda, CA: Vyaire; 2014. 14. Dräger Medical GmbH. Evita Infinity V500 operator manual. Lübeck, Germany: Dräger Medical GmbH; 2012. 15. Dräger Medical GmbH. Evita XL operator manual. Lübeck Germany: Dräger Medical GmbH; 2008. 16. General Electric (GE). CARESCAPE R860 operator manual. Fairfield, CT: General Electric Company; 2016. 17. Respironics. V60 operator manual. Carlsbad, CA: Respironics California; 2017. 18. CareFusion. 3100B operator manual. Yorba Linda, California: CareFusion; 2011. 19. Percussionaire Corporation. VDR-4 operator manual. Sandpoint, ID: Percussionaire Corporation; 2009. 20. Bunnell Incorporated. Life Pulse operator manual. Salt Lake City, UT: Bunnell Incorporated; n.d. 21. Hamilton Medical AG. HAMILTON-T1 operator manual. Bonaduz, Switzerland: Hamilton Medical AG; 2015. 22. Hamilton Medical AG. HAMILTON-MR1 operator manual. Bonaduz, Switzerland: Hamilton Medical AG; 2014. 23. Airon Corporation. pNeuton mini operator manual PN 6,591,835. Melbourne, FL: Airon Corporation; 2015. 24. Airon Corporation. pNeuton Model A operator manual PN 6,591,835. Melbourne, FL: Airon Corporation; 2015. 25. Airon Corporation. pNeuton Model S operator manual PN 6,591,835. Melbourne, FL: Airon Corporation; 2015. 26. Bio-Med Devices, Inc. Crossvent 4 brochure. Guilford, CT: Bio-Med Devices, Inc.; 2016. Available at http://www.biomeddevices.com/products/crossvent-4-infant-adult-ventilator/. 27. Vyaire. ReVel operator manual. Yorba Linda, CA: Vyaire; 2015. 28. Vyaire. LTV 1200 operator manual. Yorba Linda, CA: Vyaire; 2014. 29. Dräger Medical GmbH. Carina pocket guide. Lübeck, Germany: Dräger Medical GmbH; 2015. 30. Dräger Medical GmbH. Oxylog 3000 plus brochure. Lübeck, Germany: Dräger Medical GmbH; 2015. 31. Newport Medical Instruments, Inc. Newport HT70 plus operator manual PN 7,654,802. Costa Mesa, CA: Newport Medical Instruments, Inc.; 2013. 32. ZOLL Medical Corporation. Eagle II operator manual. Chelmsford, MA: ZOLL Medical Corporation; 2017. 33. Respironics. Trilogy operator manual. Murrysville, PA: Respironics Inc.; 2012. 34. DeVilbiss Healthcare LLC. IntelliPAP Bilevel operator manual PN 5,865,173. Somerset, PA: DeVilbiss Healthcare LLC; 2016. 35. DeVilbiss Healthcare LLC. IntelliPAP AutoBilevel operator manual PN 5,865,173. Somerset, PA: DeVilbiss Healthcare LLC; 2016. 36. ResMed Corp. Lumis Tx clinical guide PN 710989. San Diego CA: ResMed Corp; 2014. 37. ResMed Corp. Astral clinical guide PN708733. San Diego CA: ResMed Corp; 2017. 38. Dräger AG & Co. Babylog VN500 operator manual. Lübeck, Germany: Drägerwerk AG & Co. KGaA; 2017. 39. Smiths Medical. babyPAC 100 operator manual PN 5605148. Luton, UK: Pneupac Ltd; 2002.

40. Vyaire. Infant Flow SiPAP operator manual. Yorba Linda, CA: Vyaire; 2013.

CHAPTER

5 Indications for Mechanical Ventilation David C. Shelledy and Jay I. Peters

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Ventilation Ventilatory Capacity Ventilatory Requirements Assessment of Ventilation Clinical Manifestations of Respiratory Failure Goals of Mechanical Ventilatory Support Indications for Mechanical Ventilation Apnea Acute Ventilatory Failure Impending Ventilatory Failure Severe Oxygenation Problems Complications, Hazards, and Contraindications Contraindications to Mechanical Ventilation Patient Assessment for Ventilator Initiation Initial Ventilator Settings

OBJECTIVES 1. 2. 3. 4.

Explain the primary function of a mechanical ventilator. Define respiratory failure and explain the differences between hypoxemic and hypercapnic respiratory failure. Define acute ventilatory failure. Describe each of the components of ventilation, including the relationship between tidal volume, respiratory

5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.

rate, minute ventilation, physiologic dead space, and alveolar ventilation. Define ventilatory capacity and describe factors that affect ventilatory capacity. Define ventilatory requirements (aka ventilatory demand or load) and describe factors that affect ventilatory requirements. Explain the relationship between ventilatory capacity and ventilatory requirements in terms of adequacy of ventilation and development of acute ventilatory failure. Describe clinical conditions that may reduce or eliminate respiratory drive. Describe factors that may impair lung function and explain how they may reduce ventilatory capacity. Describe clinical conditions that increase ventilatory workload and may lead to ventilatory muscle fatigue and ventilatory failure. Explain how changes in ventilatory muscle strength affect ventilatory capacity. Describe the disease states or conditions that cause ventilatory muscle weakness or dysfunction and predispose patients to the development of respiratory failure, hypoventilation, and/or apnea. Explain the relationship between alveolar ventilation (V̇A), arterial carbon dioxide tension (PaCO2), metabolic rate, and carbon dioxide production (V̇CO2). Describe the normal ventilatory response to hypoxemia. Describe the effects of increased physiologic dead space on ventilatory requirements. Explain how metabolic acidosis may affect ventilatory requirements. List common causes of acute respiratory failure requiring mechanical ventilation. Describe the clinical manifestations of acute respiratory failure associated with the need for mechanical ventilatory support. Explain each of the seven primary goals of mechanical ventilatory support. Provide examples of clinical causes of each of the four primary indications for institution of mechanical ventilation. List values for bedside measures of pulmonary function that suggest the need for mechanical ventilatory support. Explain why certain neuromuscular disorders may progress to ventilatory failure requiring mechanical ventilation. Recognize the presence of severe oxygenation problems, including refractory hypoxemia. Explain how PEEP and CPAP may improve oxygenation in certain patients. Recognize patients for whom institution of mechanical ventilatory support is indicated. Describe the major complications, hazards, and contraindications of mechanical ventilation. Overview the initial ventilator settings for patients requiring mechanical ventilatory support.

KEY TERMS acute respiratory distress syndrome (ARDS) acute ventilatory failure alveolar ventilation apnea asthma exacerbation barotrauma chronic ventilatory failure continuous mandatory ventilation (CMV) continuous positive airway pressure (CPAP) continuous spontaneous ventilation (CSV) dead space ventilation hypercapnia hypercapnic respiratory failure hyperventilation hypoventilation hypoxemic respiratory failure impending ventilatory failure intermittent mandatory ventilation (IMV)

minute ventilation (V̇E) neurologic disease neuromuscular disorders positive end-expiratory pressure (PEEP) PaO2/FIO2 ratio (P/F ratio) physiologic dead space pressure control (PC) respiratory drive respiratory acidosis respiratory failure respiratory rate (f) severe oxygenation problem synchronized intermittent mandatory ventilation (SIMV) tidal volume (VT) ventilatory capacity ventilatory failure ventilatory muscle fatigue ventilatory requirements ventilatory reserve ventilatory workload volume control (VC) work of breathing (WOB)

Introduction This chapter provides an overview of the indications for mechanical ventilatory support. Mechanical ventilation may be required when spontaneous breathing is insufficient or absent. The provision of mechanical ventilatory support entails the use of sophisticated life-support technology to support tissue oxygenation and removal of carbon dioxide. Simply put, the primary function of a mechanical ventilator is to augment or replace normal ventilation. Thus, absent ventilation (apnea) or inadequate ventilation (actual or impending ventilatory failure: clinically detected by tachypnea or hypercapnea) provide major indications for the initiation of mechanical ventilatory support. The other major indication for mechanical ventilation is a severe oxygenation problem (e.g., refractory hypoxemia). In this chapter, we will review the basics of ventilation to include causes of hypoventilation and apnea. As described elsewhere, respiratory failure is the inability of the heart and lungs to maintain adequate tissue oxygenation and/or carbon dioxide removal.1–4 Respiratory failure is sometimes classified as either hypoxemic respiratory failure (Type I respiratory failure), or hypercapnic respiratory failure (Type II respiratory failure).1–4 Hypoxemic respiratory failure refers to a primary problem with oxygenation, usually due to lung failure. Hypercapnic respiratory failure is also known as ventilatory failure, and refers to a primary problem with ventilation resulting in an abnormal elevation of PaCO2.1–4 Acute ventilatory failure (aka acute hypercapnic respiratory failure) is defined as a sudden increase in arterial PCO2 with a corresponding decrease in pH.4–6 In the intensive care unit (ICU), patients often suffer from both hypoxemic and hypercapnic respiratory failure. Because respiratory failure is the most common reason for considering mechanical ventilation, we will briefly review the causes and clinical manifestations of respiratory failure. The goals of mechanical ventilation will be described, and the indications for the provision of mechanical ventilatory support will be discussed. As mechanical ventilation is not without significant risk, the contraindications, hazards, and possible complications of mechanical ventilation will be described. The chapter will conclude with a discussion of the assessment of the patient leading to the decision to initiate mechanical ventilatory support.

RC Insight Mechanical ventilation may be required when spontaneous breathing is insufficient or absent.

Ventilation Ventilation can be defined as the bulk movement of gas into and out of the lungs. Ventilation can be subdivided into tidal volume (VT), respiratory rate (f), and minute ventilation (V̇E) where V̇E = VT × f. Exhaled tidal volume is simply the volume of gas passively exhaled after a normal inspiration, and respiratory rate is simply the number of breaths taken per minute. Adequate spontaneous ventilation requires a sufficient tidal volume, respiratory rate, and minute ventilation to support oxygenation and CO2 removal, while maintaining acid-base homeostasis. While bedside measures of spontaneous breathing are sometimes useful (e.g., VT, f, and V̇E), the single best clinical index of ventilation is measurement of arterial carbon dioxide tension (PaCO2).7 For most patients, normal ventilation corresponds to a PaCO2 from 35 to 45 mmHg, while hypoventilation and hyperventilation are defined as a PaCO2 > 45 mmHg or < 35 mmHg, respectively. Since venous blood gases are frequently utilized to assess pH, a PaCO2 > 50 mmHg suggests possible hypercapnia. Box 5-1 reviews terms often used to describe ventilation.

BOX 5-1 Terms Used to Describe Ventilation ∎

Tidal volume (VT): the volume of gas exhaled passively following a normal inspiration (i.e., exhaled tidal volume). • Normal adult VT is approximately 500 mL (range 400 to 700 mL) or about 7 mL/kg of ideal body weight (IBW). • Formulas for estimating IBW vary and some (e.g., ARDSNet) use the term “predicted body weight” (PBW) where: ○ PBW males (kg) = 50 + 2.3 (height [in] – 60) ○ PBW females (kg) = 45.5 + 2.3 (height [in] – 60) • Inhaled VT: the volume of gas inhaled normally following a passive expiration. ○ Inhaled VT is sometimes measured and compared to exhaled VT in patients receiving mechanical ventilatory support in order to verify and/or quantify air leaks (e.g., endotracheal tube cuff leak, chest tube air leak) in which inhaled VT > exhaled VT. • Actual VT will vary depending on the patient’s size, gender, and overall condition.

∎

Respiratory rate (f): number of breaths taken per minute. • Normal adult respiratory rate is approximately 12 breaths/min with a range of about 12 to 18 breaths/min. • Tachypnea: elevated respiratory rate; rapid shallow breathing is a common finding in patients with acute respiratory failure. • Bradypnea: abnormally slow respiratory rate; seen with sedative or narcotic drug overdose, head trauma, CNS disease, and other causes of respiratory center depression. ∎ Minute ventilation (V̇E): VT times the respiratory rate (V̇E = VT × f). • Normal adult V̇E is approximately 6 L/min (range 5 to 10 L/min). ∎ Dead space ventilation (VD): the portion (or volume) of ventilation that does not participate in gas exchange (i.e., ventilation without perfusion). There are several types of dead space. • Anatomic dead space (VD anatomic): refers to the volume of gas in the conducting airways (i.e., from the external nares (nostrils) down to and including the terminal bronchioles). ○ Normal anatomic dead space is approximately 1 mL per pound of IBW (about 150 mL in a normal adult). ○ Anatomic dead space will vary based on the patient’s size. • Alveolar dead space (VD alveolar): volume of ventilation received by alveoli that are ventilated but not perfused. ○ Emphysema is an important cause of increased alveolar dead space (e.g., capillaries destroyed from the toxic effects of cigarette smoking). ○ Pulmonary embolus (PE) may result in severe V̇/Q̇ problems with partial occlusion of a pulmonary vessel; with complete occlusion alveolar dead space will increase. • Physiologic dead space (VD physiologic): total functional dead space volume that consists of the alveolar and anatomic dead space. ○ VD physiologic = VD anatomic + VD alveolar. ○ Normally, VD physiologic ≅ VD anatomic. ○ VD physiologic can be calculated at the bedside using the modified Bohr equation. PaCO2 and mean exhaled carbon dioxide tension (PĒCO2) are measured for calculation of the dead space to tidal volume ratio (VD/VT) where VD/VT = (PaCO2 – PĒCO2) ÷ PaCO2. ○ Normal VD/VT is 0.30 (range: 0.20 to 0.40). ○ VD physiologic = VD/VT × VT.

∎

○ VD physiologic > VD anatomic with dead space disease (e.g., emphysema or pulmonary embolus). • Mechanical dead space: the volume of rebreathed gas due to a mechanical device (e.g., large bore tubing placed between the patient “Y” and the endotracheal tube in intubated patients). Alveolar ventilation (aka effective ventilation): the volume of gas reaching alveoli that are ventilated AND perfused per breath (VA) or per minute (V̇A). • Normal adult V̇A is 4 to 5 L/min. • V̇A, CO2 production (V̇CO2) and PaCO2 are closely related where: V̇A = (0.863 × V̇CO2) ÷ PaCO2. ○ Normal V̇CO2 is about 200 mL/min. ○ Normal PaCO2 is 40 mmHg (range 35 to 45 mmHg).

•

○ 0.863 is a conversion factor to convert mmHg and mL/min to L/min. ○ PaCO2 and V̇A are inversely proportional; as V̇A decreases, PaCO2 increases. Clinically, PaCO2 is the single best index of alveolar ventilation.

∎

Normal ventilation: PaCO2 is 35 to 45 mmHg.

∎

Hypoventilation: abnormally increased level of ventilation; PaCO2 > 45 mmHg. Hyperventilation: abnormally decreased level of ventilation; PaCO2 < 35 mmHg. Hypocapnea: abnormally decreased PaCO2 (PaCO2 < 35 mmHg); the term hypocapnea is sometimes used in place of hyperventilation. Hypercapnea: abnormally elevated PaCO2 (PaCO2 > 45 mmHg); the term hypercapnia is sometimes used in place of hypoventilation. Acute ventilatory failure: a sudden (acute) increase in PaCO2 with a corresponding decrease in pH. Chronic ventilatory failure: a chronically elevated PaCO2, with a normal (compensated) or near-normal pH due to renal compensation. Note that renal compensation takes 3 to 5 days and increases HCO3- about 4 to 5 mEq/L for every 10-mmHg increase in PaCO2.

∎ ∎ ∎ ∎ ∎

∎ ∎

Acute alveolar hyperventilation: a sudden (acute) decrease in PaCO2 with a corresponding increase in pH. Chronic alveolar hyperventilation: a chronic decrease in PaCO2, with a normal or near-normal pH due to renal compensation.

Ventilatory capacity is a general term indicating the amount of air that can be moved into and out of the lungs by the ventilatory pump. Ventilatory requirements (aka ventilatory demand or load) refers to the volume of ventilation required to achieve adequate oxygenation and carbon dioxide removal. Put another way, ventilatory capacity is how much a patient can breathe, while ventilatory requirements are how much a patient must breathe in order to support oxygenation and carbon dioxide removal. The difference between ventilatory capacity and ventilatory requirements is the ventilatory reserve. In order to sustain adequate spontaneous ventilation, the patient’s ventilatory capacity must meet or exceed his or her ventilatory requirements. Ventilatory capacity is affected by a number of factors including respiratory drive, lung function, ventilatory workload, and ventilatory muscle strength. A patient’s ventilatory requirements are determined by his or her oxygenation status, carbon dioxide production, lung function (e.g., dead space volume), circulatory status (e.g., cardiac output, blood pressure) and acid-base balance. When ventilatory requirements exceed ventilatory capacity, hypercapnic respiratory failure (aka ventilatory failure) may ensue. Each of the factors affecting ventilatory capacity and level of ventilation required (i.e., ventilatory demand) are described below. RC Insight Broadly defined, respiratory failure is the inability of the heart and lungs to maintain adequate tissue oxygenation and/or CO2 removal.

Ventilatory Capacity A patient’s ventilatory capacity must be sufficient to maintain adequate tissue oxygenation and CO2 removal and preserve acid-base homeostasis. When a patient’s ventilatory capacity is insufficient to provide the level of ventilation required to maintain adequate tissue oxygenation and CO2 removal, mechanical ventilatory support may be necessary. As noted above, factors that affect ventilatory capacity include respiratory drive, lung function, workload, and ventilatory muscle strength.

Respiratory Drive The respiratory drive to breathe (aka ventilatory drive) resides primarily in the central

respiratory control centers (i.e., medullary center, pontine centers), which respond to input from the central chemoreceptors in the medulla of the brainstem and the peripheral chemoreceptors of the carotid and aortic bodies.8 Since carbon dioxide rapidly diffuses across the blood–brain barrier, an increase in PCO2 will cause a decrease in cerebrospinal fluid pH, which will stimulate the central chemoreceptors to signal the need for an increase in ventilation; decreases in PCO2 may decrease ventilatory drive, depending on whether other factors stimulating the respiratory drive are present. The peripheral chemoreceptors located in the carotid and aortic bodies are stimulated by low arterial oxygen tension (PaO2 < 50 to 55 mmHg), decreased pH, or increased PaCO2.8 Thus, hypercarbia or acidosis will stimulate the central respiratory centers, and hypoxemia, acidosis, or hypercarbia will stimulate the peripheral chemoreceptors. In addition, input from thoracic neural receptors or higher brain centers (e.g., cerebral cortex) may affect the level of ventilation. For example, stimulation of J receptors or bronchial C receptors in the lung, as may occur with consolidative lung disease (e.g., pneumonia, pulmonary edema) or inflammation, will cause an increase in respiratory rate and may result in rapid, shallow breathing.8 Other causes of an increased drive to breathe include exercise, pain, anxiety, and metabolic (hepatic or uremic) encephalopathy. Correction of problems causing central or peripheral chemoreceptor stimulation (e.g., oxygen therapy, correction of metabolic acidosis) may allow ventilation to return to normal levels. Respiratory drive can be reduced or abolished by administration of narcotics, sedatives, tranquilizers, or anesthetic gases. Other conditions that may reduce respiratory drive include metabolic alkalosis, neurologic disease, severe hypothyroidism, decreased metabolic rate, electrolyte disorders, and (possibly) very high PaCO2 (> 75 to 80 mmHg).4,8 Shock, trauma, or myocardial infarction may lead to respiratory and cardiac arrest. Certain patients with chronic obstructive pulmonary disease (COPD) develop chronic hypercapnia with hypoxemia and oxygen therapy provided to such patients may worsen CO2 retention (i.e., oxygen-associated hypercapnia).4,9–11 Certain asthma patients (known as “underpercievers”) may also exhibit a decreased respiratory drive and a reduced perception of dyspnea.12 These patients are at special risk for the development of fatal asthma exacerbation. Neuromuscular blocking agents (e.g., pancuronium [Pavulon], vercuronium

[Norcuron], atracurium [Tracium], and cistracurium [Nimbex]) block transmission of nerve impulses at the myoneural junction (aka neuromuscular junction) and may cause paralysis, apnea, and in some cases, prolonged ventilatory muscle weakness. Factors that affect respiratory drive are listed in Box 5–2.

BOX 5-2 Factors that Affect Respiratory Drive A number of factors stimulate respiratory drive including hypoxemia, hypercarbia, and acidemia. Decreased or absent respiratory drive may result in hypoventilation or apnea (e.g., acute ventilatory failure or respiratory arrest). The terms respiratory drive and ventilatory drive are often used synonymously. Patients with inadequate or absent respiratory drive often require mechanical ventilatory support. Causes of decreased or absent respiratory drive include: ∎ ∎ ∎

∎ ∎

∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

Overventilation during mechanical ventilation (induced hypocapnia) Severe hypoxia (e.g., cerebral hypoxia) Acute, severe hypercapnia (PaCO2 > 75 to 80 mmHg; initial increase in respiratory drive but may be followed by depressed level of consciousness and reduced respiratory drive) Cardiopulmonary collapse (cardiac arrest, acute MI, shock, and trauma) Neurologic disease (e.g., major stroke, brainstem tumor, cerebral hemorrhage, meningitis, encephalitis, hepatic encephalopathy, brainstem ischemia, and brain death) Head trauma Near-drowning Hypothermia Poisoning (carbon monoxide poisoning, cyanide poisoning, other) Electrical shock CNS depressants (opioids, barbiturates, benzodiazepines, and tricylic antidepressants) Intentional or accidental drug overdose (narcotics, heroin, barbiturates, and tranquilizers) Anesthesia (general) Alkalosis (respiratory alkalosis, metabolic alkalosis) Electrolyte disorders Chronic obstructive pulmonary disease (COPD) patients with chronic CO2

∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

retention and hypoxemia may have reduced respiratory drive (“blue bloater” profile) Oxygen-associated hypercapnia (sometimes seen in patients with chronic CO2 retention/COPD following administration of oxygen) Certain asthma patients with severe hypoxemia and hypercapnia Severe hypothyroidism Starvation Decreased metabolic rate Sleep disorders (e.g., central or obstructive sleep apnea) Obesity hypoventilation Central hypoventilation syndrome (Ondine’s curse) Apnea of prematurity

Causes of increased respiratory drive include: ∎ Hypoxemia ∎ Sepsis ∎ Metabolic acidosis ∎ Increased PaCO 2 ∎

Increased CO2 production (exercise, fever, agitation, seizures, and shivering)

∎

Lung receptor stimulation (e.g., J receptors, bronchial C receptors). Certain drugs (theophylline [Theolair], acetazolamide [Diamox], and salicylate intoxication) Pain and anxiety Hypotension

∎ ∎ ∎

Lung Function Ventilatory capacity is also dependent on factors that affect lung function, including the conducting airways and gas exchange units, lung compliance, thoracic compliance, and airway resistance. For example, upper airway obstruction may detrimentally affect ventilatory capacity. Bronchospasm, mucosal edema, or secretions may also reduce ventilatory capacity. Reductions in lung compliance (e.g., pneumonia, pulmonary edema, and fibrotic lung disease) or thoracic compliance (e.g., chest wall deformity, obesity, and ascites [fluid in the peritoneal cavity]) may reduce ventilatory capacity. Alveolar filling (e.g., consolidative

pneumonia, pulmonary edema), atelectasis, alveolar wall destruction (e.g., emphysema), or interstitial fibrosis may also reduce ventilatory capacity. Physiologic dead space may affect ventilatory capacity as an increase in dead space will reduce effective (alveolar) ventilation at a given tidal volume.

Workload The work performed by the respiratory muscles to provide adequate ventilation is the ventilatory workload (that is, the work of breathing [WOB]). The ventilatory workload is primarily determined by the compliance of the lungs and thorax, and resistance to gas flow.6 Ventilatory workload increases as compliance is reduced or resistance to gas flow increased. Conditions that decrease lung compliance include atelectasis, pneumonia, pulmonary edema, acute respiratory distress syndrome (ARDS), and pulmonary fibrosis. Surfactant disruption, as occurs with respiratory distress syndrome (RDS) of the neonate, will also reduce lung compliance.6 Pneumonia, pulmonary edema, ARDS, early lung dysfunction after transplant, and leakage of plasma proteins into the lung may disrupt surfactant in adults and thus reduce lung compliance. Conditions that decrease thoracic compliance include thoracic cage deformities (e.g., kyphoscoliosis, ankylosing spondylitis) or abdominal disorders (e.g., obesity or ascites).6 Causes of increased airway resistance include upper airway obstruction (e.g., epiglottitis, croup, angioedema, tumor, and foreign bodies) and lower airway disease (e.g., bronchospasm, mucosal edema, and increased secretions).6 Disease states associated with increased airway resistance include asthma, emphysema, and conditions that decrease lung volumes (e.g., atelectasis, pneumonia).6 Mechanical causes of increased resistance to air flow include artificial airways (e.g., endotracheal and tracheostomy tubes), ventilator demand flow systems, and ventilator circuits. Disease states or conditions that reduce compliance or increase resistance to gas flow will require an increase in ventilatory work in order to maintain the same level of ventilation. At some point, ventilatory workload may exceed the capacity of the respiratory muscles and respiratory failure may ensue. A high ventilatory workload may lead to ventilatory muscle fatigue, ventilatory muscle weakness, and a reduction in ventilatory capacity. Causes of increased ventilatory workload are

summarized in Box 5-3.

BOX 5-3 Causes of Increased Ventilatory Workload An increase in ventilatory workload (increased WOB) may lead to ventilatory muscle fatigue and ventilatory failure. Ventilatory workload may increase due to: ∎ Decreased lung compliance • Atelectasis, pneumonia, pulmonary edema, ARDS, pulmonary fibrosis, and surfactant disruption • Pleural effusions, hemothorax, empyema, pneumothorax, and dynamic hyperinflation (air trapping) ∎ Decreased thoracic compliance • Obesity, ascites, pregnancy, and thoracic deformity (kyphoscoliosis, ankylosing spondylitis) ∎ Increased airway resistance • Bronchospasm, mucosal edema, and increased secretions (asthma, emphysema, and chronic bronchitis) • Tumor, foreign body obstruction, epiglottitis, croup, and epiglottitis ∎ Mechanical causes of increased resistance to gas flow (i.e., imposed WOB) • Artificial airways (endotracheal tubes, tracheostomy tubes) • Mechanical ventilators (ventilator circuits, demand flow systems, and inappropriate ventilator sensitivity or flow settings) ∎ Increased level of ventilation required • Hypoxemia/tissue hypoxia • Metabolic acidosis • Pain and anxiety • Increased V̇CO2 (trauma, infection, sepsis, fever, shivering, agitation, fighting the ventilator, and struggling against restraints) • Increased physiologic dead space (emphysema, pulmonary embolus with complete vessel obstruction) • Lung receptor stimulation (e.g., rapid shallow breathing)

Ventilatory Muscles A reduction in ventilatory muscle strength or endurance will reduce ventilatory capacity. As noted above, ventilatory muscle fatigue sometimes occurs due to very

high ventilatory workloads (e.g., reduced compliance, increased airway resistance). Neuromuscular disorders may compromise ventilation by causing ventilatory muscle weakness (e.g., Guillain-Barré, myasthenia gravis, or multiple sclerosis [MS]).4,6 Poor health, inadequate nutrition or starvation, electrolyte disturbances, and advanced age may also cause ventilatory muscle weakness.4,6 Certain drugs may affect neuromuscular transmission, such as aminoglycoside antibiotics, long-term adrenocortical steroids, and calcium channel blockers.4,6 Patients with severe COPD may have a chronically elevated WOB just below the threshold which causes diaphragmatic fatigue. When these patients suffer an acute exacerbation of their COPD, the resultant ventilatory fatigue may result in acute hypercapnia, acidosis, and hypoxemia. Other major causes of ventilatory muscle dysfunction seen in the ICU include critical illness polyneuropathy, critical illness myopathy, and prolonged use of neuromuscular-blocking agents.4,6,13 Prolonged periods of controlled mechanical ventilation may also lead to ventilatory muscle discoordination and atrophy.13 Paralysis of the ventilatory muscles, as may occur with Guillain-Barré, botulism, or high cervical spinal cord injury, may result in complete cessation of effective breathing. Weakness of the diaphragm and accessory muscles of inspiration can reduce tidal volume, often with a compensatory increase in respiratory rate and rapid shallow breathing. Rapid shallow breathing may be effective in maintaining minute ventilation; however, because of increased dead space ventilation, alveolar (i.e., effective) ventilation may decline and PaCO2 may rise. Rapid shallow breathing and the associated alveolar hypoventilation are often precursors to the need for mechanical ventilatory support. An increased respiratory rate, respiratory alternations (alteration between abdominal and rib cage motion), and abdominal paradox (inward movement of the abdomen during inspiration) are sometimes seen in patients with diaphragmatic fatigue resulting in inadequate ventilation. To summarize, absent or impaired ventilatory muscle function may reduce ventilatory capacity. If ventilatory requirements exceed ventilatory capacity, respiratory failure may ensue, and mechanical ventilation may be required. Table 51 summarizes disorders that may cause ventilatory muscle weakness or dysfunction and reduced ventilatory capacity. TABLE 5-1

Causes of Ventilatory Muscle Weakness or Dysfunction Associated with the Development of Respiratory Failure, Hypoventilation, and/or Apnea Disease State or Condition

Description

Amyotrophic lateral sclerosis (ALS)

Chronic and relentless motor neuron disease resulting in progressive voluntary muscle weakness that eventually leads to respiratory failure. Patients with end-stage disease require mechanical ventilatory support in order to survive.

Botulism

Caused by ingestion of food contaminated with Clostridium botulinum, which produces a nerve toxin that affects the neuromuscular junction and may cause skeletal muscle paralysis and respiratory failure.

Critical illness myopathy and polyneuropathy

Associated with corticosteroid administration, neuromuscular-blocking agents, systemic inflammatory response, and other conditions sometimes seen in critically ill patients (e.g., sepsis). Causes generalized muscle weakness, including ventilatory muscle weakness, which may cause difficulty in weaning from mechanical ventilatory support.

Duchenne muscular dystrophy

A genetic disorder resulting in muscle weakness that progressively worsens with age. As the patient’s condition declines, nocturnal noninvasive ventilation may be needed. Eventually, tracheostomy and invasive ventilation may be required.

Guillian-Barré syndrome

A motor neuron disease that causes progressive weakness and flaccid paralysis of the arms and legs. Involvement of the diaphragm requiring mechanical ventilation occurs in up to 30% of cases; however, generally resolves in about 4 weeks.

Malnutrition

Causes generalized skeletal muscle weakness, which may predispose patients to the development of respiratory failure.

Multiple sclerosis (MS)

A central nervous system disease that damages the myelin sheath of nerves and disrupts nerve transmission from the brain to other parts of the body. In advanced cases, patients may require tracheostomy and intermittent or continuous mechanical ventilatory support.

Myasthenia gravis

An autoimmune disease that affects the neuromuscular junction and may cause relapsing, chronic respiratory muscle weakness.

Neuromuscular blocking agents

Neuromuscular-blocking agents (e.g. pancuronium, vercuronium, atracurium, and cistracurium) block nerve transmission at the myoneural junction and cause ventilatory muscle paralysis.

Poliomyelitis

Polio virus infection causes loss of motor neurons and results in varying degrees of muscle weakness and paralysis. Post-polio syndrome may cause a syndrome of new or progressive disability.

Tetanus

Caused by infection with Clostridium tetani spores, which produce a toxin that produces uncontrolled skeletal muscle contractions.

Tick paralysis

Although this disease is rare in humans, certain ticks produce a toxin that may be transmitted following a tick bite and cause life-threatening paralysis.

Ventilatory Requirements A patient’s ventilatory requirements (aka ventilatory demand or ventilatory load) are determined by his or her oxygenation needs, CO2 production, lung function, and acid-base status. The level of ventilation required to remove carbon dioxide is determined by metabolic rate, diet, and associated carbon dioxide production (V̇CO2). For example, at rest, normal V̇CO2 is about 200 mL/min and oxygen consumption (V̇O2) is about 250 mL/min requiring an alveolar ventilation (V̇A) of 4 to 5 L/min to maintain a normal PaCO2 of 40 mmHg. The relationship between V̇A, V̇CO2, and PaCO2 is as follows: V̇A = (0.863 × V̇CO2) ÷ PaCO2. The required alveolar ventilation needed to achieve a normal PaCO2 with a normal CO2 production would be: V̇A = (0.863 × V̇CO2) ÷ PaCO2. Inserting normal values for V̇CO2 and PaCO2, this becomes: V̇A = (0.863 × 200 mL/min) ÷ 40 mmHg = 4.3 L/min. If V̇CO2 increased to 300 mL/min, the required V̇A to achieve a normal PaCO2 of 40 mmHg would be: V̇A = (0.863 × V̇CO2) ÷ PaCO2. V̇A = (0.863 × 300 mL/min) ÷ 40 mmHg = 6.47 L/min This example illustrates that with increases in V̇CO2, alveolar ventilation must increase to maintain a normal PaCO2. Metabolic rate, V̇CO2, and V̇O2 are increased with fever, shivering, agitation, trauma, sepsis, and other hypermetabolic states.4,6 Overfeeding in the intensive care unit may also increase V̇CO2.6 Simply put, increased V̇CO2 will require increased ventilation to remove CO2. Put another way, an ICU patient’s ventilatory requirements may increase due to increased production of carbon dioxide caused by fever, sepsis, agitation, trauma, overfeeding, and other

hypermetabolic states. The normal ventilatory response to hypoxemia is to increase ventilation. Common causes of hypoxemia seen in the ICU include hypoventilation, ventilation–perfusion mismatch (e.g., low V̇/Q̇ and right-to left shunt), and diffusion limitations (diffusion defects alone usually only cause exercise hypoxemia; however, often are combined with low V̇/Q̇ when interstitial lung disease [ILD] progresses). Causes of decreased tissue oxygen delivery seen in critically ill patients include problems with hemoglobin (e.g., anemia, abnormal Hb), and reductions in cardiac output (e.g., circulatory hypoxia) or tissue perfusion (e.g., shock). Hyperventilation decreases alveolar and arterial PCO2 and generally will cause a corresponding increase in alveolar and arterial PO2. Hyperventilation due to hypoxemia is a normal physiologic response that typically results in small, but occasionally clinically important increases in PaO2. Hyperventilation secondary to hypoxemia represents an increase in ventilatory requirements. Lung function may affect ventilatory capacity and, in some cases, ventilatory requirements. As noted above, impaired oxygen transfer across the lung may reduce arterial oxygenation, which may trigger an increase in the level of ventilation required (e.g., hyperventilation as a response to hypoxemia). COPD and pulmonary emboli (with complete vessel blockage) may increase physiologic dead space; increased physiologic dead space will require an increase in the level of ventilation needed to remove carbon dioxide. Clinical Focus 5-1 provides an example of the effect of increased physiologic dead space on ventilatory requirements.

CLINICAL FOCUS 5-1 Effect of Increased Physiologic Dead Space on Ventilatory Requirements In this exercise, we will examine the effects of an increase in physiologic dead space on a patient’s ventilatory requirements. First, we will review normal adult minute ventilation, alveolar ventilation, and physiologic dead space. We will then calculate the effects of a significant increase in physiologic dead space on the level of ventilation required in order to maintain a normal alveolar ventilation. Question 1. Calculate normal adult minute ventilation (aka minute volume). Answer: Minute ventilation (V̇E) is simply tidal volume (VT) times respiratory rate (f):

V̇E = VT × f. Given a normal adult VT of 500 mL and f of 12 breaths/min, minute ventilation is: V̇E = VT × f = 500 mL × 12 = 6000 mL/min = 6 L/min. Question 2. Calculate normal adult alveolar ventilation. Answer: Recall that alveolar ventilation (V̇A) is simply tidal volume (VT) minus dead space (VD) times respiratory rate (f): V̇A = (VT − VD) × f. Normal VT is about 500 mL and normal f is about 12 breaths/min. Clinically, physiologic dead space is sometimes quantified by measurement of VD/VT. Normal physiologic dead space to tidal volume ratio (VD/VT) is 0.30 (range 0.20 to 0.40). Given a normal tidal volume of 500 mL and VD/VT of 0.30 (i.e., 30%), physiologic dead space volume (per breath) can be calculated as follows: VD = VD/VT × VT = 0.30 × 500 mL = 150 mL. Alveolar ventilation per minute (V̇A) can now be calculated: V̇A = (VT – VD) × f = (500 – 150) × 12 = 4200 mL/min = 4.2 L/min. Question 3. Calculate the effect of increased physiologic dead space on ventilatory requirements to maintain normal alveolar ventilation. Answer: Given an increase in VD/VT to 0.60 (i.e., 60%) due to dead space causing disease, calculate physiologic dead volume, assuming a normal VT: VD = VD/VT × VT = 0.60 × 500 mL = 300 mL Question 4. Assuming no change in VT, what respiratory rate would be needed to maintain a normal alveolar ventilation of 4.2 L/min? Answer: V̇A = (VT – VD) × f = (500 – 300) × f = 4200 mL/min (500 – 300) × f = 4200 200 × f = 4200 f = 4200 ÷ 200 = 21 breaths/min Thus, to maintain a V̇A of 4.2 L/min with a tidal volume of 500 mL per breath, and a physiologic dead space volume of 300 mL (i.e., 60% of VT), respiratory frequency (f) would have to increase to 21 breaths per minute. Question 5. Calculate the effect of increased physiologic dead space on

minute ventilation requirements to maintain normal alveolar ventilation. Answer: Minute ventilation is simply tidal volume times respiratory rate. Given the data provided above, the minute ventilation would be: V̇E = VT × f = 500 mL × 21 = 10,500 mL/min = 10.5 L/min. This means that with an increase in physiologic dead space to 60% of the tidal volume, minute ventilation would have to increase from a normal value of 6 L/min to 10.5 L/min to maintain normal alveolar ventilation. This represents a significant increase in the level of ventilation required due to dead space causing disease.

Acid-base balance may also affect the level of ventilation required. Hyperventilation is the normal compensatory response to metabolic acidosis. The expected respiratory compensation for a metabolic acidosis is a decrease in PaCO2 roughly equal to the last two digits of the pH.14 For example, if a metabolic acidosis results in a pH of 7.20, one would expect a compensatory hyperventilation resulting in a PaCO2 of about 20 mmHg. The level of ventilation required to lower PaCO2 in compensation for metabolic acidosis will vary with the severity of the acidosis and is limited by the patient’s ventilatory capacity. Causes of a metabolic acidosis sometimes seen in the ICU include lactic acidosis due to severe hypoxemia, shock, or tissue hypoperfusion; acidosis due to renal failure; ketoacidosis (e.g., diabetic ketoacidosis, starvation, and alcoholic ketoacidosis); poisoning (e.g., salicylate poisoning, ingestion of products containing methanol, ethylene glycol, propylene glycol, or toluene); loss of HCO3- (e.g., diarrhea, pancreatic fistula); hyperalimentation; administration of carbonic anhydrase inhibitors (e.g., acetazolamide); and renal tubular acidosis.15 As noted above, metabolic acidosis will increase ventilatory requirements in proportion to the severity of the acidosis.

Assessment of Ventilation Clinically, assessment of ventilation often includes the patient history, physical examination, measurement of oxygen saturation, and arterial blood gas analysis. Bedside measures of pulmonary function are sometimes performed, which may include measurement of respiratory rate (f), tidal volume (VT), minute ventilation

(V̇E), vital capacity (VC), and maximum inspiratory pressure (MIP). Calculation of the rapid shallow breathing index (RSBI = f/VT; normal is < 105 breaths/min/L) also provides a useful measure that is somewhat predictive of patients’ ability to maintain effective spontaneous breathing. Recall, however, that the single best index of effective ventilation is measurement of PaCO2. Box 5-4 provides bedside pulmonary function values suggestive of the need for mechanical ventilatory support. Clinical Focus 5-2 provides a summary of the causes of inadequate ventilation.

BOX 5-4 Assessment of Ventilation and the Need for Mechanical Ventilatory Support Bedside measures sometimes used for assessment of the adequacy of ventilation and values suggestive of the possible need for the institution of mechanical ventilatory support include: ∎ Respiratory rate (f): f > 30 or < 8 breaths/min suggests a need for mechanical ventilation. Normal adult rate is 12 to 18 breaths/min. ∎ Tidal volume (VT): VT < 5 mL/kg IBW is below normal and (along with other assessment findings) may suggest the need for mechanical ventilation. Normal adult VT is about 400 to 700 mL or about 7 mL/kg IBW. ∎ Minute ventilation (V̇E): Normal adult V̇E is 5 to 10 L/min. V̇E > 10 L/min suggests an underlying problem causing an increase in ventilation (e.g., severe hypoxemia, metabolic acidosis, or pulmonary embolus with increased dead space). ∎ Rapid shallow breathing index (RSBI = f/VT). RSVB ≥ 105 suggests the need for mechanical ventilation. ∎ Vital capacity (VC): VC < 15 to 20 mL/kg IBW suggests the need for mechanical ventilation. ∎ Maximum inspiratory pressure (MIP): MIP > –20 to –30 cm H O suggests 2 the need for mechanical ventilation. ∎ Maximum expiratory pressure (MEP): MEP < 40 cm H O is associated with 2 an inability to generate an effective cough. ∎ 20-30-40 Rule: institution of mechanical ventilation is suggested for patients with neuromuscular disorders when VC < 20 mL/kg IBW and MIP > –30 cm H2O and MEP < 40 cm H2O. ∎

Paco2 and pH: acute ventilatory failure as defined by a sudden increase in PaCO2 (> 45 to 50 mmHg) with a corresponding decrease in pH (≤ 7.25)

suggests the need for mechanical ventilation.

CLINICAL FOCUS 5-2 Causes of Inadequate Ventilation Requiring Mechanical Ventilatory Support The primary purpose of mechanical ventilation is to augment, support, or replace normal spontaneous breathing. Put another way, mechanical ventilatory support may be required for patients who won’t breathe, can’t breathe, or can’t breathe enough, as outlined below4: 1. Patients won’t breathe. Common causes of an absent or decreased respiratory drive to breathe include central nervous system (CNS) depressants (e.g., opioid narcotics, barbiturates, and tranquilizers) and CNS disease (e.g., neurologic disease, stroke, head trauma, and brain death). 2. Patients can’t breathe. Peripheral nervous system disorders, ventilatory muscle disorders, and chest wall, pleural, or upper airway problems make breathing difficult or ineffective. High cervical spine injury (e.g., C2 or C3) may result in diaphragmatic paralysis. Neuromuscular-blocking agents (e.g., pancuronium, vercuronium, atracurium, and cisatracurium) may paralyze the ventilatory muscles. Botulism produces a nerve toxin that may also cause ventilatory muscle paralysis, while tetanus toxin causes uncontrolled skeletal muscle contractions. Guillain-Barré syndrome is a motor neuron disease that causes progressive skeletal muscle weakness and paralysis. Other neuromuscular disorders may interfere with ventilatory muscle function. For example, multiple sclerosis can interfere with nerve transmission, while myasthenia gravis affects the neuromuscular junction. Ventilatory muscle weakness and fatigue may occur in the presence of very high ventilatory workloads due to pulmonary disease (e.g., decreased pulmonary compliance [ARDS, pneumonia, and interstitial lung disease], obstructive lung disease [COPD]), or thoracic disorders (e.g., decreased thoracic compliance). Massive pleural effusion may reduce the effectiveness of the ventilatory pump, and upper airway obstruction may interfere with the flow of gas into the lung while increasing WOB. 3. Patients can’t breathe enough. This is caused by increased ventilatory demand (i.e., increased ventilatory requirements) due to oxygenation problems, increased carbon dioxide production, or increased physiologic dead

space. The normal response to hypoxemia is hyperventilation. Patients with already compromised lung function (e.g., obstructive lung disease, decreased pulmonary compliance, increased airway resistance, bronchospasm, and mucosal edema), reduced ventilatory muscle strength and endurance, or ventilation/perfusion abnormalities may not be able increase ventilation sufficiently (i.e., can’t breathe enough). Increased carbon dioxide production will increase the level of ventilation required to maintain normal acid-base homeostasis. Causes of increased CO2 production seen in the ICU include fever, shivering, agitation, trauma, sepsis, overfeeding, and fighting the ventilator. Patients with compromised lung function or ventilatory muscle dysfunction may not be able to increase ventilation sufficiently. Increased physiologic dead space will require an increase in minute ventilation to maintain the same level of alveolar ventilation. Patients with otherwise compromised lung function or ventilatory muscle weakness may not be able to increase ventilation sufficiently.

RC Insight MIP > –20 to – 30 mmHg and/or VC < 15 to 20 mL/kg ideal body weight (IBW) are associated with impending or actual ventilatory failure.

In summary, when ventilatory requirements exceed ventilatory capacity, hypercapnic respiratory failure (aka ventilatory failure) may ensue, and mechanical ventilatory support may be required. Ventilatory requirements are determined by oxygenation needs, carbon dioxide production, lung function, and acid-base status. Ventilatory capacity is determined by respiratory drive, lung function, ventilatory workload, and ventilatory muscle strength. Common causes of increased ventilatory requirements include hypoxia, increased metabolic rate, increased physiologic dead space, and metabolic acidosis. Common causes of decreased ventilatory capacity include suppression or absence of ventilatory drive (e.g., opioids, neurologic disease, and cardiac arrest), increased ventilatory workload (e.g., decreased pulmonary compliance or increased airway resistance), decreased ventilatory muscle strength (e.g., ventilatory muscle fatigue), and impaired pulmonary function (e.g., airway obstruction, decreased compliance, and increased resistance). Bedside

measures of the adequacy of ventilation include tidal volume, respiratory rate, RSBI, minute ventilation, vital capacity, and maximum inspiratory pressure (MIP). However, the single best index of the adequacy of ventilation is measurement of PaCO2. RC Insight Mechanical ventilation should be considered in patients with an acute increase in PaCO2 > 45 to 50 mmHg, resulting in a pH ≤ 7.25.

Clinical Manifestations of Respiratory Failure The most common reason for initiating mechanical ventilatory support is acute respiratory failure. Common causes of acute respiratory failure requiring mechanical ventilation include pneumonia, ARDS, trauma, sepsis, postoperative respiratory failure, COPD exacerbation, heart failure, coma, neuromuscular disease, sedative or narcotic drug overdose, and pulmonary aspiration.2–4 Other causes of respiratory failure that may require mechanical ventilatory support include inhalational injury (e.g., smoke, toxic gases, and fumes), near-drowning, chest trauma (flail chest, pulmonary contusion, and pneumothorax), cardiogenic pulmonary edema, pulmonary embolism, upper airway obstruction (e.g., tumor, laryngeal edema), acute asthma exacerbation, high cervical spine injury, pulmonary hemorrhage, and massive pleural effusion.2–4 Early clinical manifestations of acute respiratory failure include tachycardia, tachypnea, diaphoresis, anxiety, and respiratory distress, followed by depressed mental status, confusion, somnolence, and coma as the patient’s condition deteriorates. Physical findings associated with increased WOB include accessory muscle use, intercostal retractions, and asynchronous chest wall to diaphragmatic movement. Alterations in ventilation initially include increased respiratory rate, and rapid shallow breathing, sometimes followed by slowed or irregular breathing and periods of apnea or respiratory arrest as the patient’s condition worsens. Initially, arterial blood gases may show hypoxemia, hyperventilation, and alkalosis, followed by hypoventilation, hypercapnia, and respiratory acidosis as the patient’s condition gets worse. Clinical Focus 5-3 summarizes the clinical manifestations of acute respiratory failure.

CLINICAL FOCUS 5-3 Clinical Manifestations of Acute Respiratory Failure Associated with the Need for Mechanical Ventilatory Support The respiratory care clinician should be alert to the presence of the clinical manifestations of acute respiratory failure, which may suggest the need for mechanical ventilatory support. These include alterations in ventilatory status, cardiac function, CNS/mental status, oxygenation, and acid-base balance, as described below. Respiratory/ventilatory status

Tachypnea (f > 20) is associated with respiratory distress and hypoxemia. f ≥ 30 is a sensitive marker of respiratory distress and is often associated with the actual or impending ventilatory failure. Bradypnea (f < 8) is associated with CNS problems (brain damage, head injury), sedatives or narcotic drug overdose, severe hypoxemia, and impending respiratory arrest. Respiratory distress/increased work of breathing Dyspnea/respiratory distress is generally due to increased respiratory drive (e.g., hypoxemia, hypercapnia, and acidosis) or impaired ventilatory mechanics (e.g., increased WOB, decreased lung compliance, increased airway resistance, and obstructive lung disease). Accessory muscle use, including contractions of the inspiratory accessory muscles (i.e., scalenes, sternocleidomastoids, and pectoralis major), are associated with respiratory distress and increased WOB. For example, palpable scalene muscle use during inspiration suggests a markedly increased WOB. Palpable abdominal muscle tensing during expiration suggests increased expiratory work associated with obstruction. Intercostal retractions are associated with significant negative pleural pressures on inspiration, sometimes seen with upper airway obstruction, decreased lung compliance, or inadequate gas flow to the mechanically ventilated patient. Chest wall to diaphragmatic asynchrony, involving asynchronous or spasmodic diaphragmatic contractions, is associated with respiratory muscle fatigue and may signal an impending respiratory arrest. Diaphoresis occurs in patients with acute distress and may be associated with increased WOB. Nasal flaring is associated with marked increased inspiratory efforts, especially in infants and children. Rapid shallow breathing is a common finding in patients with acute respiratory failure. In adults, VT < 300 mL with f > 30 is associated with the need for mechanical ventilatory support. Rapid shallow breathing index (RSBI = f/VT) quantifies the degree of rapid shallow breathing; RSBI ≥ 105 is associated with the need for mechanical ventilatory support. Reduced chest expansion with bilateral limitation is often seen with COPD and neuromuscular disease. Unilateral disorders such as lobar atelectasis or lobar pneumonia may cause unilateral limitation of chest wall movement. Slowed or irregular breathing manifests as irregular or asynchronous

breathing, periods of apnea, or rapid shallow breathing; these are all suggestive of the need for mechanical ventilatory support. Apnea is the complete cessation of breathing and provides a clear indication for mechanical ventilation. Cardiac/cardiovascular Tachycardia (heart rate [HR] > 100 in adults) is an initial (early) response to hypoxemia. Bradycardia (HR < 60) is a late response associated with severe hypoxemia that may signal impending cardiac arrest. Hypertension (blood pressure [BP] ≥ 140/90 mmHg) is an initial response to hypoxemia. Hypotension (BP < 90/60 mmHg) is associated with decreased cardiac output, peripheral vasodilation, or low circulating blood volume. Common causes include dehydration, blood loss, sepsis, heart disease, and shock. Hypotension is a late response to severe hypoxemia. Cardiac arrhythmias are a common response to severe hypoxemia and include sinus tachycardia, premature ventricular contractions (PVCs), ventricular tachycardia, irregular heartbeat, heart block, and atrial fibrillation; severe hypoxia may lead to cardiac arrest. CNS/mental status The brain is especially sensitive to hypoxia and hypercarbia. Excitement, overconfidence, restlessness, anxiety, headache, and altered mental status are early findings with acute respiratory failure. Confusion, somnolence, unconsciousness, unresponsiveness, and coma may occur as the patient’s condition deteriorates. Oxygen desaturation Oxygen desaturation is commonly assessed by pulse oximetry (SpO2) or arterial blood gas analysis (SaO2, PaO2). SpO2 85% to 90% is associated with a PaO2 of approximately 50 to 59 mmHg or moderate hypoxemia. SpO2 = 75% to 84% is associated with a PaO2 of approximately 40 to 49 mmHg or moderate to severe hypoxemia. SpO2 < 75% is associated with a PaO2 < 40 mmHg or very severe hypoxemia. Severe oxygenation problems (e.g., refractory hypoxemia) provide a possible indication for institution of mechanical ventilation and the use of PEEP or CPAP. Cyanosis is a variable finding that may not be present in hypoxemic

patients with anemia. Acid-base disturbances Hypoxemia, hyperventilation, and respiratory alkalosis are typically seen in the initial stages of acute respiratory failure. PaO2 < 60 mmHg; PaCO2 < 35 mmHg with a corresponding increase in pH > 7.45. May signal impending ventilatory failure. Impending ventilatory failure is a possible indication for institution of mechanical ventilation. Severe hypoxemia, hypoventilation, and respiratory acidosis are seen as acute respiratory failure worsens. Acute ventilatory failure (defined as a sudden increase in PaCO2 with a corresponding decrease in pH) provides a major indication for institution of mechanical ventilation. PaO2 < 40 to 60 mmHg; PaCO2 > 45 mmHg with a corresponding decrease in pH < 7.35 provides criteria for severe hypoxemia, hypoventilation, and respiratory acidosis (aka acute ventilatory failure).

Goals of Mechanical Ventilatory Support Mechanical ventilation can normalize alveolar ventilation and PaCO2, correct both respiratory and metabolic acidosis, reverse hypoxemia, relieve respiratory distress, and allow for recovery from ventilatory muscle fatigue by unloading the ventilatory muscles.2,3,16 Mechanical ventilation may also allow for deep sedation and neuromuscular blockade, in order for certain procedures to be performed.2,3,16 Deep sedation (with or without the use of neuromuscular-blocking agents) is also sometimes useful in certain cases of severe distress and agitation, delirium, or severe, refractory, or life-threatening oxygenation disorders (e.g., severe ARDS).2,3,16 In general, however, sedation should be kept to the minimum necessary for the comfort and safety of the patient and neuromuscular-blocking agents should be used only when absolutely necessary. The primary goals of mechanical ventilatory support are to: 1. 2. 3. 4. 5. 6. 7.

Provide adequate alveolar ventilation. Ensure adequate tissue oxygenation. Restore and maintain acid-base homeostasis. Reduce the WOB. Ensure patient safety and comfort. Minimize harmful side effects and complications. Promote liberation of the patient from the ventilator.

Mechanical ventilation may reduce cardiac work by supporting oxygenation and relieving the stress on the heart caused by increased cardiac output in compensation for hypoxemia.17 Mechanical ventilation may also help restore or maintain lung volumes and prevent or treat atelectasis by restoring adequate lung volumes and incorporating positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP).17 Mechanical ventilation may be helpful for internal stabilization of the chest wall in cases of severe chest trauma (e.g., flail chest) requiring mechanical ventilatory support for respiratory failure.18

Indications for Mechanical Ventilation Because mechanical ventilation supports or replaces the normal ventilatory pump, its primary indication is inadequate or absent spontaneous breathing. Mechanical ventilation will also allow for the application of PEEP or CPAP, as well as certain other techniques useful in the support of patients with severe oxygenation problems. The respiratory care clinician should be on the alert for the presence of disease states or conditions that predispose patients to the development of acute respiratory failure requiring mechanical ventilatory support. The primary indications for institution of mechanical ventilation are: 1. 2. 3. 4.

Apnea Acute ventilatory failure Impending ventilatory failure Severe/refractory oxygenation problems

Apnea Apnea is the complete cessation of breathing, and failure to institute mechanical ventilatory support in the presence of extended periods of apnea may lead to cardiac arrest and brain death in minutes. Apnea may be caused by a number of disease states or conditions, including cardiac disease, neurologic disease, shock, trauma, spinal cord injury, and sedative or narcotic drug overdose. Cardiac arrest is a common cause of apnea seen in the acute care setting. Myocardial ischemia, myocardial infarction, cardiac arrhythmias, shock, trauma, severe hypotension, and severe hypoxemia all may cause cardiac arrest. Administration of general anesthesia or neuromuscular-blocking agents may also cause apnea. Airway obstruction can completely block airflow into the lungs, although respiratory efforts will often continue until cardiac arrest ensues. Possible causes of complete airway occlusion include upper airway foreign body aspiration (e.g., food, other objects), upper airway swelling due to anaphylaxis (e.g., insect bites, medications, and food allergy), epiglottitis, airway trauma, laryngospasm post-extubation with associated swelling, and angioedema. The initial treatment of apnea in the acute care setting includes immediately securing the airway and providing ventilatory support. This may include insertion of an oral pharyngeal airway and positive-pressure ventilation using a bag-mask

manual resuscitator bag. If spontaneous breathing does not rapidly resume, endotracheal intubation should be performed and mechanical ventilatory support provided. Upper airway obstruction or acute laryngospasm occasionally requires emergent tracheostomy. While respiratory arrest occasionally occurs alone in the acute care setting, more commonly, patients suffer cardiac and respiratory arrest together. In the case of concurrent cardiac and respiratory arrest, institution of advanced cardiac life support (ACLS) protocols should begin immediately. Box 5-5 summarizes common causes of apnea. Clinical Focus 5-4 provides a discussion of a patient with apnea.

BOX 5-5 Causes of Apnea Apnea is the complete cessation of breathing, which may be caused by a number of different disease states and conditions including: ∎ Cardiac arrest due to myocardial ischemia and infarction; cardiac arrhythmias; other heart disease; shock; trauma; upper airway obstruction; acute, severe pulmonary embolus; severe electrolyte or acid-base disturbances; or acute, severe hypoxia. ∎ Brain death or severe brain injury; brain death is the irreversible loss of all brain function resulting in a coma, absence of brainstem reflexes, and apnea. ∎ Trauma, including head trauma, chest trauma, accidents, near-drowning, and electrical shock. ∎ Shock and hypotension to include cardiogenic shock, hypovolemic shock, neurogenic shock, anaphylactic shock, and septic shock. ∎ Drug overdose involving narcotic, sedative, or benzodiazepine tranquilizer drugs may result in apnea. ∎ Cervical spine injury at the level of C2, C3, or C4 may result in partial or complete paralysis of the diaphragm. ∎ Neurologic disease including massive stroke, brainstem tumor, cerebral hemorrhage, hepatic encephalopathy, meningitis, encephalitis, and other conditions causing coma. ∎ Neuromuscular disease resulting in ventilatory muscle paralysis (e.g., Guillain-Barré, ALS, poliomyelitis, botulism). ∎ Administration of general anesthesia. ∎ Paralytic drugs (i.e., neuromuscular-blocking agents). ∎ Respiratory failure with severe hypoxemia can lead to apnea.

∎

∎

Central, obstructive, and mixed sleep apneas, which generally do not require invasive mechanical ventilatory support. Nighttime noninvasive ventilatory support (i.e., BiPAP), however, is sometimes used in the treatment of obstructive sleep apnea. Apnea of prematurity is a disorder sometimes seen in premature infants.

CLINICAL FOCUS 5-4 Apnea A 62-year-old male patient is transferred to the intensive care unit following a sudden cardiac arrest that occurred on a general medical–surgical floor. The patient had been admitted to the hospital for abdominal surgery and the arrest occurred following admission. The patient was intubated, and advanced cardiac life support (ACLS) protocols were initiated. Cardiac function and blood pressure were restored; however, spontaneous breathing remains absent. The patient is being supported using a bag-valve mask manual resuscitator with supplemental oxygen. Oxygen saturation (SpO2) by pulse oximetry is 98%. Question 1. Does the patient have any of the indications for institution of invasive mechanical ventilatory support? Answer: The primary indications for institution of mechanical ventilatory support are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. Apnea is defined as the complete absence of spontaneous breathing while the term acute ventilatory failure generally is used for patients that have an inadequate level of spontaneous breathing. The term impending ventilatory failure refers to situations in which acute ventilatory failure is likely in the near future. Severe oxygenation problems are identified by the presence of inadequate arterial oxygen levels while receiving conventional oxygen therapy. The patient described above has no spontaneous breathing and meets the criteria for apnea. Assuming adequate spontaneous breathing does not rapidly resume, mechanical ventilatory support is indicated. Question 2. Are any contraindications for mechanical ventilation present? Answer: The contraindications for mechanical ventilation include: 1. Pneumothorax without chest tubes. Pneumothorax is not an uncommon complication of external chest compressions performed during basic and advanced life support (BLS/ACLS). While the information provided does not indicate the presence of a pneumothorax, the respiratory care clinician should be on the alert for the presence of any of the signs of pneumothorax. These include:

2. 3.

4.

5.

Respiratory distress. Alterations in vital signs (e.g., tachycardia, bradycardia, cardiac arrhythmia, hypotension, and tachypnea). Oxygen desaturation. Absent or reduced breath sounds on one side. Uneven chest motion on one side. Apparent unilateral lung hyperinflation. Tracheal shift and/or shift of the cardiac point of maximal impulse (PMI) may suggest development of a tension pneumothorax. Hyperresonance (tympanic) to percussion on one side or area of the chest. Development of subcutaneous emphysema. Absence of indications for mechanical ventilation. Apnea is a clear indication for mechanical ventilation. Rapid resolution of the patient’s apnea is likely without the need for continued mechanical ventilatory support. Many patients who are successfully resuscitated following cardiac arrest begin adequate spontaneous breathing very quickly. This patient, however, remains apneic even though enough time has passed for the patient to be transported to the intensive care unit. Because the patient remains apneic, institution of mechanical ventilation at this time is indicated. Institution of mechanical ventilation would be futile. The patient has been successfully resuscitated and cardiac function and blood pressure restored. Failure to provide mechanical ventilatory support in the presence of apnea could result in the rapid death of the patient. Institution of mechanical ventilation would be against the patient’s wishes. No information is provided regarding the patient’s wishes and consequently withholding mechanical ventilation at this time would be inappropriate.

Acute Ventilatory Failure Acute ventilatory failure (AVF) may be defined as a sudden increase in PaCO2 with a corresponding decrease in pH. For example, an acute increase in PaCO2 of 10 mmHg should result in a decrease in pH of about 0.08 units. Acute ventilatory failure is also known as acute hypercapnic respiratory failure; AVF initially results in an uncompensated respiratory acidosis. While arbitrary cut points should not be imposed, generally speaking, an acute increase in PaCO2 resulting in a decrease in

pH to about 7.25 or below provides a clear indication for mechanical ventilation. RC Insight Acutely, for every 1-mmHg increase in PaCO2 there will be a decrease in pH of about 0.008 units.

The respiratory care clinician should be on the alert for the presence of any of the many disease states or conditions that predispose patients for the development of acute ventilatory failure. These include problems with the conducting airways, alveolar gas exchange, respiratory drive, or ventilatory workload. Other risk factors for the development of ventilatory failure include neuromuscular disease, thoracic or abdominal surgery, chronic pulmonary disease, significant pleural disease, and cardiac disease. Shock, trauma, sepsis, severe burns, and severe obesity (BMI ≥ 40 kg/m2 or ≥ 35 kg/m2 in the presence of comorbidities) are also risk factors for the development of AVF. Box 5-6 summarizes the disease states or conditions associated with the development of acute ventilatory failure and the need to institute mechanical ventilatory support.

BOX 5-6 Conditions Predisposing Patients to the Development of Acute Ventilatory Failure (AVF) AVF occurs when ventilatory requirements exceed ventilatory capacity. Ventilatory capacity decreases because of diaphragmatic fatigue or ventilatory muscle dysfunction, neurologic or neuromuscular disease, diminished or absent respiratory drive, airway obstruction, and impaired lung function. Ventilatory requirements may increase due to hypoxemia, increased metabolic rate, increased physiologic dead space, or metabolic acidosis. Problems predisposing patients to the development of AVF include: ∎ Conducting airways problems • Upper airway obstruction, laryngeal edema [croup], epiglottis, and upper airway trauma [inhaled smoke, flames, or noxious gases]) • Lower airway disease including bronchospasm, mucosal edema, and excessive secretions ∎ Alveolar gas exchange problems • ARDS, pneumonia, atelectasis, and pulmonary edema • Aspiration

Near-drowning Pulmonary embolus ∎ Respiratory drive depression or absence • Excessive sedation • General anesthesia • Narcotic or sedative drug overdose • Head trauma • Neurologic disease (massive stroke, tumor, cerebral hemorrhage, and infectious disease) ∎ Disorders affecting neuromuscular function • Guillain-Barré, ALS, myasthenia gravis, multiple sclerosis, and polio • Spinal cord injury (C2, C3, and C4) • Botulism and tetanus ∎ Increased ventilatory workload • Decreased lung compliance ○ Atelectasis, pneumonia, pulmonary edema, and ARDS • Decreased thoracic compliance ○ Obesity, ascites, and thoracic deformity • Increased airway resistance ○ Acute asthma exacerbation, COPD exacerbation ○ Airway inflammation, mucosal edema, bronchospasm, and increased secretions ∎ Thoracic or abdominal surgery • Cardiac surgery • Lung resection ∎ Chronic pulmonary disease • COPD (emphysema, chronic bronchitis), asthma, bronchiectasis, and cystic fibrosis • Interstitial lung disease ∎ Pleural disease • Large pleural effusion, pneumothorax ∎ Cardiac disease • Congestive heart failure, myocardial ischemia and infarction, and other cardiac disease ∎ Shock, sepsis, trauma, and severe burns ∎ Severe obesity (BMI ≥ 40 kg/m2 or ≥ 35 kg/m2 in the presence of

• •

comorbidities)

Acute ventilatory failure should not be confused with chronic ventilatory failure, in which PaCO2 is chronically elevated and pH is normal or near-normal due to metabolic compensation. With chronic ventilatory failure, the acid-base state is typically compensated or partly compensated respiratory acidosis (usually back to a pH of 7.34 to 7.36). Chronic ventilatory failure is associated with chronic lung disease, such as end-stage cystic fibrosis, interstitial lung disease, or certain patients with COPD. Patients with chronic ventilatory failure may develop acute ventilatory failure superimposed on chronic ventilatory failure. For example, a COPD patient with chronic CO2 retention may experience an acute viral or bacterial infection. This acute exacerbation of COPD may result in an increase in WOB and an acute increase in PaCO2 and corresponding decrease in pH. COPD patients with markedly elevated respiratory rate, accessory muscle use, acute change in mental status, and hypoxemia that is only partially responsive to oxygen therapy have potentially life-threatening exacerbations of their chronic lung disease. Acute ventilatory failure superimposed on chronic ventilatory failure may require mechanical ventilatory support. Clinical Focus 5-5 provides an example of a patient with acute ventilatory failure.

CLINICAL FOCUS 5-5 Acute Ventilatory Failure A 26-year-old male with a history of opioid abuse arrives, unconscious and unresponsive, in the emergency department via EMS. He is suspected of taking an overdose of an unknown substance. The patient was found in a collapsed state in his apartment by a friend. His friend believes that the patient may have consumed pain medications in addition to an unknown quantity of alcohol. His vital signs include tachycardia (HR = 140), irregular pulse, bradypnea (f = 8), and decreased blood pressure (90/60 mmHg). Breath sounds are diminished. An arterial blood gas sample taken on oxygen by partial rebreathing mask reveals: pH = 7.18 PaCO2 = 70 mmHg HCO-3 = 28 mmHg Base excess (BE) = 1.0

PaO2 = 90 mmHg SaO2 = 0.96 mmHg Question 1. Based on the information now available, how would you describe this patient’s oxygenation and ventilatory status? Answer: The arterial pH in combination with an elevated PaCO2 and normal HCO-3 and base excess indicate an acute (uncompensated) respiratory acidosis; clinically this blood gas result would be described as acute ventilatory failure. The patient’s PaO2 while breathing oxygen by mask is 90 mmHg. Typical partial rebreathing oxygen masks provide an FIO2 ranging from about 40% to 70% (0.40 to 0.70). A healthy young person with normal lung function should have a significantly elevated PaO2 (> 140 mmHg) while breathing moderate to high concentrations of supplemental oxygen by mask. In this case, the patient’s PaO2 is much less than expected due to severe hypoventilation. Question 2. Is mechanical ventilatory support indicated for this patient? Answer: Acute ventilatory failure is one of the primary indications for mechanical ventilation. While specific criteria should not be arbitrarily imposed, generally speaking, mechanical ventilation should be seriously considered when pH ≤ 7.25 due to an elevated PaCO2. Based on the patient’s history, physical assessment, and arterial blood gas results, this patient meets the criteria for initiation of mechanical ventilatory support. Because the patient is unconscious and unresponsive, endotracheal intubation should be performed in order to secure and protect the airway and invasive mechanical ventilation begun. It should be noted that a number of different conditions may cause coma in adults. These include drugs and medications (e.g., sedatives, hypnotics, barbiturates, tranquilizers, opiates, and alcohol), sepsis, electrolyte disturbances, and cerebral vascular disease (e.g., cerebral vascular accident [CVA]). Other causes include infection (e.g., bacterial meningitis, viral encephalitis), metabolic disease (e.g., ketoacidosis, lactic acidosis, and hypoglycemia), and poisonings (e.g., cyanide, carbon monoxide). The patient workup should include measurement of serum glucose to verify the patient’s condition is not due to hypoglycemia. Serum acetaminophen concentration should be measured if it is thought that an opioid medication was consumed that included acetaminophen. Chest imaging is appropriate if signs of pulmonary aspiration are present (e.g., abnormal breath sounds). In cases of opioid overdose, administration of a shortacting opioid antagonist (e.g., naloxone [Narcan]) by IV route may restore spontaneous ventilation in a short period of time; however, ventilatory support should be provided until adequate spontaneous ventilation returns. Complications of opioid overdose include aspiration, lung injury, and ARDS.

Impending Ventilatory Failure The term impending ventilatory failure refers to situations where ventilatory failure is likely to occur in the immediate future. In these cases, ventilatory support may be initiated prior to the development of an acute, severe respiratory acidosis. The decision to begin ventilatory support is based on patient assessment, knowledge of the typical progression of the patient’s disease state or condition, and the clinical judgment that the patient will progress to acute ventilatory failure in the near future. Markedly elevated respiratory rates and severe distress use may signal an impending respiratory arrest.2–4 Clinical manifestations of impending ventilatory failure include extreme tachypnea (f ≥ 35), severe dyspnea, accessory muscle use, intercostal retractions, significant diaphoresis, dusky skin, and altered mental status.2–4 Patients often have difficulty speaking in complete sentences or lying supine due to dyspnea. In such cases, emergent intubation and initiation of mechanical ventilation may be appropriate. With certain diseases, such as COPD and pulmonary edema, a short course (30 to 120 minutes) of noninvasive ventilation may be attempted prior to intubation but should always be performed in the setting of close observation. Use of high-flow, heated/humidified nasal cannulas have also become popular in supporting patients with impending respiratory failure by allowing the delivery of high concentrations of oxygen and small amounts of inspiratory and expiratory pressures. RC Insight Respiratory rate ≥ 35 breaths/min, severe respiratory distress with air hunger, diaphoresis, and accessory muscle use may signal impending respiratory arrest and the need to institute mechanical ventilatory support.

Acute, severe asthma exacerbation represents a potentially life-threatening condition. The term status asthmaticus refers to severe bronchospasm that is unresponsive to routine therapy.12 Asthma patients seen in the emergency department typically show a mild respiratory alkalosis and often respond to routine therapy. Patients with acute, severe asthma that is unresponsive to conventional therapy may exhibit depressed mental status, slowed spontaneous respiratory rate, and hypoxemia despite administration of O2.12 In such patients, increasing PaCO2 is

an ominous sign because the patient’s condition may rapidly progress to acute ventilatory failure and respiratory arrest.12 Hypercapnia that fails to respond to bronchodilator therapy suggests the need for mechanical ventilation and institution of ventilatory support should be performed prior to respiratory arrest. In such cases, mechanical ventilation may be considered prior to the development of severe respiratory acidosis.19 Certain neuromuscular disorders may also progress to ventilatory failure requiring mechanical ventilation. Guillain-Barré syndrome is an acute immune-mediated polyneuropathy that sometimes occurs following a flu-like illness in otherwise healthy adults. Guillain-Barré syndrome typically, but not always, causes ascending, symmetrical muscle weakness and paralysis.20 Weakness usually begins in the legs, although the initial weakness sometimes occurs in the arms or facial muscles. Most patients have decreased or absent deep tendon reflexes, and they may experience paresthesias (tingling) in the affected arms or legs.20 Patients with suspected Guillain-Barré should be admitted to the hospital and monitored carefully for declines in vital capacity and inspiratory muscle strength. Muscle weakness and paralysis typically progresses over a period of days and may reach a plateau in about 2 weeks, with recovery occurring 2 to 4 weeks later.20 Ventilatory muscle weakness or paralysis requiring the institution of mechanical ventilation occurs in up to 30% of cases.20 Frequent (e.g., every 1 to 2 hours) bedside pulmonary function testing should be initiated in all Guillain-Barré patients and continued as the disease progresses. Impending ventilatory failure is identified by a reduction in vital capacity (VC < 20 mL/kg), maximum inspiratory pressure (MIP > –30 cm H2O), and maximum expiratory pressure (MEP < 40 cm H2O). When these measures decline below the suggested values, mechanical ventilatory support may be initiated. Others have suggested that mechanical ventilation should be instituted when the vital capacity falls to less than 1.0 L (or 15 mL/kg IBW).4 Other neuromuscular diseases that may involve the diaphragm and ventilatory muscles and require the institution of mechanical ventilatory support include myasthenia gravis, severe muscular dystrophy, and amyotrophic lateral sclerosis (ALS).4 Clinical Focus 5-6 provides an example of a patient with impending ventilatory failure due to neuromuscular disease.

CLINICAL FOCUS 5-6 Impending Ventilatory Failure A 35-year-old man has been diagnosed as having Guillain-Barré syndrome. The patient experienced a flu-like illness followed by progressive muscle weakness in his legs and difficulty walking over the past several days. The patient was admitted to the hospital this morning, and the respiratory care clinician was asked to evaluate the patient’s ventilatory status. The patient was awake and alert, resting comfortably, and in no apparent respiratory distress. Question 1. What bedside pulmonary function tests should be frequently performed in order to monitor this patient? Answer: Bedside measures of ventilatory function in patients with neuromuscular disease include maximum inspiratory pressure (MIP), vital capacity (VC), and maximum expiratory pressure (MEP). It may also be useful to measure the patient’s spontaneous tidal volume (VT), respiratory rate (f), and minute ventilation (V̇E). Initial values for bedside pulmonary function tests for this patient at 10:00 a.m. were VC = 3.5 L, MIP = –40 cm H2O, and MEP = + 50 mmHg. The patient’s weight is 70 kg, and the patient is not overweight. Question 2. What is your assessment of the results of the bedside pulmonary function tests performed at 10:00 a.m.? Answer: VC = 3.5 L. Normal vital capacity in adults is about 70 mL/kg or about 4.9 L for this patient (70 mL/kg × 70 kg = 4900 mL or 4.9 L). Vital capacity is reduced to about 71% of predicted; however, the patient’s vital capacity is still sufficient to support adequate spontaneous breathing. MIP = –40 cm H2O. Normal MIP varies with age and gender and can be as much as –100 cm H2O in healthy young men. Generally speaking, MIP < –30 cm H2O is consistent with adequate spontaneous ventilation, and MIP < –60 cm H2O can be considered normal. MEP = +50 mmHg. Maximum expiratory pressure varies with age and gender and can exceed +100 cm H2O in healthy young adults. MEP ≥ 80 to 100 cm H2O may be considered normal, and values ≥ 40 cm H2O are associated with the ability to spontaneously cough and deep breathe. VC, MIP, and MEP values are reduced; however, not to a level suggesting the need for mechanical ventilation at this time. The respiratory care clinician recommends monitoring bedside pulmonary function values to assess ventilation every 1 to 2 hours because of the progressive nature of the disease. The following data was collected that evening at 6:00 p.m. on the patient: VT = 490

f = 20 breaths/min V̇E = 9.8 L/min VC = 950 mL MIP = –18 cm H2O MEP = +30 cm H2O FIO2 = 0.21 pH = 7.45 PaO2 = 85 PaCO2 = 38 FIO2 = 0.21 HCO-3 = 26 BE = +1 SaO2 = 96% Question 3. What is your assessment of this patient’s condition at 6:00 p.m.? Answer: The patient’s tidal volume is normal, although his respiratory rate and minute ventilation are slightly elevated. The patient’s expected VC would be about 70 mL/kg of ideal body weight (IBW), which corresponds to a predicted VC of about 4.9 L. Normal values for MIP are < –30 cm H2O and normal MEP is > +40 C; the patient’s MIP and MEP are –18 cm H2O and +30 cm H2O respectively. The patient’s arterial oxygen tension and saturation while breathing room air are normal and the patient’s pH and PaCO2 are normal, indicating normal ventilatory and acid-base status. While the patient is ventilating adequately at 6:00 p.m., VC, MIP and MEP are much lower than normal. Generally speaking, when VC declines to less than 1.0 L in adults (or VC < 15 to 20 mL/kg IBW or < 60% predicted) due to neuromuscular disease with progressive muscle weakness, mechanical ventilation should be considered. Predicted VC for this patient is about 4.9 L and the patient’s current VC < 1.0 L and < 60% of predicted. Others suggest the “2030-40 Rule,” which calls for the institution of mechanical ventilation when VC < 20 mL/kg IBW, MIP > –30 cm H2O, and MEP < +40 cm H2O. Question 4. Is initiation of mechanical ventilatory support indicated for this patient at this time? Acute ventilatory failure (i.e., hypercapnia with acidosis) is not yet present based on current arterial blood gas results. However, VC, MIP, and MEP values all

suggest that mechanical ventilation should be initiated now because of impending ventilatory failure. Because the patient is not yet in acute distress, initiation of mechanical ventilation at this time will allow the process of establishing an artificial airway and beginning ventilatory support to proceed in an orderly and controlled fashion. The decision to proceed with mechanical ventilation at this time is based on the clinician’s judgment that acute hypercapnia with acidosis (i.e., ventilatory failure) will occur in the near future, and delay would place the patient at increased risk.

RC Insight Rapid shallow breathing (f > 30 breaths/min; VT ≤ 300 mL in adults) may signal impending ventilatory failure requiring mechanical ventilatory support.

To summarize, with impending ventilatory failure, intubation and the institution of mechanical ventilation may occur prior to the onset of acute respiratory acidosis. By intervening before the patient is an acute distress, establishing an artificial airway and beginning ventilatory support can proceed in a more orderly and controlled fashion. The decision to initiate mechanical ventilation is based on the diagnosis, patient assessment, and sound clinical judgment.

Severe Oxygenation Problems Hypoxemia (PaO2 < 60 mmHg; SaO2 < 90%) while breathing increased oxygen concentrations (FIO2 > 0.40) suggests a significant oxygenation problem. The term refractory hypoxemia refers to an oxygenation problem that does not respond to conventional oxygen therapy. The Pao2/Fio2 ratio (P/F ratio) provides a simple measure of the effectiveness of oxygen transfer across the lung. A normal P/F ratio is in the range of 380 to 476 mmHg, while P/F ratios ≤ 300 mmHg are associated with oxygenation problems. For patients with ARDS, the P/F ratio is used in classifying the severity of disease where: P/F ≤ 300 mmHg but > 200 mmHg (while receiving 5 cm H2O PEEP) = mild ARDS P/F ≤ 200 mmHg but > 100 mmHg (while receiving 5 cm H2O PEEP) = moderate ARDS P/F ≤ 100 mmHg (while receiving 5 cm H2O PEEP) = severe ARDS

RC Insight Refractory hypoxemia is present when an increase in FIO2 ≥ 0.10 results in an improvement of PaO2 < 5 mmHg.

Patients with severe oxygenation problems may require the use of PEEP, CPAP, or other techniques to improve arterial oxygenation (e.g., inverse ratio ventilation), which are best applied during invasive mechanical ventilation. PEEP is applied during expiration following a pressure- or volume-controlled inspiration provided by a mechanical ventilator, while CPAP is defined as spontaneous breathing with an elevated baseline pressure. Patients with ARDS have severe oxygenation problems due to increased intrapulmonary right-to-left shunt. Intrapulmonary shunt (aka physiologic shunt) occurs when venous blood is carried from the right side of the heart to the lungs via the pulmonary arteries and then to pulmonary capillaries adjacent alveoli that are not ventilated (V̇/Q̇ = 0). This unoxygenated blood is then returned to the left side of the heart without participating in gas exchange. In addition to ARDS, other causes of intrapulmonary R-to-L shunting commonly seen in the ICU include consolidative pneumonia, severe pulmonary edema with alveolar filling, significant atelectasis, complete airway obstruction, and large pneumothorax. Recall that pulmonary edema may be cardiogenic or noncardiogenic and noncardiogenic causes of pulmonary edema include ARDS and neurogenic pulmonary edema. Patients with large intrapulmonary shunts experience significant hypoxemia that does not respond well to low to moderate concentrations of oxygen therapy (i.e., refractory hypoxemia). PEEP or CPAP may restore functional residual capacity (FRC), keep alveoli open throughout the ventilatory cycle, increase alveolar volume, improve lung compliance, improve P/F ratio, and reduce intrapulmonary shunt.17 PEEP or CPAP may increase PaO2 at a given FIO2 in patients with severe oxygenation problems and these patients may require PEEP or CPAP in order to achieve an adequate PaO2 using a safe FIO2 (i.e., PaO2 ≥ 60 mmHg and FIO2 ≤ 0.50). Increased WOB due to decreased lung compliance is common in patients with acute, restrictive lung disease (e.g., pneumonia, ARDS). Although adequate spontaneous breathing may be present, these patients often tire, and hypoventilation and ventilatory failure ensue. Early initiation of mechanical ventilation in such

patients allows for the use of PEEP or CPAP, pressure support, pressure control, or other techniques that may improve oxygenation and reduce the WOB. Institution of mechanical ventilatory support also allows for the use of sophisticated alarms and monitoring systems that are incorporated in modern critical care ventilators. It should be noted that CPAP alone may be useful to improve oxygenation in patients with refractory hypoxemia in the presence of adequate spontaneous ventilation. CPAP may reduce the WOB while improving PaO2. CPAP may be delivered using a spontaneous breathing apparatus and a face mask; however, in the ICU setting CPAP is sometimes applied using a conventional mechanical ventilator in the “spontaneous” mode. Other techniques applied during mechanical ventilation that may be helpful in improving oxygenation include use of prolonged inspiratory times, inverse ratio ventilation, prone positioning, and rotational therapy.21,22 Patients with “nonpulmonary” oxygenation problems including inadequate arterial blood oxygen content (e.g., carbon monoxide poisoning, severe anemia due to blood loss), inadequate oxygen delivery (e.g., heart failure, sepsis, and shock) or inadequate tissue utilization (e.g., cyanide poisoning) may also require mechanical ventilatory support. Clinical Focus 5-7 provides an example of a patient with severe oxygenation problems. Clinical Focus 5-8 provides an example of a patient with acute ventilatory failure superimposed on chronic ventilatory failure.

CLINICAL FOCUS 5-7 Severe Oxygenation Problems A 24-year-old female patient is admitted to the hospital with severe bilateral pneumonia. The patient is awake and alert, but in severe respiratory distress. Blood gases on a partial rebreathing mask at 10 L/min are as follows: pH = 7.52 PaCO2 = 28 mmHg PaO2 = 48 mmHg Respiratory rate = 28 breaths/min HCO-3 = 23 mEq/L BE = 2 SaO2 = 0.89 Heart rate = 118

Question 1. What is your assessment of this patient? Answer: The patient currently exhibits tachycardia, tachypnea, and respiratory distress, which are consistent with acute respiratory failure. The patient’s oxygenation status suggests refractory hypoxemia. The FIO2 delivered via partial rebreathing mask at 5 to 10 L/min is in the range of 40% to 70%, yet the resultant PaO2 is only 48 mmHg at 10 L/min of O2. Arterial blood gases indicate acute alveolar hyperventilation (aka uncompensated respiratory alkalosis) with severe hypoxemia (the patient’s PaO2 on room air would be < 40 mmHg). The patient is able to ventilate adequately, and she is currently hyperventilating (PaCO2 = 28), probably due to severe hypoxemia. Additional assessment information and review of the patient’s chest imaging results would be helpful. Question 2. Is mechanical ventilatory support indicated for this patient? Answer: Indications for mechanical ventilation are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. Currently, the patient is hyperventilating (probably due to acute, severe hypoxemia) and is experiencing severe oxygenation problems (i.e., refractory hypoxemia). PEEP or CPAP is indicated for the severe hypoxemia. PEEP/CPAP improves oxygen transfer across the lung by increasing FRC and reducing or eliminating end-expiratory alveolar collapse. PEEP is indicated in most patients with hypoxemic respiratory failure, including ARDS. A trial of CPAP by mask or noninvasive ventilation (NIV) with PEEP/CPAP may be considered; acute hypoxemic respiratory failure sometimes responds to NIV. Invasive mechanical ventilation with PEEP should be considered if ventilatory failure is imminent due to ventilatory muscle fatigue and worsening ventilatory status.

CLINICAL FOCUS 5-8 Acute Ventilatory Failure Superimposed on Chronic Ventilatory Failure A 68-year-old male patient with a longstanding history of COPD with chronic CO2 retention enters the emergency department. The patient is diaphoretic, confused, and hypotensive. Heart rate and respiratory rate are elevated (tachycardia and tachypnea) and the patient appears to be in respiratory distress with accessory muscle use and oxygen desaturation (SpO2 = 62%). An arterial blood gas sample is analyzed with the following results: FIO2 = 0.21 pH = 7.23 PaCO2 = 85 mmHg

PaO2 = 38 mmHg SaO2 = 0.60 HCO-3 = 37 mEq/L BE (base excess) = +5 Question 1. What disease state or condition (other than COPD) should the respiratory care clinician be concerned about in this case? Answer: Common causes of acute respiratory failure requiring mechanical ventilation include pneumonia, ARDS, trauma, sepsis, postoperative respiratory failure, COPD exacerbation, heart failure, neurologic disease, neuromuscular disease, and sedative or narcotic drug overdose. This patient has a longstanding history of COPD with chronic CO2 retention and is predisposed to the development of acute respiratory failure due to COPD exacerbation. Early clinical manifestations of acute respiratory failure include tachycardia, tachypnea, diaphoresis, anxiety, and respiratory distress followed by depressed mental status, confusion, somnolence, and coma as the patient’s condition deteriorates. Physical findings associated with increased WOB are common, and rapid shallow breathing or slowed or irregular breathing may be present. This patient is currently exhibiting many of the clinical manifestations of acute respiratory failure. Question 2. What is your assessment of the patient’s blood gas data? Answer: Suspected respiratory failure is best evaluated by analysis of arterial blood gases. The patient is currently breathing room air with a PaO2 of 38 mmHg and SaO2 of 0.60, which would be classified as severe hypoxemia (normal PaO2 and SaO2 while breathing room air are 80 to 100 mmHg and 0.96 to 0.98, respectively). The patient’s acid-base status is as follows: pH = 7.23 → acidosis (normal pH is 7.35 to 7.45) PaCO2 = 85 mmHg → respiratory acidosis (normal PaCO2 is 35 to 45 mmHg; PaCO2 > 45 mmHg is respiratory acidosis while PaCO2 < 35 mmHg is respiratory alkalosis) HCO-3 = 37 mEq/L → metabolic alkalosis (normal HCO-3 is 22 to 28 mEq/L: HCO-3 < 22 mEq/L is metabolic acidosis, while HCO-3 > 28 mEq/L is metabolic alkalosis) BE = +5 → metabolic alkalosis (normal base excess or deficit [BE/BD] is ± 2.0 mEq/L; BD < –2.0 is metabolic acidosis while BE > +2.0 is metabolic alkalosis) Using conventional nomenclature, this blood gas result would be classified as a partially compensated respiratory acidosis. However, this patient has a long-

standing history of chronic CO2 retention and his “normal” acid-base status probably is chronic ventilatory failure (i.e., chronically elevated PaCO2 with normal or near-normal pH due to renal compensation). Chronic ventilatory failure is also known as chronic hypercapnic respiratory failure. Patients with chronic ventilatory failure who become acutely ill may develop acute ventilatory failure superimposed on chronic ventilatory failure (aka acute on chronic hypercapnia). Question 3. What respiratory care would you suggest for this patient at this time? Answer: The patient most likely is experiencing an acute exacerbation of his COPD with severe hypoxemia while breathing room air. Further evaluation should include a patient history and physical assessment; imaging studies, complete blood count (CBC), serum electrolytes, and serum glucose should be obtained. Hospital treatment should include oxygen therapy, inhaled bronchodilators, glucocorticoids, antibiotics, and supportive care. Institution of mechanical ventilatory support should be considered if the patient’s condition continues to deteriorate. Assessment of follow-up care: The patient is placed on a nasal cannula at 2 L/min, given a short acting beta-2 adrenergic bronchodilator and observed closely. Two hours later, the patient’s condition has not improved. Blood gases at this time reveal: Oxygen: 2 L/min cannula pH = 7.22 PaCO2 = 90 mmHg PaO2 = 48 mmHg HCO-3 = 36 mEq/L BE = +8 SaO2 = 75% Question 4. What is your assessment of the patient’s condition at this time? Answer: Moderately severe hypoxemia is present while breathing lowconcentration oxygen therapy via nasal cannula. The patient’s hypercapnia and acidosis have worsened, and acute ventilatory failure superimposed on chronic ventilatory failure continues (aka acute on chronic hypercapnia). Mechanical ventilatory support is now indicated, although a trial of noninvasive ventilation (NIV) may be a good place to begin.

Complications, Hazards, and Contraindications Mechanical ventilation has a number of potential complications and hazards that may result in increased patient morbidity and mortality. These include barotrauma, airway injury, infection, ventilator–associated pneumonia, pulmonary embolus, and gastrointestinal bleeding. Common forms of barotrauma associated with mechanical ventilation include pneumothorax, pneumomediastinum, and subcutaneous emphysema. Ventilatory muscle atrophy and dysfunction can occur, particularly with prolonged controlled mechanical ventilation and the use of neuromuscular-blocking agents.13,23 The addition of positive pressure to the airways reduces venous return to the right side of the heart (since right atrial pressure equals central venous pressure [CVP] minus pleural pressure). Thus, in the setting of hypovolemia, initiation of mechanical ventilation may result in hypotension. In addition, catastrophic failure of the ventilator or artificial airway can result in life-threatening complications, including death.

Contraindications to Mechanical Ventilation While there are a number of relative contraindications to mechanical ventilation, failure to provide mechanical ventilatory support when needed may result in the patient’s death. Contraindications may include pneumothorax without chest tubes, an absence of indications for mechanical ventilation, rapid resolution of the underlying condition, situations in which life-support interventions are futile, and situations in which mechanical ventilation is contrary to the patient’s wishes. Pneumothorax without chest tubes is considered a contraindication for the use of positive-pressure ventilation because a tension pneumothorax may result. In such cases, prompt recognition, decompression, and insertion of chest tubes will allow for safe administration of positive-pressure ventilation. Initiation of mechanical ventilation without clear indications exposes patients to the potentially serious hazards and complications associated with mechanical ventilation. Some conditions resolve rapidly and may only require bag-valve mask manual resuscitator support in the interim. In these cases, intubation and initiation of mechanical ventilation may not be required. In other cases, life-support interventions may be futile; however, the decision to withhold mechanical ventilatory support may be fraught with legal and

ethical implications. Lastly, some patients may not wish to have extraordinary lifesupport measures. Careful attention to any advanced directives in place regarding end-of-life care may provide guidance in cases where the patient is unable to communicate directly. Thus, the decision to initiate mechanical ventilatory support is not without risk and careful consideration of the indications, contraindications, clinical goals, and potential hazards and complications is required. Box 5-7 summarizes the contraindications, potential complications, and hazards of mechanical ventilation.

BOX 5-7 Complications and Hazards of Mechanical Ventilation Adverse pulmonary effects ∎

Ventilator-associated lung injury (VALI) is lung injury associated with mechanical ventilation thought to be due to cyclic alveolar distention and collapse resulting in alveolar edema and hemorrhage indistinguishable from ARDS; a lung protective ventilation strategy may help avoid VALI. ∎ Barotrauma is most often due to alveolar rupture and release of air into the pleural space. It includes: • Pneumothorax • Pneumomediastinum • Pneumoperitoneum • Subcutaneous emphysema ∎ Ventilator-associated pneumonia (VAP) is a type of nosocomial pneumonia that develops following institution of mechanical ventilation. ∎ Atelectasis may be caused by mucus plugging or use of low tidal volumes with normal pulmonary mechanics. ∎ Decreased mucociliary transport (decreased mucus clearance). ∎ Hyperventilation (decreased PaCO , respiratory alkalosis). 2 ∎

Hypoventilation (increased PaCO2, respiratory acidosis).

∎

Increased physiologic dead space. Uneven distribution of inspired gas (overventilation of nondependent portions of the lung). Redistribution of pulmonary blood flow (due to positive pressure). AutoPEEP. Increased WOB (often due to inappropriate ventilator settings). Patient–ventilator asynchrony.

∎ ∎ ∎ ∎ ∎

∎ ∎

Diaphragmatic muscle atrophy (associated with controlled ventilation). Oxygen toxicity (associated with FIO2 > 0.50 for prolonged periods of time).

Artificial airways ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

Cuff leaks Aspiration (often due to leakage around airway cuffs) Excessive cuff pressures Inadvertent extubation Accidental bronchial intubation Airway occlusion (partial or complete) Esophageal intubation Airway trauma (may be associated with traumatic intubation) Sore throat, hoarse voice, and stridor (following extubation) Laryngeal edema (e.g., glottic and subglottic edema), vocal cord paralysis, and granuloma formation Tracheal stenosis or other tracheal lesions (e.g., tracheomalacia, tracheoesophageal fistula, and innominate artery erosion) Tracheostomy complications (stomal infection, hemorrhage, subcutaneous emphysema, and pneumomediastinum)

Ventilator system failure ∎ ∎ ∎ ∎ ∎ ∎ ∎

Patient disconnect Air leaks in the ventilator system or patient circuit Power failure or power disconnect Alarm failure or improper alarm settings Humidification system failure (inadequate humidification, overheating) Improper assembly of the ventilator circuit Inappropriate ventilator settings (hypoventilation, hyperventilation, increased WOB, and patient– ventilator asynchrony)

Cardiac and cardiovascular adverse effects of positive-pressure ventilation ∎ ∎ ∎ ∎

Reduced venous return to the right heart Decreased right ventricular output Decreased cardiac output Hypotension

Other organs and systems

∎

Renal failure ∎ Increased intracranial pressure ∎ Gastrointestinal (GI) complications • GI tract bleeding • Decreased splanchnic perfusion • GI hypomotility ∎ Generalized skeletal muscle weakness (associated with prolonged immobilization) ∎ Generalized inflammation ∎ Sleep deprivation ∎ Psychological distress—posttraumatic stress disorder

Patient Assessment for Ventilator Initiation The decision to initiate mechanical ventilatory support should be based on a thorough patient assessment, sound clinical judgment, and understanding of the indications and associated contraindications, complications, and hazards of mechanical ventilation. As noted, the most common reason for initiating mechanical ventilation is acute respiratory failure and the respiratory care clinician must be on the alert for the presence of disease states or conditions that predispose patients for the development of respiratory failure. Recall also that respiratory failure may be classified as hypoxemic respiratory failure, which may cause severe oxygenation problems and hypercapnic respiratory failure, commonly referred to as ventilatory failure. Conditions that may cause ventilatory failure include those that reduce or eliminate the normal respiratory drive to breathe (see Box 5-2), conditions that increase ventilatory workload beyond ventilatory capacity (see Box 5-3), and conditions that result in ventilatory muscle weakness or dysfunction (see Table 5-1). Generally speaking, causes of inadequate ventilation requiring mechanical ventilatory support can be classified as conditions in which the patient won’t breathe (i.e., absent or decreased respiratory drive), can’t breathe (e.g., high cervical spine injury, ventilatory muscle dysfunction, and impairment of the ventilatory pump) or can’t breathe enough (e.g., hypoxemia, compromised lung function, and ventilatory muscle weakness).4 Conditions predisposing patients to the development of acute ventilatory failure can be further classified as problems with the conducting airways (e.g., upper airway obstruction, bronchospasm, mucosal edema, and excessive secretions), alveolar gas exchange problems (e.g., ARDS, pneumonia, atelectasis pulmonary, and edema), disorders affecting neuromuscular function or ventilatory drive (e.g., neuromuscular disease, spinal cord injury, botulism, tetanus, and narcotic or sedative drug overdose), and increased ventilatory workload (e.g., decreased compliance, increased airway resistance). Other at-risk groups for the development of respiratory failure requiring mechanical ventilatory support include patients following thoracic or abdominal surgery, and those with chronic lung disease (e.g., COPD, severe asthma, and interstitial pulmonary fibrosis), pleural disease (e.g., pneumothorax, large pleural effusion), or cardiac disease (see Box 5-6). Patients with sepsis, shock, and trauma; poisoning (e.g., carbon monoxide, cyanide, opiods,

and botulism); severe burns; and severe obesity are also at high risk for development of acute respiratory failure. Assessment of patients for the clinical manifestations of acute respiratory failure include review of patients’ oxygenation and ventilatory status, acid-base balance, cardiac and cardiovascular function, and CNS and mental status. Abnormal respiratory rate (f ≥ 30 to 35 or f ≤ 8 to 10 in adults), respiratory distress (e.g., severe dyspnea, accessory muscle use, intercostal retractions, chest wall to diaphragm asynchrony, and sweating), rapid shallow breathing, reduced chest expansion, and slowed or irregular breathing or periods of apnea suggest the possible need for mechanical ventilatory support.1–4 Abnormal bedside measures of pulmonary function including reduced vital capacity (VC < 15–20 mL/kg), inadequate maximum inspiratory pressure (MIP > –20 to –30 cm H2O), reduced maximum expiratory pressure (MEP < 40 cm H2O), or increased rapid shallow breathing index (RSBI [f/VT] ≥ 105) are also suggestive of the need for the institution of mechanical ventilatory support. Cardiac and cardiovascular assessment findings suggestive of the possible need for mechanical ventilatory support include tachycardia, bradycardia, abnormal blood pressure, and the presence of cardiac arrhythmias. The brain is especially sensitive to hypoxia and agitation, confusion, somnolence, unconsciousness, unresponsiveness, and coma all suggest the possible need for mechanical ventilatory support. Wherever possible, the presence of respiratory failure should be confirmed by measurement of arterial oxygen saturation (SaO2), arterial oxygen tension (PaO2) and oxygen content (CaO2), and arterial blood gas analysis for assessment of acid-base balance. To summarize, respiratory failure is suspected based on the patient’s history, presence of conditions that predispose the development of respiratory failure, and related assessment findings. The presence of oxygen desaturation is commonly determined by pulse oximetry or arterial blood gas analysis. Assessment of acidbase balance and PaCO2 requires arterial blood gas analysis, or the use of venous blood gases. Acute respiratory failure is defined as a sudden fall in arterial oxygenation with or without CO2 retention. Apnea is defined as complete cessation of breathing. Acute ventilatory failure is defined as a sudden rise in arterial carbon dioxide tension (PaCO2) with a corresponding decrease in pH. It may also be

considered when a normal end-tidal CO2 (35 to 40) acutely rises on capnography, although clinicians must be aware of the limitations of capnography for the assessment of ventilation. Impending ventilatory failure is a clinical judgment in which the development of acute respiratory acidosis is thought to be imminent. Severe oxygenation problems generally are associated with refractory hypoxemia, often caused by large intrapulmonary (physiologic) shunts. The decision to institute mechanical ventilatory support is based on clinical assessment and evaluation of the factors listed below. Predisposing factors for the development of acute respiratory failure are present. Acute lung disease (e.g., ARDS, pneumonia, pulmonary embolus, airway obstruction, and pulmonary aspiration) Chronic lung disease (e.g., asthma, COPD, and interstitial lung disease) Cardiac disease (e.g., myocardial ischemia, myocardial infarction, and heart failure) Sepsis Shock (cardiogenic, septic, neurogenic, hypovolemic, and anaphylactic Trauma (e.g., chest trauma, head trauma, near-drowning, and smoke inhalation) Poisoning (e.g., carbon monoxide, cyanide) Neurologic disease (e.g., brain stem tumor, cerebral hemorrhage, massive stroke, meningitis, and coma) Neuromuscular disease (e.g., Guillain-Barré, myasthenia gravis, ALS, critical illness, and myopathy) Sedative, tranquilizer, or narcotic drug overdose Postoperative abdominal or thoracic surgery Clinical manifestations of acute respiratory failure are present. Tachycardia, bradycardia, arrhythmias, hypertension, and hypotension Tachypnea, rapid shallow breathing, irregular breathing, bradypnea, and periods of apnea Anxiety, dyspnea, and respiratory distress Accessory muscle use, intercostal retractions, asynchronous chest wall to diaphragm movement, and reduced chest wall movement Sweating, cyanosis, and pallor Depressed mental status, confusion, somnolence, and coma Indications for mechanical ventilation are present. Apnea Acute ventilatory failure Impending ventilatory failure

Severe oxygenation problems Other possible indications include: General anesthesia administration Need for deep sedation and/or neuromuscular blockade Contraindications to mechanical ventilation: Indications for mechanical ventilation are not present. Rapid resolution of underlying condition occurs. For example, narcotic overdose patients may be given an opioid antagonist (e.g., naloxone) and supported in the interim using a bag-valve mask manual resuscitator until adequate spontaneous ventilation returns. Pneumothorax without chest tubes. Life-support interventions are futile. Mechanical ventilation is contrary to the patient’s wishes. Consideration of possible complications and hazards including: Ventilator-associated lung injury, barotrauma, and ventilator-associated pneumonia Inappropriate ventilator settings, hyperventilation, hypoventilation, and increased WOB Airway problems (accidental extubation, bronchial intubation, cuff leaks, and airway trauma) Ventilator system failure Impaired cardiac output, hypotension Increased intracranial pressure Other organ system complications (GI bleeding, renal failure, and generalized inflammation) Generalized skeletal muscle weakness Psychological distress, sleep deprivation, and traumatic stress disorder

Initial Ventilator Settings A number of choices must be made following the decision to institute mechanical ventilatory support. For example, certain patients may do well with noninvasive ventilation (NIV), while others may require invasive mechanical ventilation. Many ventilators allow the clinician to choose between providing partial and full ventilatory support. Apneic patients require full ventilatory support, while partial ventilatory support using some form of synchronized intermittent mandatory ventilation (SIMV) may be useful in certain patients who are spontaneously breathing. A large number of different ventilator modes are currently available, and the clinician must choose between continuous mandatory ventilation (CMV), intermittent inventory ventilation (IMV), and continuous spontaneous ventilation (CSV).24 Initiation of ventilator breaths may be time triggered or patient triggered, and patient-triggered breaths may be initiated based on a pressure or flow signal (i.e., pressure triggered or flow triggered). Ventilator breaths may be volume limited, pressure limited, or time limited. Ventilator breaths may be terminated following delivery of a specific volume (volume cycled), achievement of an inspiratory pressure (pressure cycled), when the inspiratory flow drops to a certain value (flow cycled), or following a preset time interval (time cycled). Spontaneous breathing may be allowed, which may or may not include some form of pressure support. A recommended taxonomy for mechanical ventilation suggests five basic ventilatory patterns or modes, as follows.24

Volume Control-Continuous Mandatory Ventilation (VC-CMV) For volume-control (VC) ventilation, the control variable is volume and both volume and flow are preset prior to inspiration and volume delivery is not affected by changes in lung compliance or airway resistance. CMV indicates that all breaths are mandatory, but may be patient or machine (i.e., time) triggered to inspiration. If the ventilator is set up to allow for patient triggered or machine-triggered, volumetargeted mandatory breaths, the mode is commonly referred to as assist/control (A/C) volume ventilation (aka patient-triggered or time-triggered CMV). If only machine-triggered, volume-targeted breaths are allowed, the ventilator is in the control mode (aka time-triggered CMV).

Volume Control-Intermittent Mandatory Ventilation (VC-IMV) IMV and synchronized intermittent mandatory ventilation (SIMV) may be used to provide partial or full ventilatory support. VC indicates the control variable is volume; during mandatory breaths, volume delivery remains constant. IMV indicates that patients may breathe spontaneously between mandatory breaths. As originally introduced, IMV only allowed for time-triggered mandatory breaths. SIMV is the most common form of IMV in which the mandatory breaths may be time or patient triggered. SIMV also allows patients to breathe spontaneously between mandatory breaths and the mandatory breaths are “synchronized” to the end of the patient’s exhalation.

Pressure Control-Continuous Mandatory Ventilation (PC-CMV) Pressure control (PC) indicates that the control variable is pressure and inspiratory pressure is preset as either a constant value or proportional to the patient’s inspiratory effort. CMV indicates that all breaths are mandatory. Breaths may be machine or patient triggered. A commonly used form of this mode delivers a predetermined minimum mandatory rate and allows the patient to trigger the ventilator at a higher rate (i.e., assist/control mode); inspiration is pressure limited and time cycled.

Pressure Control-Intermittent Mandatory Ventilation (PC-IMV) PC indicates that the control variable is pressure while IMV indicates that the patient may breathe spontaneously in between mandatory breaths.

Pressure Control-Continuous Spontaneous Ventilation (PC-CSV) PC indicates that the control variable is pressure while CSV indicates all breaths are spontaneous. A commonly used form of this mode is referred to as pressure-support ventilation (PSV) in which each breath is patient triggered, inspiratory pressure is preset, and inspiration is flow cycled to expiration. Qualifying subscripts are then added to further describe the ventilatory pattern targeting scheme (e.g., set-point [s], dual [d], adaptive [a], etc.).24 The suggested taxonomy thus becomes complex and somewhat difficult for clinicians to apply. To further complicate initial ventilator setup, manufacturers use a dizzying array of

different terms to describe the modes available on their ventilators. For example, the Covidien Puritan Bennett 840 lists the following modes: bilevel, pressure control assist/control, pressure control synchronized intermittent mandatory ventilation, pressure support, proportional assist ventilation plus, spontaneous, tube compensation, volume control assist/control, volume control plus assist/control, volume control plus synchronized intermittent mandatory ventilation, and volume ventilation plus synchronized intermittent mandatory ventilation. Two other common critical care ventilators, the Dräger Evita X and HAMILTON Medical G5, have similar, but not the same, naming taxonomies for the modes available on those machines. Despite the large number of modes available on current critical care ventilators, most patients in the ICU will do quite well using volume or pressure ventilation with set point targeting in the assist/control mode (aka VC-CMVs or PC-CMVs). PSV or SIMV with pressure support can also be effectively applied to patients. Positive endexpiratory pressure (PEEP) or continuous positive airway pressure (CPAP) may be added to these common modes. Choice of ventilator mode will be further discussed in Chapter 6, Ventilator Initiation. The respiratory care clinician must also choose other important ventilator settings including tidal volume (or pressure limit), respiratory rate, trigger method and sensitivity, inspiratory flow rate (or inspiratory time), and adjustable inspiratory flow pattern (with VC ventilation) or rise time and flow termination criteria (with pressure support ventilation). Oxygen concentration (FIO2), and PEEP/CPAP level must also be selected. Tidal volume should be selected based on the patient’s condition and clinical goals. Large tidal volumes may result in high airway pressures, which may cause ventilator-induced lung injury. Generally speaking, the initial tidal volume should be such that plateau pressure (Pplateau) ≤ 30 cm H2O. ARDS patients have reduced lung compliance and initial tidal volume may be set at 8 mL/kg and then gradually reduced to 6 mL/kg over the next 1 to 3 hours to maintain Pplateau ≤ 30 cm H2O.25 Patients with neuromuscular disease, on the other hand, may have normal lung compliance and initial tidal volume may be set in the range of 8 to 10 mL/kg.26 Smaller tidal volumes in these patients may promote the development of atelectasis and some centers titrate tidal volume to higher levels as long as the Pplateau remains ≤ 30 cm H2O. Respiratory rate in combination with tidal volume will determine minute ventilation

and PaCO2. An approximate minute ventilation goal to achieve full ventilatory support for most adult patients is about 100 mL/kg IBW.26 For patient-triggered breaths, sensitivity must be set at a level where patient triggering requires minimal patient effort without autocycling. Inspiratory flow, tidal volume (or pressure), and respiratory rate will determine inspiratory and expiratory time and I:E ratio. Inspiratory flows should be sufficient to meet or exceed patients’ inspiratory demand and expiratory time should be sufficient to avoid the development of autoPEEP. Care should be taken to ensure patient comfort, minimize the WOB, and avoid patient–ventilator asynchrony. Inspiratory flow pattern may have an impact on inspiratory time as well as peak and mean airway pressures and distribution of the inspired gas. Oxygen concentration generally is set at the lowest level required to correct hypoxemia and avoid oxygen toxicity. PEEP/CPAP is often added to prevent end-expiratory alveolar collapse and improve V̇/Q̇ and arterial oxygenation while allowing for reduction in FIO2. Each of these initial ventilator settings will be discussed in detail in Chapter 6, Ventilator Initiation. Once the decision has been made to institute mechanical ventilatory support, the respiratory care clinician must adjust the level of support provided to achieve adequate alveolar ventilation, maintain acid-base homeostasis, and insure adequate tissue oxygenation. Ventilator settings should be selected that reduce the patient’s WOB, ensure patient comfort, and avoid patient–ventilator breathing asynchrony. Patient safety must be ensured, and avoidance of the complications and hazards of mechanical ventilation, wherever possible, must occur. Last but not least, patient management should promote liberation of the patient from the ventilator as soon as reasonably prudent. In summary, the four primary indications for mechanical ventilation are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. Acute respiratory failure is the most common diagnosis requiring mechanical ventilation. Other common diagnoses include acute exacerbation of COPD, coma, and neuromuscular disease. Clinical manifestations of respiratory failure include respiratory distress, dyspnea, accessory muscle use, retractions, and tachypnea. Rapid shallow breathing is a common finding in patients with respiratory failure. Tachycardia and other arrhythmias are signs of cardiac distress. Bradycardia is an ominous finding. Initially patients may be anxious and restless followed by

confusion, somnolence, and coma. Bedside pulmonary function measures associated with ventilatory failure and the need to initiate mechanical ventilation include elevated respiratory rate, reduced tidal volume, rapid shallow breathing index ≥ 105, vital capacity < 15 to 20 mL per kg or 1.0 L, and maximum inspiratory pressure > –30 mmHg. Acute ventilatory failure is defined as a sudden rise in arterial PaCO2 with a corresponding decrease in pH. Severe oxygenation problems are best identified by evaluation of arterial blood oxygenation versus FIO2. P/F ratios provide a convenient estimate of the effectiveness of gas transfer across the lung.

Key Points The primary function of the mechanical ventilator is to augment or replace normal ventilation. Respiratory failure is the inability of the heart and lungs to maintain adequate tissue oxygenation and/or carbon dioxide removal; hypoxemic respiratory failure (aka lung failure) is a problem with oxygenation while hypercapneic ventilatory failure (aka pump failure) is a problem with ventilation resulting in an abnormal increase in PaCO2. Mechanical ventilation may be required when spontaneous breathing is insufficient or absent. Respiratory failure is the most common reason for initiating mechanical ventilatory support. Acute ventilatory failure (aka acute hypercapnic respiratory failure) is a sudden rise in PaCO2 with a corresponding decrease in pH. The major components of ventilation are tidal volume, respiratory rate, and minute ventilation. Alveolar ventilation is determined by tidal volume, respiratory rate, and physiologic dead space. Ventilatory capacity refers to the amount of air that can be moved into and out of the lungs by the ventilatory pump. Ventilatory requirements (aka ventilatory demand) is the volume of ventilation required to achieve adequate oxygenation and carbon dioxide removal. Ventilatory capacity may be reduced due to absent or decreased respiratory drive, increased work of breathing resulting in ventilatory muscle fatigue, neuromuscular disease, and impaired lung function. Ventilatory requirements may increase due to hypoxia, increased metabolic rate, metabolic acidosis, or increased physiologic dead space. When ventilatory requirements exceed ventilatory capacity, mechanical ventilatory support may be necessary. Respiratory drive may be reduced or absent in the presence of severe hypoxemia, severe hypercapnia, cardiac arrest, neurologic disease, head trauma, near-drowning, poisoning, severe electrical shock, drug overdose (e.g., narcotics, barbiturates, and tranquilizers), general anesthesia, alkalosis, electrolyte disorders, severe hypothyroidism, and certain other disease states and conditions. Ventilatory capacity may be reduced due to upper airway obstruction; lower airway bronchospasm, mucosal edema, or secretions; reductions in lung or thoracic compliance; alveolar filling or collapse; interstitial pulmonary fibrosis; or increased physiologic dead space. Increased ventilatory workload may result in ventilatory muscle fatigue, reduced

ventilatory capacity, and the development of acute ventilatory failure. Causes of increased ventilatory workload include decreased lung compliance, decreased thoracic compliance, increased airway resistance, and increased level of ventilation required. Causes of ventilatory muscle weakness or dysfunction include amyotrophic lateral sclerosis, botulism, critical illness myopathy and polyneuropathy, muscular dystrophy, Guillain-Barré syndrome, multiple sclerosis, malnutrition, myasthenia gravis, poliomyelitis, tetanus, and tick paralysis. Neuromuscular-blocking agents block nerve transmission at the myoneural junction (aka neuromuscular junction) and cause ventilatory muscle paralysis. Arterial carbon dioxide tension (PaCO2) is inversely proportional to alveolar ventilation (V̇A) and directly proportional to carbon dioxide production (V̇CO2). Clinically, the single best index of alveolar ventilation is measurement of PaCO2. Clinical manifestations of acute respiratory failure include tachycardia, tachypnea, diaphoresis, anxiety, respiratory distress, accessory muscle use, and intercostal retractions. Manifestations of severe respiratory failure may include markedly increased respiratory rate, rapid shallow breathing, slowed or irregular breathing, periods of apnea, asynchronous chest wall to diaphragm movement, confusion, somnolence, and coma. Goals of mechanical ventilation include providing adequate alveolar ventilation and oxygenation, restoring and maintaining acid-base homeostasis, reducing the work of breathing, ensuring patient safety and comfort, minimizing harmful side effects and complications, and promoting liberation of the patient from the ventilator. The primary indications for institution of mechanical ventilation are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. Apnea is the complete cessation of breathing and failure to provide mechanical ventilatory support in the presence of prolonged apnea will lead to cardiac arrest and brain death in minutes. Acute ventilatory failure in which an acute increase in PaCO2 results in a pH ≤ 7.25 provides an indication for mechanical ventilation. Impending ventilatory failure refers to situations where ventilatory failure is likely to occur in the immediate future. Refractory hypoxemia refers to an oxygenation problem that does not respond conventional oxygen therapy. Patients with refractory hypoxemia may require the use of PEEP or CPAP. Complications of mechanical ventilation include barotrauma, ventilatorassociated lung injury, airway injury, infection, ventilator-associated pneumonia, pulmonary embolus, hypotension, and stress ulcers (gastrointestinal bleeding). Contraindications to mechanical ventilation include pneumothorax without chest

tubes, absence of clear indications, rapid resolution of apnea or ventilatory failure, futility of intervention, or when mechanical ventilation is against the patient’s wishes. The decision to initiate mechanical ventilatory support should be based on a thorough patient assessment, sound clinical judgment, and an understanding of the indications, contraindications, complications, and hazards of mechanical ventilation. Decisions regarding initial ventilator setup include use of invasive or noninvasive ventilation, use of full or partial ventilatory support, choice of mode, and selection of initial ventilator settings.

References 1. Selvakumar N, Casserly B, Rounds S. Essentials in critical care medicine. In: Benjamin IJ, Griggs RC, Wings EJ, Figgs JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016: 259–265. 2. Aboussovan LS. Respiratory failure and the need for ventilator support. In: Kacmarek RM, Stoller JK, Heuer AJ (eds.). Egan’s Fundamentals of Respiratory Care, 11th ed. St. Louis, MO: Elsevier; 2017: 972– 986. 3. Cairo JM. Establishing the need for mechanical ventilation. In: Cairo JM (ed.). Pilbeam’s Mechanical Ventilation: Physiological and Clinical Applications. 6th ed. St. Louis, MO: Elsevier; 2016: 43–57. 4. Feller-Kopman DJ, Schwartzstein RM. The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnia respiratory failure. In: Stoller JK, Finlay G (eds.). UpToDate; July 20, 2017. 5. Maloney JP. Acute ventilatory failure. In: Hanley ME, Welsh CH (eds.). Current Diagnosis and Treatment in Pulmonary Medicine. Columbus, OH: McGraw Hill Education; 2003. Access Medicine. Available at http://accessmedicine.mhmedical.com. Accessed April 11, 2017. 6. Hall JB, McShane. Ventilatory failure. In: Critical Care Medicine: Respiratory Failure and Mechanical Ventilation, Merck Manual Professional Version. Kenilworth, NJ; 2017. Available at https://www.merckmanuals.com/professional/critical-care-medicine/respiratory-failure-and-mechanicalventilation/ventilatory-failure. Accessed April 11, 2017. 7. Piraino T. Monitoring the patient in the intensive care unit. In: Kacmarek RM, Stoller JK, Heuer AJ (eds). Egan’s Fundamentals of Respiratory Care, 11th ed. St. Louis, MO: Elsevier; 2017: 1154–1189. 8. Johnson DC. Control of ventilation. In: Flaherty KR, Manaker S, Finlay G (eds). UpToDate; August 1, 2017. 9. Stoller JK. Management of exacerbations of chronic obstructive pulmonary disease. In: Barnes PJ, Hollingsworth H (eds.). UpToDate; 2016. 10. Jankowich MD. Obstructive lung disease. In: Benjamin IJ, Griggs RC, Wings EJ, Figgs JG (eds.). Andreoli and Carpenter’s Cecil Essentials of Medicine, 9th ed. Philadelphia, PA: Elsevier-Saunders; 2016: 207–221. 11. Global Initiative for Chronic Obstructive Lung Disease (GOLD). GOLD 2017 global strategy for the diagnosis, management and prevention of COPD. January 2017. Available at http://goldcopd.org/gold2017-global-strategy-diagnosis-management-prevention-copd/. Accessed April 11, 2017. 12. Fanta CH. Management of acute exacerbations of asthma in adults. In: Bochner BS, Hockberger RS, Hollingsworth H (eds.). UpToDate; 2017. 13. Hyzy RC. Physiologic and pathophysiologic consequences of mechanical ventilation. In: Parsons PE, Finlay G (eds.). UpToDate; 2017. 14. Emmett M, Palmer BF. Simple and mixed acid-base disorders. In: Sterns RH, Forman JP (eds.). UpToDate; 2016. 15. Emmett M, Szerlip H. Approach to the adult with metabolic acidosis. In: Sterns RH, Forman JP (eds.). UpToDate; 2016. 16. Courey AJ, Hyzy RC,. Overview of mechanical ventilation. In: Parsons PE, Finlay G (eds.). UpToDate; 2016. 17. Kacmarek RM. Physiology of ventilatory support. In: Kacmarek RM, Stoller JK, Heuer AJ, (eds). Egan’s Fundamentals of Respiratory Care, 11th ed. St. Louis, MO. Elsevier; 2017: 1016–1057. 18. Sarani B. Inpatient management of traumatic rib fractures. In: Bulger EM, Friedburg JS, Collings KA (eds.). UpToDate; 2017. 19. Camargo CA, Krishnan JA. Invasive ventilation in adults with acute exacerbations of asthma. In: Manaker S, Hollingsworth H (eds.). UpToDate; 2016. 20. Vriesendorp FJ. Guillain-Barré syndrome in adults: clinical features and diagnosis. In: Shefner JM, Targoff IN, Dashe JF (eds.). UpToDate; 2017. 21. Schwartz DR, Malhotra A, Kacmarek RM. Prone ventilation for adult patients with acute respiratory distress syndrome. In: Parsons PE, Finlay G (eds.). UpToDate; 2017. 22. Kacmerek RM. Initiating and adjusting invasive ventilatory support. In: Kacmarek RM, Stoller JK, Heuer AJ (eds.). Egan’s Fundamentals of Respiratory Care, 11th ed. St. Louis, MO. Elsevier; 2017:1078–1110. 23. Lacomis D. Neuromuscular weakness related to critical illness. In: Shefner JM, Dashe JF (eds.). UpToDate; 2017. 24. Chatburn Rl, El-Khatib M, Mireles-Cabodevila E. A taxonomy for mechanical ventilation: 10 fundamental maxims. Respir Care. 2014;59(11):1747–1763.

25. Siegel MD, Hyzy RC. Mechanical ventilation of adults in acute respiratory distress syndrome. In: Parsons PE, Finlay G (eds.). UpToDate; 2016. 26. Hou P, Baez AA. Mechanical ventilation of adults in the emergency department. In: Walls RM, Grayzel J (eds.). UpToDate; 2016.

CHAPTER

6 Ventilator Initiation David C. Shelledy and Jay I. Peters

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Goals of Mechanical Ventilation Methods of Ventilation Negative-Pressure Ventilation Positive-Pressure Ventilation Establishment of the Airway Endotracheal Intubation Tracheostomy Choice of a Ventilator Choice of Mode More on Nomenclature Full and Partial Ventilatory Support Major Modes of Ventilation Other Modes of Ventilation Initial Ventilator Settings Mode Tidal Volume and Rate Breath Trigger Inspiratory Phase, Expiratory Phase, and I:E Ratio PEEP and CPAP Alarms and Limits Humidification Patient Assessment Management of Specific Disease States and Conditions Asthma Acute Exacerbation of COPD Severe Pneumonia

Acute Respiratory Distress Syndrome Neuromuscular Disease Summary

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

22.

Describe the primary function of a mechanical ventilator. Identify the four major indications for mechanical ventilation. Describe the major goals of mechanical ventilation. Overview the historical development of negative-pressure ventilation. Explain the advantages and disadvantages of negative-pressure ventilation. Define the term trigger variable and compare time-triggered ventilation to patient-triggered ventilation. Explain each of the following terms related to the trigger variable: flow trigger, pressure trigger, and autotrigger. Define each of the following commonly used terms: assist breath, control breath, assist/control, and controlled ventilation in terms of the trigger variable associated with each term. Explain how each of the following cycle variables terminates the inspiratory phase: volume cycled, pressure cycled, time cycled, and flow cycled. Compare volume-control (VC) and pressure-control ventilation (PC). Compare pressure-support ventilation (PSV) and pressure-control ventilation (PCV). Define each of the following: continuous mandatory ventilation (CMV), intermittent mandatory ventilation (IMV), and continuous spontaneous ventilation (CSV). Explain the indications, contraindications, advantages, and disadvantages of noninvasive ventilation (NIV). Describe initial ventilator settings for NIV. Describe methods and steps to establish the airway for invasive mechanical ventilation. Contrast endotracheal intubation and tracheostomy when used to provide invasive mechanical ventilation. Summarize the factors that should be considered when choosing a mechanical ventilator. Explain each of the following terms used to define the mode of ventilation employed: control variable, breath sequence, and targeting scheme. Explain methods for providing full and partial ventilatory support and contrast advantages and disadvantages of each. Define each of the five major modes of ventilation and explain the advantages and disadvantages of each. Explain the use of other modes of ventilation to include adaptive pressure control (APC), mandatory minute ventilation (MMV), adaptive support ventilation (ASV), airway pressure-release ventilation (APRV), proportional assist ventilation (PAV), automode, neutrally adjusted ventilatory assist (NAVA), and highfrequency ventilation (HFV). Describe initial ventilator setup for adult patients to include mode, tidal volume, rate, inspiratory pressure, breath trigger, pressure rise time or slope, inspiratory time, expiratory time and I:E ratio, oxygen concentration, PEEP/CPAP, alarms and limits, and humidification.

KEY TERMS adaptive pressure control (APC) adaptive support ventilation (ASV) adaptive targeting (a) airway pressure-release ventilation (APRV) assist/control volume ventilation autotriggering automode biovariable targeting (b) continuous positive airway pressure (CPAP) controlled ventilation dual targeting (d) flow cycled

full ventilatory support high-frequency jet ventilation (HFJV) high-frequency oscillatory ventilation (HFOV) high-frequency percussive ventilation (HFPV) high-frequency positive-pressure ventilation (HFPPV) high-frequency ventilation (HFV) imposed work of breathing (WOBI) intelligent targeting (i) intermittent mandatory ventilation (IMV) invasive ventilation lung-protective ventilatory strategy mandatory breaths mandatory minute ventilation (MMV) negative-pressure ventilation neurally adjusted ventilatory assist (NAVA) noninvasive ventilation (NIV) optimal targeting (o) partial ventilatory support patient-triggered breaths positive end-expiratory pressure (PEEP) positive-pressure ventilation pressure control-continuous mandatory ventilation (PC-CMV) pressure control-continuous spontaneous ventilation (PC-CSV) pressure control intermittent mandatory ventilation (PC-IMV) pressure-control ventilation (PCV) pressure cycled pressure-regulated volume control (PRVC) pressure-support ventilation (PSV) primary breaths proportional assist ventilation (PAV) rapid sequence intubation (RSI) secondary breaths servo targeting (r) set-point targeting (s) spontaneous breaths synchronized intermittent mandatory ventilation (SIMV) targeting scheme time cycled time-triggered breaths volume control-continuous mandatory ventilation (VC-CMV) volume control intermittent mandatory ventilation (VC-IMV) volume control (VC) volume cycled volume support (VS) work of breathing (WOB)

Introduction The primary function of a mechanical ventilator is to augment or replace normal ventilation. Thus, mechanical ventilation may be required when spontaneous breathing is insufficient or absent. The decision to initiate mechanical ventilatory support should be based on a thorough patient assessment, sound clinical judgment, and an understanding of the indications, contraindications, complications, and hazards of mechanical ventilation. The most common reason for initiation of mechanical ventilatory support is acute respiratory failure. Other common diagnoses associated with the need for mechanical ventilatory support include acute exacerbation of chronic obstructive pulmonary disease (COPD), coma, multiple trauma, and neuromuscular disease. The respiratory care clinician should be aware of predisposing factors for the development of acute respiratory failure, the clinical manifestations of acute respiratory failure, and the indications for mechanical ventilation. These indications include: Apnea Acute ventilatory failure Impending ventilatory failure Severe oxygenation problems (refractory hypoxemia) Other possible indications include the administration of general anesthesia, protection of the airway in the absence of a gag reflex, and the need for deep sedation and/or neuromuscular blockade. The decision to initiate mechanical ventilatory support must also consider contraindications to mechanical ventilation, and possible complications and hazards. Hazards of mechanical ventilation include ventilator-associated lung injury (VALI), ventilator-associated pneumonia (VAP), and increased work of breathing (WOB) and ventilatory muscle dysfunction due to inappropriate ventilator settings. Positivepressure ventilation may result in reduced venous return to the right heart, decreased cardiac output, and hypotension. Other possible adverse effects of mechanical ventilation include the development of barotrauma (e.g., pneumothorax, pneumomediastinum), airway problems (e.g., accidental bronchial intubation, airway occlusion), and ventilator system failure. Chapter 2 reviews respiratory failure, while Chapter 5 provides a discussion of the indications for mechanical ventilation.

Once the decision has been made to institute mechanical ventilatory support, a number of choices must be made. Most patients will receive some form of positivepressure ventilation, although negative-pressure ventilation may be appropriate in a few select cases. Certain patients may do well with noninvasive positive-pressure ventilation (NPPV), while others may require endotracheal (ET) intubation and invasive mechanical ventilation. Many modern ventilators allow the clinician to choose between providing partial and full ventilatory support, and a large number of different ventilator modes are currently available. Following selection of the appropriate mechanical ventilator and initial mode of ventilation, the respiratory care clinician must choose the initial ventilator settings. Each of these choices will be discussed in this chapter. RC Insight Major indications for ventilator initiation include apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems.

Goals of Mechanical Ventilation Mechanical ventilation can normalize alveolar ventilation and PaCO2, reverse hypoxemia, relieve respiratory distress, and allow for recovery from ventilatory muscle fatigue. Properly applied, mechanical ventilation may decrease ventilatory muscle and myocardial oxygen consumption and improve oxygen delivery to the tissues. Mechanical ventilation may also allow for deep sedation and neuromuscular blockade for certain procedures to be performed or in cases of severe distress and agitation, delirium, or severe, refractory hypoxemia. However, for most patients, sedation should only be applied as necessary for patient comfort and effective ventilation. In the presence of a closed head injury (e.g., severe traumatic brain injury) or cerebral edema, mechanical ventilation may be used for a short period of time to reduce the PaCO2, cause cerebral vasoconstriction, and reduce intracranial pressure (ICP). Initial hyperventilation should be avoided in such patients except as a life-saving measure when cerebral herniation has occurred or is imminent. The primary goals of mechanical ventilation are to provide adequate alveolar ventilation, ensure adequate tissue oxygenation, restore and maintain acid-base homeostasis, and reduce the WOB. Mechanical ventilatory support should be adjusted to ensure patient comfort and safety and minimize harmful side effects and complications. Mechanical ventilatory support should also be applied in such a fashion as to promote prompt liberation of the patient from the ventilator. It should also be noted that mechanical ventilation may reduce cardiac work by supporting oxygenation and relieving stress on the heart. Mechanical ventilation may also incorporate positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) to help restore or maintain lung volumes, improve compliance, and prevent or treat atelectasis. In cases of severe thoracic trauma with a flail chest requiring ventilatory support, mechanical ventilation may be helpful for internal stabilization of the thorax. Initiation of mechanical ventilation is not without risk. Hazards include ventilatorassociated lung injury (VALI), increased WOB (which may be caused by patient– ventilator asynchrony), ventilatory muscle dysfunction, and decreased venous return and cardiac output. Other hazards include barotrauma, ventilator-associated pneumonia (VAP), oxygen toxicity, and ventilator system failure.

VALI may be caused by elevated transpulmonary pressures during positivepressure breathing. During mechanical ventilation, plateau pressure (Pplateau) reflects alveolar pressure and, in turn, transpulmonary pressure. A lung-protective ventilatory strategy should be employed, which includes limiting plateau pressure to less than 30 cm H2O for most patients.1,2 It should be noted, however, that patients with decreased thoracic compliance may have decreased transpulmonary pressures; in such cases, higher Pplateau may be applied (if needed) without causing overdistention. Smaller tidal volumes (e.g., 6 to 8 mL/kg) and appropriate levels of PEEP are used in patients with acute respiratory distress syndrome (ARDS) to avoid ventilator-induced lung injury (VILI). An extensive review suggested that with ARDS, if Pplateau remained < 30 cm H2O, a slightly larger tidal volume (VT) (8 to 10 mL/kg ideal body weight [IBW]) did not affect outcomes.3 Properly applied, PEEP can stabilize unstable lung units and avoid repetitive inflation and deflation of alveoli, thus reducing the likelihood of additional injury. As a point of interest, the term ventilator-induced lung injury (VILI) is used when the ventilator can be clearly identified as the source of the injury. Because it can be difficult to be sure that the ventilator caused any lung injury observed (e.g., VILI), the term ventilator-associated lung injury (VALI) is commonly used.

Methods of Ventilation Methods of providing mechanical ventilatory support include negative-pressure ventilation, positive-pressure ventilation, partial ventilatory support, full ventilatory support, volume-control ventilation, pressure-control ventilation, and various ventilatory modes that employ automated targeting schemes (e.g., proportional assist ventilation [PAV], pressure-regulated volume control [PRVC], or adaptive support ventilation [ASV]).

Negative-Pressure Ventilation The tank ventilator or “iron lung” was developed by Drinker, McKhann, and Shaw at Harvard University in 1928; an improved commercial version was introduced by John H. Emerson in 1932. The Emerson iron lung was in widespread use during the polio epidemics in the United States in the 1940s and 1950s and continued to be manufactured until 1970. Other forms of negative-pressure ventilation include the Port-a-Lung, chest cuirass, and bodysuit. These devices have been used to provide intermittent or continuous negative-pressure ventilatory support to patients with chronic conditions (e.g., polio, other neuromuscular disease, or chronic restrictive disorders). Negative-pressure devices do not require the placement of an artificial airway and are relatively easy to use to support patients with chronic ventilatory failure. Negative-pressure ventilators enclose the thorax within a chamber, shell, or body suit and apply a negative pressure to effect inspiration. This negative pressure is then released to allow for expiration. Initial settings for adults were at a rate of 12 to 24 breaths/min with a negative inspiratory pressure of –10 to –35 cm H2O. The level of negative pressure applied determines the degree of inspiratory support and resultant tidal volume. Advantages of negative-pressure ventilators included the maintenance of the natural airway, which allowed patients to talk or eat, and the relative simplicity of the ventilator controls. Problems associated with negative-pressure ventilation include difficulties in accessing the patient for procedures, bathing, or turning. Most devices were large and bulky and difficult to move. Maintaining ventilation could be difficult because of leaks. In the case of full-body tanks, abdominal venous blood pooling could occur, resulting in reduced venous return and acute hypotension or “tank

shock.” In the absence of an artificial airway, negative-pressure ventilation could result in upper airway soft tissue obstruction, and negative pressure ventilation is contraindicated in patients with obstructive sleep apnea. Because of these problems, negative-pressure ventilators are inappropriate in most modern acute care and ICU settings. Although negative-pressure ventilation may be useful in a handful of longterm care patients based on patient preference, its use has been largely replaced by noninvasive positive-pressure ventilation (NPPV). As late as 2014, a few negativepressure ventilators remained in use in the United States. Other devices that have been used in the past to noninvasively support ventilation include the rocking bed and pneumobelt. Diaphragmatic pacing (aka phrenic nerve pacing) provides another example of ventilatory support that does not require insertion of an endotracheal or tracheostomy tube for patients with apnea or severe hypoventilation due to bilateral diaphragmatic paralysis.

Positive-Pressure Ventilation During positive-pressure ventilation, the ventilator applies a positive pressure via mask, endotracheal tube, tracheostomy tube, or other interface during inspiration. This positive proximal airway pressure (PAW) creates a pressure gradient between the mouth or airway and the alveoli (PA), and inspiration occurs. The peak inspiratory pressure (PIP) is the highest pressure reached during the inspiratory phase. In general, PIP occurs at the end of inspiration during volume-control ventilation. PIP occurs early in the inspiratory phase during pressure-control ventilation and continues until the cycle variable criterion is reached (e.g., time or flow cycle). Occasionally an inspiratory pause or hold of 0.5 to 1.5 seconds may be mechanically applied at the end of inspiration, and airway pressure will fall to a plateau during this inspiratory pause. This plateau pressure (Pplateau) represents the point at which PAW and PA have equilibrated (assuming no spontaneous breathing efforts are made during the inspiratory pause). Monitoring PIP and Pplateau during mechanical ventilation in the volume-control mode provides valuable information used to detect important clinical changes as well as allowing for the calculation of the patient’s static total compliance (CsT) and airway resistance (RAW). Following the inspiratory phase, the ventilator allows airway pressure to fall to a

baseline value, and expiration occurs due to the natural elastic recoil of the lungs. Baseline pressure may be ambient barometric pressure (conventionally referred to as zero) or elevated with the application of PEEP or CPAP. When properly applied, positive-pressure breathing can be accomplished with little or no work on the part of the patient.

Terminology Terminology used to describe positive-pressure ventilation can be confusing, due to the wide variety of terms in common in use. To further complicate the taxonomy for mechanical ventilation, different ventilator manufacturers use different terms to refer to the same modes.4,5 The trigger variable refers to the method that begins inspiration (i.e., the changeover from expiration to inspiration). The two most common trigger variables are time and patient effort (i.e., patient triggered), which may be further described as a (negative) pressure trigger or flow trigger. Patient-triggered breaths are initiated by the patient independent of the ventilator rate settings. Patient-triggered breaths are commonly referred to as assisted breaths, although using this terminology for patient-triggered breaths has been discouraged by some authors.4,5 Autotriggering refers to unintentional initiation of breath delivery by the ventilator, most often due to inappropriate trigger sensitivity settings and/or movement of the ventilator circuit. As noted, in common clinical parlance, the term assisted breath is often used to refer to breaths that are patient triggered. In a similar fashion, control breaths commonly refer to breaths that are time triggered, and the term assist/control is commonly used to refer to a mode of ventilation that may be patient or time triggered, depending on which occurs first. Controlled ventilation, in this context, is used to refer to a mode of ventilation in which every breath is time triggered. These latter terms should probably be avoided in favor of simply describing the trigger method that starts a breath (e.g., patient or time triggered).5 It should be noted that other trigger variables may be employed with certain modes of ventilation. Examples of other trigger variables include preset apnea interval set as a backup safety feature in the event of apnea, and electrical signals from the diaphragm (see neurally adjusted ventilatory assist [NAVA]). Mandatory minute volume (MMV) ventilation may automatically increase the respiratory rate (or pressure-support level, depending on

the ventilator employed) to meet a minimum minute ventilation goal. The cycle variable refers to the method by which inspiration is cycled off or stops (i.e., the changeover from inspiration to expiration). Common cycle variables include inspiratory time, inspiratory pressure (i.e., peak airway pressure), volume, and flow (e.g., percentage of peak inspiratory flow). Thus, a breath may be volume cycled, pressure cycled, time cycled, or flow cycled. It should also be noted that a breath may be pressure limited and pressure cycled, pressure limited and time cycled (e.g., pressure-control ventilation), or pressure limited and flow cycled (e.g., pressuresupport ventilation), as described below. Volume control (VC) occurs when volume delivery is fixed, and airway pressure varies with changes in resistance and compliance. Put another way, with VC the preset tidal volume is delivered regardless of patient effort, resistance, or compliance and peak airway pressure varies (assuming the ventilator’s set pressure limit is not reached). Other terms often used to refer to VC include volume ventilation, volumetargeted ventilation, and volume-limited ventilation. Both volume and flow are preset prior to inspiration during VC. It should be noted that the targeting scheme employed refers to the characteristics that distinguish the ventilatory pattern in use.4,5 For example, a volume-control mode in which the operator sets all parameters for volume and flow waveforms, is known as set-point targeting. A targeting scheme that allows the ventilator to automatically adjust pressure between breaths to achieve an average tidal volume over several breaths would be referred to as adaptive targeting (e.g., adaptive pressure ventilation [APV] or pressure-regulated volume control [PRVC]). With dual targeting, the ventilator can automatically switch between volume control and pressure control during a single breath. Other targeting schemes include servo, optimal, biovariable, and intelligent targeting discussed below under modes of ventilation.4,5 Pressure control (PC) occurs when inspiratory airway pressure remains constant despite changes in patient effort, resistance and compliance. With PC, tidal volume varies and is dependent on the driving pressure, inspiratory time, patient effort, compliance, resistance, and presence (or absence) of PEEP. Inspiratory pressure is predetermined with PC. It should be noted that a PC breath may be triggered by time or patient effort and cycled to expiration by time (i.e., time-cycled ventilation) or flow (i.e., flow-cycled ventilation). It should be noted that older ventilators (e.g., Bird Mark

series) allowing for pressure-cycled ventilation are no longer in common use, although pressure-cycled breath termination may occur if the ventilator’s set pressure limit is reached. Other terms sometimes used to refer to PC include pressure ventilation, pressure-targeted ventilation, and pressure-limited ventilation. Pressure-support ventilation (PSV) is a form of spontaneous ventilation (see definition below) in which the beginning of inspiration is patient triggered and the inspiratory pressure rapidly rises to a preset value. With PSV, the change over from inspiration to expiration is flow cycledd. Pressure-control ventilation (PCV) is the term employed for PC ventilation in which the beginning of inspiration is time or patient triggered (aka assist/control) and the change over from inspiration to expiration is time cycled. Although the term pressure-support ventilation is commonly used, it should be noted that the recommended taxonomy for PSV is pressure control-continuous spontaneous ventilation (PC-CSV).4,5 In a similar fashion, while the term pressurecontrol ventilation is in common use, the preferred taxonomy for PCV is pressure control-continuous mandatory ventilation (PC-CMV).4,5 This taxonomy is described further below. Mandatory breaths occur when the ventilator delivers the same breath type with every cycle, regardless of whether the breath is patient or time triggered to inspiration.5 Mandatory breaths may be VC or PC breaths. Terms sometimes used to refer to mandatory breaths include machine breaths, or mechanical breaths, although these terms are not recommended. Spontaneous breaths occur when the start and end of inspiration are determined by the patient, independent of other ventilator settings.5 Put another way, during spontaneous breathing, the patient triggers the breath to inspiration and cycles the breath to expiration. Spontaneous breaths may or may not be pressure supported (i.e., pressure-support ventilation) and may or may not occur with an elevated baseline pressure (i.e., continuous positive airway pressure or CPAP). Some authors have suggested that if the ventilator does some or all the WOB, the breath is assisted.5 Normal spontaneous breathing is unassisted, while spontaneous breathing with pressure support is assisted.5 The use of the term assisted breathing in this context should not be confused with the term assist/control, which indicates the trigger method.

Continuous spontaneous ventilation (CSV) occurs when all breaths are initiated and ended by the patient.5 Common examples of CSV modes include normal spontaneous breathing, PSV, and CPAP. Other forms of CSV include automatic tube compensation (ATC), proportional assist ventilation (PAV), and neurally adjusted ventilatory assist (NAVA).4,5 The term continuous mandatory ventilation (CMV) is used when every breath is a mandatory breath, regardless of whether the breath is patient or time triggered (aka assist/control).4 CMV breaths may be pressure control-continuous mandatory ventilation (PC-CMV) breaths or volume control-continuous mandatory ventilation (VC-CMV) breaths. VC-CMV is commonly referred to as assist/control (A/C) volume ventilation. To add to the confusion, the terms controlled-volume ventilation or volume ventilation in the control mode are commonly used to refer to time-triggered VC-CMV. These latter terms should be avoided in favor of timetriggered VC-CMV. Intermittent mandatory ventilation (IMV) occurs when patients can breathe spontaneously between mandatory breaths. Synchronized intermittent mandatory ventilation (SIMV) is a form of IMV in which the mandatory breaths may be time or patient triggered. With SIMV, spontaneous breaths may be pressure supported (i.e., SIMV with pressure support). SIMV may also be provided with (or without) an elevated baseline pressure (i.e., PEEP/CPAP). Note the term IMV has been suggested for mode classification purposes regardless whether intermittent mandatory breaths are time or patient triggered.4,5 That said, the term SIMV remains in common use by both clinicians and manufacturers. Table 6-1 summarizes terminology in use to describe common modes of ventilation. Box 6-1 lists additional modes available on certain ventilators. TABLE 6-1 Terminology Used to Describe Modes of Ventilation

Mandatory breaths occur when the ventilator delivers the same breath type with every breath. Mandatory breaths may be time or patient triggered and pressure or volume controlled (PC or VC). The term assisted breath is commonly used to refer to PC or VC breaths that are patient triggered. In a similar fashion, the term control breaths is commonly used to refer to PC or VC breaths that are time triggered. When every breath is a mandatory breath, the mode is referred to as continuous mandatory ventilation (CMV). CMV may be volume or pressure controlled (VC-CMV or PC-CMV). Spontaneous breaths are initiated by the patient and the patient determines when the end of inspiration occurs (i.e., patient cycled). Pressure support (PS) or automatic tube compensation (ATC) may be applied during spontaneous breaths and support some of the work of inspiration. When used alone, PSV is a form of pressure control-continuous spontaneous ventilation (PC-CSV).

PEEP, positive end-expiratory pressure; CPAP, continuous positive airway pressure. 1. 2. 3. 4. 5. 6.

AC (or A/C) indicates assist/control, which may be time or patient triggered. VC indicates volume control. PC indicates pressure control. PA indicates pressure assist. PS indicates pressure support. Modes available using this simplified nomenclature are volume assist/control (VAC); pressure assist/control (PAC); volume-synchronized intermittent mandatory ventilation (V-SIMV); pressure-synchronized intermittent mandatory ventilation (P-SIMV); and pressure-support ventilation (PSV).

BOX 6-1 Other Available Modes of Ventilation ∎

Noninvasive ventilation (NIV) is sometimes referred to as noninvasive positive-pressure ventilation (NPPV). • The ventilator is connected to the patient using a nasal mask or pillows, full face mask, mouthpiece, or helmet interface. • The ventilator is typically patient triggered, pressure limited, and flow cycled. • NIV is currently available on most critical care ventilators. ∎ Bi-level positive airway pressure (BiPAP). • Often used to deliver noninvasive ventilation, BiPAP delivers a preset inspiratory pressure (IPAP) that is patient triggered to inspiration and flow cycled to expiration similar to pressure support (PSV). • Inspiratory positive airway pressure (IPAP) refers to the pressure delivered during inspiration. • Expiratory positive airway pressure (EPAP) refers to the baseline pressure maintained during expiration. • Along with compliance, resistance, and patient effort, the difference between IPAP and EPAP determines the tidal volume delivered. ∎ Pressure-control inverse-ratio ventilation (PCIRV). • Typically, the ventilator is time triggered, pressure limited, and time cycled in a manner such that inspiration is longer than expiration (I:E ratio > 1:1; e.g., 1.5:1, 2:1). • Inverse-ratio ventilation (IRV) increases mean airway pressure and may improve oxygenation in certain patients (e.g., severe ARDS). ∎ Pressure-regulated volume control (PRVC). • PRVC is a form of adaptive pressure control (see below). • Provides a volume-targeted, pressure-control breath. • Inspiration is patient or time triggered, pressure limited, and time cycled. Pressure is automatically adjusted breath to breath to achieve a volume

target. • Delivered tidal volume is measured and compared to the set (targeted) tidal volume; pressure control is gradually increased or decreased until the target tidal volume is reached. • PRVC is available under that name on the Maquet Servo-i and Servo-u; Yvaire AVEA and VELA; and eVent Inspiration 7i (eVent Medical, Lake Forest, CA). • Other proprietary names for PRVC include Autoflow (Dräger Evita E-4, Infinity V500 Elite), VC+ (Covidien PB 840, PB 980) and adaptive pressure ventilation (HAMILTON G5 and G3). ∎ Volume support (VS). • Like pressure support, breaths are patient triggered and flow cycled. The pressure-support level is adjusted automatically breath to breath to achieve a volume target. • Inspiration is patient triggered; spontaneous breathing is required. • VS is a form of adaptive pressure control (see below). ∎ Adaptive pressure control (APC) automatically adjusts pressure control or pressure support to achieve the target tidal volume. • Inspiratory pressure varies automatically between breaths to achieve the target tidal volume. • Maintains tidal volume with changes in ventilatory mechanics. • May improve patient–ventilator synchrony due to variable inspiratory flow provided. • APC is also known as PRVC (Servo-i, Servo-u), adaptive pressure ventilation (HAMILTON Galileo), AutoFlow (Dräger), volume control plus (Puritan Bennett), and volume-targeted pressure control (General Electric). • Support is reduced if the patient’s tidal volume consistently exceeds the target. ∎ Adaptive support ventilation (ASV) makes automatic adjustments in respiratory rate and inspiratory pressure based on measurements of respiratory mechanics to deliver the desired minute ventilation and minimize the WOB. • Desired minute ventilation is calculated based on the patient’s ideal body weight and estimated dead space where target V̇E = 0.1 L/min/kg or 100 mL/min/kg. • The level of ventilatory support to be provided is set by the clinician as a percentage of the target V̇E. • The ventilator uses an algorithm to determine optimal breathing frequency

∎

∎

(f) and a target tidal volume is calculated based on V̇E and f (VT = V̇E/f) • Pressure control is then adjusted automatically to achieve the targeted tidal volume. Airway pressure-release ventilation (APRV). • APRV provides two levels of CPAP, which are time triggered and time cycled. APRV allows for spontaneous breathing at both levels. • APRV is typically used as a form of pressure-control inverse-ratio ventilation (PCIRV) in which the high-pressure time exceeds the lowpressure time. • APRV may reduce shunt and improve oxygenation and gas exchange as compared to conventional ventilation in ARDS patients; improved patient outcomes have not been clearly demonstrated. Automatic tube compensation (ATC). • Imposed airway resistance due to the endotracheal tube or tracheostomy tube is estimated. • Pressure-support level is automatically adjusted to compensate for the WOBI.

The clinician may choose 100% tube compensation or a lower value. ∎ Proportional assist ventilation (PAV). • PAV incorporates an algorithm to calculate the pressure required to ventilate based on the patient’s tidal volume, elastance, resistance, and gas flow. ○ The ventilator estimates WOB based on inspiratory flow, volume, pressure, compliance, resistance, and pressure. • Breaths are patient triggered, pressure limited, and flow cycled. • Pressure, flow, and volume are proportional to the patient’s spontaneous effort and clinician-set parameters. ○ Pressure varies depending on the amount of inspiratory flow and volume demanded by the patient and the amplification level selected by the clinician. ○ Flow increases proportionally as patient’s inspiratory effort increases. • The clinician adjusts the percentage of support (from 5% to 95%) to achieve WOB in the range of 0.5 to 1.0 joules per liter. • Applied pressure and inspiratory time vary breath by breath and within each breath depending on changes in compliance, resistance, and flow demand. Inspiratory time is determined by the flow cycle setting. • PAV may be more comfortable for some patients and improves patient– ventilator synchrony by matching the patient’s inspiratory demand.

•

PAV has not been shown to improve patient outcomes. ∎ Neurally adjusted ventilatory assist (NAVA) uses the electrical discharge from the diaphragm (i.e., electromyography [EMG]) to trigger and cycle mechanical breaths. • NAVA requires an esophageal catheter that incorporates a multiple array esophageal electrode. • NAVA increases ventilator pressure as patient effort increases. • NAVA may improve patient–ventilator synchrony. ∎ Mandatory minute volume ventilation (MMV) is aka mandatory minute ventilation, minimum minute ventilation, or augmented minute ventilation). • Designed to promote ventilator weaning. • A minimum minute ventilation (V̇E) is set for spontaneously breathing patients. • The ventilator monitors the patient’s spontaneous minute volume and provides additional ventilatory support as needed to achieve the set minimal minute volume. • With increased spontaneous V̇E, the ventilator reduces the level of support provided. • Additional ventilatory support may be in the form of increased pressure support or increased IMV rate, depending on the ventilator employed. • MMV using automatic adjustments in SIMV rate can vary the number of mandatory breaths from 0 to the set SIMV rate, depending on the patient’s spontaneous V̇E. ∎ High-frequency ventilation (HFV) delivers small tidal volumes at a very high respiratory frequency. Possible indications for HFV include ARDS, bronchopleural fistula, and air leaks. HFV is not recommended as a first choice for mode of ventilation and should be avoided in patients with obstructive lung disease. • High-frequency oscillatory ventilation (HFOV) is delivered using an oscillator to provide a respiratory frequency in the range of 3 to 15 Hz (180 to 900 breaths/min). ○ HFOV may minimize alveolar over distention and derecruitment. ○ HFOV seems to be effective in neonatal respiratory failure. ○ HFOV may be considered for refractory hypoxemic respiratory failure in adults, although better patient outcomes have not been demonstrated. • High-frequency jet ventilation (HFJV) is delivered using a jet gas flow delivered to the endotracheal tube via a small cannula. • High-frequency percussive ventilation (HFPV) combines time-cycled

•

∎

pressure-control ventilation with a phasitron to provide oscillatory or percussive ventilation throughout inspiration and expiration. HFPV may improve secretion clearance, improve oxygenation and ventilation, and lower airway pressures. • High-frequency positive-pressure ventilation (HFPPV) uses a conventional ventilator with a low tidal volume setting and a very rapid respiratory rate. Continuous positive airway pressure (CPAP). • CPAP allows for spontaneous breathing at elevated baseline pressure. • CPAP increases functional residual capacity (FRC) and may improve compliance, oxygenation, and ventilation in patients with acute restrictive lung disease.

WOBI - imposed work of breathing

Noninvasive Ventilation Noninvasive ventilation (NIV) refers to techniques that do not require insertion of an invasive artificial airway (e.g., endotracheal intubation or tracheostomy). NPPV is the most common form of NIV in use today. CPAP and bilevel positive airway pressure (BiPAP) have been used in the home for management of obstructive sleep apnea (OSA) for many years. BiPAP combines inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). The routine use of NIV for patients with acute respiratory failure has been a relatively recent development. NIV requires the use of a nasal mask, oronasal mask, nasal pillows, mouthpiece, or helmet interface. Properly applying the interface to avoid excessive leaks without causing patient discomfort or skin breakdown is one of the more important and challenging aspects of NIV. The oronasal or full-face mask is the most common interface for use in patients with acute respiratory failure. NIV may be delivered by volume-limited or pressure-limited ventilators. Most BiPAP devices are flow triggered to inspiration, flow cycled to expiration, and pressure limited. Newer critical care ventilators may also have an NIV mode built in. Indications for NIV include acute exacerbation of COPD with hypercapnic acidosis, cardiogenic pulmonary edema, and acute hypoxemic respiratory failure.6 NIV may also be useful to prevent postextubation respiratory failure. Nocturnal NIV may be

useful for stable COPD patients with chronic respiratory failure and daytime hypercapnia. NIV may also be useful for acute or impending respiratory failure in pediatric patients who do not require emergency endotracheal intubation.7 RC Insight Indications for NIV in the acute care setting include acute exacerbation of COPD with hypercapnic acidosis, cardiogenic pulmonary edema, and acute hypoxemic respiratory failure. NIV may also be used to prevent extubation failure.

NIV is also commonly used to support ventilation in patients with chronic hypoventilation due to neuromuscular or chest wall disease (e.g., muscular dystrophy, post-polio syndrome, other slowly progressing neuromuscular diseases, or chest wall deformity).8 Such patients may be candidates for nocturnal or sustained NIV, especially if they have either daytime hypercapnia or nocturnal hypoventilation with sustained oxygen desaturation.8 Contraindications for NIV include cardiac or respiratory arrest; hemodynamic or cardiac instability (e.g., unstable cardiac arrhythmias), or severely impaired consciousness (Glasgow coma score [GCS] < 10).6 NIV may also be contraindicated in the presence of facial trauma, facial surgery, or facial deformity. Upper airway obstruction, inability to protect the airway or clear secretions, and high risk for aspiration are relative contraindications for the use of NIV. For example, patients with upper gastrointestinal bleeds are not good candidates for NIV. Patients with acute respiratory failure who are likely to require prolonged mechanical ventilatory support may be best treated with invasive mechanical ventilation. Patients with encephalopathy (i.e., brain dysfunction) caused by hypercapnia may respond to NIV, but these patients must be carefully monitored; if there is no prompt response, intubation and invasive mechanical ventilation should occur.6 NIV can result in gastric inflation at pressures above 20 to 25 cm H2O; NIV is also contraindicated in patients who have recently received esophageal surgery or in the presence of a tracheal-esophageal fistula.6 NIV may be provided using BiPAP, PSV, assist/control (A/C) volume ventilation (aka VC-CMV), PAV, and NAVA. Initial NIV ventilator settings using BiPAP, PSV, or volume ventilation typically include:6,8 Lower initial pressures for BiPAP and PSV to allow for patient adaptation to the device and interface.

IPAP 8 to 20 cm H2O (begin at 8 to 12 cm H2O for most patients). EPAP 3 to 5 cm H2O. Delta P (∆P = IPAP – EPAP) should be adjusted to about 5 to 15 cm H2O to ensure adequate tidal volume. IPAP should be maintained < 25 to 30 cm H2O in order to avoid gastric insufflation and ventilator-induced lung injury. For volume ventilation, larger initial tidal volumes of 6 to 10 mL/kg have been suggested to compensate for air leaks during NIV. Trigger effort should be set for minimal patient work without autocycling. A backup respiratory rate may be set 2 to 4 breaths/min below the patient’s spontaneous rate. Patients often initially hyperventilate, and the backup rate may be adjusted accordingly. Patients’ rates may slow within 6 to 12 hours as they become accustomed to NIV, and the backup rate may need to be decreased at that time. Initial FIO2 should be selected to avoid hypoxemia without administration of excessive oxygen concentrations. Following initial ventilator setup, the ventilator is adjusted to ensure adequate oxygenation, ventilation, and patient comfort while avoiding patient–ventilator asynchrony. Chapter 10 provides additional information regarding NIV.

Invasive Ventilation Invasive mechanical ventilation is provided via an artificial airway whose tip is located in the trachea (e.g., endotracheal tube or tracheostomy tube). Invasive ventilation has the advantage of securing and protecting the airway and providing a more dependable form of ventilatory support for unstable, critically ill patients. For example, in patients requiring mechanical ventilatory support, the loss of protective airway reflexes are an important indication for endotracheal intubation. On the other hand, patients who can swallow and speak may not require endotracheal intubation to protect the lower airway; these patients may be candidates for NIV. Patients with depressed mental status (e.g., unconsciousness, coma), hemodynamic instability, severe oxygenation disorders, and those requiring (or likely to require) sophisticated mechanical ventilatory support probably are best served by invasive mechanical ventilation. The placement of an endotracheal tube or tracheostomy tube may also facilitate suctioning of airway secretions.

RC Insight Invasive ventilation has the advantage of securing and protecting the airway and providing a more dependable form of ventilatory support for unstable, critically ill patients.

Establishment of the Airway Nasopharyngeal or oral pharyngeal airways may be helpful in certain patients with soft tissue obstruction; however, they do little to protect the lower airway and do not allow for invasive mechanical ventilatory support. Extraglottic airways (aka supraglottic airways) have been sometimes used during general anesthesia or as an adjunct to manage difficult and emergency airways.9 An example of an extraglottic airway is the laryngeal mask airway (LMA). Most patients requiring invasive mechanical ventilation, however, are endotracheally intubated, and the clear majority (95%) of these intubations are done orally; the remaining endotracheal tubes are placed nasally. A subset of patients requiring extended invasive mechanical ventilation will receive a tracheostomy at some point (most often > 10 to 14 days, but earlier in some patients).

Endotracheal Intubation Indications for endotracheal intubation include the inability to maintain a patent airway, inability to protect the airway against aspiration, failure to ventilate, failure to oxygenate, and anticipation of deterioration in the patient’s condition that will lead to respiratory failure.10 Contraindications to endotracheal intubation generally are those in which the procedure for tube insertion is likely to cause additional airway trauma or is likely to be unsuccessful. NIV may be helpful in such situations, although an emergency tracheostomy (or in rare cases cricothyrotomy) may be necessary if ventilation is compromised. Box 6-2 summarizes indications, contraindications, and hazards associated with endotracheal intubation.

BOX 6-2 Indications, Contraindications, and Complications of Endotracheal Intubation Indications ∎ Cardiac arrest ∎ Apnea (e.g., respiratory arrest) ∎ Upper airway obstruction ∎ Need to provide a patent airway (e.g., coma, depressed mental status) ∎ Need to protect the airway (e.g., high risk of aspiration, lack of gag reflex)

∎ ∎ ∎

Respiratory failure (failure to oxygenate and/or ventilate) Need to provide mechanical ventilatory support to critically ill patients (i.e., invasive mechanical ventilation; NIV contraindicated or impractical) Anticipated deterioration in the patient’s condition that will lead to respiratory failure

Contraindications ∎ ∎ ∎ ∎

Supraglottic or subglottic pathology (e.g., blunt trauma with laryngeal fracture) Penetrating trauma of the upper airway (e.g., hematoma, airway transection) Severe laryngeal edema or supralaryngeal edema (e.g., anaphylaxis, bacterial infection, or burns) Difficult airway due to anatomic features or injuries

Complications During the Procedure ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎ ∎

Difficult intubation may result in complications Prolonged intubation attempts Hypoxemia, hypercarbia, and acidosis Trauma to the upper airway Glottis, vocal cord, or laryngeal trauma Aspiration of stomach contents (patient may gag and vomit) Inadvertent mainstem bronchial intubation Inadvertent esophageal intubation Airway obstruction

Complications Following the Procedure ∎

Accidental extubation Airway malfunction • Obstruction • Secretions • Kinks • Cuff leaks • Pilot balloon failure • Aspiration of secretions due to cuff failure or improper inflation ∎ Complications associated with suctioning • Hypoxemia • Arrhythmias

∎

Vagal stimulation Bradycardia Hypotension Cardiac arrest ∎ Ventilator-associated pneumonia (VAP) ∎ Tracheobronchitis ∎ Nasal complications (due to nasal endotracheal intubation) • Sinusitis due to impaired sinus drainage • Nasal necrosis (following nasal intubation) ∎ Laryngeal injury due to ETT • Vocal cord ulceration • Glottic edema • Subglottic edema • Vocal cord ulceration • Vocal cord paralysis • Laryngeal inflammation • Granuloma formation • Laryngotracheal stenosis ∎ Tracheomalacia ∎ Tracheal arterial fistula ∎ Tracheoesophageal fistula ∎ Complications discovered following extubation • Swallowing disorders • Hoarseness • Sore throat • Speech impairment • Tracheal stenosis • Extubation failure requiring re-intubation or NIV

• • • •

Rapid-sequence intubation (RSI) is performed for emergency airway management. Completion of RSI includes the administration of an induction agent (e.g., ketamine [Ketalar], etomidate [Amidate], midazolam [Versed], and propofol [Diprivan]) resulting in unconsciousness immediately followed by a paralytic agent (e.g., rocuronium [Zemuron], succinylcholine [Anectine]) for neuromuscular

blockade.10 Initial medication dosage is based on the patient’s weight and designed to achieve unconsciousness and paralysis within 1 minute.10 Induction and paralysis may not be necessary in already unconscious and apneic patients (e.g., a crash airway). Specific indications for emergency endotracheal intubation include cardiac arrest, respiratory arrest, and upper airway obstruction not relieved by other methods. Direct laryngoscopy is often employed to achieve endotracheal intubation. Prior to intubation, the patient is assessed and the appropriate equipment, supplies, and medications are gathered.9,11 The patient is prepared, positioned, and preoxygenated with 100% oxygen using a bag-valve mask system with a PEEP valve.9,11 For oral intubation, the patient’s mouth is opened and the laryngoscope is introduced and advanced until the epiglottis and glottis can be visualized. The endotracheal tube is then guided to the glottis and inserted between and past the vocal cords into the trachea. Recent advances in intubation include the common use of a video laryngoscope (e.g., the Glide Scope), where the entire glottis can be visualized from the level of the pharynx and a specialized stylet allows the ET tube to be placed past the level of the vocal cords. Following insertion to an appropriate depth (e.g., 21 cm for most adult females or 23 cm for most adult males) the tube is secured, and the patient is mechanically supported using the manual resuscitator bag and 100% oxygen.9,11 Equal and bilateral breath sounds should be confirmed by auscultating the patient’s chest and assessment for the presence of exhaled CO2 using capnography should be promptly performed to confirm proper tube placement.9,11 Once proper placement of the endotracheal tube has been assured and the tube secured, mechanical ventilation can begin. Figure 6-1 describes assessment of the difficult airway. The modified Mallampati Classification system for airway assessment is described below.

FIGURE 6-1 Modified Mallampati Classification. The modified Mallampati difficulty classification is based on structures visible during oropharyngeal examination via direct laryngoscopy. Class I is least difficult intubation, while Class IV is most difficult intubation.

Description Class I: Visible structures include the tongue, hard palate, soft palate, uvula, and posterior pharynx. Class II: Visible structures include the tongue, hard palate, soft palate, and part of the uvula, and posterior pharynx. Class III: Visible structures include the tongue, hard palate, soft palate; posterior pharynx NOT visible. Class IV: Visible structures include only the anterior tongue and hard palate. Portable chest x-rays taken shortly after intubation are often useful in confirming proper tube placement. The tip of the endotracheal tube generally should lie in the middle one-third of the trachea and be at least 2 cm above the carina. Following tube placement, bedside ultrasound may be useful to confirm bilateral lung ventilation by observing the lung sliding sign on each side (i.e., movement of the parietal and visceral pleura as the lung expands and contracts).11 If the lung sliding sign is present on only one side, bronchial intubation may have occurred. Absence of sliding is also seen with a pneumothorax or scarring between the visceral and parietal pleura. Box 6-3 summarizes key points regarding endotracheal intubation. Chapter 9 provides additional information regarding patient assessment and the procedure for endotracheal intubation.

BOX 6-3 Endotracheal Intubation The following steps are recommended in order to perform successful and safe endotracheal intubations. 1. Assess the airway – HAND • History of difficult intubation? • Anatomic considerations present? ○ 3-3-2 rule assessment. A difficult to intubate airway may be present if one of or more of the following are present: • Patient’s mouth cannot be opened to permit placement of three fingers between the upper and lower teeth. • Three fingers do not fit under the chin between the tip of the jaw and the beginning of the neck. • There is not enough space for two fingers between the thyroid notch and the floor of the mandible. ○ Modified Mallampati classification is employed to assess probable difficulty of intubation. • Oropharyngeal examination of the tongue, hard palate, soft palate, uvula, and posterior pharynx during laryngoscopy. • Classification (I through IV) is based on structures visible during the oral pharyngeal exam. • Class I indicates least difficult airway to intubate. • Class IV indicates most difficult airway to intubate. ○ Other risk factors present for airway distortion, any obstruction? • Neck mobility. • Difficult airway should be considered if concerns with any of the factors above. 2. Preoxygenate using 100% oxygen, bag-valve mask with PEEP valve. 3. Prepare. • Patient: Sniffing position, headboard off and patient head just below intubator’s xyphoid process • Medications: Free-flowing IV, premedication, induction, paralytic and vasopressor agents • Right side: Suction, endotracheal tube with stylet and syringe attached • Left side: Laryngoscope handle, blades, oral and nasal airways end-tidal CO2 detector 4. Review team member roles, primary and backup intubation plans.

5. Oxygen cut offs: Identify signals to abort; reinitiate bag-valve mask ventilation. 6. Administer medication, if indicated. 7. Confirm endotracheal tube placement using two indicators (including endtidal CO2). 8. Hold endotracheal tube until secured. Data from the American College of Chest Physicians Airway Management Program Curriculum, 2013.

RC Insight Endotracheal intubation can maintain a patent airway, protect the airway against aspiration, and allow for ventilation and oxygenation.

Tracheostomy Indications for tracheostomy include long-term mechanical ventilation, weaning failure, upper airway obstruction, and for the management of copious secretions.12 A surgical tracheostomy is performed in the region of the second to fourth tracheal cartilages, while percutaneous tracheostomy is done between the first and second or the second and third tracheal cartilages.13 Percutaneous tracheostomy is simpler, quicker, and has a lower rate of early complications. Because of this, well over half (66% to 86%) of tracheostomies performed are now percutaneous tracheostomies.12,13 Advantages of tracheostomy (as compared to endotracheal intubation) include improved patient comfort, less sedation/analgesia required, reduced oral/laryngeal injury, and improved oral care.14 Tracheostomy can also improve patient communication by enabling lip-reading or the use of speaking valves. Tracheostomy better preserves the swallow, allowing for earlier feeding and helps maintain glottic competence, which may have some benefit in avoiding aspiration and the development of ventilator-associated pneumonia.14 Tracheostomy may also slightly reduce anatomic dead space (due to bypass of the upper airway), decrease airway resistance and WOB, improve secretion clearance, reduce the need for sedation, and decrease the risk of aspiration.15,16 Because of these advantages, some have speculated that tracheostomy may facilitate ventilator weaning in certain patients.15,17,18 Tracheostomy should be

considered after an initial period of stabilization on the ventilator when it becomes apparent that the patient will require prolonged ventilatory assistance. Early tracheostomy may be beneficial in patients who require high levels of sedation to tolerate the endotracheal tube. As noted, tracheostomy placement may slightly reduce airway resistance and anatomic dead space and reduce WOB. Patients may derive benefit from the ability to eat orally, communicate by articulated speech, and enhanced mobility. Tracheostomy is not without complications, which may include infection of the wound site, pneumothorax, subcutaneous emphysema, tube obstruction, and accidental decannulation.16–18 Later complications include aspiration (30% to 50% of patients), pneumonia, tracheal stenosis, tracheoarterial fistula (most commonly tracheoinnominate artery fistula), tracheoesophageal fistula, and tracheomalacia.12,14,16,19,20 Tracheostomy bypasses the natural warming, filtration, and humidification provided by the upper airway. Inadequate humidification can lead to chronic inflammatory changes, squamous metaplasia, desiccation of the tracheal mucosa, and reduced ciliary function. Tracheostomy also diminishes cough effectiveness and may hamper an effective swallow. Although rare (especially with the higher position of tracheostomy tubes done percutaneously), innominate artery erosion (i.e., tracheoarterial fistula) can lead to massive hemorrhage and death. Immediate recognition and maneuvers to sustain the patient until surgical repair can be done should be applied.16 For example, the tube cuff may be overinflated to compress the innominate artery, or an endotracheal tube inserted allowing for removal of the tracheostomy tube. The ETT tip is then advanced distal to the tracheostomy stoma and the cuff inflated.16 As a last resort, the artery may be digitally compressed using a finger placed through the stoma.16 In summary, the effect of early tracheostomy on hospital mortality, duration of mechanical ventilation, and development of ventilator-associated pneumonia remains unclear.21,22 Tracheostomy appears to have benefits in terms of reduced sedation requirements, patient comfort, resumption of oral feeding, decreased oral and laryngeal injury, and reduced WOB. Early tracheostomy should be considered in patients likely to require prolonged mechanical ventilation. Box 6-4 lists the indications, contraindications, and hazards of tracheostomy.

BOX 6-4 Indications, Contraindications, and Complications of Tracheostomy Indications ∎ Provide secure airway for mechanical ventilation (especially prolonged mechanical ventilation). ∎ Failure to wean from the ventilator in 1 to 3 weeks following endotracheal intubation. Advantages ∎ Improve weaning parameters (e.g., rapid shallow breathing index [RSBI]). ∎ Reduce WOB. ∎ Improve patient comfort. ∎ Reduce need for sedation and analgesia. ∎ Improved patient mobility. ∎ Improved patient communication (speaking tubes, lip-reading). ∎ Allow patient to eat orally. ∎ Improved secretion clearance and ease of suctioning. ∎ Easier nursing care. ∎ Percutaneous tracheostomy is faster, less expensive, and may be performed at the bedside. Contraindications ∎ Age < 15 years (percutaneous tracheostomy) ∎ Bleeding diathesis (tendency to bleed, e.g., clotting disorder) ∎ Neck tumor ∎ Thyromegaly (enlarged thyroid) ∎ Tracheomalacia (weak, soft, floppy tracheal cartilages) ∎ Soft-tissue infection ∎ Obesity ∎ Cervical spine instability ∎ Short neck Complications During the Procedure ∎ Bleeding ∎ Airway obstruction/malfunction ∎ Hypoxemia/hypoventilation Complications Following the Procedure

∎

Airway malfunction • Obstruction • Secretions • Cuff leaks • Pilot balloon failure • Aspiration of secretions due to cuff failure or improper inflation • Accidental decannulation • Migration of the tube ∎ Pneumothorax; subcutaneous emphysema ∎ Postoperative hemorrhage ∎ Infection ∎ Nosocomial pneumonia ∎ Reduced or lost phonation (vocal fold sound production, speech) ∎ Tracheoarterial fistula (e.g., tracheal innominate artery erosion) ∎ Wound infection ∎ Oral secretion aspiration (cuff failure or poor cuff maintenance) ∎ Complications at the cuff site • Tracheomalacia • Tracheoesophageal fistula (more common with endotracheal intubation) • Tracheal stenosis ∎ Complications associated with suctioning (e.g., hypoxemia, arrhythmias, vagal stimulation, bradycardia, hypotension, and cardiac arrest)

Choice of a Ventilator Prior to initiation of mechanical ventilation, the respiratory care clinician must choose an appropriate ventilator. Ventilator choice should be driven by consideration of the patient’s needs, the goals to be achieved, patient safety, and the clinician’s familiarity with the ventilator to be employed. For example, an unstable, critically ill patient in acute ventilatory failure with severe, refractory hypoxemia may require a ventilator with in-depth monitoring and graphics capabilities able to apply sophisticated modes of ventilation. On the other hand, a long-term high cervical spinal cord injury patient with little or no lung injury may require a dependable and reliable ventilator able to safely support the patient; sophisticated graphics packages and modes of ventilation may not be needed. Patients expected to continue to make spontaneous ventilatory efforts during ventilatory support may do well with a ventilator able to provide a mode of ventilation that better promotes patient–ventilator synchrony. An apneic patient generally will require time-triggered volume ventilation (aka control mode), while a COPD patient with acute respiratory failure may do well with NIV. When choosing a specific ventilator, features, modes available, pressure and flow capabilities, and integrated alarms and monitoring systems should be considered. Reliability, cost, and familiarity with the ventilator are also important factors in ventilator choice. Most modern ventilators have sufficient pressure and flow capabilities to ventilate patients with low compliance, high resistance, or markedly increased inspiratory flow demands. The ventilator chosen should adequately and safely ventilate patients under changing conditions and provide the features and modes required. Most ventilator manufacturers offer several ventilators with different capabilities and features. Typically, manufacturers will offer a sophisticated, high-end ventilator for critical care use that incorporates a number of modes and special features. The same manufacturer may also offer an intermediate critical care ventilator that does not include some modes of ventilation and/or some specific features. These intermediate ventilators are often less expensive and may be easier to operate by personnel unfamiliar with newer and more sophisticated modes of ventilation. Manufacturers also often offer specific ventilators for patient transport or very short-term use. While most of the newer critical care ventilators have NIV capability, some manufacturers offer ventilators that are designed primarily for NIV. In a similar fashion, some ventilators are designed primarily for use in the neonatal

intensive care unit, while other ventilators are able to support infants, children, and adults. Several manufacturers offer ventilators particularly suited for long-term or home-care use. As manufacturers develop and market newer ventilators, older models are often gradually phased out, and may be acquired at a reduced cost. Current adult critical care ventilators in common use include the Covidien Puritan Bennett series (PB 840, PB 980), Dräger Evita series (Evita XL, Evita Infinity V500), GE Healthcare CARESCAPE R860, Getinge Group Maquet Servo ventilators (Servo-s, Servo-i, Servo-u), HAMILTON Medical Ventilators (HAMILTON G-5, HAMILTON C-3), and Vyaire ventilators (AVEA, VELA). Other ventilators for use in acute and postacute care include the Covidien Newport e360 ventilator and the Vyaire LTV 1200 and LTV 1150. Ventilators especially well-suited to provide NIV include the Philips Respironics ventilators (e.g., V60, V200, BiPAP, and Trilogy series) and Devilbiss ventilators (e.g., Intelli PAP AutoBilevel and Bilevel S). Highfrequency ventilators include the Vyaire 3100B Oscillator, Percussionaire VDR-4, and Bunnell Life Pulse high-frequency ventilator. There are also transport and home care ventilators available, although these ventilators in general are not appropriate for continuing support of patients in the ICU. To summarize, factors that should be considered when choosing a ventilator include: Clinical goals and patient’s needs Availability Reliability Ventilator features Alarms and monitoring capabilities Modes available Cost Clinician’s familiarity with the ventilator Chapter 4 provides additional information regarding specific critical care ventilators currently available. RC Insight The most important factor in choice of ventilator is the clinician’s familiarity with the device.

Choice of Mode The mode of ventilation is determined by the control variable (e.g., volume control [VC] or pressure control [PC]), breath sequence (e.g., continuous mandatory ventilation [CMV] or intermittent mandatory ventilation [IMV]), and targeting scheme employed.4,5 Mandatory breaths occur when the start and/or end of inspiration is determined by the ventilator, independent of the patient. A mandatory breath may be patient or time triggered to inspiration but is cycled to expiration by ventilatordetermined parameters, which may be set by the clinician or automatically determined by the ventilator. For example, continuous mandatory ventilation (CMV) may incorporate mandatory breaths that are time or patient triggered to inspiration (assist/control) and volume or time cycled to expiration. IMV intersperses mandatory breaths with spontaneous breaths. By definition, spontaneous breaths are initiated by the patient and the patient determines when the end of inspiration occurs. In order to allow for spontaneous breathing through the ventilator circuit, modern ventilators incorporate a patient trigger to provide inspiratory gas flow and a cycle mechanism to allow flow to be patient cycled to expiration. Spontaneous breaths provided by the ventilator may include pressure support or automatic tube compensation during inspiration and may include CPAP during inspiration and expiration. The only requirement for a breath to be classified as spontaneous is that the breath is patient triggered to inspiration and patient cycled to expiration. Recall that PSV is patient triggered to inspiration and cycled to expiration when the patient’s inspiratory flow rate declines to a preset value; thus, PSV can be considered a form of spontaneous ventilation.4,5 To review, the common control variables are PC or VC for the primary breath. The primary breath is defined as either the spontaneous breath in continuous spontaneous ventilation (CSV), the mandatory breath in continuous mandatory ventilation (CMV), or the mandatory breath in intermittent mandatory ventilation. With CSV, all breaths are spontaneous. With CMV, all breaths are mandatory. With IMV, spontaneous breaths are interspersed with mandatory breaths. Using the breath sequence of either CSV, CMV, or IMV coupled with the control variable of either pressure or volume, the clinician can describe the basic mode of ventilation being employed. Using this system, the five basic modes of ventilation available are: VCCMV, VC-IMV, PC-CMV, PC-IMV, and PC-CSV.5

Within these broad modes, there are several variations that can be distinguished by their targeting schemes. There are seven targeting schemes in current use: setpoint (s), dual (d), servo (r), adaptive (a), bio-variable (b), optimal (o), and intelligent (i).5 The mode of ventilation can be further described by placing the targeting scheme subscripts after the basic mode description. For example, assist/control volume ventilation (aka volume control-continuous mandatory ventilation) with setpoint breath targeting can be further described as VC-CMVs. Volume control-SIMV with set-point breath targeting for both mandatory and spontaneous breaths would be described as VC-IMVs,s. These targeting schemes are further described in Table 6-2. TABLE 6-2 Ventilator Modes and Targeting Schemes

The mode of ventilation is determined by the control variable (e.g., VC or PC), breath sequence (e.g., CMV or IMV), and targeting scheme employed. * Note: the targeting scheme is indicated by the abbreviation following the major mode description. For example, volume-controlled continuous mechanical ventilation with set-point targeting would be described as VC-CMVs. Targeting schemes for mandatory and spontaneous breaths are listed for IMV modes. For example, SIMV volume control with pressure support (PB840 and 980) using set-point targeting for spontaneous and mandatory breaths would be described as VC-IMVs,s, indicating set-point targeting for both spontaneous and mandatory breaths. Targeting schemes can be mixed in the IMV mode. For example, adaptive pressure ventilation SIMV (HAMILTON G5) would be described as PC-IMVa,s, indicating adaptive targeting for pressurecontrol breaths and set-point targeting for spontaneous breaths.

Currently, there are very large number of modes of ventilation available. While many of these modes have distinct advantages from a theoretical point of view, research demonstrating that a specific mode is more effective in improving patient outcomes is often lacking. Consequently, we will focus on common modes used to provide adult ventilatory support. Other, newer modes will be discussed later in this section.

More on Nomenclature Nomenclature for different modes of ventilation can be confusing and specific manufacturers often use different terms to refer to the same mode. As noted, what distinguishes different modes of ventilation are the control variables (pressure or volume), breath sequence (CMV, IMV, or CSV), and the targeting scheme or schemes used for the primary and secondary breaths.4,5 The primary breath generally refers to mandatory breaths (CMV or IMV) although with continuous spontaneous breathing (absent mandatory breaths) spontaneous breaths would be considered primary. The secondary breaths are those that occur in addition to the primary breaths. For example, IMV combines mandatory breaths with spontaneous breaths. To further complicate the nomenclature, there are seven basic targeting schemes (set point [s], dual [d], biovariable [b], servo [r], adaptive [a], optimal [o], and intelligent [i]).4,5 For example, for the Covidien PB 840 and PB 980, in the assist/control (A/C) volume-control mode the clinician sets the tidal volume, peak

flow, and trigger sensitivity. The tidal volume and flow waveform are set by the clinician and not adjusted automatically by the ventilator. This is referred to as setpoint targeting; the recommended nomenclature for this mode would be VC-CMVs where the s indicates the set-point targeting scheme.4,5 Other names used for VCCMVs include CMV and VC-CMV (Dräger Evita XL and Evita Infinity V500 respectively [VC-CMV provided by the V500 is time triggered only]), and synchronized controlled mandatory ventilation (HAMILTON G5, HAMILTON C-3). The Maquet Servo-i and Servo-u have a similar mode called volume control; this mode allows patient or time triggering (i.e., assist/control). For the Covidien PB 840 and PB 980 in the SIMV volume control with pressure support mode, the clinician sets the tidal volume, peak flow, and trigger sensitivity for the mandatory breaths and the pressure-support level for spontaneous breaths. The recommended nomenclature for this mode of ventilation would be VC-IMVs,s, indicating a set-point targeting scheme for both primary and secondary breaths. VCIMVs,s is simply called SIMV by Dräger and HAMILTON (Dräger Evita XL, Dräger Evita Infinity V500, and HAMILTON Medical G5 and C-3). Dual targeting allows the ventilator to automatically switch between volume control and pressure control during a single breath.4,5 The Maquet Servo-i and Servo-u incorporate dual targeting when using AutoMode for PC, VC, and PRVC. In this case, dual targeting allows the ventilator to automatically switch between volume or pressure control and pressure support during a single breath.

Full and Partial Ventilatory Support Mechanical ventilation may be employed to provide 100% of the WOB required to meet the patient’s ventilatory needs. In such cases, the patient is receiving full ventilatory support. Other modes of ventilation may be selected that do not provide 100% of the patient’s ventilatory needs and require the patient to provide some portion of the WOB in order to achieve effective ventilation. When less than 100% of the WOB is performed by the ventilator, this is known as partial ventilatory support. Advantages and disadvantages of these two approaches are discussed below.

Full Ventilatory Support When mechanical ventilation is initiated to provide full ventilatory support, adequate

alveolar ventilation is maintained even if the patient makes no spontaneous breathing efforts. Full ventilatory support can be provided using volume- or pressurecontrolled ventilation. The key to providing full ventilatory support is ventilator settings that deliver a tidal volume, respiratory rate, and resultant minute ventilation sufficient to provide 100% of the patient’s needs with little or no work on the part of the patient. In the case of spontaneously breathing patients in the CMV mode, the patient can trigger the ventilator (aka assist breaths); care must be taken to minimize trigger work and maximize patient–ventilator synchrony. In the event of apnea, the set ventilator rate, tidal volume, and minute ventilation are sufficient, and the patient’s WOB is zero. The term controlled ventilation is sometimes used to refer to time-triggered continuous mandatory ventilation and should not be confused with volume control or pressure control. Full ventilatory support is required in the presence of apnea. Causes of apnea include anesthesia, sedative or narcotic drugs, cardiac arrest, heart failure, shock, trauma, head injury, cerebral hypoxia, neurologic/neuromuscular disease (e.g., major stroke, spinal cord injury, and brain death), poisoning (e.g., carbon monoxide, cyanide) and administration of neuromuscular-blocking agents (e.g., succinylcholine, rocuronium). Full ventilatory support is also generally indicated as an initial approach for patients with severe respiratory failure and increased WOB. Properly applied, full ventilatory support may allow for ventilatory muscle rest and recovery in cases of diaphragmatic fatigue. Controlled ventilation is a time-triggered form of full ventilatory support that requires apnea. Controlled ventilation eliminates the WOB and allows for complete control over the patient’s ventilatory pressures, volumes, and flows. Controlled ventilation will reduce oxygen consumption of the ventilatory muscles and provide ventilatory muscle rest. Administration of sedatives and (in some cases) neuromuscular-blocking agents (aka paralytic drugs) may be needed to achieve controlled ventilation. Neuromuscular-blocking agents paralyze the voluntary muscles, including the diaphragm. In the event of a ventilator malfunction or disconnect, the patient will be unable to breathe spontaneously, and a catastrophic outcome may follow. It should also be noted that paralytic agents do not alter cognitive function, perception, or the experience of pain.23 Because of this, neuromuscular-blocking agents should be given in conjunction with sedatives and

appropriate analgesics for pain and anxiety. Neuromuscular-blocking agents can also cause anaphylaxis, hypotension, cardiac arrhythmias, electrolyte disturbances, and prolonged paralysis and muscle weakness.23 Neuromuscular-blocking agents used in the ICU include vercuronium (Norcuron), pancuronium (Pavulon), and cisatracurium (Nimbex). Neuromuscular-blocking agents should be used cautiously, and other options should be considered for managing patient agitation, excessive movement, or ventilator asynchrony.23 Prolonged controlled ventilation may also result in ventilatory muscle atrophy and reductions in diaphragmatic muscle strength and endurance.24 To summarize, full ventilatory support provides 100% of the patient’s ventilatory needs. Full ventilatory support can be provided using assist/control volume-control ventilation (aka VC-CMV), assist/control pressure-control ventilation (PC-CMV), and volume- or pressure-control SIMV (e.g., VC-IMV or PC-SIMV).

Partial Ventilatory Support When mechanical ventilation is initiated to provide partial ventilatory support, the ventilator settings and mode require that the patient provide a portion of the ventilation and associated work required to maintain an acceptable PaCO2. The most common form of partial ventilatory support is IMV with mandatory rates less than 8 to 10 breaths/min. This requires the patient to breathe spontaneously between mandatory breaths at a spontaneous rate and tidal volume sufficient (in combination with the ventilator’s support) to maintain effective alveolar ventilation. With partial ventilatory support in the IMV mode, should the patient’s spontaneous breathing cease or become inadequate, acute hypercapnia and respiratory acidosis may occur. Full ventilatory support can be provided using IMV if the mandatory rate, tidal volume, and resultant minute ventilation meets all the patient’s needs (e.g., VT ≥ 6 to 8 mL/kg and f ≥10 to 12 breaths/min). There are several other modes of ventilation that require the patient to breathe spontaneously. These include PSV, volume support (VS), PAV, and NAVA, all of which can be used to provide partial ventilatory support. Mandatory minute ventilation (MMV) and adaptive support ventilation (ASV) automatically vary the level of mechanical ventilatory support with changes in the patient’s spontaneous minute ventilation. Thus, MMV and ASV adjust automatically

to provide partial or full ventilatory support as the patient’s spontaneous minute ventilation varies. In summary, partial ventilatory support requires the patient to continue to breathe spontaneously to maintain adequate alveolar ventilation. Modes sometimes used to provide partial ventilatory support include IMV/SIMV, PSV as a standalone mode, VS, PAV, and NAVA. Partial ventilatory support may help maintain ventilatory muscle function and reduce the loss of ventilatory muscle strength that sometimes occurs with mechanical ventilation.24,25 Partial ventilatory support may require less sedation and improve patient–ventilator synchrony in some patients. Because spontaneous breathing occurs during partial ventilatory support, there may be some advantages in stabilizing and recruiting alveoli because of the negative intrathoracic pressures that occur during spontaneous breathing. A major disadvantage of partial ventilatory support is that it may not allow for adequate ventilatory muscle rest and recovery in cases where diaphragmatic fatigue has occurred.

Major Modes of Ventilation As noted, there are five basic ventilatory modes at the clinician’s disposal: volume control-continuous mandatory ventilation (VC-CMV), pressure control-continuous mandatory ventilation (PC-CMV), volume control-intermittent mandatory ventilation (VC-IMV), pressure control-intermittent mandatory ventilation (PC-IMV), and pressure control-continuous spontaneous ventilation (PC-CSV). VC-CMV and VC-IMV are the most frequently used forms of ventilation for adult patients at many institutions and most clinicians are familiar with these two modes.25,26 While multiple breath-targeting schemes are used in various adaptations of these five basic modes, we will focus our discussion to use of these modes where the clinician determines most ventilator parameters (i.e., set-point breath targeting). Advantages and disadvantages of each of these major modes are discussed below.

Volume Control-Continuous Mandatory Ventilation (VC-CMV) VC-CMV with set-point breath targeting is commonly referred to as volume-limited ventilation, volume-targeted ventilation, volume-cycled ventilation, volume assist/control (VA/C), or just plain volume ventilation. VC-CMV may be patient or time triggered to inspiration and is volume cycled to expiration. Typically, the clinician

sets the desired tidal volume, minimum mandatory (machine) rate, inspiratory peak flow, and trigger sensitivity. Other ventilators instead have the clinician set the desired tidal volume, mandatory (machine) rate and inspiratory time, or inspiratory percentage time. Most ventilators also allow the clinician to select the inspiratory flow waveform, typically as a square wave or down ramp, although some ventilators have a sinewave option (e.g., HAMILTON G5). A square flow waveform (aka constant flow waveform) may reduce mean airway pressure, which may be useful in patients who are hemodynamically compromised.27 A down-ramp flow waveform (aka decreasing flow waveform) may increase mean airway pressure, reduce peak inspiratory pressure, and improve distribution of inspired gases.27 With VC-CMV, every breath is a mandatory breath delivered at the clinicianselected VT. Commonly referred to as assist/control volume ventilation, the patient can trigger the primary breath (aka assist breath). If no spontaneous effort is detected during the respiratory cycle time, the ventilator will provide a timetriggered breath (aka control breath). Figure 6-2 illustrates patient- and timetriggered VC-CMV.

FIGURE 6-2 Continuous Mandatory Ventilation Illustrating Ventilator-Triggered and Patient-Triggered Breaths.

Description Volume-control ventilation is available as A/C volume control (Covidien PB 840 and PB P980), CMV and VC-CMV (Dräger Evita XL and Evita Infinity V500) and synchronized controlled mandatory ventilation [(S)CMV] (HAMILTON G-5). The Maquet Servo-i and Servo-u also feature a volume control mode, which (in the absence of Automode) functions as VC-CMV. A major advantage of VC-CMV is the fact that it will deliver a constant VT in the face of changes in compliance and resistance limited only by the clinician-set maximum pressure alarm limit and the machine’s pressure and flow capabilities. A minimum guaranteed minute ventilation (V̇E) will be delivered based on the VT and set backup rate. In the assist/control mode, the patient can trigger the ventilator above the set minimum respiratory rate; a minimum V̇E will be provided in the

absence of a patient trigger (e.g., apnea due to sedation or CNS problems). Properly applied assist/control volume ventilation provides full ventilatory support with a lower WOB then partial ventilatory support modes. Ventilatory muscle fatigue occurs due to high ventilatory workloads, such as may occur in patients with acute respiratory failure. Because VC-CMV can reduce or eliminate the WOB, it is especially wellsuited to allow for ventilatory muscle rest and recovery from ventilatory muscle dysfunction. It must be noted, however, that prolonged ventilatory muscle inactivity may result in ventilatory muscle weakness and atrophy.24 VC-CMV is easy to understand and apply and is well-suited for most patients. Disadvantages of VC-CMV include the possible delivery of unsafe peak and plateau pressures (PIP and Pplateau) in the presence of decreasing compliance or increasing airway resistance. Use of large tidal volumes may also result in excessive PIP and Pplateau and excessive airway pressures may result in barotrauma or VILI. This emphasizes the need for setting the ventilator alarms at appropriate levels to alert the respiratory therapist to make ventilator adjustments, when needed. It is also important to note that with patient-triggered breaths, patients continue to actively inspire even though the machine breath has been triggered. This can result in an increase in WOB, especially if inspiratory time or peak inspiratory flow rates are set improperly. Problems with patient–ventilator asynchrony may also occur due to inappropriate trigger-sensitivity settings, high patient trigger rates, or inadequate peak inspiratory flow rates. For example, a patient in distress may trigger the ventilator at a rapid assist rate resulting in decreased expiratory time and increased mean airway pressures. Excessive patient effort required to trigger a mandatory breath will increase the patient’s WOB. This can be caused by inappropriate trigger sensitivity or autoPEEP, both of which may increase trigger work. Inappropriate peak inspiratory flow rate settings that do not meet or exceed the patient’s inspiratory flow demand may increase the patient’s WOB and result in patient–ventilator asynchrony. Inadequate expiratory times may cause the development of autoPEEP, especially in patients with obstructive lung disease. High mean airway pressures may impede venous return and reduce cardiac output in hemodynamically compromised patients. Some patients who are awake, alert, and anxious do not tolerate VC-CMV well, and other forms of ventilatory support may be considered.

Controlled ventilation (time-triggered VC-CMV) requires patient apnea, which in turn may require the administration of sedative and possibly paralytic agents, which can delay ventilator weaning and discontinuance. Controlled ventilation may be required in patients with an absent ventilatory drive due to CNS problems (e.g., coma), spinal cord injury, or neuromuscular paralysis. Provision of a relatively high minute ventilation via time-triggered VC-CMV that meets all the patient’s physiologic needs may reduce the drive to breathe and cause an absence of patient-triggered breaths. Time-triggered VC-CMV eliminates diaphragmatic activity and the WOB. Patients may also develop ventilatory muscle weakness, and atrophy and neuromuscular weakness related to critical illness is not uncommon.24 Diaphragmatic inactivity can cause atrophy in as little as 18 to 69 hours.28 Careful monitoring of the apneic patient is required as a ventilator malfunction or disconnect can be catastrophic in patients unable to spontaneously breathe. Box 6-5 summarizes the advantages and disadvantages of patient- and time-triggered VC-CMV (aka assist/control volume ventilation).

BOX 6-5 Advantages and Disadvantages of Volume Control-Continuous Mandatory Ventilation (VC-CMV) VC-CMV, commonly known as assist/control volume ventilation, allows the clinician to set the desired tidal volume (VT), minimum mandatory (machine) rate (f), inspiratory peak flow, and trigger sensitivity. Other ventilators have the clinician set tidal volume, mandatory (machine) rate, and inspiratory time or inspiratory percentage time and trigger sensitivity. VC-CMV allows for control of the FIO2 and the addition of PEEP. Assist/control volume ventilation allows for a patient or time trigger, whichever occurs first. Controlled volume ventilation is time triggered and requires apnea. Advantages of VC-CMV ∎ VT constant in the face of changes in compliance and resistance (within the clinician-set maximum pressure limit and the machine’s pressure and flow capabilities). ∎ Guaranteed minimum minute ventilation delivered (V̇E) based on set minimum f and VT. ∎ Provides full ventilatory support. ∎ Minimizes or eliminates the WOB.

Patient-triggered (assist) breaths should have minimal work if proper trigger sensitivity and appropriate peak inspiratory flowrates are set in spontaneously breathing patients. • Time-triggered ventilation (control mode) eliminates the WOB but requires apnea. Allows for ventilatory muscle rest and recovery from ventilatory muscle dysfunction. Flow waveform is adjustable on some ventilators. • Square wave flow waveform (aka constant flow waveform) may reduce mean airway pressure and inspiratory time (in ventilators with peak flow control) but increase peak inspiratory pressure (PIP). This flow waveform may be useful in patients who are hemodynamically compromised. • Down ramp (aka decreasing flow waveform) may increase mean airway pressure, reduce PIP, and increase inspiratory time in ventilators with the peak flow control. This may improve the distribution of inspired gases and oxygenation. Assist/control volume ventilation is easy to understand and apply and is a type of ventilation familiar to most clinicians. Mode is well-suited for most patients.

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Disadvantages of VC-CMV ∎ Unsafe peak inspiratory pressures (PIP > 35 to 40 cm H O) may occur with 2 reduced compliance or increased airway resistance as the ventilator attempts to maintain delivered VT. ∎ Unsafe plateau pressures (P plateau > 28 to 30 cm H2O) may occur with inappropriate tidal volume settings and/or reduced lung compliance, which may result in alveolar overdistention. ∎ Improper trigger sensitivity may increase the WOB. ∎ Inspiratory flow rate is typically fixed and does not vary with patient effort. This may cause patient–ventilator asynchrony. ∎ Inadequate ventilator flow rates may increase the WOB in spontaneously breathing patients and result in patient–ventilator asynchrony. • Low inspiratory flow rates also increase inspiratory time and (assuming a constant respiratory rate) decrease expiratory time. ∎ Inadequate expiratory times may result in auto PEEP, particularly in patients with obstructive lung disease. ∎ With patient-triggered breaths, patients continue to actively inspire even though the ventilator has begun to provide support; this may increase the WOB especially in cases of inappropriate ventilator peak flow settings.

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High mean airway pressures may reduce venous return and impede cardiac output in hemodynamically unstable patients. High pressures may result in barotrauma (e.g., pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema) or ventilator-induced lung injury (VILI). VILI is caused by alveolar overdistention (aka volume trauma), cyclic alveolar expansion and collapse (aka atlectrauma), or inflammation associated with mechanical ventilation (aka biotrauma). Patients may trigger the ventilator at a rapid rate resulting in respiratory alkalosis, patient–ventilator asynchrony, and increased peak and mean airway pressures. Inappropriate inspiratory flow rates that do not meet the patient’s inspiratory flow demand in spontaneously breathing patients may increase the WOB. Assist/control volume ventilation may be poorly tolerated in patients who are awake, anxious, or in pain; this may result in the patient fighting the ventilator. Controlled ventilation (time-triggered VC-CMV) requires apnea. • Sedative and (possibly) paralytic drugs may be required. • Paralytic drugs should not be administered alone and require the addition of sedatives for pain and anxiety. Prolonged use of paralytic agents is uncommon in the modern ICU. • Ventilator malfunction or disconnect can be catastrophic in the presence of apnea. Development of ventilatory muscle weakness and atrophy is associated with controlled ventilation, prolonged use of sedatives, and use of neuromuscularblocking agents.

Pressure Control-Continuous Mandatory Ventilation Pressure control-continuous mandatory ventilation (PC-CMV) with set-point breath targeting is patient- or time triggered to inspiration, pressure limited and time cycled to expiration. Other terms employed for PC-CMV include pressure assist/control, pressure A/C, pressure-control ventilation (PCV), and (when used with an inverse I:E ratio) pressure-control inverse-ratio ventilation (PCIRV). With PC-CMV, the respiratory care clinician sets the respiratory rate, inspiratory time (or inspiratory percent time), and inspiratory pressure limit. The clinician also determines the patient trigger sensitivity and may adjust the inspiratory rise time or ramp. During inspiration, airway pressure rises to a preset value; inspiration is terminated when

the inspiratory time limit is reached. Normal adult inspiratory time (TI) is set at 0.6 to 1.0 seconds with a respiratory rate of 12 to 20 breaths/min and I:E ratio of 1:2 or lower. Some patients do well with slightly longer TI (e.g., 0.8 to 1.2 seconds). Typically, PC-CMV results in a square wave-like inspiratory pressure waveform and a decreasing or decelerating inspiratory flow waveform, which may improve patient comfort and improve the distribution of inspired gases. The square wave pressure pattern will also increase mean airway pressure, which may improve oxygenation. Recall, however, that increased mean airway pressure may impede venous return and reduce cardiac output in patients with hemodynamic instability. Properly applied, PC-CMV provides full ventilatory support and minimizes the WOB, which may be helpful to rest the ventilatory muscles in the presence of ventilatory muscle fatigue. RC Insight With PC-CMV, tidal volume is adjusted by adjusting the pressure gradient (ΔP = PIP–PEEP) to obtain the desired VT.

With PC-CMV, the clinician sets the pressure-control level, which assures (if properly set) that airway pressures remain in a safe range (Pplateau ≤ 28 to 30 cm H2O). PC-CMV provides a decreasing flow waveform that varies flow with patient demand. For example, gas flow to the patient will increase with increased patient effort. This variable flow may better match patient inspiratory demand, improve patient comfort, provide better patient–ventilator synchrony and allow for earlier liberation from the ventilator. As noted, the square wave inspiratory pressure waveform results in a decreasing flow waveform. The square wave inspiratory pressure waveform also results in more sustained inspiratory pressure, which may improve alveolar recruitment, as well as improve distribution of inspired gases. Pressure rise time or slope may be adjusted by the clinician to adjust the rate at which inspiratory gas flow increases from baseline to peak flow during the first part of the inspiratory phase. Rise time should be adjusted so that inspiratory gas flow meets or exceeds patient demand. Slow rise times may not provide adequate flow and increase the WOB. Rapid rise times may provide more flow than necessary and result in an inspiratory pressure spike near the beginning of the inspiratory phase. VT is determined by the pressure gradient (ΔP = PIP – PEEP), inspiratory time,

patient effort, and pulmonary mechanics (compliance and resistance). In general, VT increases as the inspiratory pressure increases (assuming ventilatory mechanics, patient effort, inspiratory time, and PEEP are constant); decreases in inspiratory pressure generally reduce VT. Changes in PEEP will affect delivered VT if inspiratory pressure is not simultaneously adjusted, although most ventilators in the pressurecontrol mode will automatically adjust inspiratory pressure with changes in PEEP to maintain a constant ΔP. For initial ventilator setup, inspiratory pressure generally is adjusted to achieve a VT in the range of 6 to 8 mL/kg of ideal body weight (IBW) while maintaining a safe plateau pressure (Pplateau ≤ 28 to 30 cm H2O). With PC-CMV, as inspiratory time (TI) increases, inspiratory flow to the patient decreases because of the decreasing flow waveform provided. If sufficient inspiratory time is provided, flow will decrease to zero and any remaining inspiratory time will provide an inspiratory hold or plateau. Increases in inspiratory time generally will increase VT up until the point at which flow reaches zero. Initial ventilator set up for PC-CMV includes selecting a TI that provides enough time for the inspiratory flow to decrease to zero before beginning the expiratory phase. In cases where inspiratory flow does not reach zero at end inspiration, increasing inspiratory time will tend to increase VT. As noted, if inspiratory time continues past the point of zero gas flow, an inspiratory pause or hold will ensue, which may further improve the distribution of inspired gases. That said, with patients making spontaneous respiratory efforts, excessive inspiratory times may cause patient–ventilator asynchrony. Care should also be taken to ensure adequate expiratory time to avoid autoPEEP and gas trapping, especially in patients with obstructive lung disease. Disadvantages of PC-CMV include variable tidal volume delivery in the face of changes in the level of patient effort, system compliance, or airway resistance and this may result in inadvertent hypo- or hyperventilation. This requires the clinician to pay careful attention to delivered VT and V̇E and set the ventilator’s alarms appropriately. Changes in inspiratory time may also affect delivered VT. PC-CMV may also result in a higher mean airway pressures, which may decrease venous return and impair cardiac output in hemodynamically unstable patients. As with other modes, improper trigger sensitivity may increase WOB. Inadequate inspiratory flow

rates, which may occur with inappropriate rise time settings, may also increase WOB and cause patient–ventilator asynchrony. As with other modes of ventilation, excessive airway pressures may cause barotrauma or VILI and inadequate expiratory times may result in the development of auto PEEP and air trapping. Some awake and alert patients will not tolerate PC-CMV. For example, pain and anxiety may result in rapid patient-triggering rates, increased airway pressures, respiratory alkalosis, and patient–ventilator asynchrony. Controlled ventilation (time-triggered PC-CMV) requires apnea, which in turn may require the use of sedatives and possibly paralytic agents. Pressure-control inverse-ratio ventilation (PCIRV) is a form of PC-CMV in which the ventilator is adjusted so that inspiratory time is longer than expiratory time. PCIRV increases mean airway pressure and may improve oxygenation in certain patients with severe hypoxemic respiratory failure despite optimal PEEP and appropriate FIO2. While PCIRV can improve oxygenation, evidence of improvement in other important outcomes (e.g., time on the ventilator, time in the ICU, and mortality) is lacking.26 PCIRV often requires the use of sedatives and (sometimes) paralytic agents, as spontaneously breathing patients generally do not tolerate the use of inverse-ratio ventilatory patterns well and may fight the ventilator. The clinician should also be aware that increased mean airway pressures may reduce venous return and cardiac output in hemodynamically compromised patients. PC-CMV is available as A/C pressure control (Covidien PB 840 and PB 980); pressure-control ventilation plus assisted, CMV with Autoflow, and CMV with Autoflow and tube compensation,(Dräger Evita XL); pressure control assist/control, and volume control assist/control with Autoflow (Evita Infinity V500); pressure control CMV, pressure-control CMV with tube-resistance compensation, adaptive pressure ventilation CMV, and adaptive pressure ventilation and CMV with tube-resistance compensation (HAMILTON G-5). The Maquet Servo-i and Servo-u also feature pressure control and pressure-regulated volume control modes. Box 6-6 summarizes the advantages and disadvantages of PC-CMV.

BOX 6-6 Advantages and Disadvantages of Pressure Control-Continuous Mandatory Ventilation (PC-CMV)

PC-CMV, commonly known as assist/control pressure-control ventilation (PCV), allows the clinician to set the desired inspiratory pressure, minimum mandatory (machine) rate (f), inspiratory time (or inspiratory percentage time), and trigger sensitivity. PC-CMV allows for control of the FIO2 and the addition of PEEP. Assist/control PCV allows for a patient or time trigger, whichever occurs first. Time–triggered control mode PCV requires patient apnea. Advantages of PC-CMV ∎ Inspiratory pressure is constant in the face of changes in compliance and resistance. • Plateau pressure can be maintained at safe levels (Pplateau ≤ 28 to 30 cm H2O). Resultant PIP may be lower than can be achieved with VC-CMV (square wave). • Risk of alveolar overdistention is reduced with changes in compliance. • Square wave-like inspiratory pressure waveform results in more sustained inspiratory pressure, which may improve alveolar recruitment. Desired VT may be achieved by adjusting pressure control level (PIP) or inspiratory time. • VT is determined by the pressure gradient (ΔP = PIP – PEEP), patient effort, inspiratory time (TI), and pulmonary mechanics (compliance and resistance). • Increasing ΔP by increasing PIP generally increases VT and vice versa. • In cases where inspiratory flow does not reach zero at end inspiration, increasing inspiratory time will tend to increase VT. • PEEP changes may affect ΔP and delivered VT. PEEP alterations will require attention to alterations in PIP to maintain the same ΔP and tidal volume delivery. • Increased patient inspiratory effort will generally increase VT; decreased effort tends to decrease VT. Properly applied, PC-CMV can provide full ventilatory support. PC-CMV may minimize or eliminate the WOB. • Patient-triggered (assist) breaths should have minimal work if proper trigger sensitivity is set and adequate inspiratory gas flow is provided to meet or exceed the patient’s inspiratory demand (i.e., appropriate rise time settings). • Time-triggered ventilation (control mode) eliminates the WOB but requires apnea. Allows for ventilatory muscle rest and recovery from ventilatory muscle

•

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dysfunction if properly applied. Decreasing flow waveform varies flow based on patients’ inspiratory effort. • Patient comfort and patient–ventilator synchrony may improve with PCCMV because inspiratory flow varies with patient effort. • Decreasing flow waveform (aka down ramp) increases mean airway pressure and may improve inspired gas distribution and oxygenation. • Decreasing flow waveform results in a square wave pressure pattern, which may open alveoli earlier in the inspiratory phase, improve inspired gas distribution, and improve oxygenation. • Improved gas distribution may allow for use of a lower VT. • Pressure rise time or slope can be adjusted. Rise time allows the clinician to adjust the rate at which inspiratory gas flow increases from baseline to peak flow. Rise time should be adjusted to ensure that machine gas flow meets or exceeds patient demand. • Rise time adjustment of the pressure waveform can be made to avoid a pressure spike at the beginning of inspiration due to rapid rise times in which the flow to the patient exceeds patient demand. • Rise time should also be adjusted to ensure that inspiratory gas flow is not too slow and meets or exceeds patient demand. Slow rise times may increase WOB. Pressure-control inverse-ratio-ventilation (PCIRV) has been suggested for severe hypoxemic respiratory failure (e.g., severe ARDS) where optimal PEEP and FIO2 have been ineffective in providing adequate oxygenation. While PCIRV may improve oxygenation, cardiac output may be compromised due to increased mean airway pressures and decreased venous return. Assist/control PCV is relatively easy to understand and apply. Mode is well-suited for most patients, assuming skilled clinicians and careful monitoring of delivered volumes.

Disadvantages of PC-CMV ∎ VT will vary with changes in compliance, resistance, or patient effort. • Decreased compliance, increased resistance, or decreased patient effort will reduce delivered VT. • Increased compliance, decreased resistance, or increased patient effort will increase delivered VT. • Careful monitoring of exhaled VT is required to avoid inadvertent hyperventilation or hypoventilation associated with changes in pulmonary mechanics or patient effort. ∎ Because VT is determined by the pressure gradient (ΔP = PIP – PEEP),

∎ ∎ ∎ ∎ ∎

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increases in PEEP without increases in PIP will decrease ΔP and decrease delivered VT. Most ventilators make this adjustment automatically (i.e., PC is maintained at the set value above PEEP). No guaranteed minimum minute ventilation (V̇E) because VT may change due to changes in compliance, resistance, or patient effort. Improper trigger sensitivity may increase the WOB. Inadequate inspiratory flow rates may increase the WOB in spontaneously breathing patients and result in patient–ventilator asynchrony. High mean airway pressures may reduce venous return and impede cardiac output in hemodynamically unstable patients. Pressure-control inverse-ratio ventilation (PCIRV) will further increase mean airway pressure and may reduce venous return and cardiac output. PCIRV may also cause autoPEEP due to short expiratory times resulting in further decreases in venous return and impairment of cardiac output. PIP and Pplateau > 28 to 30 cm H2O may result in barotrauma (e.g., pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema) or VILI. VILI is caused by alveolar overdistention (aka volume trauma), cyclic alveolar expansion and collapse (aka atelectrauma), or inflammation associated with mechanical ventilation (biotrauma). Patients may trigger the ventilator at a rapid rate resulting in respiratory alkalosis and patient–ventilator asynchrony. Inappropriate inspiratory flow rates that do not meet the patient’s inspiratory flow demand in spontaneously breathing patients may increase the WOB. Pressure rise time or slope may be improperly set. Rise time allows the clinician to adjust the rate at which inspiratory gas flow increases from baseline to peak flow at the beginning of the inspiratory phase. • If inspiratory flow exceeds patient demand, a pressure spike may occur early in the inspiratory phase. Adjustment of the rise time can eliminate a pressure spike at the beginning of inspiration due to inappropriately high initial machine flow rates. • If inspiratory flow is reduced to the point at which patient demand exceeds machine flow, the pressure waveform will be deformed. Adjustment of rise time can increase inspiratory flow to meet or exceed patient demand. Assist/control PC ventilation may be poorly tolerated in patients who are awake, anxious, or in pain; this may result in the patient fighting the ventilator. Inadequate expiratory times may result in auto PEEP, particularly in patients with obstructive lung disease. Controlled ventilation (time-triggered PC-CMV) requires apnea.

Sedative and paralytic drugs may be required. Paralytic drugs should not be administered alone and require the addition of sedatives for pain and anxiety. Development of ventilatory muscle weakness and atrophy is associated with controlled ventilation, prolonged use of sedatives, and use of neuromuscularblocking agents. Pressure control is a less familiar type of ventilation for some clinicians (as compared volume control).

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Volume-Controlled Intermittent Mandatory Ventilation Volume-controlled intermittent mandatory ventilation (VC-IMV) intersperses volumetargeted mandatory breaths with spontaneous breathing. VC-IMV is commonly referred to as volume-targeted SIMV or V-SIMV. With SIMV mandatory breaths may be time or patient triggered. Older forms of IMV did not allow for patient-triggered mandatory breaths. With SIMV, if the patient does not trigger a breath during the time window provided, the ventilator will provide a time-triggered mandatory breath. SIMV was introduced to help avoid breath stacking and reduce patient–ventilator asynchrony, which can occur with time-triggered IMV. Most modern ventilators today provide SIMV. For VC-SIMV, the clinician sets VT and mandatory rate, inspiratory peak flow or inspiratory time, trigger sensitivity, and FIO2. Spontaneous breaths may include pressure augmentation (e.g., pressure support or automatic tube compensation). PEEP/CPAP may be added to provide an elevated baseline pressure. VC-IMV probably was the most popular and widely used mode of ventilation in United States from the late 1970s through the 1990s, and most clinicians from that era have had a great deal of experience in the use of IMV and/or SIMV. SIMV is currently available as SIMV volume control with pressure support or tube compensation (Covidien PB 840 and PB 980), SIMV and SIMV with automatic tube compensation (Dräger Evita XL), volume-control SIMV (Evita Infinity V500), and SIMV and SIMV with tube resistance compensation (HAMILTON G-5). The Maquet Servo-i and Servo-u also feature SIMV (volume control). IMV was originally advanced as a preferred mode of ventilation because IMV was thought to result in more rapid ventilator weaning. It has subsequently become

apparent that when the support level approaches 50% of that required for full ventilatory support, the patient’s WOB during VC-IMV can approach that of unsupported spontaneous ventilation. Put another way, the degree of ventilatory muscle rest with VC-IMV is not proportional to the level of ventilatory support provided.29 Today, it generally is accepted that VC-IMV may prolong ventilator weaning as compared to other methods (e.g., spontaneous breathing trials [SBTs] or pressure support).26,29 Advantages of IMV include reduced mean airway pressures (as compared to VCCMV); maintenance of ventilatory muscle activity, strength, and coordination; and reduction in the need for sedation or administration of paralytic drugs. There is some evidence that the lower mean airway pressures associated with VC-IMV may be helpful in maintaining cardiac output and blood pressure in some patients.26 During IMV, the patient continues to breathe spontaneously interspersed with mandatory machine breaths and spontaneous breathing is thought to be more physiologic than positive pressure breathing. The level of ventilatory support provided can be easily titrated up and down based on the patient’s needs by simply increasing or decreasing the mandatory rate. The level of support provided can range from full ventilatory support, to partial support, to no support, depending on the set mandatory (machine) rate. Rapidly breathing patients may adapt more readily to IMV, without the problem of triggering mandatory breaths at a rapid rate resulting in a respiratory alkalosis, which may occur with patient-triggered VC-CMV. VC-IMV may improve patient tolerance and patient–ventilator synchrony as compared to VC-CMV and the development of autoPEEP is less likely. Disadvantages of VC-IMV include the WOBI associated with endotracheal and tracheostomy tubes during spontaneous breathing requiring the addition of PSV or automatic tube compensation (ATC). Spontaneous breathing with high ventilatory workloads may result in ventilatory muscle fatigue and dysfunction, which may prolong the need for mechanical ventilatory support. The addition of PSV or ATC will reduce the WOB, but increase mean airway pressure, which may reduce venous return and impair cardiac output in hemodynamically unstable patients. As noted above, when the level of ventilatory support provided using IMV is decreased to about 50% that needed for full ventilatory support, the patient’s WOB can approach that of spontaneous unsupported breathing. Also, as noted, VC-IMV may prolong

ventilator weaning and discontinuance as compared to spontaneous breathing trials (SBTs) or PSV. When used to provide partial ventilatory support, sudden hypoventilation or apnea may result in an acute respiratory acidosis. Lastly, some patients who are experiencing rapid shallow breathing may continue to make respiratory efforts throughout the mandatory breath cycle resulting in an increase in WOB and patient– ventilator asynchrony Automated modes of ventilation that provide a form of VC IMV include mandatory minute volume ventilation, mandatory minute volume ventilation with automatic tube compensation, mandatory minute volume ventilation with pressure-limited ventilation, and mandatory minute volume ventilation with pressure-limited ventilation and automatic tube compensation available with the Dräger Evita XL and Evita Infinity V500. Automode (available with the Maquet Servo-i and Servo-u) also provides a form of VC-IMV. These newer modes of ventilation are discussed later in this chapter. Box 6-7 summarizes the advantages and disadvantages of VC-IMV.

BOX 6-7 Advantages and Disadvantages of VC-IMV VC-IMV intersperses volume-targeted mandatory breaths with spontaneous breathing. Mandatory breaths may be time or patient triggered in the case of synchronized intermittent mandatory ventilation (SIMV). Pressure augmentation in the form of pressure support or automatic tube compensation may be provided to overcome the imposed work of breathing (WOBI) associated with endotracheal and tracheostomy tubes. PEEP/CPAP may be added in order to improve oxygenation, increase FRC, and prevent cyclic alveolar recruitment– derecruitment as sometimes seen in patients with severe hypoxemic respiratory failure (e.g., ARDS). Advantages of VC-IMV ∎ Incorporates spontaneous breathing that maintains ventilatory muscle activity and may help maintain ventilatory muscle strength and coordination. ∎ Incorporation of spontaneous breathing allows for more physiologic alveolar and intrathoracic pressures during spontaneous breaths and lower mean airway pressures (as compared to VC-CMV). ∎ Mandatory respiratory rate can be easily titrated up and down to vary the level of support provided based on the patient’s needs.

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May provide partial or full ventilatory support, depending on the set mandatory rate. • Level of support provided can be easily titrated from full ventilatory support (mandatory rate ≥ 10 to 12 breaths/min) to no ventilatory support (mandatory rate = 0). • Lower levels of support may be beneficial in certain patients to maintain cardiac output and blood pressure. Patients often adjust easily to IMV, which may improve patient tolerance and patient–ventilator synchrony. PSV or ATC may be added to overcome the WOBI associated with endotracheal or tracheostomy tubes. No need for excessive sedation or administration of neuromuscular-blocking agents. Patients who rapidly trigger the ventilator in the VC-CMV mode, resulting in hyperventilation and respiratory alkalosis, may benefit from a trial of VC-IMV. Development of autoPEEP may be less likely.

Disadvantages of VC-IMV ∎ Patients requiring full ventilatory support and constant tidal volume delivery may do better on VC-CMV. ∎ Imposed work of breathing (WOB ) due to the artificial airway during I spontaneous breathing may be high. ∎ The addition of PSV or ATC to overcome WOB increases mean airway I pressure. ∎ Spontaneous breathing with high ventilatory workloads may result in ventilatory muscle fatigue, especially in patients with rapid shallow breathing and impaired pulmonary mechanics (e.g., reduced compliance, increased resistance). ∎ With partial ventilatory support and lower set mandatory rates (f < 8 to 10 breaths/min) acute respiratory acidosis may occur if the patient becomes apneic or hypoventilates. ∎ With lower mandatory rates (f < 6 to 8 breaths/min or 50% of the full ventilatory support value) WOB can approach that of spontaneous breathing. ∎ The degree of respiratory muscle rest during VC-IMV is not proportional to the level of ventilatory support provided. ∎ Some patients have difficulty adjusting to the ventilator and their spontaneous breathing pattern may conflict with the ventilator settings. ∎ VC-IMV may prolong ventilator weaning.

Pressure Control-Intermittent Mandatory Ventilation Pressure control-intermittent mandatory ventilation (PC-IMV) intersperses mandatory pressure-control breaths with spontaneous breaths. The pressure-control breaths may be time or patient triggered and are pressure limited and time cycled to expiration. Spontaneous breaths may be provided with or without pressure augmentation (e.g., pressure-support ventilation [PSV] or automatic tube compensation [ATC]. FIO2 is selected and PEEP/CPAP may also be employed. The respiratory care clinician typically sets the pressure-control level, inspiratory time, and mandatory rate. The clinician also will set the trigger sensitivity and inspiratory rise time for the mandatory pressure-control breaths. For spontaneous breaths, the clinician may add pressure support or automatic tube compensation. Minimal PEEP/CPAP (3 to 5 cm H2O) generally is used to maintain FRC and provide physiologic PEEP. Higher PEEP levels may be required in patients with hypoxemic respiratory failure. Pressure-control SIMV is currently available as SIMV pressure control with pressure support or tube compensation (Covidien PB 840 and PB 980), PCV+ with pressure support or automatic tube compensation (Dräger Evita XL), pressurecontrol SIMV and pressure-control SIMV+ (Evita Infinity V500), and pressure-control SIMV with pressure support or tube resistance compensation (HAMILTON G-5). The Maquet Servo-i and Servo-u also feature SIMV (pressure control). There are several more exotic PC-IMV variations that incorporate multiple targeting schemes (e.g., servo, adaptive, and adaptive with servo). Recall that adaptive targeting schemes can maintain a stable tidal volume by adjusting pressure-control levels between breaths as lung mechanics or inspiratory patient effort vary. Servo-targeting schemes vary the support provided by the ventilator proportional to inspiratory effort. Forms of PC-IMV that incorporate adaptive targeting to maintain stable VT delivery include SIMV volume control plus, SIMV volume control plus with pressure support, and SIMV volume control plus with tube compensation (Covidien PB 840 and PB 980), SIMV with autoflow (Dräger Evita XL), VC-SIMV with autoflow and PC-SIMV with volume guarantee (Evita Infinity V500), and SIMV pressure-regulated volume control (Maquet Servo-i and Servo-u). These modes use pressure control with automatic adjustment to achieve a target VT. Other forms of PC-IMV include bilevel with pressure support, bilevel with tube

compensation (Covidien PB 840 and PB 980) and APRV and APRV with tube compensation (Dräger Evita XL and Evita Infinity V500). PC-IMV incorporates the advantages and disadvantages of pressure-control ventilation with IMV. As with PC-CMV, mandatory breath VT will vary with changes in patients’ pulmonary mechanics and inspiratory effort. PC-IMV will allow the clinician to set an appropriate and safe inspiratory pressure to maintain Pplateau ≤ 28 to 30 cm H2O and avoid ventilator-induced lung injury. Tidal volume for pressure-control breaths is determined by the pressure gradient (ΔP = PIP – PEEP), patient effort, inspiratory time (TI), and pulmonary mechanics (compliance and resistance). Normally the PIP is adjusted to achieve a mandatory breath tidal volume in the range of 6 to 8 mL/kg IBW, although larger tidal volumes may be appropriate for some patients. Inspiratory time (TI) may also affect VT provided during pressure-control breaths. Typical adult TI for mandatory pressure-control breaths is in the range of 0.6 to 1.0 seconds, although many patients do well with a slightly longer TI (e.g., 0.8 to 1.2 seconds). On initial setup, inspiratory time is usually adjusted so that inspiratory flow declines to zero at end inspiration. This should optimize VT delivery (at the set pressure-control value) and improve distribution of inspired gas. The decreasing flow waveform provided with pressure control will vary inspiratory flow with patient inspiratory effort, which may improve patient comfort and patient–ventilator synchrony. The square wave-like pressure waveform provided will increase mean airway pressure and may improve distribution of inspired gases and oxygenation. As with PC-CMV, higher mean airway pressures may impair venous return and cardiac output in hemodynamically unstable patients. That said, the inclusion of IMV should lower mean airway pressures compared to PC-CMV. Pressure rise time or slope should be adjusted to ensure inspiratory flow provided meets or exceeds the patient’s inspiratory demand. Recall, however, that too rapid rise times can result in a pressure spike at the beginning of inspiration. PC-IMV can provide full or partial ventilatory support by adjusting the mandatory rate. For full ventilatory support, pressures generally are adjusted to achieve an acceptable VT and mandatory IMV rate is set in the range of 12 to 20 breaths/min. Partial ventilatory support is provided by using a lower IMV rate. Because PC-IMV incorporates spontaneous breathing, ventilatory muscle activity is maintained, which

may help preserve ventilatory muscle strength and coordination. Allowing the patient to spontaneously breathe between pressure-control breaths may have other physiologic benefits (e.g., more normal alveolar and intrathoracic pressures during spontaneous breaths). Pressure support provided during spontaneous breaths should be adjusted to minimize the WOBI associated with the artificial airway. Recall, however, that PSV and ATC will increase mean airway pressure. Some patients adjust easily to IMV, which may further improve patient tolerance and patient– ventilator synchrony. Patients with rapid shallow breathing may have difficulty tolerating PC-IMV and at lower mandatory rates, sudden apnea or hypoventilation can result in acute respiratory acidosis. It should also be recalled that at low mandatory IMV rates, WOB can approach that of spontaneous unsupported breathing. Appropriate levels of PSV should help reduce WOB when low mandatory rates are employed. Like VC-IMV, PC-IMV has not been shown to be a superior mode for ventilator weaning and may prolong the weaning process as comparted to PSV or SBTs.29

Pressure Control-Continuous Spontaneous Ventilation Forms of pressure control-continuous spontanteous ventilation (PC-CSV) include pressure support, automatic tube compensation and continuous positive airway pressure. While pressure support and CPAP can be used with IMV, they may also be used as stand alone, primary modes.

Continuous Spontaneous Ventilation (CSV) Some modes of ventilation allow for spontaneous breathing through the ventilator circuit. Spontaneous breathing during mechanical ventilatory support can be defined by the method a breath is triggered and cycled. With IMV, some breaths are mandatory (i.e., time or patient triggered, but machine cycled) and some breaths are spontaneous (i.e., patient triggered and patient cycled). With continuous spontaneous ventilation (CSV) every breath is patient triggered and patient cycled. Put another way, every breath is spontaneous. Spontaneous breaths during mechanical ventilation can be provided with or without pressure augmentation. The most common forms of pressure augmentation are PSV and automatic tube compensation (ATC). CPAP can be defined as spontaneous breathing with an

elevated baseline pressure. Thus, during inspiration CPAP also provides a form of inspiratory pressure augmentation.

Pressure-Support Ventilation (PSV) PSV provides patient-triggered, pressure-limited, flow-cycled ventilation. When used as a primary mode of ventilation, PSV is a form of pressure control-continuous spontaneous ventilation (PC-CSV). Every breath is patient triggered and patient cycled and inspiratory pressure augmentation is provided with every breath. Thus, during PSV patients can vary their respiratory rate, inspiratory flow, inspiratory time, and tidal volume. The respiratory care clinician sets the trigger sensitivity and pressure-support level. Most modern critical care ventilators also allow the clinician to set the inspiratory rise time and flow termination criteria (i.e., cycle sensitivity) during PSV. The level of pressure augmentation (i.e., pressure-support level) provided will vary, depending on the clinical goals. As the pressure-support level increases, so will the patient’s spontaneous tidal volume. Assuming adequate inspiratory flow rates are provided, as PSV increases, tidal volume increases and WOB declines. Figure 6-3 illustrates patient-triggered, pressure-limited, flow-cycled pressure-support ventilation (aka PC-CSV).

FIGURE 6-3 Pressure Support.

Description During PSV, expiration may be passive to ambient pressure (0 cm H2O baseline) or to an elevated baseline pressure (PEEP/CPAP). Modest levels of pressure support (5 to 15 cm H2O) can be used to overcome the WOBI due to the ventilator circuit and artificial airway. Low levels of PSV (e.g., 5 to 8 cm H2O) are often combined with CPAP during IMV and during spontaneous breathing trials (SBTs) to evaluate the patient’s readiness for ventilator discontinuance and extubation. While commonly used in conjunction with IMV, PSV can also be used as a primary mode of ventilation. As a primary mode of ventilation, PSV may improve patient– ventilator synchrony and patient comfort. When used as the primary mode of ventilation, the pressure-support level generally is adjusted to achieve a tidal volume

in the range of 4 to 8 mL/kg IBW with the patient-triggered respiratory rate ≤ 25 breaths/min. Generally speaking, as the pressure-support level increases, WOB decreases. While often employed during SBTs to overcome the WOBI due to the endotracheal or tracheostomy tube, PSV may also be used as an alternative ventilator weaning method. When used as a primary weaning method, PSV generally is initiated at a relatively high level to achieve an adequate VT and respiratory rate (f). When the patient meets readiness criteria, PSV is reduced 2 to 4 cm H2O in a stepwise fashion followed by assessment for signs of distress (e.g., f > 30 to 35 breath/min, SpO2 < 90%, heart rate [HR] > 120 to 140 bpm, systolic blood pressure [BP] < 90 or > 180 mmHg). If the patient displays signs of distress, PSV is returned to its previous level. In the absence of distress, reductions in the level of PSV continue to the point at which extubation is considered (e.g., PSV of 5 to 8 cm H2O is well tolerated). However, if full ventilatory support only requires 10 cm of H2O, then PSV at 5 cm is not truly considered a SBT and some clinicians suggest a trial of ATC without PSV to assess the patients readiness for extubation. To summarize, PSV may be used as a standalone mode or in conjunction with IMV. When used with IMV, low levels of PSV are often employed to reduce or eliminate the WOBI of spontaneous breaths in between mandatory breaths. PSV values needed to eliminate the WOBI will vary with the patient’s ventilatory pattern and endotracheal or tracheostomy tube diameter but usually are in the range of 5 to 15 cm H2O. PSV may also be used during SBTs, often in combination with CPAP, to assess the patient’s readiness for ventilator discontinuance. PSV is sometimes used as the primary mode of ventilation and may improve patient–ventilator synchrony and comfort, reduce the WOB, and provide an alternative method for ventilator weaning. When used as a primary, standalone mode PSV is a form of PC-CSV. Automatic tube compensation (ATC) is designed to overcome the WOBI due to an endotracheal tube or tracheostomy tube during spontaneous breathing. ATC automatically applies inspiratory positive pressure proportional to the measured resistance of the artificial airway. The respiratory care clinician sets the percentage of compensation to be applied, ranging from partial to full compensation. While ATC does reduce the patient’s WOB, it has not been shown to improve patient outcomes.2 ATC incorporates a set point with servo-(s,r) targeting scheme and is

commonly used with IMV.4 Recall that servo-targeting schemes vary the output of the ventilator automatically following a varying input and can vary support provided proportional to inspiratory effort. Setpoint targeting simply refers to the ability of the clinician to set specific parameters (e.g., level of compensation provided). Ventilators that offer ATC include the Covidien PB 840 and PB 980 (as tube compensation), Dräger Evita XL and Evita Infinity V500 (as automatic tube compensation), and HAMILTON G-5 (as tube resistance compensation). When used alone (e.g., IMV rate = 0) ATC is a form of PC-CSV.

Continuous Positive Airway Pressure CPAP describes spontaneous breathing at a constant elevated pressure. With CPAP, the patient initiates and terminates each breath. CPAP may be used during continuous spontaneous ventilation (CSV) or with IMV. CPAP may also be combined with PSV. CPAP may be provided through the ventilator or independently using a high-flow, blended and humidified gas source and a PEEP valve. CPAP may be provided by a well-fitted facemask or invasively, via endotracheal or tracheostomy tube. Like PEEP, CPAP increases mean airway pressure, mean intrathoracic pressure, and FRC. Figure 6-4 illustrates pressure, volume, and flow curves seen with CPAP.

FIGURE 6-4 Continuous Positive Airway Pressure.

Description CPAP may increase the lung surface area for gas exchange, improve oxygenation, and help prevent alveolar collapse and atelectasis. CPAP may be useful to maintain alveolar recruitment in patients with acute restrictive lung disease (e.g., mild to moderate pulmonary edema, parenchymal lung injury).2 With CPAP, pressure is elevated during inspiration and expiration, thus providing a form of inspiratory pressure augmentation that may reduce the WOB during spontaneous ventilation. CPAP is often used during spontaneous breathing trials (SBTs) for evaluation of ventilator discontinuance and extubation. CPAP may also be useful in maintaining FRC in intubated patients, who may otherwise have slight reductions in FRC due to the loss of glottic function; thus, CPAP levels of 3 to 5 cm H2O for intubated patients may be considered physiologic. CPAP should be used cautiously

in patients with obstructive lung disease and those with hemodynamic instability.

Other Modes of Ventilation There are a number of alternative modes of ventilation which incorporate feedback mechanisms to adjust the level or type of support provided. In addition, APRV and high frequency ventilation provide alternative modes which may be useful for certain patients (e.g., severe ARDS).

Adaptive Pressure Control Adaptive pressure control (APC) provides an adaptive feedback mechanism for pressure control or pressure support. With APC the desired tidal volume (VT) is set but the breath type is pressure control or pressure support. The ventilator then automatically adjusts the pressure level from breath to breath to achieve the targeted VT. This allows the ventilator to maintain a relatively stable VT in the face of changes in compliance, resistance, or patient effort. If delivered VT decreases, the ventilator automatically increases the pressure provided and vice versa. On the other hand, if patient demand and associated effort increases resulting in a larger than desired VT, the ventilator automatically decreases the pressure-control level, which may be inappropriate. APC provides many of the advantages of pressure-control ventilation while maintaining a relatively stable clinician-selected VT. Decreases in compliance, increases in resistance, or reductions in patient effort will cause the ventilator to increase the pressure automatically. Clinicians must be aware, however, that peak inspiratory pressures (PIP) and plateau pressures (Pplateau) may rise above acceptable levels as the ventilator attempts to automatically maintain a target VT in the face of changes in ventilatory mechanics or decreased patient effort. On the other hand, increasing patient effort may result in an inappropriate decreased level of support for patients in distress. Manufacturers’ names for adaptive pressure control include pressure-regulated volume control (PRVC) provided with the Maquet Servo-i and Servo-u (see below), auto-flow provided with the Dräger Evita XL and Evita Infinity V500, volume control plus (Covidien PB 840 and PB 980), and adaptive pressure ventilation (HAMILTON

G5 and C-3). We will discuss a few of these versions of APC below.

Pressure-Regulated Volume Control Pressure-regulated volume control (PRVC) is a form of APC first introduced on the Servo 300 ventilator in the 1990s. This form of APC is currently available on the Maquet Servo-i and Servo-u and Yvaire AVEA ventilators as pressure-regulated volume control. PRVC provides volume-targeted pressure-control breaths using an adaptive (a) targeting scheme that automatically adjusts the pressure between breaths to reach the targeted tidal volume in response to varying patient conditions. Delivered VT is measured and compared with target VT and the pressure-control value is then gradually increased or decreased until the target VT is reached. PRVC allows for patient-triggered or time-triggered breaths (aka assist/control ventilation). PRVC with IMV is also offered with the Servo-i and Servo-u ventilators as SIMV pressure-regulated volume control. PRVC can be classified as pressure control-continuous mechanical ventilation with adaptive targeting (PC-CMVa) where the “a” notation indicates an adaptive targeting scheme. As a form of APC, PRVC provides relatively stable tidal volume delivery with changes in compliance, resistance, or patient effort. Patients may trigger the ventilator (aka assist breaths) and set their own rate. In the absence of a patient trigger within the time interval provided, the ventilator will initiate a timetriggered breath (aka control breath). If the delivered VT for a breath is less than the target, the pressure-control value will automatically increase for the next breath. If VT is greater than target, the pressure-control value will automatically decrease for the next breath. As noted earlier, adaptive targeting has the advantage of allowing for automatic adjustments in pressure control to achieve a volume target. Adaptive targeting, however, can make inappropriate ventilator adjustments in cases where algorithm assumptions are incorrect, or the assumptions do not match the patient’s physiology. For example, an increase in patient effort may be interpreted as an increase in compliance. This may result in an inappropriate decrease in support. Functionally, the Servo-i and Servo-u ventilators in the PRVC mode will deliver a test breath VT with an inspiratory breath hold to measure the plateau pressure (Pplateau). The measured Pplateau pressure is then used for the next breath and the

resultant exhaled VT is compared to the target VT. The pressure is then regulated to provide the clinician-set VT from breath to breath. The pressure will increase or decrease in increments of ± 3 cm H2O per breath as needed to achieve the target tidal volume. The pressures possible, however, cannot exceed the clinician-selected peak pressure alarm setting minus 5 cm H2O (e.g., if the peak pressure alarm is set at 30 cm H2O, the ventilator cannot increase PIP beyond 25 cm H2O).30 As with other forms of PC-CMV, PRVC incorporates a decreasing flow waveform and square wave pressure waveform. As compared to VC-CMV with fixed inspiratory flow rates, PRVC shares many of the advantages of PC-CMV in that it may reduce the WOB and improve patient comfort, and increased mean airway pressure may improve oxygenation. Inspiratory gas flow varies with patient inspiratory effort, which may improve patient–ventilator synchrony. As described above, PRVC is a form of adaptive pressure control (APC) that is available on several other ventilators under different proprietary names (e.g., autoflow: Dräger Evita XL and Evita Infinity V500, volume control plus: Covidien PB 840 and PB 980, and adaptive pressure ventilation: HAMILTON G5 and C-3).

Volume Support Volume support (VS) is like PSV with the addition of a clinician-set volume target. Like PSV, volume support requires spontaneous breathing. All breaths are patient triggered, pressure limited, and flow cycled to expiration. Upon initial setup the ventilator delivers a test pulse at 10 cm H2O above PEEP and measures compliance and exhaled VT. The ventilator than automatically adjusts the pressure-support level up or down on a breath-to-breath basis to achieve the clinician-selected tidal volume. Volume support is a form of pressure-control ventilation with adaptive breath targeting. As described earlier, adaptive breath targeting allows the ventilator to automatically vary pressure to achieve the desired VT. Like PSV, the patient triggers and cycles each breath; because of this, VS can be classified as a form of pressure control-continuous spontaneous ventilation, specifically PC-CSVa. With adaptive (a) breath targeting, however, inappropriate changes may occur if algorithm assumptions are violated or do not match the patient’s actual physiology. For example, the ventilator cannot distinguish between changes in patient effort and changes in compliance; an increase in patient effort may be misinterpreted as an

improvement in compliance and the ventilator may decrease support inappropriately. In summary, volume support has many of the advantages of pressure support but provides more stable tidal volume delivery in the face of changes in compliance, resistance, or patient effort. Volume support can be classified as PC-CSVa.4,5 All breaths are initiated and terminated by the patient (i.e., patient triggered and flow cycled). In the absence of a patient trigger, no time-triggered breaths will be provided; an apnea alarm and backup apnea ventilation mode should be employed. For example, in the volume-support mode the Maquet Servo-i ventilator will automatically switch from volume support to volume control in the event of apnea. Volume support is available on the Servo-i, Servo-u, Covidien PB 840 and PB 980, and Newport e360.

Mandatory Minute Ventilation (MVV) Mandatory minute ventilation (MVV) is an older form of automated ventilation that compares the patient’s actual minute ventilation (V̇E) to a targeted value and automatically increases or decreases the level of support provided. As originally introduced in 1977, MMV was a form of intermittent mandatory ventilation that automatically increased or decreased the mandatory breath rate to achieve the desired minute ventilation. MMV was initially introduced as a form of automated ventilator weaning. As the patient’s level of spontaneous ventilation increased, the ventilator would automatically dial back the number of mandatory breaths delivered. If the patient’s spontaneous ventilation decreased, the ventilator would automatically increase the number of mandatory breaths provided to maintain the desired V̇E. Other forms of MMV later introduced would vary the level of pressure support provided (vs. IMV rate) to maintain a stable V̇E. Advantages of MMV include assuring a more stable level of ventilation during IMV in the face of changes in patients’ spontaneous breathing; avoidance of episodes of acute hypoventilation; and providing a smooth, systematic, automated method of weaning ventilatory support. An important disadvantage of MMV is that patients may develop rapid shallow spontaneous breathing, which can result in high V̇E but inadequate alveolar ventilation. Recall that many patients in respiratory failure develop rapid shallow breathing patterns that maintain a relatively high minute ventilation. This is especially true for patients with acute restrictive pulmonary

disease (e.g., severe pneumonia, ARDS). For example, a very sick patient breathing 40 breaths/min with VT = 150 mL would have a minute ventilation of 6 L/min: V̇E = VT × f = 150 mL × 40 breaths/min = 6000 mL/min = 6 L/min In such a case, the MMV system would assume that spontaneous minute ventilation was adequate and dial back the mandatory IMV rate, even though very shallow tidal volumes provide minimal effective alveolar ventilation due to dead space. Recall also that IMV has the potential to prolong ventilator weaning, and spontaneous breathing trials (SBTs) have supplanted IMV as the most appropriate approach to ventilator discontinuance for most patients. MMV is currently available on the Dräger Evita XL and Evita Infinity V500 as mandatory minute volume ventilation (VC-IMVa,s, that is, adaptive and set-point breath targeting) and mandatory minute volume with pressure-limited ventilation (VC-IMVda,s indicates dual adaptive and set-point breath targeting).31 Despite being available since the late 1970s, MMV has not been shown to consistently improve ventilator weaning success as compared to newer techniques and has not been shown to improve other important patient outcomes.

Adaptive Support Ventilation (ASV) Adaptive support ventilation (ASV) is a closed-loop, automatic ventilation mode that combines aspects of pressure control IMV with pressure support (i.e., PC-IMV) to achieve a target minute ventilation (V̇E). ASV incorporates optimal targeting of both mandatory and spontaneous breaths.4,5 With ASV the pressure-control level is adjusted automatically to achieve a specific tidal volume (VT) at a specific frequency for mandatory breaths.4,5 Target tidal volume for spontaneous breaths is based on respiratory system mechanics and target minute ventilation.4,5 Mandatory breaths are time triggered at a preset frequency and inspiratory pressure and are time cycled to expiration (i.e., pressure control). Spontaneous breaths are patient triggered and flow cycled to expiration (i.e., pressure support). Simply put, ASV allows for the delivery of patient-triggered pressure-supported spontaneous breaths or time-triggered mandatory pressure-control breaths to achieve a minimum minute ventilation at an optimal level of WOB. The ventilator automatically adjusts the level of support provided based on respiratory system

mechanics, targeted minute ventilation (V̇E), and clinician-selected level of support. Target minute ventilation is calculated by the ventilator based on the patient’s ideal body weight (IBW) at 0.1 L/min/kg (or 100 mL/min/kg). For example, a patient with an ideal body weight of 70 kg would have a target minute ventilation of 7 L/min (V̇E = 0.1 L/min/kg × 70 kg = 7 L/min). The clinician could then select to provide from 20% to 200% of the calculated V̇E. If 100% support was selected, in this example the target V̇E would be 7 L/min. A level of support of up to 200% could be selected for patients with increased ventilatory needs. Examples of patients who may have increased ventilatory needs include those with sepsis, increased physiologic dead space, or increased metabolic rate. Less than 100% support could be selected for ventilator weaning. With ASV, the ventilator uses an algorithm to determine the optimal breathing frequency (f) and tidal volume (VT). The ventilator’s goal is to provide tidal volumes and frequencies that are physiologically beneficial for the patient in terms of WOB. The optimal breathing frequency (f) to minimize WOB based on the estimated dead space (VD) and measured expiratory time constant is calculated.2 Ventilatory dead space (VD) is estimated at 2.2 mL/kg IBW. Tidal volume (VT) is calculated based on the target V̇E and optimal calculated breathing frequency where VT = V̇E/f. The clinician sets the inspiratory pressure-support level, rise time, and expiratory cycle sensitivities for spontaneous breaths.

CLINICAL FOCUS 6-1 Estimated Minute Volume and Dead Space Volume A patient with acute respiratory failure is to receive adaptive support ventilation (ASV). The clinician calculates her ideal body weight at 70 kg. Question 1. Estimate the required minute ventilation for this patient using the formula integrated into the ASV system. The patient’s required minute ventilation (V̇E) can be estimated using the following formula: V̇E = 100 mL/min/kg × IBW (kg). Assuming IBW = 70 kg, this becomes: V̇E = 100 mL/min/kg × 70 kg = 7000 mL/min or 7 L/min.

Question 2. Estimate this patient’s dead space volume using the formula integrated into the ASV system. Ventilatory dead space volume (VD) is estimated at 2.2 mL/kg: VD = 2.2. mL/kg IBW × IBW (kg). In this example for a 70 kg (IBW) patient the estimated dead space volume would be: VD = 2.2 mL/kg × 70 kg = 154 mL.

To initiate ASV the clinician enters the patient’s ideal body weight, high pressure limit, PEEP, FIO2, rise time, flow cycle, and percentage of predicted minute ventilation to support (i.e., 20% to 200%). The ventilator incorporates algorithms that automatically adjust the respiratory rate, pressure limit, and tidal volume to optimize the patient’s WOB based on measurement of specific variables (e.g., flows, times, compliance, resistance, and expiratory time constant) to maintain an appropriate level of support based on calculated V̇E.32 The ventilator uses a test breath to calculate compliance, resistance, and autoPEEP. The ventilator automatically sets minimum and maximum values for VT, mandatory breath frequency, inspiratory pressure, and inspiratory/expiratory time. VT is adjusted with changes in compliance to maintain a lung-protective strategy. For example, a decrease in compliance may result in a decrease in VT. ASV automatically adjusts mandatory breath frequency (f) and I:E ratio to maintain an expiratory time at least three time constants in length and reduce the risk of autoPEEP. ASV will alter the amount of support provided to achieve the target V̇E. With spontaneously breathing patients, ASV will deliver patient-triggered, pressurelimited, flow-cycled pressure-support breaths while monitoring the patient’s lung mechanics and minute ventilation. If the level of spontaneous ventilation is sufficient to meet the target V̇E, no mandatory breaths will be delivered. If the level of spontaneous ventilation is insufficient to meet the V̇E, the ventilator will automatically increase the level of support provided. ASV can be an effective approach to ventilation in patients with acute respiratory failure.2 Patients with normal or near-normal lungs (e.g., opiod drug overdose without

aspiration) who require ventilatory support may receive unnecessarily large tidal volumes with ASV.2 ASV can adjust to changing lung compliance and patient inspiratory effort; however, automatic adjustment may be inappropriate if algorithm assumptions are violated or if they do not match the patient’s physiology.5 ASV while may provide a safe and effective method for automated ventilator weaning.32 Because of the algorithms in play, patients with extended expiratory time constants (e.g., long expiratory time as seen in COPD) may receive larger tidal volumes and lower frequencies as compared to patients with shorter time expiratory constants (e.g., short expiratory time as may occur with ARDS).26 ASV has not been shown to improve specific clinically important patient outcomes.26 ASV is available on the HAMILTON G5, C-3, C-1, T-1, and MR-1 ventilators. IntelliVent ASV (HAMILTON S1 ventilator) provides a form of ASV that adds a closed-loop system to control oxygenation based on the ARDSNet PEEP tables and SpO2 to adjust FIO2 and PEEP.2

Airway Pressure-Release Ventilation Airway pressure-release ventilation (APRV) employs two levels of pressure, which are time triggered and time cycled. Patients may breathe spontaneously at both levels not unlike providing two levels of CPAP. The high-pressure level may be set to last several seconds (e.g., 3 to 6 sec) to promote alveolar stabilization and alveolar recruitment in patients with severe hypoxemic respiratory failure (e.g., ARDS). The ventilator then cycles to the low-pressure setting for a brief period (e.g., 0.5 to 0.8 sec) to aid in CO2 removal, lower mean airway pressures, and reduce the risk of cardiovascular compromise. Figure 6-5 illustrates high and low airway pressures and times during APRV.

FIGURE 6-5 Airway Pressure-Release Ventilation.

Ventilator settings during APRV include high airway pressure (Phigh), high-pressure time (Thigh), low airway pressure (Plow), and low-pressure time (Tlow). Phigh and Plow are the two levels of pressure provided and function like two levels of CPAP in the presence of spontaneous breathing. Thigh and Tlow represent the time periods set for each pressure level. Plow and Tlow represent the airway pressure-release level and airway pressure-release time. APRV can be classified as a form of PC-IMV. In the absence of spontaneous breathing, however, APRV functions as time-triggered pressure control-continuous mechanical ventilation (PC-CMV). As noted, Thigh generally is > Tlow and in the absence of spontaneous breathing, APRV can provide pressure-controlled inverse-ratio ventilation (PCIRV). Tidal volume (VT) provided by the ventilator during APRV is determined by the pressure gradient between the two pressure levels (ΔP = Phigh – Plow), the duration of high pressure (Thigh), and the patient’s pulmonary mechanics (i.e., compliance and resistance). Put another way, the transition from Plow to Phigh inflates the lungs while

the transition from Phigh to Plow allows the lungs to deflate. The patient’s alveolar ventilation and PaCO2 are determined by the VT, frequency of the airway pressurerelease maneuver, and level of the patient’s spontaneous breathing. For example, if Thigh is 4.2 seconds and Tlow is 0.8 seconds, the cycle time would be 5 seconds and provide 12 inspiratory/expiratory cycles per minute. APRV may decrease peak airway pressures, improve alveolar recruitment, improve oxygenation, and increase ventilation in dependent lung zones in patients with ARDS (as compared to conventional ventilatory support).26 Because spontaneous breathing is allowed during APRV, there may be some physiologic benefits (e.g., spontaneous breathing may promote recruitment of dependent alveoli, improve gas exchange, and improve cardiac filling). There is also some evidence that APRV has the potential to decrease the need for sedation and administration of paralytic agents, decrease the time on the ventilator, and reduce ICU length of stay as compared to conventional approaches.26 Like other forms of pressure-control ventilation, tidal volume may vary during APRV with changes in the patient’s condition and a minimum minute ventilation is not guaranteed. As with PCIRV, short expiratory times can result in the development of autoPEEP and higher mean airway pressures can reduce venous return and compromise cardiac output in patients with hemodynamic compromise. APRV generally is not indicated for use in patients with severe obstructive lung disease due to the potential for air trapping and barotrauma. APRV has not been shown to improve mortality or other important outcomes as compared to more conventional modes of ventilation.2, 26 APRV is available as APRV (Dräger Evita XL, Evita Infinity V500), Bi-level (Covidien PB 840 and 980), BiVent and BiVent/APRV (Maquet Servo-i and Servo-u), APRV and DuoPAP (HAMILTON G-5 and C-3), and BiPhasic (Yvaire AVEA).

Proportional Assist Ventilation Proportional assist ventilation (PAV) automatically adjusts the level of ventilatory support based on estimated WOB and feedback measures associated with the neural output of the respiratory center.2 Specifically, the patient’s spontaneous inspiratory effort (as inspiratory gas flow) reflects the patient’s respiratory drive. The ventilator calculates delivered volume and estimates resistance and compliance (as elastance) by applying a brief end-inspiratory pause and expiratory pause every few

seconds.2 Inspiratory pressure is varied automatically depending on the patient’s inspiratory effort, calculated WOB, and the clinician-set percentage of support. Inspiratory pressure and inspiratory time may vary breath to breath and within each breath.2 Work is simply force times distance; WOB is a function of pressure times volume (see Box 6-8). The level of support provided can be adjusted from 5% to 95% so that the WOB is in the range of approximately 0.5 to 1.0 J/L.2 The ventilator monitors the patient’s inspiratory flow and calculates the pressure required for ventilation based on the equation of motion. Recall that the equation of motion describes the pressure required to overcome the elastic and resistive properties or loads of the lung–thorax system. Recall also that compliance is the inverse of elastance and that work is required to overcome these elastic and resistive forces. The elastic forces are proportional to tidal volume and the resistive forces are proportional to the airflow.

BOX 6-8 Work of Breathing Work of breathing (WOB) is the work done by the ventilatory muscles and/or mechanical ventilator to overcome elastic and resistive forces opposing ventilation. Work is force × distance and work units are kilograms × meters (kg × m) or joules (1 joule = 0.1 kg × m). Pressure is force per unit surface area (force/surface area) while volume is distance cubed (m3 or cm3). ∎ WOB is a function of the pressure change × volume change (ΔP × ΔV): • Work = force × distance. • Pressure is force per unit surface area (force/cm2). • Surface area is distance2 often reported as cm2. • Volume may be recorded in cm3 (i.e., cc or mL). • WOB = ΔP × ΔV = force/cm2 × cm3 = force × cm = force × distance. ∎ WOB can be measured as pressure units (cm H O) × volume units (L) and 2 then converted to kg × m or joules OR normalized to volume (i.e., joules/L) where: 1 joule = 0.1 kg × m. 1 joule per liter = joule/L = 0.1 kg × m/L ∎

Normally work occurs during inspiration and is performed by the diaphragm

∎ ∎

and accessory muscles of inspiration; expiration is normally passive requiring only the elastic recoil of the lung tissue (i.e., no work). With severe obstructive lung disease, the accessory muscles of expiration may be engaged increasing WOB during exhalation. Normal WOB normalized to volume is about 0.5 to 1.0 joules per liter; > 1.5 joules/L may be an excessive workload. Proportional assist ventilation (PAV) is typically set so WOB is 0.5 to 1.0 joules per liter.

The required WOB can be performed by the patient or the ventilator, or both may contribute to the total work necessary. Put another way, the equation of motion describes the elastic and resistive loads contributing to the WOB and predicts the pressures needed to overcome these workloads. The ventilator can perform some or all this work thus unloading the ventilatory muscles. In the presence of ventilatory work provided by the ventilator and work provided by the respiratory muscles, the equation of motion can be simplified, where P is the pressure needed to overcome the elastic and resistive loads of the lung. This pressure may be provided by the ventilator or the respiratory muscles, or both. P ventilator + P respiratory muscles = elastance × volume + resistance × flow As noted, the patient’s spontaneous inspiratory flow provides an estimate of the neural output of the respiratory centers and inspiratory effort. Thus, PAV adjusts the level of support based on the patient’s inspiratory effort and changing lung mechanics (i.e., compliance and resistance). Pressure may vary from breath to breath depending on changes in the patient’s pulmonary mechanics and inspiratory flow demand. Breaths are cycled to expiration by flow, similar to breath cycling with pressure-support ventilation; the flow termination criterion is adjustable. Box 6-8 provides additional information about WOB. Box 3-11 (Chapter 3) provides additional information about the equation of motion. PAV may improve patient–ventilator synchrony and patient comfort.2 PAV assumes intact neural control of respiration and no leaks in the system (a system leak can be misinterpreted as increased patient effort and increased inspiratory effort). A runaway phenomenon may occur, resulting in in excessive volume and pressure

delivery if the clinician has set the percentage of support too high; if the percentage of support is too low, WOB may be excessive.2 It must also be noted that PAV does not provide an automatic minimal support level and alarms and backup ventilation modes must be activated in the event of apnea or otherwise absent or minimal patient effort. It must also be noted that calculated WOB may not reflect actual patient effort. For example, a patient may make a large effort that results in little or no volume or flow. In this case, while the patient effort is large, the calculated WOB will not reflect that effort because the volume change is small. PAV is not useful in patients with a weak ventilatory drive or weak respiratory muscles. PAV is available on the Covidien PB 840 and PB 980 as spontaneous proportional assist. The Dräger Evita V 500 offers spontaneous proportional pressure support, which allows the clinician to set the amount of resistance to be supported as flow assist and the amount of elastance to be supported as volume assist.31 The Phillips Respironics V60 ventilator provides a noninvasive form of PAV as proportional pressure support, which may be useful in treating patients with sleep disorders. Proportional assist ventilation can be classified as a form of pressure controlcontinuous spontaneous ventilation with servo breath targeting (PC-CSVr).4 The proportional pressure-support mode available with the Respironics V 60, however, would be best classified as a form of pressure control-intermittent mandatory ventilation (PV-IMVs,r).4 PAV has not yet been shown to significantly improve important clinical outcomes.2

Automode Automode is a form of IMV that incorporates a targeting scheme for both primary and secondary breaths based on the modes selected. Automode uses IMV to synchronize mandatory and spontaneous breaths by automatically switching between two modes of ventilation based on specific feedback measures.4 This allows the ventilator to automatically titrate the level of support provided between control and support modes dependent on the patient’s level of spontaneous ventilation. In the event of apnea, the ventilator will automatically switch to a timetriggered control mode. Automode may be especially useful in patients who have a variable respiratory drive due to fatigue, pain, changing lung mechanics, or intermittent apnea. Automode can be used to provide an automated form of

ventilator weaning. Automode can be set to titrate the level of ventilation provided between the following modes: Volume control (VC) and volume support (VS). Used in this fashion, automode can be classified as VC-IMVd,a using dual targeting for VC and adaptive targeting for VS. Pressure control (PC) and pressure support (PS). Used in this fashion, automode can be classified as PC-IMVs,s using set-point targeting for PC and PS. Pressure-regulated volume control (PRVC) and volume support (VS). Used in this fashion, auto-mode can be classified as PC-IMVa,a using adaptive targeting for both PRVC and VS. As noted, automode can be set to the alternate between PRVC and VS with a target minute ventilation based on the set tidal volume and respiratory rate. Used in this manner, the ventilator monitors the patient’s tidal volume and automatically adjusts inspiratory pressure between breaths to achieve an average exhaled tidal volume at the set target. If the spontaneous respiratory rate does not achieve the minimum minute ventilation target, mandatory time-triggered breaths are provided. Inappropriate sensitivity settings, resulting in autotriggering, can mislead the ventilator regarding the level of spontaneous breathing present. As with other modes of ventilation, attention to appropriate alarm settings is required. Automode is available on the Maquet Servo-i and Servo-u.

Neurally Adjusted Ventilatory Assist (NAVA) NAVA incorporates an esophageal catheter with a multiple array electrode to detect the electrical discharge from the diaphragm (Edi). Edi provides a reflection of the respiratory center’s neural output to the diaphragm.28 This diaphragmatic signal is used to trigger, adjust flow, and cycle the ventilator.2 Because the strength of the diaphragmatic signal varies throughout inspiration, pressure will also vary throughout inspiration.28 NAVA may provide better coordination between the patient’s central respiratory drive and the ventilator’s inspiratory trigger, flow, and cycle. The degree of support provided varies with the amplitude of the diaphragmatic signal and assist level set by the respiratory care clinician.6 Tidal volume will vary from breath to

breath in proportion to the patient’s inspiratory demand. NAVA can be classified as a form of pressure control-continuous spontaneous ventilation with servo breath targeting (PC-CSVr), not unlike proportional assist ventilation (PAV). Up to 25% of ventilator patients experience patient–ventilator asynchrony.33 Patient–ventilator asynchrony may lead to patient discomfort, increased WOB, diaphragmatic dysfunction, the need for increased sedation, and delayed liberation from the ventilator. NAVA was developed to provide spontaneously breathing patients greater control of their ventilatory pattern during mechanical ventilatory support.28 NAVA’s intent is to achieve neural-ventilatory coupling, which should improve trigger synchrony and cycle synchrony. Neural–ventilatory coupling refers to the time between the spontaneous breath and the delivery of a mechanical breath. Neural–ventilatory coupling is faster with NAVA than with conventional flow or pressure-triggered ventilatory support.26 Another advantage of NAVA is ventilator triggering should not be adversely affected in patients with flow limitations and autoPEEP and this may be helpful in patients with COPD.2 As described, the degree of support provided with NAVA varies with the amplitude of the diaphragmatic signal and the assist level set by the clinician. As the set NAVA level is increased, the inspiratory pressure provided in proportion to the diaphragmatic signal also increases.28 Initially, NAVA settings should be adjusted to produce the same or slightly lower inspiratory pressures as the patient was receiving during conventional ventilation. Settings may then be adjusted until a comfortable and consistent tidal volume is achieved while observing the diaphragmatic signal displayed on the ventilator screen. In general, as NAVA levels are increased, peak pressure and tidal volume will increase, although this is dependent on patient effort and the strength of the diaphragmatic signal. The ventilator can be set to cycle to expiration when the diaphragmatic signal decreases to 40% to 70% of its maximum signal strength. Normally, the diaphragmatic signal decreases as inspiratory effort decreases, and expiration begins. The goal is to avoid continued inflation when the patient’s central respiratory control centers have switched to the expiratory phase. Cycling criteria is normally set at 70% of peak inspiratory diaphragmatic activity. With inadequate levels of support, the patient may exhibit signs of distress with increased respiratory rate; ventilatory muscle fatigue may ensue. If support provided is greater than necessary, large tidal

volumes may result with suppression of the diaphragmatic signal. Optimal NAVA support will allow the patients to comfortably choose their respiratory rate and tidal volume and maintain adequate alveolar ventilation while unloading the respiratory muscles. Drawbacks of NAVA include the expense and invasive nature of the esophageal catheter, which may cause discomfort; catheter displacement and signal loss are other potential problems. Contraindications for the placement of an esophageal catheter precludes the use of NAVA. In the case of the loss of the catheter signal, the ventilator will automatically switch to conventional, patient-triggered pressuresupport mode.28 Spontaneous breathing is required with NAVA, and it should not be used in patients who are heavily sedated or otherwise have respiratory center depression. NAVA is also contraindicated in patients with spinal cord injury, brain center damage, absent phrenic nerve activity, neuromuscular transmission problems or blockade, or apnea.28 Should a patient become apneic during NAVA, the ventilator will automatically switch to time-triggered pressure control.28 NAVA also depends on adequate neurotransmission via the phrenic nerve to the diaphragm and an intact vagal reflex.28 It should be noted that lung transplant patients may not have an intact vagal reflex and are not candidates for NAVA. As with any ventilatory mode, proper alarm settings are an important consideration. In addition to an audible alarm for diaphragmatic signal loss (e.g., catheter displacement) or apnea, alarms are also available for high pressure, PEEP, minute ventilation, and rate.28 As noted above, NAVA requires spontaneous breathing with an intact ventilatory drive and is not appropriate for patients who are heavily sedated or have other CNS problems that depress spontaneous ventilation. NAVA does not provide a minimal support level and alarms and apnea backup ventilation modes must be employed. Also, as noted should apnea occur the ventilator will automatically switch to time-triggered pressure control (PC-CMV) as a safety feature. The respiratory care clinician can set the backup PC-CMV pressure, rate, and inspiratory time.28 NAVA has been safely used in adults, children, and neonates and there is evidence that NAVA may improve patient–ventilator trigger and cycle synchrony and reduce the need for sedation.2 Patients may be more comfortable as NAVA allows

them to determine their own ventilatory pressures, volumes, and respiratory rates.28 The level of support provided varies based on the patients’ respiratory drive. Outcomes data that NAVA improves important clinical outcomes such as liberation from the ventilator or survival are not currently available.26 NAVA is available on the Maquet Servo-i and Servo-u. Recently an option to provide noninvasive ventilatory support using NAVA has been developed and newer Servo ventilators allow NAVA to be used to provide invasive or noninvasive ventilatory support.28 RC Insight Newer modes of ventilation have been shown to be safe and effective; however, they do not significantly improve important patient outcomes.

High-Frequency Ventilation High-frequency ventilation (HFV) employs very rapid respiratory rates (> 60 to 3000 breaths/min) and very small tidal volumes at or below that of anatomic dead space volume. HFV has been used in neonatal, pediatric, and adult patients as a lungprotective strategy. Its primary use in adults is as a rescue mode for patients with severe ARDS who have failed to respond to conventional ventilation using a lungprotective strategy. Routine use of HFV for patients with ARDS is not supported by current evidence.2 HFV has been suggested for several other conditions including bronchopleural fistula, neonatal respiratory distress syndrome (RDS), burns with inhalational injury, and head trauma with increased intracranial pressure (ICP). HFV can successfully ventilate patients with large air leaks (e.g., tracheoesophageal fistula, bronchopleural fistula) and may be helpful in cases of major airway disruption that cannot be successfully managed with conventional ventilation. HFV has been used extensively to support neonates with RDS and in those with pulmonary air leaks and bronchopulmonary dysplasia with generally good results.2 Currently there are four major types of HFV available as described below. High-frequency positive-pressure ventilation (HFPPV) as applied to adults uses tidal volumes in the range of 100 to 200 mL with respiratory rates of 60 to 120 breaths/min. HFPPV can be accomplished using current conventional ventilators and

can be effective in ventilating patients with large air leaks. HFPPV is rarely used in the modern intensive care unit. High-frequency percussive ventilation (HFPV) was developed by Forrest Bird in the mid-1980s. HFPV incorporates a sliding Venturi device or Phasitron and combines high-frequency oscillatory pulses (200 to 900 beats per minute) and small tidal volumes with more traditional pressure-control ventilation. HFPV may improve oxygenation and ventilation and reduce the risk of barotrauma and hemodynamic compromise. HFPV may also be useful in promoting secretion clearance. HFPV has been advocated for ventilation of burn patients with inhalational injury to maintain lower peak airway pressures, facilitate clearance of soot and secretions, and to facilitate reinflation of collapsed alveoli.34 HFPV may reduce the incidence of pneumonia in patients with smoke inhalation and decrease ICP in patients with head injuries. HFPV is available for critical-care applications as the Percussionaire VDR-4 volumetric diffusive respirator (Percussionaire Corporation). The Percussionaire IPV1C is primarily a therapy device to aid in secretion removal, although it may be used in-line with other ventilators. High-frequency jet ventilation (HFJV) employs a jet delivered through a special endotracheal tube adapter. HFJV uses constant gas flow interrupters that are time cycled and pressure limited.35 Tidal volume is dependent on amplitude, jet driving pressure, jet orifice size, length of inspiratory jet valve time on, and the patient’s compliance and resistance. HFJV is used in conjunction with a conventional ventilator, which can provide adjustable FIO2, PEEP, and 2 to 10 sigh breaths/min.35 The clinician selects peak inspiratory pressure (PIP), jet frequency, and inspiratory jet valve time on.35 HFJV is available with the Bunnell Life Pulse jet ventilator, which can deliver frequencies in the range of 240 to 660 cycles per minute. HFJV is commonly employed in preterm neonates with RDS, although evidence that routine use of HFJV improves patient outcomes as compared to conventional ventilation is lacking. High-frequency oscillatory ventilation (HFOV) uses very high frequencies in the range of 180 to 900 cycles/min (3 to 15 Hz; 1 Hz = 60 cycles/min) and very small tidal volumes (50 to 250 mL). HFOV is the most commonly used form of highfrequency ventilation in neonates and adults. HFOV creates a rapidly oscillating bias

flow that affects gas transport through complex, incompletely understood mechanisms.2 These mechanisms may include conventional bulk flow, Taylor dispersion, pendeluft, asymmetric velocity profiles, cardiogenic mixing, and/or enhanced molecular diffusion.27 HFOV provides relatively high mean alveolar pressures with minimal fluctuation (as compared to conventional mechanical ventilation).2 This may help prevent cyclic alveolar inflation—deflation (i.e., cyclic recruitment–derecruitment), which may contribute to alveolar injury in patients with ARDS. HFOV may also minimize alveolar overdistention and help maintain alveolar patency.2 HFOV has frequently been used in preterm neonates in respiratory failure and may be useful as rescue therapy when PIP ≥ 28 to 30 cm H2O or when mean airway pressure > 10 cm H2O.35 In adults, HFOV is primarily used as a rescue mode for ARDS patients with refractory hypoxemia that has failed to respond to conventional mechanical ventilation using a lung-protective strategy. HFOV is available for ventilation of neonates, infants, and small children using the Vyaire 3100A. The Vyaire 3100B is designed to provide HFOV for adults and larger children (> 35 kg). In summary, high-frequency ventilation may be provided using high-frequency positive-pressure ventilation (HFPPV), high-frequency percussive ventilation (HFPV), high-frequency jet ventilation (HFJV), and high-frequency oscillatory ventilation (HFOV). HFOV has been the most commonly employed method to provide high-frequency ventilation in neonates and adults. HFV should be only employed by skilled clinicians well familiar with its use. Management of ventilatory parameters with HFV can be complex. HFV may cause autoPEEP due to reduced expiratory times and probably should be avoided in patients with obstructive lung disease. HFV can be safe and effective in maintaining oxygenation and ventilation in various settings.26 However, no form of HFV has been shown to be consistently superior to conventional ventilation in reducing mortality or improving outcomes. Chapter 3 provides additional information regarding HFV. Chapter 11 describes the use of HFOV for adults with ARDS.

Initial Ventilator Settings Once the decision has been made to initiate mechanical ventilation, several important choices must be made. As noted, mechanical ventilatory support can be invasive or noninvasive. Initiation of NIV was discussed earlier in this chapter and additional information is provided in Chapter 10. Invasive mechanical ventilation requires establishment of an artificial airway, and mechanical ventilation is most commonly initiated following oral endotracheal intubation. An appropriate ventilator must be available based on the patient’s needs and the expertise and experience of the respiratory care clinician. The clinician must then choose the mode of ventilation and make important decisions about the tidal volume, respiratory rate, breath trigger, inspiratory pressures, flows, and time. The clinician must also choose an appropriate FIO2 and whether to implement PEEP or CPAP. Humidification, alarms, limits, and backup apnea ventilation must then be selected. Each of these choices is discussed below.

Mode While there are several mode choices that may be appropriate in specific situations, we recommend that the initial mode for most adult and pediatric patients be volume control-continuous mandatory ventilation (VC-CMV) allowing for patient-triggered or time-triggered ventilation. This mode is commonly referred to as assist/control volume ventilation. VC-CMV assures that the patient will receive a minimum minute ventilation (V̇E) based on the set tidal volume (VT) and respiratory rate (f). The set VT is delivered consistently, even in the face of changes in the patient’s compliance or resistance. Allowing for patient triggering enables the patient to set his or her respiratory rate at a value above the minimum set rate. In the event of apnea, sedation, or respiratory center depression VT, f, and V̇E are assured. VC-CMV also provides full ventilatory support and when properly applied may significantly reduce the WOB. The main disadvantages of VC-CMV are the variability of PIP and Pplateau, introducing the possibility of inappropriately high pressures being delivered to the patient. Patient triggering sometimes results in an unacceptably high ventilatory rate resulting in a respiratory alkalosis, especially in patients who are anxious or in pain.

Inappropriately high triggering rates can also cause inadequate expiratory time resulting in air trapping and autoPEEP. VC-CMV is also provided using a fixed inspiratory flow rate, which can result in an increased WOB in spontaneously breathing patients if the set inspiratory flow does not meet or exceed the patient’s inspiratory demand. Improper ventilator settings can also lead to patient–ventilator asynchrony. That said, VC-CMV generally is the best initial choice for most critically ill adult patients. An acceptable alternative to VC-CMV for initial mode choice is PC-CMV set to allow patient-triggered or time-triggered breath initiation. This mode is commonly referred to as assist/control pressure-control ventilation (PCV). With PC-CMV, inspiratory pressure will not exceed the set pressure-control level, thus assuring that PIP and Pplateau remain in a safe range, despite changes in the patient’s respiratory mechanics. PC-CMV also incorporates a variable inspiratory flow, which may be more comfortable and better tolerated by some patients. The major disadvantage of PC-CMV is that delivered VT will vary with changes in the patient’s compliance, resistance, or inspiratory effort. Adjustment of PC-CMV to ensure tidal volume delivery also requires that the respiratory care clinician fully understand the interactions between inspiratory pressure, inspiratory time, respiratory mechanics, and patient effort. If apnea is present, PC-CMV will provide time-triggered ventilation (aka controlled ventilation). Volume-targeted forms of PC-CMV (e.g., PRVC) provide good options for clinicians familiar with these modes. A third option sometimes appropriate for initial choice of mode in spontaneously breathing patients with an intact respiratory drive is PSV. Used as a primary standalone mode, PSV may be classified as pressure control-continuous spontaneous ventilation (PC-CSV). PSV generally is well tolerated by spontaneously breathing patients and the pressure level can be adjusted to achieve a desired tidal volume. PSV allows the patient to initiate and terminate each breath and it delivers a variable flow based on the patient’s inspiratory effort. Thus, PSV may improve patient–ventilator synchrony and comfort while reducing the WOB. Two major drawbacks of PSV as a primary mode of ventilation are present. If apnea or bradypnea occur, there is no backup ventilatory rate provided. Attention to ventilator alarms and properly setting apnea backup ventilation is very important. As with other forms of pressure control, tidal volume will vary with changes in compliance,

resistance, or patient effort. SIMV is also a serviceable option for initial ventilator setup and can be provided as volume control-intermittent mandatory ventilation (VC-IMV) or pressure controlintermittent mandatory ventilation (PC-IMV). SIMV, when properly applied, can provide full ventilatory support, while allowing the patient to breathe spontaneously in between mandatory breaths. Spontaneous breaths can be pressure augmented using pressure support or automatic tube compensation to reduce the WOB associated with the artificial airway. While SIMV has largely fallen out of favor in recent years, it can be useful as an alternative for patients with rapid spontaneous respiratory rates that would otherwise trigger the ventilator much too frequently when using a mode in which every patient trigger results in a mandatory breath. It is used by some clinicians in patients with status asthmaticus to limit the minute ventilation to around 10 L/min and minimize air trapping. Following initiation of mechanical ventilation and patient stabilization using one of the above modes, the respiratory care clinician must thoroughly assess the patient. It may then become apparent that an alternative mode should be considered.

Tidal Volume and Rate Tidal volume, respiratory rate, and minute ventilation determine the effectiveness of the ventilatory support provided. Each of these parameters may be set directly or indirectly as described below.

Normal Tidal Volume, Rate, and Minute Ventilation A normal adult’s resting spontaneous tidal volume (VT) is about 5 to 7 mL/kg of ideal body weight (IBW) or about 400 to 700 mL with a respiratory rate (f) in the range of 12 to 18 breaths/min. Minute ventilation (V̇E) is simply tidal volume (VT) × rate (f): V̇E = VT × f Assuming a normal adult tidal volume (500 mL) and respiratory rate (12 breaths/min), minute ventilation would be: V̇E = VT × f = 500 mL × 12 breaths/min = 6000 mL/min or 6 L/min.

The normal range (for adults) for V̇E is 5 to 10 L/min or about 100 mL/kg IBW. Note that there are several formulas for estimating IBW (e.g., Broca formula, Devine formula, and Hamwi formula). We use the formulas suggested by ARDSNet, which are based on the Devine formula for IBW calculation: Males: IBW = 50 + 2.3 (height in inches – 60) Females: IBW = 45.5 + 2.3 (height in inches – 60) Note: ARDSNet uses the term predicted body weight or PBW instead of IBW; the terms can be used interchangeably. Table 6-3 illustrates the calculation of tidal volume and minute ventilation based on ideal body weight. TABLE 6-3 Tidal Volume and Minute Ventilation Based on Ideal Body Weight

Description Males: IBW = 50 + 2.3 (height in inches – 60).

Females: IBW = 45.5 + 2.3 (height in inches – 60). Note: ARDSNet uses the term predicted body weight or PBW instead of IBW; the terms can be used interchangeably. Set ventilator tidal volumes may be rounded, as appropriate.

Initial Ventilator Settings for Tidal Volume and Rate With VC-CMV using set-point breath targeting (aka assist/control volume ventilation) the clinician sets the desired VT and f. For ventilator initiation in the VC-CMV mode, we suggest an initial tidal volume of 8 mL/kg IBW with a rate of 12 to 16 breaths/min for most patients. Tidal volume should be then adjusted (if necessary) to maintain a Pplateau ≤ 28 to 30 cm H2O. Slightly larger tidal volumes (e.g., 8 to 10 mL/kg) may be acceptable if Pplateau ≤ 28 to 30 cm H2O.3 ARDS patients may require smaller tidal volumes (e.g., 6 mL/kg IBW or less) to maintain Pplateau ≤ 28 to 30 cm H2O. Patients with neuromuscular diseases may require larger tidal volumes to prevent atelectasis. The spontaneously breathing patient may trigger the ventilator at a rate greater than the set minimum rate. If smaller tidal volumes are required to maintain Pplateau ≤ 28 to 30 cm H2O (e.g., ARDS, severe pneumonia), higher initial respiratory rates may be required. For PC-CMV using set-point breath targeting (aka assist/control pressure-control ventilation [PCV]) we suggest an initial pressure-control setting of 12 to 15 cm H2O (above PEEP) followed by immediate observation of the resultant tidal volume. The pressure-control level is then quickly adjusted up or down to achieve the desired VT while ensuring Pplateau ≤ 28 to 30 cm H2O. Initial rate is set in the range of 12 to 16 breaths/min. Spontaneously breathing patients may trigger the ventilator at a rate greater than the set minimum rate. If smaller tidal volumes are required to maintain Pplateau ≤ 28 to 30 cm H2O to prevent alveolar overdistention (e.g., ARDS), higher initial respiratory rates may be required. For PC-CSV using set-point breath targeting (aka standalone pressure-support ventilation [PSV]), we suggest an initial PSV setting of 12 to 15 cm H2O (above PEEP) followed by immediate observation of the resultant tidal volume. PSV is then adjusted to achieve an acceptable tidal volume, usually in the range of 4 to 8 mL/kg IBW and resulting in a patient-triggered respiratory rate of ≤ 25 breaths/min. Typically, this requires PSV levels of ≤ 20 cm H2O (above PEEP). Recall that with PSV all breaths are patient triggered and no time-triggered rate is set. In the event of apnea, an automatic backup apnea ventilation function should be set, as well as

setting other appropriate alarms and limits. With VC-IMV and PC-IMV, mandatory breath tidal volume Pressure and rate are set in a similar fashion as volume control- and pressure control-continuous mandatory ventilation (VC-CMV and P-CMV) as described above.

Inspiratory Pressure High inspiratory pressures are associated with barotrauma and lung injury. In general, Pplateau ≤ 28 to 30 cm H2O is thought to reduce the likelihood of ventilatorinduced lung injury and lower plateau pressures are associated with better patient outcomes. It should be noted, however, that patients with decreased thoracic compliance (e.g., chest wall deformity, obesity, and ascites) may tolerate Pplateau > 28 to 30 cm H2O without causing alveolar overdistention. With VC-CMV, peak inspiratory pressure (PIP) and plateau pressure (Pplateau) will vary with changes in patients’ compliance and resistance. In general, PIP should be ≤ 40 cm H2O while maintaining Pplateau ≤ 28 to 30 cm H2O. Ventilator adjustments that may reduce PIP during volume ventilation include lowering the set tidal volume, decreasing the inspiratory peak flow, and changing the inspiratory flow waveform from a square wave to a down ramp. Pplateau can be reduced by lowering the set tidal. With PC-CMV, PC-CSV, and PC-IMV the pressure-control level is set by the clinician to achieve an acceptable VT while maintaining Pplateau ≤ 28 to 30 cm H2O.

Intermittent Sigh Breaths Normal spontaneously breathing subjects take an intermittent deep breath or sigh every 6 to 10 minutes. Monotonous shallow tidal breathing (< 7 mL/kg IBW) without an intermittent deep breath may cause progressive atelectasis, and intermittent deep breaths (sighs) will reverse this trend. Often modern critical care ventilators incorporate a sigh function, which may be set by the clinician to deliver an intermittent deep breath or sigh volume at a specific interval. Traditionally, sigh breaths were set at 1.5 to 2 times the tidal volume to be delivered every 6 to 10 minutes. We suggest that almost all patients receive a minimal level of PEEP (e.g., 5 to 8 cm H2O), which should make institution of intermittent sigh breaths unnecessary. That said, recruitment maneuvers are sometimes used in patients with ARDS and function somewhat like an intermittent sigh. There is also some evidence that the

use of intermittent sighs may improve alveolar recruitment in ARDS.2 Chapters 7 and 8 provide additional discussion of the use of recruitment maneuvers in ARDS.

Breath Trigger Patient-triggered breaths may be (negative) pressure or flow triggered. With pressure triggering, a patient inspiratory effort decreases the ventilator circuit pressure to a clinician-selected level, thus triggering inspiration. With flow triggering, a constant flow of gas during the expiratory phase is disrupted by the patient’s inspiratory effort, triggering inspiration. In either case, the trigger sensitivity should be adjusted to minimize trigger work while avoiding autotriggering. For pressure triggering, the trigger generally is set between –0.5 and –1.5 cm H2O, although some circuits may require trigger sensitivity be set at –2.0 cm H2O to avoid autotriggering.2,27 With flow triggering the trigger sensitivity generally is set at the range of 1 to 2 L/min below the baseline or bias flow, although some systems may require flow triggers as high as 3 to 4 L/min below baseline or bias flow to avoid autotriggering.2,27 Inappropriate trigger sensitivity settings and autoPEEP can increase trigger work. Trigger asynchrony occurs when the patient’s inspiratory effort becomes decoupled from the ventilator trigger. With the current generation of critical care ventilators there are no clinically important differences between a pressure and flow trigger.2,27 NAVA may also improve patient–trigger synchrony. RC Insight Patient-trigger sensitivity should be adjusted to minimize trigger work without autocycling.

Inspiratory Phase, Expiratory Phase, and I:E Ratio Various ventilator controls will effect inspiratory time, expiratory time, and I:E ratio, and these effects vary depending on the mode of ventilation employed. Initial ventilator settings are discussed further below.

Volume Control With VC-CMV and VC-IMV using set-point breath targeting (aka assist/control volume ventilation and volume SIMV), the clinician sets the desired VT and f for

mandatory breaths. With these modes, the clinician also sets either the peak flow and flow waveform or the inspiratory time and flow waveform. For assist/control ventilation, the clinician also sets trigger sensitivity. In ventilators with a peak flow control, peak flow, flow waveform, and tidal volume determine inspiratory time. As peak flow increases, inspiratory time decreases and vice versa. In ventilators with an inspiratory time setting, inspiratory time, tidal volume, and flow waveform determine peak flow. Inspiratory time is set directly in these ventilators and inspiratory flow varies to ensure tidal volume delivery within the set inspiratory time. Many ventilators allow the clinician to choose between a square wave (constant flow) flow waveform and a down ramp (decreasing flow waveform). In ventilators with peak flow controls, a square wave will result in a shorter inspiratory time, higher PIP, and lower mean airway pressure (as compared to a down ramp). In ventilators with peak flow controls, a down-ramp waveform will result in a longer inspiratory time, lower PIP, and higher mean airway pressure (as compared to a square wave). Ventilators with inspiratory time controls will vary the inspiratory flow based on the set tidal volume and inspiratory time. Changes in flow waveform in these ventilators will affect PIP and mean airway pressure. In general, flow waveforms that increase mean airway pressure will tend to decrease PIP and vice versa. For VC-CMV, inspiratory time and respiratory rate determine the expiratory time and I:E ratio. In general, an I:E ratio of 1:2 or lower is preferred. For VC-IMV, mandatory and spontaneous breaths are interspersed allowing the patient to initiate a spontaneous inspiration following a mandatory breath. Thus, the patient has control of his or her spontaneous inspiratory time, spontaneous expiratory time, and spontaneous I:E ratio. We suggest an initial mandatory breath peak flow setting for VC-CMV and VC-IMV of 60 L/min with a range of 40 to 80 L/min for adult patients.27 In ventilators with an inspiratory time setting, we suggest an initial inspiratory time of 0.8 seconds with a range of 0.6 to 1.0 seconds for adult patients,27 although many patients do well with a slightly longer TI (e.g., 0.8 to 1.2 seconds). We also suggest using a down-ramp flow waveform for initial ventilator setup. This may later be adjusted based on patient assessment results. Box 6-9 summarizes initial ventilator settings for most adult patients when using assist/control volume ventilation (aka patient- or time-triggered VC-CMV). Clinical Focus 6-2 provides an example using VC-CMV.

BOX 6-9 Initial Ventilator Settings for Assist/Control Volume Ventilation (VC-CMV) Initial ventilator settings for most adults receiving volume ventilation in the assist/control mode are summarized as follows. Ventilator Control

Initial Setting

Tidal volume (VT)

8 mL/kg IBW (range 6 to 8 mL/kg); adjust to ensure Pplateau ≤ 28 to 30 cm H2O. ARDS patients may require smaller tidal volumes to maintain Pplateau ≤ 28 to 30 cm H2O. Some patients with neuromuscular disease may require larger tidal volume.

Rate

For assist/control (patient- or time-triggered ventilation), set the rate in the range of 12 to 14 breaths/min.

Peak flow or inspiratory time

For ventilators with peak flow control begin at 60 L/min (range 40 to 80 L/min). Adjust peak flow to ensure inspiratory flow meets or exceeds patient inspiratory demand. For ventilators with inspiratory time control, begin with an inspiratory time setting of 0.8 sec (range 0.6 to 1.0 sec). Adjust inspiratory time to ensure resultant flows meet or exceed patient demand and avoid patient–ventilator asynchrony.

Trigger sensitivity

Set pressure trigger –0.05 to –1.5 cm H2O. For flow, trigger set sensitivity at 1 to 2 L/min below baseline flow. Adjust trigger sensitivity to minimize trigger work without autocycling.

Flow waveform

Begin with a decreasing flow waveform (down ramp). A decreasing flow waveform will reduce PIP and increase inspiratory time (in ventilators with a peak flow control) and mean airway pressure and may improve distribution of inspired gases. Consider square wave to decrease inspiratory time and decrease mean airway pressures.

FIO2 (O2 percentage)

Begin with 100% O2 for patients in obvious distress or conditions that may require high initial O2 concentrations (e.g., multiple trauma, severe pneumonia, ARDS, carbon monoxide poisoning, pulmonary edema, and post-resuscitation cardiac arrest). If recent arterial blood gases and the patient’s condition (e.g., COPD) suggest that 100% O2 will not be necessary, you may begin with a moderate to high FIO2 (e.g., 0.40 to 0.70.) Careful assessment and monitoring (including continuous SPO2) should guide appropriate adjustment in FIO2 to obtain adequate arterial oxygenation at a safe oxygen concentration.

PEEP

Initial PEEP setting for most patients is 5 cm H2O.

Humidification

For heated humidification, adjust to obtain a temperature at the proximal airway of 35° to 37°C. A heat moisture exchanger may suffice for some patients.

Alarms and limits

Set appropriate volume and pressure alarms and limits to ensure safe and effective ventilation (see Table 6-4)

TABLE 6-4

Initial Ventilator Alarm Settings for Adult Patients* Alarm

Initial setting

Adjusted value

Low-pressure limit

8 cm H2O

5 to 10 cm H2O below PIP

High-pressure limit

40 cm H2O

10 cm H2O above PIP; avoid PIP exceeding 40 cm H2O

Low PEEP/CPAP

3 to 5 cm H2O below initial PEEP setting to begin

2 cm H2O below PEEP/CPAP

Low VT

100 mL below set VT

100 mL below actual VT

Low V̇E

1 to 2 L/min below set V̇E

1 to 2 L/min < actual V̇E

High V̇E

5 L/min or 50% above set V̇E

5 L/min or 50% above actual V̇E

Apnea

20 seconds

20 seconds

Apnea backup ventilation

Set VT and f for full ventilatory support in the event of apnea

Set VT and f for full ventilatory support in the event of apnea

High oxygen percentage

5% > set O2%

5% > actual O2%

Low oxygen percentage

5% < set O2%

5% < actual O2%

Humidifier temperature

35° to 37°C

35° to 37°C

Low humidifier temperature alarm

2°C below set temperature

2°C < actual temperature

High humidifier temperature alarm

1°C above set temperature

1°C above set temperature; do not exceed delivered temperature > 37°C

*The initial alarm settings should be set prior to patient connection to the ventilator. Ventilator alarms and limits should then be adjusted based on the patient’s response. Data from Hyzy RC. Modes of mechanical ventilation. In: Parsons PE, Finlay G (eds.) UpToDate; October 2018.

CLINICAL FOCUS 6-2 Initiating Assist/Control Volume Ventilation (aka VCCMV) A 50-year-old man presented to the emergency department complaining of shortness of breath, cough, yellow-colored sputum, and fever with chills for 2 weeks. The patient was extremely short of breath and on examination, the respiratory care clinician noted respiratory accessory muscle use, diaphoresis, and course crackles upon auscultation. Vital signs were heart rate of 126, respirations of 35, blood pressure 160/92 mmHg, SpO2 84% (while breathing room air), and oral temperature of 102° F. Chest radiographs demonstrated

bilateral infiltrates. Arterial blood gas was obtained after the patient was placed on a nasal cannula at 5 L/min: pH: 7.24 PaCO2: 68 mmHg PaO2: 48 mmHg SaO2: 0.83 HCO3-: 27 mEq/L NIV was considered; however, the decision was made to initiate invasive mechanical ventilatory support. Question 1: What initial mode of ventilation is appropriate for this patient? Assist/control volume ventilation (aka VC-CMV) to provide full ventilatory support is a good initial choice for most patients. Assist/control pressure-control ventilation (PC-CMV) or volume control-SIMV (VC-SIMV) could also be used to provide full ventilatory support for this patient. Question 2: With assist/control volume ventilation, what are appropriate choices for initial tidal volume (VT) and respiratory rate (f)? Initial tidal volume should be 8 mL/kg IBW (range 6 to 8 mL/kg) with a respiratory rate of 12 to 14 breaths/min. A rate in the range of 8 to 12/min may be necessary to ensure adequate expiratory time. Ideal body weight can be estimated based on the patient’s height using the following formula for males: IBW = 50 + 2.3 (height in inches – 60) If this patient is 5 ft 10 in tall (70 in) his estimated IBW would be: IBW = 50 + 2.3 (70 – 60) = 73 kg (or 168 lb). VT (desired) will be 8 mL/kg × 73 kg = 584 mL. Question 3. What’s an appropriate initial respiratory rate for this patient? While an initial respiratory rate of 12 to 14 breath/min should suffice, the respiratory care clinician can estimate the rate (f) based on the desired VT and minute ventilation (V̇E), where: V̇E = VT × f and f = V̇E ÷ VT Given the patient’s IBW of 73 kg, the target minute ventilation can be estimated at 100 mL/kg/min: Desired V̇E = IBW × 100 mL/kg/min = 73 kg ×

100 mL/kg/min = 7300 mL/min (7.3 L/min). Given a tidal volume of 584 mL, the rate needed to achieve this minute ventilation would be: f = V̇E ÷ VT = 7300 mL ÷ 584 mL = 12.5 breaths/min. The respiratory care clinician would then set the rate at 12 or 13 breaths/min. A rate as low as 8 to 12 breaths/min may be necessary to increase expiratory time and avoid air trapping. Initial FIO2 of 0.50 to 0.70 with a PEEP of ≤ 5 cm H2O (or as needed to offset autoPEEP) is a good place to start followed by rapid adjustment based on SpO2. Initial peak flow (e.g., ≥ 80 L/min) and inspiratory time (e.g., should allow for an expiratory time sufficient to allow complete exhalation, and avoid air trappingg and autoPEEP. As a point of interest, if initial time volume is 8 mL/kg IBW and initial rate is 12.5 breaths/min for any patient, the target minute ventilation will be 100 mL/kg.

Pressure Control With PC-CMV and PC-IMV using set-point breath targeting (aka assist/control pressure-control ventilation [PCV] and pressure-control SIMV) the clinician sets the inspiratory pressure, inspiratory time, and rate (f) for mandatory breaths. With these two modes, the inspiratory pressure waveform is a square wave while the inspiratory flow waveform is a decreasing flow that varies with the patient’s inspiratory effort. As noted above, inspiratory pressure is set to achieve the desired tidal volume while maintaining Pplateau ≤ 28 to 30 cm H2O. The inspiratory time setting and rate determine the expiratory time and I:E ratio. Inspiratory time may be set initially in the range of 0.6 to 1.0 seconds. For example, with an inspiratory time of 1.0 second and respiratory rate of 15 breaths per min, the respiratory cycle time will be 4 sec (60/15 = 4 sec); expiratory time will be 3 sec resulting in an I:E ratio of 1:3. Pressure-control inverse-ratio ventilation (PCIRV) may begin with an I:E ratio 1:1 and increase the I:E ratio based on patient response. We suggest that more conventional modes of lungprotective ventilation with appropriate levels of PEEP be applied before attempting PCIRV. With PC-CMV, the patient may trigger the ventilator more frequently than the set rate. In such cases, the inspiratory time will remain constant, while the expiratory time will decrease and I:E ratio will increase. With PC-IMV, the patient may intersperse spontaneous breaths with mandatory breaths. In such cases, the patient

will have control over his or her spontaneous inspiratory time, spontaneous expiratory time, and spontaneous I:E ratio. Box 6-10 summarizes initial ventilator settings for most adult patients when using assist/control pressure-control ventilation (aka patient- or time-triggered PC-CMV). Clinical Focus 6-3 provides an example of a ventilator initiation using PC-CMV.

BOX 6-10 Initial Ventilator Settings for Assist/Control Pressure-Control Ventilation (PC-CMV) Initial ventilator settings for most adults receiving pressure-control ventilation (PCV) in the assist/control mode are summarized as follows. Ventilator Control

Initial Setting

Pressure control

Begin at 15 to 20 cm H2O and adjust to obtain an expired tidal volume of 8 mL/kg IBW (range 6 to 8 mL/kg). Do not exceed Pplateau > 28 to 30 cm H2O. ARDS patients may require smaller tidal volumes as described in the ARDS Clinical Network Mechanical Ventilation Protocol Summary.a

Inspiratory time

Begin with an inspiratory time setting of 0.8 sec (range 0.6–1.0 sec, although many patients do well with TI 0.8 to 1.2 sec. Adjust inspiratory time to ensure resultant flow meets or exceeds patient demand; avoid patient–ventilator asynchrony. If possible, the inspiratory time and pressure-control settings should allow the inspiratory flow to decrease to zero prior to the initiation of the expiratory phase, as observed on the ventilator’s graphics flow–time display.

Rate

For assist/control (patient- or time-triggered ventilation) set the rate in the range of 12 to 14 breaths/min.

Trigger sensitivity

Set pressure trigger –0.05 to –1.5 cm H2O. For flow, trigger set sensitivity at 1 to 2 L/min below baseline flow. Adjust trigger sensitivity to minimize trigger work without autocycling.

Flow waveform and pressure rise time or slope

PCV results in a square wave pressure pattern and a decreasing flow waveform. Pressure rise time should be adjusted based on observation of the ventilator graphics pressure–time curve to ensure that there is not a pressure overshoot or spike at the beginning of inspiration, but that pressure rises quickly enough to meet the patient’s spontaneous inspiratory demand in spontaneously breathing patients.

FIO2 (O2 percentage)

Begin with 100% O2 for patients in obvious distress or conditions that may require high initial O2 concentrations (e.g., multiple trauma, severe pneumonia, ARDS, carbon monoxide poisoning, pulmonary edema, and post-resuscitation cardiac arrest). If recent arterial blood gases and the patient’s condition (e.g., COPD) suggest that 100% O2 will not be necessary, you may begin with a moderate to high FIO2 (e.g., 0.40 to 0.70.) Careful assessment and monitoring, (including continuous SPO2) should guide appropriate adjustment in FIO2 to obtain adequate arterial oxygenation at a safe oxygen concentration.

PEEP

Initial PEEP setting for most patients is 5 cm H2O.

Humidification

For heated humidification adjust to obtain a temperature at the proximal airway of 35°C–37°C. A heat moisture exchanger (HME) may suffice for some patients.

Alarms and limits

Set appropriate volume and pressure alarms and limits to ensure safe and effective ventilation (see Table 6-4).

aThe ARDSNet Protocol may be found at the ARDSNet website:

www.ardsnet.org/files/ventilator_protocol_2008-07.pdf.

CLINICAL FOCUS 6-3 Initiating Assist/Control Pressure-Control Ventilation (aka PC-CMV) The decision is made to intubate and ventilate a female ARDS patient using assist/control pressure control ventilation (aka PC-CMV). The patient is 65 inches (165 cm) in height. Question 1. What is an appropriate initial tidal volume goal for this patient? Initial tidal volume should be 8 mL/kg IBW with a respiratory rate to achieve an appropriate minute ventilation V̇E). Ideal body weight can be estimated based on the patient’s height using the following formula for females: IBW = 45.5 + 2.3 (height in inches – 60) If this patient is 65 in tall, her estimated IBW would be: IBW = 45.5 + 2.3 (65 – 60) = 57 kg (or 125 lb). VT (desired) will be 8 mL/kg × 57 kg = 456 mL. Question 2. What is an appropriate initial respiratory rate for this patient? While an initial respiratory rate of 12 to 14 breath/min may suffice, the respiratory care clinician can estimate the rate (f) based on the desired VT and minute ventilation (V̇E) where: and f = V̇E ÷ VT Given the patient’s IBW of 57 kg, the target minute ventilation can be estimated at 100 mL/kg/min: Desired V̇E = IBW × 100 mL/kg/min = 57 kg × 100 mL/kg/min = 5700 mL/min (5.7 L/min). Given a target tidal volume of 456 mL, the rate needed to achieve this minute ventilation would be: f = V̇E ÷ VT = 5700 mL ÷ 456 mL = 12.5 breaths/min. The respiratory care clinician would then set the rate at 12 or 13 breaths/min.

Question 3. What is an appropriate initial pressure control, inspiratory time, and PEEP for this patient? Pressure control can be initially set at 15 cm H2O above PEEP; initial PEEP should be set at 5 cm H2O. Tidal volume delivery should then be immediately assessed, and pressure-control level adjusted to achieve the target VT of about 460 mL, while at the same time assuring that Pplateau < 30 cm H2O. The ARDSNet Protocola suggests that VT then be reduced by 1 mL/kg at intervals of ≤ 2 hours until VT is 6 mL/kg, or about 340 mL for this patient. As VT is reduced, appropriate increases in rate (up to 35 breaths /min) should be made to maintain V̇E. aThe ARDSNet Protocol may be found at the ARDSNet website:

www.ardsnet.org/files/ventilator_protocol_2008-07.pdf.

With PSV (aka PC-CSV), when used as a primary mode of ventilation, the clinician sets the inspiratory pressure-support level to achieve a desired tidal volume. The patient triggers and cycles each breath and thus controls his or her inspiratory time, expiratory time, I:E ratio, and rate. RC Insight Pressure-control ventilation is a good option for patients with ARDS to maintain safe airway pressures, while providing effective ventilation.

Pressure Rise Time or Slope Most modern ventilators allow for adjustment of rise time (aka pressure slope) and expiratory sensitivity during PSV and these adjustments will alter the inspiratory pressure and flow waveforms. The inspiratory pressure rise time control adjusts the rate at which gas flow increases during inspiration. Normally, the rise time is adjusted so that there is not a pressure spike on the pressure–time scalar at the beginning of inspiration. Rise time should also be adjusted such that initial gas flow to the patient meets or exceeds the patient’s inspiratory demand. With PSV inspiratory gas flow declines until the flow termination criteria is met (e.g., 5% to 25% of peak inspiratory flow). Expiratory sensitivity allows for adjustment of the flow termination criterion to ensure the ventilator and patient cycle are in sync in terms of the beginning of the expiratory phase and cycle asynchrony does not occur.

With pressure-control ventilation, the clinician can set the rise time; the cycle variable is time.

Inspiratory Pause With VC-CMV and VC-IMV using set-point breath targeting (aka assist/control volume ventilation and volume SIMV) the clinician may set an inspiratory pause or inspiratory hold. Clinicians and automated monitoring systems routinely use a brief inspiratory pause (0.5 to 2.0 sec) to measure patients’ Pplateau and calculate compliance and resistance. The application of an inspiratory pause will increase inspiratory time, decrease expiratory time, increase I:E ratio, and increase mean airway pressure. A brief inspiratory pause (e.g., 10%) may improve distribution of inspired gases, improve PaO2, and improve aerosol medication delivery.27 An inspiratory pause may also be used to ensure a full inspiration (e.g., 1-sec inspiratory pause) before a chest radiograph is obtained.27 Caution should be employed beyond intermittent use of an inspiratory pause to measure Pplateau in spontaneously breathing patients to avoid causing or worsening patient–ventilator asynchrony. An inspiratory pause will also increase mean airway pressure, which could be problematic in patients with hemodynamic instability.

Expiratory Time Expiratory time for continuous mandatory ventilation is a function of inspiratory time, and respiratory rate. Depending on the ventilator employed and the mode in use, inspiratory time may be set directly OR be determined by the tidal volume, peak flow, and flow waveform. Expiratory time should allow for complete exhalation of inspired gases prior to the initiation of the next breath. This is especially important in patients with obstructive lung disease (e.g., asthma, COPD) to avoid the development of autoPEEP and pulmonary over inflation. AutoPEEP may also cause patients to have difficulty triggering the ventilator. Steps to correct for autoPEEP include using smaller tidal volumes, decreasing inspiratory time, increasing expiratory time, and reducing mandatory breath rate. Small amounts of extrinsic PEEP to balance autoPEEP may be useful in patients have triggering difficulty.

I:E Ratio

For ventilator initiation, we recommend that adjustments in inspiratory time, expiratory time, and respiratory rate achieve an initial I:E ratio of 1:2 or lower. Methods to alter expiratory time and I:E ratio will vary, depending on the mode in use and available controls (e.g., peak flow, respiratory rate, and inspiratory time). Box 611 summarizes initial ventilator settings for most adult patients when using volume control or pressure control intermittent mandatory ventilation (aka VC-SIMV or PCSIMV). Clinical Focus 6-4 provides an example using IMV/SIMV.

BOX 6-11 Initial Ventilator Settings for Intermittent Mandatory Ventilation (VC-IMV or PC-IMV) Intermittent mandatory ventilation (IMV) intersperses mandatory breaths with spontaneous breathing. Spontaneous breaths may be pressure supported using pressure-support ventilation (PSV) or automatic tube compensation (ATC). IMV is most commonly provided as volume-SIMV (aka VC-SIMV), although many modern critical care ventilators allow for the use of pressure control-SIMV (aka PC-IMV) or various other targeting schemes. With SIMV, the ventilator is often initially adjusted to provide full ventilatory support. Initial ventilator settings for VC-IMV and PC-IMV are described below. Ventilator Control

Initial Setting

Tidal volume (VT) and inspiratory pressure

For VC-IMV initial VT may be set at 8 mL/kg IBW (range 6 to 8 mL/kg); adjust to ensure Pplateau ≤ 28 to 30 cm H2O. For PC-IMV set initial pressure-control value in the range of 15 to 20 cm H2O and adjust to achieve an adequate VT.

Rate

Initially set the IMV rate in the range of 12 to 14 breaths/min to achieve full ventilatory support.

Peak flow or inspiratory time

For volume ventilators with peak flow control begin at 60 L/min (range 40 to 80 L/min). Adjust peak flow to ensure mandatory breath inspiratory flow meets or exceeds patient inspiratory demand. For ventilators with inspiratory time control, begin with an inspiratory time setting of 0.8 sec (range 0.6 to 1.0 sec although some patients do well with a TI 0.8 to 1.2 sec. Adjust inspiratory time to ensure resultant flows meet or exceed patient demand and avoid patient–ventilator asynchrony.

Trigger sensitivity

Set pressure trigger –0.05 to –1.5 cm H2O. For flow, trigger set sensitivity at 1 to 2 L/min below baseline flow. Adjust trigger sensitivity to minimize trigger work without autocycling.

Flow waveform for the mandatory breaths

For VC-IMV begin with a decreasing flow waveform (down ramp) and adjust, if needed. PC-IMV provides a square wave-like pressure pattern with a decreasing flow waveform. The pressure waveform may be modified by adjusting the pressure rise time or slope.

Pressure support

PSV generally is provided for spontaneous breaths in the range of 5 to 15 cm H2O to overcome the WOBI due to artificial airways. Automatic tube compensation (ATC) is also available on most modern critical care ventilators when used in the IMV/SIMV mode.

FIO2 (O2 percentage)

Begin with 100% O2 for patients in obvious distress or conditions that may require high initial O2 concentrations (e.g., multiple trauma, severe pneumonia, ARDS, carbon monoxide poisoning, pulmonary edema, and post-resuscitation cardiac arrest). If recent arterial blood gases and the patient’s condition (e.g., COPD) suggest that 100% O2 will not be necessary, you may begin with a moderate to high FIO2 (e.g., 0.40 to 0.70). Careful assessment and monitoring (including continuous SpO2) should guide appropriate adjustment in FIO2 to obtain adequate arterial oxygenation at a safe oxygen concentration.

PEEP

Initial PEEP setting for most patients is 5 cm H2O.

Humidification

For heated humidification adjust to obtain a temperature at the proximal airway of 35°C to 37°C. A heat moisture exchanger (HME) may suffice for some patients.

Alarms and limits

Set appropriate volume and pressure alarms and limits to ensure safe and effective ventilation (see Table 6-4).

CLINICAL FOCUS 6-4 Initiating Volume SIMV (VC-IMV) A 38-year-old male arrived unresponsive in the emergency department. He was suspected of taking an overdose of an unknown substance. An arterial blood gas sample taken on room air reveals: pH: 7.15 PaCO2: 80 mmHg PaO2: 38 mmHg SaO2: 0.78 HCO3–: 28 mEq/L The decision is made to intubate and ventilate this patient using volume SIMV (aka VC-IMV). The patient is approximately 72 inches in height (6 ft). Question 1. What are appropriate initial ventilator settings for rate (f) and tidal volume (VT) this patient? Initial VT should be 8 mL/kg IBW. The patient’s ideal body weight can be calculated using the following formula for males: IBW = 50 + 2.3 (height in inches – 60) IBW = 50 + 2.3 (72 – 60) = 77.6 kg (or 168 lb).

VT (desired) will be 8 mL/kg × 77.6 kg = 620.8 mL. SIMV rate can be set in the range of 12 to 14 breaths/min to achieve a V̇E of 100 mL/min/kg IBW or 7760 mL/min. Question 2. What are appropriate initial ventilator settings for this patient for peak flow, flow wave form, trigger sensitivity, and FIO2? The peak flow should be initially set at 60 L/min (range 40 to 80 L/min) and then adjusted to ensure that peak flow meets or exceeds the patient’s inspiratory flow demand. In ventilators with inspiratory time control, an initial setting of 0.8 seconds (range 0.6 to 1.0 sec) is a good place to start. Most modern critical care ventilators allow the respiratory care clinician to choose between a square wave and down ramp flow waveform. We suggest Initiating ventilation with a down ramp. This may then be adjusted following ventilator initiation. Trigger sensitivity should be adjusted to ensure minimal trigger work without autocycling. This generally corresponds to a pressure trigger of 0.5 to –1.5 cm H2O or flow trigger of 1 to 2 L/min below baseline bias flow. This patient was experiencing severe hypoxemia while breathing room air. FIO2 should be initiated at 1.0 or 100% O2. Question 3. What is an appropriate initial ventilator setting for PSV? SIMV allows for spontaneous breathing to be interspersed with mandatory IMV breaths. Some form of pressure augmentation should be provided with SIMV to compensate for the WOBI due to the endotracheal tube. Pressure augmentation may be provided using PSV or automatic tube compensation. For PSV an initial setting of 5 to 15 cm H2O is appropriate. Following ventilator initiation, the PSV needed to overcome the resistance of the endotracheal tube can be estimated as follows: PSV = (PIP – Pplateau) × the patient’s spontaneous inspiratory flow rate. Following ventilator initiation, the patient’s peak inspiratory pressure (PIP) was 35 cm H2O and plateau pressure (Pplateau) was 21 cm H2O. During spontaneous breathing in between mandatory SIMV breaths, the patient’s spontaneous inspiratory flow rate was 0.5 L/sec or 30 L/min. PSV needed to overcome the WOBI for this patient was: PSV = (PIP – Pplateau) × the patient’s spontaneous inspiratory flow rate. PSV = (35 cm H2O – 21 cm H2O) × 0.5 L/sec = 7 cm H2O.

FIO2 (Oxygen Percentage) In general, the safest option for initial oxygen concentration (FIO2) is 1.0 (100% O2) followed by patient assessment, observation of changes in pulse oximetry values (SpO2), and arterial blood gas measurement.2 Beginning with 100% oxygen is especially important in patients for whom little information is available or those in obvious distress. Disease states or conditions that may require high initial oxygen concentrations include severe pneumonia, ARDS, cardiac arrest following resuscitation, severe trauma, acute pulmonary edema, near-drowning, smoke inhalation, suspected aspiration, and carbon monoxide poisoning.27 Many of these conditions increase pulmonary shunt, which generally is less responsive to oxygen therapy. FIO2 should then be quickly reduced (if possible) to avoid the development of absorption atelectasis and oxygen toxicity. In many patients FIO2 may be rapidly titrated downward based on SpO2 monitoring and clinical assessment. The end goal is to achieve an adequate arterial oxygen level (PaO2 ≥ 60 mmHg, SaO2 ≥ 0.90) at a safe FIO2 (≤ 0.50 to 0.60). PEEP or CPAP may help achieve this goal. Some patients require mechanical ventilatory support due to extra pulmonary conditions (e.g., anesthesia, drug overdose, head trauma, neuromuscular disease, and spinal cord injury). These patients may have normal or near-normal lungs and may respond well to low to moderate initial concentrations of oxygen (e.g., FIO2 of 0.40 to 0.50). Certain disease states associated with low V̇/Q̇ (but not shunt) also often respond well to low to moderate concentrations of oxygen therapy. These include asthma, emphysema, chronic bronchitis, and COPD. There may also be patients for whom a great deal of information is available including recent arterial blood gases, suggesting adequate arterial oxygenation can be achieved with low to moderate concentrations of oxygen. In such cases, the clinician may choose to begin with a moderate concentration of oxygen (e.g., 40% to 50%) based on prior blood gases and the patient’s clinical condition. That said, when in doubt begin with 100% O2 and titrate down based on the patient’s oxygen saturation. RC Insight In general, the safest option for initial oxygen concentration is 100% O2.

PEEP and CPAP As described earlier, patients with acute restrictive pulmonary disease (e.g., ARDS, severe pneumonia, or pulmonary edema) may develop hypoxemia due to unstable alveolar units that are collapsed. PEEP and CPAP can restore FRC, improve and maintain lung volumes, and improve oxygenation in such patients. PEEP/CPAP should be considered in such patients with inadequate arterial oxygen levels (PaO2 < 60 mmHg, SaO2 < 0.90) on moderate to high oxygen concentrations (FIO2 ≥ 0.40). Smaller tidal volumes and appropriate levels of PEEP are used in patients with ARDS to avoid VILI. With ARDS, properly applied PEEP can stabilize unstable lung units and avoid repetitive inflation and deflation of alveoli, thus reducing the likelihood of additional injury. Minimal PEEP/CPAP (3 to 5 cm H2O) generally is used to maintain FRC and provide physiologic PEEP. PEEP/CPAP may also be useful to offset autoPEEP and reduce trigger work in some patients. PEEP and CPAP must be used cautiously in patients with an already elevated FRC as may occur with obstructive lung disease (e.g., COPD, acute asthma). There are several approaches to the use of PEEP. These include minimal PEEP, optimal or best PEEP, compliance titrated PEEP, and the use of pressure–volume curves as part of a lung-protective strategy. For initial ventilator setup, however, we suggest that almost all patients initially receive 5 cm H2O of PEEP/CPAP.

Alarms and Limits Modern critical care ventilators have sophisticated alarms and monitoring systems. Ventilator alarms audibly and visually notify ICU personnel that specific parameters are not met, and the patient–ventilator system should be assessed. Ventilator malfunction alarms are normally set by the manufacturer, and include alarms for power loss, gas supply loss, electronic malfunction, or pneumatic malfunction. Certain patient status alarms can be set by the respiratory care clinician. These include alarms for maximum inspiratory pressure, low pressure, low PEEP, high and low tidal volume, high and low minute ventilation, high and low respiratory rate, oxygen percentage, humidification (temperature), and apnea.27 The respiratory care clinician should adjust the ventilator alarms to ensure patient safety without

becoming a nuisance that may be ignored. Limits should be adjusted prior to ventilator initiation. The high-pressure limit and high-pressure alarm may can be set at 40 cm H2O prior to connecting the patient to the ventilator to ensure that excessive pressures are not unintentionally delivered. Pressures are then reassessed and readjusted following initiation of mechanical ventilation with the goal of maintaining safe inspiratory pressures (e.g., Pplateau ≤ 28 to 30 cm H2O, PIP ≤40 cm H2O). Ventilator adjustments can be made to reduce Pplateau and PIP if necessary following ventilator initiation. Table 6-4 lists suggested initial alarm settings for adult mechanical ventilation.

Humidification Humidification should be provided for all patients receiving invasive mechanical ventilatory support. Clinical practice guidelines for heated humidifiers suggest an inspired gas temperature of 35°C ± 2°C to provide humidity of 33 to 44 mg H2O/L at the patient Y connection. Heat and moisture exchangers (HME) may be appropriate for some patients. HMEs should not be used in patients receiving low tidal volumes as they add additional mechanical dead space. HMEs are also not recommended for use with noninvasive ventilation.

Patient Assessment Following initiation of mechanical ventilation, the patient and patient–ventilator system should be carefully assessed. This should include physical assessment, breath sounds, oximetry, heart rate, blood pressure, and observation of the cardiac monitor for cardiac rhythm. The patient–ventilator system should be assessed for ventilatory pressures, volumes, and flows. Arterial blood gases are usually obtained following initial patient stabilization. Following assessment, necessary changes in ventilatory parameters should be made to ensure patient safety, comfort, oxygenation, and ventilation. Chapter 7 describes patient stabilization and ventilator adjustments following ventilator initiation.

Management of Specific Disease States and Conditions Management of patients with specific disease states and conditions can be complex. A few of the key factors that should be considered for mechanical ventilation in specific situations are described below.

Asthma Ventilation of patients with severe asthma can be extremely challenging. Lower tidal volumes (e.g., 6 to 8 mL/kg IBW) should be used to reduce airway pressures and avoid barotrauma; Pplateau should be maintained ≤ 30 cm H2O.36,37 Care must be taken to ensure adequate I:E ratios and sufficient expiratory time to allow for complete exhalation in the presence of airway obstruction. Lower respiratory rates (e.g., 10 to 12 breaths/min) and higher inspiratory flow (e.g., 60 to 80 L/min) should be employed.36,37 Patient–ventilator asynchrony should be avoided, and adjustment of tidal volume, respiratory rate, inspiratory flow, inspiratory time, and trigger sensitivity may be necessary. PEEP may be set at ≤ 5 cm H2O or at 50% to 80% of measured autoPEEP, if present. Some patients may require the use of paralytic agents to control ventilation and permissive hypercapnia may sometimes be used to ensure airway pressures are not excessive. Oxygen concentrations should be adjusted to achieve adequate arterial oxygenation (e.g., SPO2 ≥ 90%).

Acute Exacerbation of COPD Mechanical ventilatory support may be necessary for patients with severe exacerbation of COPD.36,38 NIV is often a good option for these patients in the presence of acute respiratory acidosis. Other indications for NIV include severe dyspnea with respiratory muscle fatigue, increased WOB, or persistent hypoxemia unresponsive to supplemental oxygen therapy36,38 NIV can be delivered by facemask, nasal mask, or nasal pillows. Initial settings may include patient-triggered breaths with inspiratory pressure in the range of 8 to 20 cm H2O and end-expiratory pressure in the range of 3 to 5 cm H2O.36,38 Inspiratory pressure is then adjusted based on measured tidal volume and respiratory rate. Some patients may be unable to tolerate NIV and require invasive mechanical ventilation. Initial ventilator settings generally include assist/control volume

ventilation with a tidal volume in the range of 6 to 8 mL/kg, backup rate of 10 to 12 breaths/min, and inspiratory flow of 60 to 80 L/min.36,38 Lower tidal volumes (e.g., 6 mL/kg), lower rates (e.g., 8 to 10), and higher initial peak flow (≥ 80 L/min or inspiratory time of 0.6 to 0.80 sec) may be necessary to allow for sufficient expiratory time. Care should be taken to avoid excessive pressures (e.g., maintain Pplateau ≤ 30 cm H2O). Trigger sensitivity should be set to minimize trigger work without autotriggering. Adequate expiratory time should be provided to avoid air trapping and autoPEEP. Moderate FIO2s will often suffice (e.g., 0.40 to 0.50). FIO2 is adjusted to maintain adequate arterial oxygen levels (e.g., SpO2 ≥ 92%, PaO2 ≥ 60 mmHg). Patients who rapidly trigger the ventilator in the assist/control mode may do well with SIMV. If SIMV is employed, tidal volume, inspiratory peak flow, and inspiratory time should be set at values similar to those used for assist/control volume ventilation. Pressure support (5 to 10 cm H2O) should be added to reduce the WOBI due to the endotracheal tube. In the presence of autoPEEP resulting in triggering difficulty, small amounts of extrinsic PEEP (3 to 5 cm H2O) may be applied, generally at about 50% to 80% of the measured autoPEEP level.

Severe Pneumonia Mechanical ventilation may be necessary in pneumonia patients with severe respiratory failure to maintain oxygenation, ventilation, and acid-base balance.36,39 Assist/control volume ventilation (VC-CMV) or volume-SIMV with pressure support will be effective for most patients. Initial VT and f may be set at 8 mL/kg IBW and 14 to 16 breaths/min (respectively) with sufficient inspiratory flow and time settings (e.g., 60 to 80 L/min or 0.6 to 0.8 sec) to meet or exceed the patient’s inspiratory demand.36,39 Unless recent blood gases and the patient’s condition indicate otherwise, it is usually best to begin FIO2 at 1.0 and PEEP of 5 cm H2O. FIO2 and PEEP are then titrated to achieve an adequate arterial oxygenation at a safe FIO2. Respiratory rate and tidal volume are adjusted to maintain adequate alveolar ventilation, while avoiding excessive pressures (e.g., keep Pplateau < 30 cm H2O). A lung-protective ventilation strategy is then employed (see ARDS below).36,39

Acute Respiratory Distress Syndrome

Patients with severe ARDS often require intubation and mechanical ventilation. Initially, very high oxygen concentrations may be required, and it generally is best to begin ventilation with 100% O2. As soon as is feasible, FIO2 and PEEP are titrated to achieve adequate oxygenation at a safe FIO2. Lower tidal volumes are used as part of a lung-protective strategy to avoid ventilator-associated lung injury.36,39 Ventilation is usually initiated to achieve full ventilatory support. Assist/control volume ventilation (aka VC-CMV) or assist/control pressure/control ventilation (aka PC-CMV) generally is effective. Initial tidal volume may be set at 8 mL/kg IBW and respiratory rate adjusted to achieve an adequate minute ventilation (e.g., 100 mL/min/kg IBW).36,39 Tidal volume is then progressively reduced to 7 mL/kg and then to 6 mL/kg over the next 1 to 3 hours.36,39 As tidal volume is reduced, respiratory rate is increased to maintain minute ventilation. Respiratory rate may be adjusted up to 35 breaths/min. Additional tidal volume adjustments may be made to maintain Pplateau < 30 cm H2O. PEEP is employed to facilitate alveolar recruitment and reduce end expiratory alveolar collapse. Several PEEP strategies have been suggested for ARDS patients. A good strategy for most patients is to adjust the PEEP to the lowest level that results in an adequate PaO2 with an FIO2 ≤ 0.60. To begin, we suggest in initial PEEP of 5 to 8 cm H2O. Other strategies to improve oxygenation include recruitment maneuvers, pressure-control inverse-ratio ventilation, and prone positioning. Various open lung and PEEP strategies are discussed in Chapters 7 and 8. Slightly larger tidal volumes (e.g., 8 to 10 mL/kg) may be acceptable if Pplateau remains ≤ 28 to 30 cm H2O.3

Neuromuscular Disease Mechanical ventilatory support is sometimes required in patients with neuromuscular disease. NIV can often be effective in these patients and should be considered. Acutely ill patients, however, may require invasive mechanical ventilatory support.35 Assist/control volume ventilation (aka VC-CMV) or volume SIMV (VC-IMV) to provide full ventilatory support generally is effective. Initially, tidal volume may be set at 8 mL/kg IBW with a respiratory rate of 12 to 16 breaths/min to achieve a desired minute ventilation (e.g., 100 mL/kg/min).35 Initial inspiratory peak flow or inspiratory time may be set at 60 to 80 L/min (0.8 to 1.0 sec inspiratory time) with a down ramp

flow waveform. Trigger sensitivity should be adjusted to ensure minimal trigger effort without autocycling. If IMV/SIMV is employed, pressure support starting at 5 cm H2O or automatic tube compensation should be used to overcome the WOBI associated with the artificial airway. Often, patients with neuromuscular disease, head trauma, or spinal cord injury have otherwise normal lungs. These patients may initially only require moderate concentrations of oxygen (e.g., 0.40 to 0.50). Initial FIO2 may be 1.0 if the patient is in distress or recent oximetry or blood gases suggest the need for a high initial oxygen concentration. Patients with neuromuscular disease and otherwise normal or near-normal lungs may benefit from the use of slightly larger tidal volumes (e.g., 8 to 10 mL/kg) to prevent the development of atelectasis. Some neuromuscular care units begin with tidal volumes in the range of 10 to 12 mL/kg IBW and quadriplegic patients with high spinal cord injury (C3 to C4) may achieve more rapid ventilator weaning with larger tidal volumes (> 20 mL/kg IBW).40

Summary Indications for mechanical ventilation include apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. Mechanical ventilatory support may be provided using noninvasive ventilation or invasive ventilation requiring endotracheal intubation or tracheostomy. Mechanical ventilation is usually initiated to provide full ventilatory support; partial ventilatory support modes may be appropriate in certain circumstances. Conventional modes of ventilation include assist/control volume ventilation, also known as volume control-continuous mandatory ventilation (VC-CMV); assist/control pressure-control ventilation, also known as pressure control-continuous mandatory ventilation (PC-CMV) and intermittent mandatory ventilation (IMV/SIMV). There are also a large number of alternative modes that have been used to safely and effectively provide ventilatory support to critically ill patients. While these newer modes may have theoretic advantages, none has been shown to consistently improve patient outcomes as compared to more conventional approaches. Ventilator initiation requires important choices, including whether to provide invasive or noninvasive ventilation, type of airway or ventilator interface, and whether to provide full or partial ventilatory support. The respiratory care clinician must also select the mode of ventilation and specific ventilator to be employed and the initial ventilator settings. These include initial pressures, volumes, and flows provided, as well as oxygen concentration, PEEP/CPAP, humidification, and ventilator alarms and limits. Careful patient observation and assessment must follow ventilator initiation and appropriate adjustments made. The goal is to ensure safe, comfortable support that achieves adequate tissue oxygenation, alveolar ventilation, and acid-base homeostasis while minimizing the WOB.

Key Points The primary function of a mechanical ventilator is to augment or replace normal ventilation. The four major indications for mechanical ventilation are apnea, acute ventilatory failure, impending ventilatory failure, and severe oxygenation problems. The major goals of mechanical ventilation are to provide adequate alveolar ventilation, ensure adequate tissue oxygenation, restore and maintain acid-base balance, and reduce the work of breathing. The tank ventilator or iron lung was developed by Drinker, McCann, and Shaw at Harvard University in 1928 and saw widespread use as the Emerson iron lung during the polio epidemics in the 1940s and 50s. Negative-pressure ventilators maintain the natural airway, which allows patients to talk and eat; however, it is challenging to access the patient for procedures, bathing, or turning and they are large, bulky, and difficult to maneuver. The most common trigger variables are time and patient effort (i.e., patient triggered). The common types of patient triggers are flow trigger and pressure trigger. Commonly used terms include assist breath, which is patient triggered, control breath, which is time triggered, and assist/control, which can be patient or time triggered. Controlled ventilation refers to time-triggered ventilation and requires apnea. Cycle variables include volume, pressure, flow, and time. With volume-control ventilation, a constant tidal volume is delivered; however, inspiratory pressure varies with changes in the patient’s compliance and resistance. With pressure-control ventilation, a constant inspiratory pressure is delivered; however, tidal volume varies with changes in the patient’s compliance, resistance, and inspiratory effort. Pressure-support ventilation (PSV) is patient triggered, pressure limited, and flow cycled. Pressure-control ventilation (PCV) may be time or patient triggered and is pressure limited and time cycled. With continuous mandatory ventilation (CMV), every breath is a mandatory breath. With intermittent mandatory ventilation (IMV), mandatory breaths are interspersed with spontaneous breaths. With continuous spontaneous ventilation (CSV), the patient initiates and terminates each breath; however, inspiratory pressure augmentation may be provided (e.g., PSV or automatic tube compensation [ATC]). Noninvasive ventilation (NIV) may be indicated for patients with acute

exacerbation of COPD with hypercapnic acidosis, cardiogenic pulmonary edema, and acute hypoxemic respiratory failure. NIV may also be useful to prevent postextubation respiratory failure and in the support of patients with chronic hypoventilation due to neuromuscular or chest wall disease. NIV should not be used in patients with cardiac or respiratory arrest, hemodynamic or cardiac instability, or severely impaired consciousness. Indications for endotracheal intubation include the inability to maintain a patent airway, inability to protect the airway against aspiration, failure to ventilate, failure to oxygenate, and anticipation of deterioration in the patient’s condition that will lead to respiratory failure. Endotracheal intubation is the most common method to achieve invasive ventilatory support; however, tracheostomy should be considered in certain patients. Factors that should be considered when choosing a ventilator include clinical goals, the patient’s needs, availability, reliability, ventilator features, alarms and monitoring capabilities, modes available, cost, and (most importantly) clinician’s familiarity with the ventilator. The mode of ventilation can be described by the control variable, breath sequence, and targeting scheme employed. Common control variables are pressure control (PC) and volume control (VC) for the primary breath. With full ventilatory support, adequate alveolar ventilation is achieved even if the patient makes no spontaneous breathing efforts. Partial ventilatory support requires the patient to provide a portion of the work needed to maintain an acceptable PaCO2. High airway pressures may result in barotrauma or VILI. The five major modes of ventilation are VC-CMV, PC-CMV, VC-IMV, PC-IMV, and PC-CSV. These modes may be supplemented with PEEP or CPAP. Advantages of VC-CMV include constant tidal volume delivery in the face of changes in compliance and resistance, provision of full ventilatory support, and reduced or eliminated work of breathing; however, unsafe airway pressures may result. Advantages of PC-CMV include a constant inspiratory pressure in the face of changes in compliance and resistance, allowing for maintenance of a safe Pplateau ≤ 28 to 30 cm H2O. IMV incorporates spontaneous breathing, which maintains ventilatory muscle activity and may help maintain ventilatory muscle strength and coordination. IMV may be used to provide full or partial ventilatory support; IMV may delay weaning as compared to spontaneous breathing trials (SBTs). Pressure-control inverse-ratio ventilation (PCIRV) is a form of PC-CMV that may

improve oxygenation in patients with acute, severe hypoxemia that is unresponsive to conventional ventilation. Automatic tube compensation (ATC) is designed to overcome the imposed work of breathing due to an endotracheal or tracheostomy tube during spontaneous breathing. CPAP may help maintain FRC and improve oxygenation in spontaneously breathing patients. Other modes of ventilation include adaptive pressure control, (APC), mandatory minute ventilation (MMV), adaptive support ventilation (ASV), airway pressurerelease ventilation (APRV), proportional assist ventilation (PAV), automode, neutrally adjusted ventilatory assist (NAVA), and high-frequency ventilation. Adaptive pressure control (APC) automatically adjusts pressure-control or pressure-support levels to achieve the desired tidal volume. Pressure-regulated volume control (PRVC) and volume support (VS) are considered forms of APC. Mandatory minute ventilation (MVV) automatically adjusts the level of support provided to achieve a target minute ventilation. Adaptive support ventilation (ASV) automatically adjusts respiratory rate and inspiratory pressure to deliver the desired minute ventilation and minimize the work of breathing. Airway pressure-release ventilation (APRV) allows for two levels of CPAP that are time triggered and time cycled. Proportional assist ventilation (PAV) automatically adjusts the level of ventilatory support based on the patient’s inspiratory effort, calculated work of breathing, and clinician-set percentage of support to be provided. Automode is a form of IMV that incorporates a targeting scheme for both primary and secondary breaths based on the modes selected. Neurally adjusted ventilatory assist (NAVA) uses the electrical discharge from the diaphragm to trigger and cycle ventilator breaths. High-frequency ventilation uses small tidal volumes and very high respiratory rates; possible indications include ARDS, bronchopleural fistula, and air leaks. There are currently four major types of HFV: high-frequency positive-pressure ventilation (HFPPV), high-frequency percussive ventilation (HFPV), highfrequency jet ventilation (HFJV), and high-frequency oscillatory ventilation (HFOV). Assist/control volume ventilation, also known as VC-CMV, is a good initial mode choice for most patients. An acceptable alternative to assist/control volume ventilation is assist/control pressure-control ventilation (also known as PC-CMV); this mode requires careful attention to the delivered tidal volume. Pressure-support ventilation (PSV) can be used as the primary mode of

ventilation when patients have a consistent, stable, spontaneous ventilatory pattern. SIMV is a serviceable option for initial ventilator setup, although it is used less commonly. Initial tidal volume (adults) may be set in the range of VT 6 to 8 mL/kg IBW with the rate of 12 to 16 breaths/min; smaller tidal volumes and faster rates may be required for some ARDS patients. Tidal volume should be adjusted to ensure that Pplateau ≤ 28 to 30 cm H2O with a peak inspiratory pressure (PIP) < 40 cm H2O. Intermittent sigh breaths have been used in the past to prevent development of atelectasis; routine use of PEEP may eliminate the need for an intermittent sigh. Patient-triggered breaths may be negative pressure or flow triggered; trigger sensitivity should be set to minimize trigger work while avoiding autotriggering. Most modern ventilators allow for the adjustment of rise time and expiratory sensitivity during PSV. An inspiratory pause allows for the measurement of the plateau pressure (Pplateau) and calculation of compliance and resistance. I:E ratio should be 1:2 or lower for most patients. In general, the safest option for initial oxygen concentration is 100%. PEEP/CPAP may improve and maintain lung volumes and improve oxygenation in patients with acute restrictive pulmonary disease. Initial PEEP/CPAP of 5 cm H2O is appropriate for most patients. Ventilator alarms and limits are to ensure patient safety and should be adjusted to alert ICU personnel that the patient–ventilator system should be assessed. Heated humidification should be provided at 35°C ± 2°C; heat and moisture exchangers (HME) may be appropriate for some patients. A careful assessment should be done immediately following ventilator initiation and appropriate ventilator adjustments should be made to ensure patient safety, comfort and effective gas exchange.

References 1. Kacmarek RM, Stoller JK, Heuer AJ. Physiology of ventilatory support. In: Kacmarek RM, Stroller JK, Heuer AJ, Chatburn RL, Kallet RH (eds.). Egan’s Fundamentals of Respiratory Care. 11th ed. St. Louis, MO: Elsevier; 2017: 1016–1057. 2. Hess DR, MacIntyre NR, Galvin WF, Mishoe SC. Mechanical ventilation. In: Hess DR, MacIntyre NR, Galvin WF, Mishoe SC (eds.). Respiratory Care: Principles and Practice. 3rd ed. Burlington, MA: Jones & Bartlett Learning; 2016: 493–531. 3. Petrucci N, Feo CD, Iacovelli W. Lung protective ventilation strategy for the acute respiratory distress syndrome. Cochrane Database Syst Rev. 2007;3:1–32. doi:10.1002/14651858.cd003844.pub3. 4. Chatburn RL, Volsko TA, Hess DR, et al. Mechanical ventilators: classification and principles of operation. In: Hess DR, MacIntyre NR, Galvin WF, Mishoe SC (eds.). Respiratory Care: Principles and Practice. 3rd ed. Burlington, MA: Jones & Bartlett Learning; 2016: 462–492. 5. Chatburn RL, El-Khatib M, Mireles-Cabodevila E. A taxonomy for mechanical ventilation: 10 fundamental maxims. Respir Care. 2014;59(11):1747–1763. doi:10.4187/respcare.03057. 6. Hyzy RC, McSparron JI. Noninvasive ventilation in acute respiratory failure in adults. In: Parsons PE, Finlay G (eds.). UpToDate; July 2018. 7. Nagler J, Cheifetz IM. Noninvasive ventilation for acute and impending respiratory failure in children. In: Randolph AG, Wiley JF (eds.). UpToDate; May 2018. 8. Hill NS, Kramer NR. Practical aspects of nocturnal noninvasive ventilation in neuromuscular and chest wall disease. In: Shefner JM, Parsons PE (eds.). UpToDate; October 2018. 9. Davies JD, Niven AS, Hess DR, et al. Airway management. In: Hess DR, MacIntyre NR, Galvin WF, Mishoe SC (eds.). Respiratory Care: Principles and Practice. 3rd ed. Burlington, MA: Jones & Bartlett Learning; 2016: 380–430. 10. Lafferty KA, Dillinger R. Rapid sequence intubation: background, indications, contraindications. Medscape. May 24, 2018. Available at emedicine.medscape.com/article/80222-overview. 11. Orebaugh S, Snyder JV. Direct laryngoscopy and endotracheal intubation in adults. In: Wolfson AB, Hagberg CA (eds.). UpToDate; 2018 12. De Leyn P, Bedert L, Delcroix M, et al. Tracheotomy: clinical review and guidelines. Eur J Cardio-Thoracic Surg. 2007;32:412–421. 13. Silvestri GA, Colice GL. Deciding timing and technique for tracheostomy. Contemp Intern Med. 1993;5(3):20–31. 14. Epstein S. Anatomy and physiology of tracheostomy. Respir Care. 2005;50(3):476–482. 15. Pierson, DJ. Tracheostomy and weaning. Respir Care. 2005;50(4):526–533. 16. Hyzy RC, McSparron JI. Overview of tracheostomy. In: King TE, Finlay G (eds.). UpToDate; July 2018. 17. Blot F, Melot C. Indications, timing, and techniques of tracheostomy in 152 French ICUs. Chest. 2005;127(4):1347–1352. 18. Griffiths J, Barber VS, Morgan J, Young JD. Systematic review and meta-analysis of studies of timing of tracheostomy in adult patients undergoing artificial ventilation. Br Med J. 2005;330(7502):1243. doi:10.1136/bmj.38467.485671.ED 19. Littlewood KE. Evidence-based management of tracheostomies in hospitalized patients, Respir Care. 2005;50(4):516–518. 20. Goldenberg D, Ari EG, Golz A, et al. Tracheotomy complications: a retrospective study of 1,130 cases. Otolaryngol Head Neck Surg. 2000;123(4):495–500. 21. Trouillet JL, Luyt CE, Guiguet M, et al. Early percutaneous tracheotomy versus prolonged intubation of mechanically ventilated patients after cardiac surgery: a randomized trial. Ann Intern Med. 2011;154(6):373–383. 22. Rumbak MJ, Newton M, Truncale T, et al. A prospective, randomized, study comparing early percutaneous dilatonal tracheotomy to prolonged translaryngeal intubation (delayed tracheotomy) in critically ill medical patients. Crit Care Med. 2004;32(8):1689–1694. 23. Bittner EA. Clinical use of neuromuscular blocking agents in critically ill patients. In: Parsons PE, Finlay G, Crowley M (eds.). UpToDate; December 2017. 24. Hyzy RC. Physiologic and pathophysiologic consequences of mechanical ventilation. In: Parsons PE, Finlay G (eds.). UpToDate; April 2018. 25. Hyzy RC, McSparron JI. Overview of mechanical ventilation. In: Parsons PE, Finlay G (eds.). UpToDate;

November 2018. 26. Hyzy RC. Modes of mechanical ventilation. In: Parsons PE, Finlay G (eds.). UpToDate; 2018. 27. Kacmarek RM, Stoller JK, Heuer AJ. Initiating and adjusting invasive ventilatory support. In: Kacmarek RM, Stroller JK, Heuer AJ, Chatburn RL, Kallet RH (eds.). Egan’s Fundamentals of Respiratory Care. 11th ed. St. Louis, MO: Elsevier; 2017:1078–1110. 28. Cairo JM. Special techniques and ventilatory support. In: Cairo JM (ed.). Pilbeam Mechanical Ventilation: Physiological and Clinical Applications. 6th ed. Maryland Heights, MO: Elsevier; 2016:443–485. 29. Epstein SK, Walkey A. Methods of weaning from mechanical ventilation. In: Parsons PE, Finlay G (eds.). UpToDate; July 2018. 30. Cairo JM. Selecting the ventilator and the mode. In: Pilbeam Mechanical Ventilation: Physiological and Clinical Applications. 6th ed. Maryland Heights, MO: Elsevier; 2016: 58–79. 31. Chatburn RL, Zhou S. Mechanical ventilation. In: Volscow TA, Chatburn RL, El-Khatib MF (eds.). Equipment for Respiratory Care. Burlington, MA: Jones & Bartlett Learning; 2016: 271–448. 32. Cairo JM. Weaning and discontinuation from mechanical ventilation. In: Cairo JM (ed.). Pilbeam Mechanical Ventilation: Physiological and Clinical Applications. 6th ed. Maryland Heights, MO: Elsevier; 2016: 387– 412. 33. Verbrugghe W, Jorens PG. Neurally adjusted ventilatory assist: a ventilation tool or a ventilation toy? Respir Care. 2011;56(3):327–335. doi:10.4187/respcare.00775. 34. Harrington D. Volumetric diffusive ventilator. J Burn Care Res. 2009;1(1):175–176. https://doi.org/10.1097/BCR.0b013e3181923c44. 35. Eichenwald EC. Mechanical ventilation in neonates. In: Martin R, Kim MS (eds.). UpToDate; June 2018. 36. Hou P, Baez AA. Mechanical ventilation of adults in the emergency department. In: Walls RM, Grayzel J (eds.). UpToDate; September 2017. 37. Thomson CC, Hasegawa K. Invasive mechanical ventilation in adults with acute exacerbations of asthma. In: Manaker S, Hollingsworth H (eds.). UpToDate; September 2018. 38. Allen GB. Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease. In: Stoller JK, Parsons PE, Finlay G (eds.). UpToDate; November 2016. 39. Siegel MD, Hyzy RC. Mechanical ventilation of adults in acute respiratory distress syndrome. In: Parsons PE, Finlay G (eds.). UpToDate; November 2017. 40. Peterson W, Barbalata L, Brooks C, et al. The effect of tidal volumes on the time to wean persons with high tetraplegia from ventilators. Spinal Cord. 1999;37(4):284–288. doi:10.1038/sj.sc.3100818.

CHAPTER

7 Patient Stabilization: Adjusting Ventilatory Support David C. Shelledy and Jay I. Peters

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Initiation of Mechanical Ventilation Patient–Ventilator Interaction Trigger Asynchrony Flow Asynchrony Cycle Asynchrony Mode Asynchrony Oxygenation FIO2 PEEP/CPAP Recruitment Maneuvers Prone Positioning Bronchial Hygiene Ventilation Tidal Volume, Rate, and Minute Ventilation Alveolar Ventilation Alveolar Ventilation and PaCO2 PaCO2 During Mechanical Ventilation Acid-Base Balance Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis Cardiac and Cardiovascular Support

Use of Sedation and Neuromuscular Blockade Summary

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31.

Describe items that should be assessed immediately following ventilator initiation. List respiratory problems sometimes encountered following ventilator initiation. Define the term patient–ventilator interaction and explain what is meant by patient–ventilator asynchrony. Describe the adverse effects of patient–ventilator asynchrony. Describe each of the types of trigger asynchrony and explain how to recognize and correct each. Explain how to recognize and correct flow asynchrony. Explain the importance of correctly adjusting rise time and expiratory sensitivity when using PSV. Explain what is meant by the term mode asynchrony and explain how NAVA and PAV may improve patient– ventilator interaction. Explain each of the factors that determine tissue oxygen delivery. Describe appropriate clinical goals for most patients for PaO2, SaO2, and FIO2. Describe methods to titrate FIO2 down from 1.0 in ventilated patients. Differentiate each of the following types of PEEP and explain how to apply each: minimum PEEP, compliance-titrated PEEP, optimal PEEP for oxygen delivery, PEEP–FIO2 tables, static pressure–volume curves, and slow-flow pressure–volume curves. Explain how to perform a decremental PEEP trial to include appropriate use of a lung recruitment maneuver. Explain causes, recognition, and correction of autoPEEP. Explain the purpose of prone positioning and describe its application. Explain the purpose of lung recruitment maneuvers and describe the possible risks and benefits. Describe bronchial hygiene techniques that may be beneficial in improving oxygenation. Explain the relationships between tidal volume, dead space, respiratory rate, and alveolar ventilation. Describe the relationship between alveolar ventilation, CO2 production, and PaCO2. Describe alterations in spontaneous breathing commonly seen in ICU patients. Explain methods to alter ventilation and PaCO2 during time-triggered controlled ventilation. Describe factors that affect PaCO2 when using each of the major modes of ventilation. Explain the use of permissive hypercapnia. Describe the purpose of intentional hyperventilation for patients with cerebral edema. Explain the effects of PaCO2 on acid-base balance during mechanical ventilation. Describe causes of metabolic acidosis and alkalosis and explain expected respiratory compensation. List normal values for arterial blood gases and hemodynamic measures often monitored in the intensive care unit (ICU). Describe major cardiac and cardiovascular abnormalities that will reduce oxygen delivery to the tissues. Summarize hemodynamic changes associated with ARDS, volume overload, left ventricular failure, hypovolemic shock, septic shock, and cardiogenic shock. Explain the importance of appropriate pain management and sedation protocols. List possible indications for and hazards of neuromuscular blockade.

KEY TERMS airway pressure-release ventilation (APRV) assist/control pressure-control ventilation (PC A/C) assist/control volume-control ventilation (VC A/C) autotriggering autoPEEP barotrauma baseline (bias) flow

bronchial hygiene cycle asynchrony decremental PEEP trial diaphragmatic dysfunction double cycling double triggering dynamic autoPEEP electrical discharge from the diaphragm (EDI) flail chest flow asynchrony flow trigger inspiratory waveform long cycling lower inflection point (LIP) minimum PEEP missed triggering mode asynchrony neural–ventilatory coupling neurally adjusted ventilatory assist (NAVA) neuro-inspiratory time neuromuscular blockade obstructive lung disease open lung ventilation optimal PEEP overdistention patient–ventilator asynchrony physiologic PEEP pressure control–synchronized intermittent mandatory ventilation (PC-SIMV) pressure-control ventilation (PCV) pressure-regulated volume control (PRVC) pressure-support ventilation (PSV) pressure trigger prone positioning proportional assist ventilation (PAV) recruitment maneuvers reverse triggering rise time short cycling static autoPEEP terminal flow titrate trigger asynchrony trigger delay trigger sensitivity trigger work upper inflection point (UIP)

Introduction Following establishment of an artificial airway and initiation of mechanical ventilation, the respiratory care clinician must assess the patient–ventilator system to assure appropriate ventilator function and patient–ventilator interaction. Support must provide adequate oxygenation and ventilation and reduce the work of breathing (WOB). Support must be adjusted to ensure patient comfort and safety and minimize harmful side effects. Support should also promote prompt patient liberation from the ventilator. Based on the clinician’s initial assessment, adjustments in ventilatory support may be necessary to reach these goals. A word about modes of ventilation: A sophisticated taxonomy has been developed to describe various modes of ventilation.1,2 Manufacturers and clinicians, however, often use less rigorous and sometimes conflicting terminology. This chapter will focus on use of common clinical terminology to describe the most common modes of ventilation in use, specifically: Assist/control volume-control ventilation (VC A/C, aka patient- or timetriggered VC-CMV with set-point breath targeting) Assist/control pressure-control ventilation (PCV or PC A/C, aka patient- or time-triggered PC-CMV with set-point breath targeting) Pressure-support ventilation (PSV, aka PC-CSV) Volume control-synchronized intermittent mandatory ventilation (V-SIMV, aka VC-IMV with set-point breath targeting) and Pressure control-synchronized intermittent mandatory ventilation (PSIMV, aka PC-IMV with set-point breath targeting). A more formal taxonomy for description of ventilatory modes is described in Chapter 6. Using that taxonomy, VC indicates volume control, PC indicates pressure control, CMV indicates continuous mandatory ventilation, IMV indicates intermittent mandatory ventilation, and CSV indicates continuous spontaneous ventilation.1,2

Initiation of Mechanical Ventilation Initiation of mechanical ventilation should be immediately followed by assessment of the patient and patient–ventilator system, including physical assessment of the patient, assessment of ventilator settings and patient–ventilator interaction, cardiovascular assessment, oximetry, and measurement of arterial blood gases. Ventilator adjustments are often needed to meet oxygenation and ventilation goals while maintaining optimal acid-base balance and minimizing harmful cardiovascular side effects. The ventilation provided must be safe and effective, minimize the WOB, and assure patient comfort. The initial assessment should alert the respiratory care clinician to specific areas of concern. These may include signs of hypoxemia or inadequate ventilation, increased WOB, respiratory distress, and diaphragmatic fatigue. Findings associated with heart failure, volume overload, shock, blood loss, or sepsis should be addressed. Impaired central nervous system (CNS) or neurologic function, including depressed level of consciousness, heavy sedation, and signs of neuromuscular disease or paralysis, should be noted. Respiratory problems sometimes encountered following ventilator initiation include inadvertent right mainstem intubation, misplaced endotracheal tube (e.g., esophageal intubation), cuff leak or malfunction, large air leak, inappropriate ventilator settings, and ventilator malfunction or disconnect. Other common problems include bronchospasm, mucosal edema, or secretions in a large airway. The clinician should be alert for the development or worsening of pulmonary edema, consolidation, pneumothorax, pleural effusion, or atelectasis. Based on this initial assessment, the respiratory care clinician should make appropriate ventilator adjustments to optimize oxygenation and ventilation, maintain acid-base homeostasis, reduce the WOB, minimize harmful cardiovascular side effects, and assure patient safety and comfort. Box 7-1 summarizes the items that should be reviewed as part of the initial assessment of the patient following ventilator initiation.

BOX 7-1 Initial Assessment of the Patient Following ventilator initiation, the patient should be assessed to ensure adequate oxygenation and ventilation while avoiding patient–ventilator asynchrony, increased WOB, or cardiovascular compromise. Assessment

should include review of the following to include findings of concern: ∎ Physical findings and monitored information • General appearance: head and neck: normal or reduced level of consciousness (confusion, somnolent, or coma); signs of restlessness, anxiety, pain, discomfort, distress, or dyspnea; cyanotic lips and gums; pupils abnormally dilated or contracted; jugular venous distention • Extremities: warm and moist or pale, cold, clammy, edematous, or cyanotic • Respiratory rate and pattern: normal or abnormal, e.g., tachypnea, bradypnea, rapid shallow breathing, periods of apnea, ventilator–patient asynchrony • Heart rate, blood pressure, and presence of arrhythmia on cardiac monitor (normal or abnormal) • Pulse oximetry • Breath sounds: good bilateral aeration or absent, diminished, unilateral, or abnormal breath sounds • Chest exam: bilateral chest expansion vs. unilateral chest expansion, accessory muscle use, intercostal retractions, chest/abdomen asynchrony ○ Palpation for tracheal position, chest wall motion, presence of subcutaneous air ○ Percussion for resonance, dullness, or hyperresonance • Artificial airway ○ Placement, patency, and cuff inflation (pressure and volume) ○ Tube diameter and depth of insertion • Monitoring equipment ∎ Ventilator settings • Mode of ventilation • Ventilatory graphics display (pressure, flow, and volume waveforms) • Peak, plateau, and mean airway pressures • Exhaled volumes and rate (spontaneous and mandatory VT, f, and V̇E) • Baseline pressure (PEEP/CPAP) • Trigger effort, trigger synchrony/asynchrony • Oxygen concentration • Inspiratory time, flow, and I:E ratio • Humidification and airway temperature ∎ Bedside equipment and supplies • Suctioning equipment and supplies

• • • •

Manual resuscitator bag, oxygen supply, positive end-expiratory pressure (PEEP) valve, extra airways Other equipment and supplies (e.g., chest tubes, urinary catheter collection bags). Crash cart location. Ancillary equipment (e.g., mechanical circulatory assistance devices, extracorporeal membrane oxygenation [ECMO], inhaled nitric oxide [NO])

Patient–Ventilator Interaction With patient-triggered modes of ventilation (e.g., assist/control volume or pressurecontrol ventilation) and modes that incorporate spontaneous breathing (e.g., SIMV, pressure support) the patient and ventilator must interact. Patient–ventilator interaction refers to patient–ventilator synchrony, comfort, and WOB during ventilator-assisted breaths. This interaction may be good, resulting in adequate oxygenation and ventilation, while decreasing the WOB and promoting patient comfort. Poor patient–ventilator interaction can result in patient–ventilator asynchrony, which may increase the WOB, cause patient discomfort, and threaten effective oxygenation and ventilation. Patients in ventilatory failure often experience diaphragmatic dysfunction, which may prolong the need for mechanical ventilation and lengthen ICU stay.3 A sustained increase in ventilatory workload can lead to ventilatory muscle fatigue and structural injury. Once ventilatory muscle fatigue occurs, at least 24 hours is required for recovery. Ventilatory support should be adjusted to minimize the WOB and allow for ventilatory muscle rest. Absence of ventilatory activity as seen with controlled ventilation results in near-complete ventilatory rest. Controlled ventilation, however, may lead to ventilatory muscle weakness, deconditioning, and atrophy.3 The development of diaphragmatic dysfunction while receiving mechanical ventilatory support may be correlated with the degree of support provided and the quality of the patient–ventilator interaction. Diaphragmatic dysfunction can develop within hours and worsen with the duration of mechanical ventilation. Appropriate selection of ventilatory mode and associated ventilator settings can reduce the ventilatory work load without resulting in deconditioning and atrophy of the ventilatory muscles. Assist/control volume ventilation, assist/control pressurecontrol ventilation, synchronized intermittent mandatory ventilation (SIMV) with pressure support, and standalone pressure-support ventilation can reduce inspiratory work without eliminating respiratory muscle activity. Newer modes of ventilation (e.g., proportional assist ventilation [PAV], neurally adjusted ventilatory assist [NAVA]) may be especially useful in enhancing patient–ventilator interaction. Immediately following initiation of mechanical ventilation, the patient should be assessed for the presence of patient–ventilator asynchrony. Patient–ventilator

asynchrony occurs when the timing of the ventilator does not coincide with the patient’s respiratory center neurologic inspiratory/expiratory cycle. Patient–ventilator asynchrony may be detected via physical assessment and observation of the ventilator pressure, flow, and volume waveforms. The degree of patient–ventilator asynchrony can vary from mild to very severe. The quality of the patient–ventilator interaction may also vary over time. For example, periods of sleep or sedation may improve patient–ventilator synchrony, while pain, anxiety, procedural interventions, and other clinician–patient interactions may worsen patient–ventilator asynchrony. It has been estimated that up to 25% of patients experience severe patient–ventilator asynchrony, while some have suggested that asynchrony occurs at some point in almost all patients receiving patient-triggered ventilatory support.4,5 Box 7-2 describes some of the adverse effects of patient–ventilator asynchrony.

BOX 7-2 Effects of Patient–Ventilator Asynchrony Patient–ventilator asynchrony is associated with adverse effects, including: ∎ Increased WOB • Diaphragmatic fatigue • Structural damage to the diaphragm ∎ Hypoxemia due to decreased V̇/Q ̇ or increased shunt ∎ Inadequate or ineffective ventilation • Hypoventilation (abnormally increased PaCO2)

• • •

Hyperventilation (abnormally decreased PaCO2)

Tachypnea, rapid shallow breathing (IMV/SIMV mode) Slowed spontaneous breathing rate (sedation) ∎ Hemodynamic compromise • Tachycardia or bradycardia • Hypertension or hypotension ∎ Increased likelihood of complications • Increased peak inspiratory pressure (PIP) • Pneumothorax/tension pneumothorax, other forms of barotrauma • Increased mean airway pressure ○ Decreased venous return, decreased cardiac output

∎

○ Increased likelihood of ventilator-associated lung injury (VALI) Prolonged duration of ventilation • Increased time to extubation • Increased need for tracheostomy • Increased time in the ICU • Increased hospital length of stay • Increased mortality

Types of patient–ventilator asynchrony include trigger asynchrony, flow asynchrony, cycle asynchrony, and mode asynchrony, as described below.

Trigger Asynchrony Patient-triggered breaths may be pressure triggered or flow triggered. Trigger sensitivity should be adjusted so that trigger work is minimal without autocycling. For pressure triggering, the trigger is generally set at –0.5 to –1.5 cm H2O below the baseline expiratory pressure, although some circuits may require trigger sensitivity be set at –2.0 cm H2O to avoid autotriggering.2,26 With flow triggering, the trigger sensitivity is generally set in the range of 1 to 2 L/min below the baseline or bias flow, although some systems may require flow triggers as high as 3 to 4 L/min below baseline (bias) flow to avoid autotriggering.2,6 There are no clinically important differences between pressure trigger and flow trigger when using the current generation of critical care ventilators.2,6 Trigger asynchrony occurs when the patient’s inspiratory effort and the initiation of a ventilator-supported breath are poorly coordinated. RC Insight Trigger sensitivity should be adjusted so that trigger work is minimal without autocycling.

Trigger Work Trigger work refers to that portion of the WOB performed by the patient to trigger the ventilator to the inspiratory phase. Inappropriate trigger sensitivity settings and autoPEEP can increase trigger work. For example, if pressure trigger sensitivity

threshold is adjusted from –1.5 cm H2O to –3.0 cm H2O, the required patient effort (work) to trigger the ventilator will increase and the patient may not be able to generate this effort consistently. AutoPEEP may also increase trigger work. For example, if the expiratory baseline pressure at the proximal airway is 0 cm H2O, and the pressure trigger sensitivity is set at –2 cm H2O, the patient must generate an inspiratory effort to decrease proximal airway pressure 2 cm H2O to trigger the ventilator in the absence of autoPEEP. However, if the autoPEEP is +4 cm H2O the patient would have to generate a pressure decrease from +4 cm H2O to –2 cm H2O in order to trigger the ventilator, a decrease of 6 cm H2O significantly increasing trigger work. If patients are having trouble triggering the ventilator in the presence of autoPEEP, extrinsic PEEP may be applied to reduce trigger work, usually at 50% to 80% of the measured autoPEEP level. Trigger asynchrony occurs when the patient’s inspiratory effort becomes decoupled from the ventilator trigger. There are five types of trigger asynchrony: missed triggering, trigger delay, double triggering, reverse triggering, and autotriggering. Most forms of trigger asynchrony may occur in any mode that includes patient-triggered ventilation. Reverse triggering, however, occurs only with time-triggered “control mode” ventilation.

Missed Triggering A patient inspiratory effort that does not trigger the ventilator is called missed triggering. This is typically detected by observing inspiratory muscle contraction that is not followed by a “machine” breath. The pressure–time curve observed on the ventilator’s graphics display will indicate a dip in the baseline pressure caused by the patient’s inspiratory effort that is not followed by a positive-pressure breath. Figure 7-1 illustrates missed triggering.

FIGURE 7-1 Missed Trigger Threshold.

Description Typically, missed triggering occurs intermittently. For example, two unsuccessful patient inspiratory efforts may be followed by a third effort that successfully triggers the ventilator to inspiration.5 Missed triggering is most commonly caused by the presence of autoPEEP. AutoPEEP is caused by incomplete exhalation and most commonly occurs in patients with obstructive lung disease. AutoPEEP can be documented by observing the patient’s expiratory flow curve; expiratory gas flow does not reach zero prior to the initiation of the next breath. Application of intrinsic PEEP (e.g., 50% to 80% of measured autoPEEP) to balance autoPEEP may correct missed triggering. One approach involves gradually increasing extrinsic PEEP by 1 to 2 cm H2O and observing the effect on patient triggering. The appropriate extrinsic PEEP level to balance autoPEEP has been reached when each patient inspiratory effort results in effective ventilator triggering.5 Following the application of extrinsic PEEP in this fashion, autoPEEP should be reevaluated to ensure it has not also

increased. PEEP increases mean airway pressure and may reduce venous return and cardiac output. Studies show that application of extrinsic PEEP in patients with obstructive lung disease can improve or occasionally worsen WOB. PEEP is contraindicated with untreated pneumothorax and should be used with caution in patients with hemodynamic compromise or elevated intracranial pressure (ICP).5 Figure 7-2 illustrates autoPEEP as seen on a flow–time curve during mechanical ventilation.

FIGURE 7-2 AutoPEEP.

Description Other steps to reduce or eliminate autoPEEP include increasing expiratory time, decreasing tidal volume, use of larger diameter endotracheal tubes, bronchodilator administration, and secretion management. Inappropriate trigger sensitivity settings may also cause missed triggering. Inappropriate sensitivity settings should be corrected.

Trigger Delay Trigger delay occurs when there is an increased time interval between the neurologic inspiratory signal from the patient’s respiratory control center and the ventilator’s initiation of breath. A trigger delay > 100 ms may increase the patient’s perception of the delay and increase ventilatory drive.5 Trigger delay can be best observed using an esophageal catheter with a multiple array electrode to detect the electrical

discharge from the diaphragm (Edi). The Edi signal is displayed graphically and provides a reflection of the respiratory center’s neural output to the diaphragm. NAVA was developed to provide better neural–ventilatory coupling and to improve trigger and cycle synchrony. Trigger delay is most commonly caused by inappropriate sensitivity settings, and adjustment of trigger sensitivity can often correct trigger delay. Trigger delay may also be caused by autoPEEP or ventilator malfunction. AutoPEEP should be measured; the application of extrinsic PEEP at 50% to 80% of the autoPEEP level may correct trigger delay. In the case of a ventilator malfunction, the ventilator should be replaced.

Double Triggering Patients may try to breathe in longer or deeper than the ventilator is set to provide. This occurs most often in the volume-control mode when the set tidal volume or inspiratory time is less than the patient’s neurologic ventilatory control center demands. In these cases, the ventilator may cycle to the expiratory phase while the patient continues to make an inspiratory effort, resulting in double triggering. Double triggering may cause the patient to receive two consecutive tidal breaths from the ventilator before exhaling. Double triggering may be corrected by increasing the inspiratory time to match the patient’s neuro-inspiratory time, increasing the tidal volume to better match the patient’s demand or considering a different mode of ventilation (e.g., pressure support or assist/control PCV). If double triggering continues, sedation may be considered.

Reverse Triggering Reverse triggering may occur during controlled ventilation in which a time-triggered ventilator breath stimulates the diaphragm, resulting in diaphragmatic contraction, which then triggers the next breath.6 Reverse triggering has been observed in deeply sedated patients with acute respiratory distress syndrome (ARDS), and it may be promoted by sedation or sedation may make reverse triggering more apparent.

Autotriggering Autotriggering occurs when the ventilator initiates inspiration without a corresponding

patient effort due to inappropriate ventilator trigger sensitivity settings. Autotriggering most often occurs when trigger sensitivity thresholds are such that even minor fluctuations in ventilator circuit pressure and flow result in a breath trigger. With inappropriate sensitivity settings, autotriggering can occur due to ambient vibration (e.g., moving the breathing circuit), water in the circuit tubing, hyperdynamic cardiogenic contractions, system leaks, or endotracheal cuff leaks. Autotriggering can often be corrected by adjusting the ventilator trigger sensitivity setting, correcting any system leaks (e.g., replacing ventilator circuit), or draining water from the circuit.

Flow Asynchrony Flow asynchrony occurs when the inspiratory gas flow from the ventilator is unable to match the patient’s inspiratory flow demand. With a patient trigger, the patient initiates inspiration by contraction of the respiratory muscles. Although the ventilator responds by delivering gas flow to the patient, contraction of the respiratory muscles continues throughout the inspiratory phase. If the gas flow from the ventilator does not meet or exceed the patient’s inspiratory flow demand, the WOB may increase substantially. With assist/control volume ventilation, this work may exceed that of spontaneous breathing.7 With assist/control volume ventilation, the clinician sets the tidal volume, inspiratory peak flowrate or inspiratory time (I-time), and inspiratory flow waveform. Peak flow values ≥ 60 to 80 L/min are sometimes required to meet inspiratory demand in adult patients. Inspiratory time should match the patient’s respiratory center neuro-inspiratory time; typical adult inspiratory times are 0.8 to 1.0 seconds. Flow asynchrony most commonly occurs during volume ventilation with inappropriately low peak flow settings or high inspiratory time settings. When ventilator settings are adjusted by increasing the peak flow (e.g., 60 to 80 L/min) and decreasing inspiratory time (e.g., 0.6 to 0.8 seconds) to match the patient’s inspiratory flow demand and neuro-inspiratory time, the patient’s WOB and flow asynchrony will decrease. Most modern critical care ventilators allow the respiratory care clinician to select the inspiratory flow waveform during volume ventilation. In ventilators with clinician-selected peak flow controls, a down-ramp or decelerating flow waveform produces a high initial peak flow but increased inspiratory time (as compared to a

square wave). In ventilators with a clinician-selected peak flow control, a squarewave or constant flow waveform results in a lower peak flow and decreased inspiratory time (as compared to a decreasing flow waveform). Increases in tidal volume increase inspiratory time, while decreases in tidal volume decrease inspiratory time in ventilators with a selectable peak flow control. During volume ventilation with ventilators incorporating a clinician-selected inspiratory time, the set tidal volume and I-time will determine peak flow. Most clinicians prefer a down-ramp or decreasing (aka decelerating) flow waveform because of the high initial peak flow, which then decreases throughout inspiration. With pressure-support ventilation (PSV) or pressure-control ventilation (PCV), modern critical care ventilators incorporate an inspiratory pressure rise time or pressure slope control. This control allows the clinician to adjust the rate at which flow increases from baseline to peak during pressure-supported or pressure-control breaths.5 Rise time should be set to avoid a spike in inspiratory pressure at the beginning of the inspiratory phase, yet provide sufficient inspiratory gas flow to meet the patient’s inspiratory demand. A rise time or pressure slope control is provided for pressure-limited breaths provided during PSV, PCV, pressure-control SIMV, volume support (VS), pressure-regulated volume control (PRVC) and airway pressurerelease ventilation (APRV).5 Figure 7-3 illustrates a fast rise time, slow rise time, and appropriate rise time with pressure-control ventilation.

FIGURE 7-3 Pressure-Control Ventilation.

Description With volume ventilation, if the patient’s inspiratory effort increases, the work performed by the ventilator decreases and vice versa. With pressure-control ventilation, the work performed by the ventilator remains constant with changes in patients’ inspiratory demand. RC Insight During volume ventilation peak flow should be adjusted to a value that meets or exceeds the patient’s inspiratory flow demand.

Cycle Asynchrony Cycle asynchrony occurs when the patient’s respiratory center neurologic output and

the ventilator do not match. Put another way, with cycle asynchrony there is poor coordination between the patient’s desire to exhale and the ventilator’s response.5 Cycle asynchrony is most common during PCV, although it can occur in other modes.8 If the ventilator’s set inspiratory time exceeds the patient’s neuro-inspiratory time, long cycling (delayed ventilator cycling) may occur. With delayed cycling, inspiratory times are excessive and the patient may attempt to actively exhale while the ventilator is still in the inspiratory phase, resulting in a spike in pressure at the end of the pressure-targeted breath. If the ventilator’s set inspiratory time is less than the patient’s neuro-inspiratory time, short cycling (premature ventilator cycling) or double cycling may occur. With premature ventilator cycling, inspiratory times are too short. Double cycling typically occurs with volume ventilation when the ventilator’s set inspiratory time and tidal volume are insufficient. During volume ventilation using ventilators with a clinician-selected inspiratory time control, cycle asynchrony can often be corrected by altering the set inspiratory time to match the patient’s respiratory center neuro-inspiratory time. In ventilators with peak flow controls, inspiratory time is a function of the set tidal volume and peak flow; increasing peak flow reduces inspiratory time and vice versa. Figure 7-4 illustrates a mismatch between the patient’s inspiratory time and the ventilator’s inspiratory time in which the patient begins exhalation early resulting in a pressure spike at end inspiration in the pressure–time curve. Steps should be taken to match the patient’s neuro-inspiratory time with the ventilator’s inspiratory time. Inspiratory times (adults) are often set in the range of 0.8 to 1.0 seconds. Patients with high inspiratory demand may require shorter inspiratory times (e.g., 0.6 to 0.8 seconds).

FIGURE 7-4 Cycling Asynchrony.

Description With PSV, the ventilator cycles to expiration when the inspiratory flow decreases to a preset value (e.g., 10% to 25% of the inspiratory peak flow). This value works well for some patients; however, certain patients may attempt to terminate inspiration at a higher terminal flow (e.g., 50% of peak flow).5 For example, a chronic obstructive pulmonary disease (COPD) patient with high levels of PSV may attempt to exhale before the machine has completed the inspiratory phase. When this occurs, the accessory muscles of expiration are employed to cycle the ventilator to the

expiratory phase. Put another way, the ventilator remains in the inspiratory phase as the patient attempts to breathe out, resulting in cycle asynchrony and increased patient work. Careful observation of the pressure–time curve may reveal a spike in inspiratory pressure caused by the patient’s active exhalation. This type of cycle asynchrony most commonly occurs in patients in distress and those with COPD.5 Modern critical care ventilators allow the clinician to adjust the PSV expiratory cycling criteria; this function may be used to correct cycle asynchrony. This function goes under various names for various ventilators, including expiratory sensitivity (Esens: PB 840, PB 980; range 1% to 80% peak flow); expiratory trigger sensitivity (ETS: Hamilton G5; range 5% to 70% peak flow); end flow (GE CareStation; range 5% to 80% peak flow), expiratory termination (Drager Evita V500; range 1% to 80% peak flow), and inspiratory cycle off % (Maquet Servo-i and Servo-u; range 1% to 80% peak flow). When using PSV, the respiratory care clinician should assess the patient to ensure that there is no increase in expiratory work due to cycle asynchrony and adjust the expiratory sensitivity as needed. Figure 7-5 illustrates the effects of different flow termination criteria on the flow–time and pressure–time curves.

FIGURE 7-5 Effect of Changing the Flow Termination Criteria During Pressure-Support Ventilation. Note the effect on inspiratory time when a change in flow termination criteria as a percentage of peak flow is made.

Description NAVA and PAV are designed to vary the level of support provided based on the

patient’s demand. NAVA uses electrical signals from the diaphragm to trigger and cycle inspiration and should minimize patient–ventilator asynchrony. The drawback to these two modes is that they will attempt to match the patient’s ventilatory pattern, even if it is problematic. For example, patients with acute restrictive lung disease in respiratory failure (e.g., severe pneumonia, ARDS) often choose a rapid shallow breathing pattern.

Mode Asynchrony Mode asynchrony occurs when the mode of ventilation selected is unable to match the patient’s spontaneous ventilatory pattern.5 Modes that increase the patient’s control over of his or her own ventilatory pattern improve patient–ventilator interaction and reduce patient–ventilator asynchrony. For example, with PSV, each breath is patient triggered, pressure limited, and flow cycled. The patient initiates and terminates each breath and inspiratory flow varies with the patient’s inspiratory effort; inspiratory pressure is constant, regardless of patient effort. With assist/control volume ventilation, the patient may trigger each breath; however, the inspiratory flow, flow waveform, inspiratory time, and tidal volume are determined by the clinician. While assist/control volume ventilation will deliver a consistent tidal volume breath to breath, pressures provided may decrease with increases in patient effort. Thus, PSV should improve patient–ventilator interactions and provide a more consistent level of support as compared to assist/control volume ventilation. Proportional assist ventilation (PAV) and neurally adjusted ventilatory assist (NAVA) provide a proportional assist based on patients’ inspiratory demand; as patient effort increases, ventilatory support increases, and vice versa. With PAV and NAVA, the patient triggers each breath and has control over his or her respiratory rate, inspiratory gas flow, tidal volume, inspiratory time, and expiratory time, which should improve patient–ventilator synchrony. The level of support provided by the ventilator varies with patient effort. NAVA uses a special esophageal catheter to detect the electrical discharge from the diaphragm as a reflection of the respiratory center’s neural output to the diaphragm. As noted above, NAVA is specifically designed to achieve neural-ventilatory coupling to improve trigger and cycle synchrony. As noted, breathing modes that increase patients control over their ventilatory

pattern reduce the likelihood of patient–ventilator asynchrony. Modes providing patients the most control include NAVA and PAV followed by PSV. Assist/control PCV provides less patient control over their ventilatory pattern while assist/control volume ventilation provides patients with the least control. If mode asynchrony occurs, the respiratory care clinician may institute a different mode of ventilation that provides the patient better control of his or her ventilatory pattern. In summary, following initiation of mechanical ventilatory support the patient should be immediately assessed for the quality of the patient–ventilator interaction by observing for trigger effort, accessory muscle use, patient–ventilator inspiratory time matching, respiratory rate, and signs of distress. Trigger work should be adjusted to minimize patient effort without autotriggering. The clinician should also carefully observe for the presence of patient efforts that do not result in a ventilator trigger or other triggering abnormalities. Inspiratory flow should meet or exceed the patient’s ventilatory needs. Inadequate inspiratory flow will increase the WOB while excessive inspiratory flow may result in immediate and persistent tachypnea. Mode of ventilation can also have a significant effect on the patient–ventilator interaction. Assist/control volume ventilation may result in an excessive trigger rate, hyperventilation, and patient–ventilator asynchrony in patients with increased respiratory drive. Inspiratory flows and times must match the patient’s needs and neurologic respiratory cycle. With assist/control PCV, pressure must be adjusted to provide an adequate inspiratory volume and inspiratory time must be adjusted to match the patient’s neuro-inspiratory time. SIMV can be problematic as it combines mandatory and spontaneous breaths. SIMV mandatory breaths should be adjusted to match the patient and spontaneous breaths should be pressure supported as the absence of pressure support may worsen ventilatory muscle dysfunction. PSV may improve patient–ventilator synchrony but does not guarantee tidal volume delivery. Newer adaptive modes combine the benefits of pressure control while assuring tidal volume delivery (e.g., pressure-regulated volume control [PRVC], volume support [VS]) while other newer modes (PAV, NAVA) vary the level of support provided based on the patient demand.

Oxygenation Adequate tissue oxygenation requires adequate arterial oxygen content, sufficient cardiac output, and peripheral tissue perfusion. Arterial oxygen content (CaO2) is dependent on arterial oxygen tension (PaO2), arterial oxygen saturation (SaO2), and hemoglobin level (Hb) where: CaO2 = 1.34 × SaO2 × Hb + 0.003 × PaO2. Tissue oxygen delivery (ḊO2) is dependent on the arterial oxygen content (CaO2) and cardiac output (Q̇T; total cardiac output) where: ḊO2 = CaO2 × Q̇T. Cardiac output (Q̇T; also noted as CO) is dependent on stroke volume (SV) and heart rate (HR) where: Q̇T = SV × HR. Normal values for each of these variables is listed in Table 7-1. TABLE 7-1 Normal Values for Variables Affecting Tissue Oxygenation

Arterial oxygen saturation: Sao2. Arterial oxygen tension: Pao2. Body surface area (BSA): normal BSA is 18.5 to 24.9 m2. Cardiac index: CI; normal 3.5 +/– 0.7 L/min/m2. Cardiac output: Q̇T. Oxygen content: Cao2. Oxygen delivery: ḊO2 = Cao2 x Q̇T.

Tissue oxygenation is dependent on multiple factors including inspired oxygen concentration, alveolar ventilation, ventilation–perfusion relationships, diffusion across the alveolar–capillary membrane, arterial oxygen content, cardiac output, and peripheral perfusion. Problems in any of these areas should be identified and treated (if possible). The primary ventilator adjustments available to alter arterial oxygenation are inspired oxygen concentration (FIO2) and PEEP/CPAP. Other ventilatory techniques that may improve oxygenation in certain patients include recruitment maneuvers, open lung ventilation, and prone positioning. Basic respiratory care, including suctioning and airway care, bronchial hygiene, and bronchodilator and other inhaled medication administration, may be helpful. Less common techniques that may improve oxygenation in certain critically ill patients include inhaled nitric oxide (NO) and extracorporeal membrane oxygenation (ECMO).

FIO2 Ventilator initiation often includes providing 100% oxygen (FIO2 = 1.0) as a safeguard against development of severe hypoxemia. FIO2 should be rapidly titrated down (if possible) to avoid oxygen toxicity and related complications. These possible complications include absorption atelectasis, cellular injury, accentuation of hypercapnia, airway injury, parenchymal injury, and potentiation by bleomycin (Blenoxane).8 Retinopathy of prematurity is a complication associated with PaO2 > 80 mmHg in premature infants. For most critically ill patients, the goal is to achieve adequate arterial oxygen levels (PaO2 ≥ 60 mmHg, SaO2 ≥ 90%) at a safe oxygen concentration (FIO2 ≤ 0.50 to 0.60). RC Insight A clinical goal of PaO2 = 60 to 80 mmHg and SaO2 = 90% to 95% at FIO2 ≤ 0.50 to 0.60 is appropriate for

most patients.

Titration of FIO2 is usually based on continuous pulse oximetry measurement (SpO2), which should reflect SaO2 under most circumstances. Clinicians should be aware of factors that may cause SpO2 to be a poor surrogate for SaO2. These include increased levels of abnormal hemoglobin (e.g., carboxyhemoglobin [CoHb], methemoglobin [MetHb], sulfhemoglobin), high glycohemoglobin A1c in diabetics, and poor signal quality (e.g., low blood pressure, vasoconstriction, motion artifact, and probe position). SpO2 values should be compared to measured SaO2 via cooximetry to verify that the values correlate; SpO2 values should correspond to SaO2 values ± 2 to 3%.9 Table 7-2 compares PaO2 to SpO2 assuming a normal oxyhemoglobin dissociation curve to give a sense of the oxygen tensions (PaO2) associated with specific pulse-oximetry values. TABLE 7-2 Relationship Between Pao2 and Sao2* Pao2

Sao2

Spo2 (Sao2 ± 2%)

100

98

100 to 96

95

97

99 to 95

90

96.9

98 to 95

85

96.4

98 to 94

80

95.7

98 to 94

75

94.9

97 to 93

70

93.8

96 to 92

65

92.4

94 to 90

60

90.6

93 to 87

55

88.2

90 to 86

50

85

87 to 83

45

80

82 to 78

40

75

77 to 73

FIO2 in ventilated patients is often titrated based on continuous oximetry monitoring (Spo2). Spo2 values

should be correlated with measured Sao2 via co-oximetry. Normal Spo2 accuracy is ± 2%. Accuracy declines when Sao2 < 90% and is especially poor when Sao2 < 80%. The relationship between Sao2 and Pao2 displayed assumes a normal oxygen saturation curve and adjustments must be made based on changes in the patient’s pH, Paco2, body temperature, and 2 to 3 DPG. Green = clinically acceptable values for most patients. Yellow = moderate hypoxemia. Red = moderate to severe hypoxemia. Abbreviations: Pao2, the partial pressure of oxygen in the arterial blood; Paco2, partial pressure of carbon dioxide in the arterial blood; Sao2, arterial oxyhemoglobin saturation; Spo2, oxygen saturation as measured by pulse oximetry. *Sao2 values are estimates and will vary depending on the blood’s chemical environment (pH, Pco2, temperature, and 2 to 3 DPG).

FIO2 is titrated down from 1.0 in decrements of not more than 0.20 (20% O2). Following each decrease the clinician should allow oxygen levels to stabilize for period of at least 10 minutes prior to the next decrease; COPD patients may take longer to stabilize. As the oxygen level approaches a more moderate value (e.g., 50% to 60%), alterations in FIO2 should be in steps of 0.05 to 0.10 (5% to 10%) followed by assessment of SpO2. When the desired SpO2 is reached on a safe FIO2, arterial blood gases should be drawn and analyzed. The goal is a PaO2 of 60 to 80 mmHg and SaO2 ≥ 90% and/or SpO2 ≥ 90% to 92% on 40% to 60% O2. In cases where adequate arterial oxygenation cannot be achieved at a safe FIO2, PEEP or other techniques may be employed (see below). Table 7-3 illustrates the titration of oxygen concentration down from an initial FIO2 of 1.0 based on PaO2 and SpO2. TABLE 7-3 FIO2 Titration

Description Patients often receive 100% O2 upon initiation of mechanical ventilation. FIO2 is then rapidly titrated down based on oximetry (Spo2) and patient observation. If an initial arterial blood gas (ABG) study demonstrates initial Pao2 values ≥ 150 mmHg while receiving 100% O2, FIO2 generally can be titrated down in increments of 0.20 for the first several steps followed by patient assessment and continued monitoring of Spo2. The clinician should wait 10 to 30 minutes after each decrease in FIO2 to allow oxygenation values to stabilize before making any additional decreases. If the patient appears to be in distress or Spo2 falls to < 90% to 92% FIO2 should be immediately returned to its previous value (or 100%) and the patient reassessed. If initial ABGs on 100% O2 are not available, although Spo2 is 100%, it is reasonable to cautiously assume that this corresponds to a Pao2 > 150 mmHg and make appropriate adjustments based on patient observation and continued Spo2 monitoring. It is generally acceptable to continue to decrease FIO2 if Spo2 remains > 95%. If at any point Spo2 falls to < 90%, immediately return to the previous FIO2 (or 100% O2) and reassess the patient.

In cases where initial blood gases are available, FIO2 requirements to obtain a desired PaO2 can be estimated using the following formula derived from the alveolar air equation and the assumption that the arterial (PaO2) to alveolar (PAO2) oxygen tension ratio (aka a/A ratio) remains relatively constant with recent changes in FIO2: Required FIO2 = ([PaO2 desired ÷ a/A ratio] + PaCO2 × 1.25] × (1/[PB – PH2O]) Where a/A ratio is the initial measured PaO2 divided by calculated initial alveolar oxygen tension (PAO2); PB and PH2O are the barometric pressure and water vapor pressure, respectively.

A simpler, but less accurate estimate of the required FIO2 to achieve a desired PaO2 is: Required FIO2 = (Initial FIO2 ÷ Initial PaO2) × Desired PaO2. Clinical Focus 7-1 illustrates use of these formulas for estimating FIO2 based on PaO2.

CLINICAL FOCUS 7-1 Oxygen Titration Invasive mechanical ventilation is instituted for a patient in acute respiratory failure with the following settings: Mode: assist/control volume ventilation (V-AC aka patient- or time-triggered VC-CMV) Tidal volume: 8 mL/kg IBW Set rate: 14 breaths/minute FIO2: 1.0 PEEP: + 5 cm H2O Arterial blood gases are obtained shortly after initiation of mechanical ventilatory support: pH: 7.36 PaCO2: 35 mmHg PaO2: 182 mmHg SaO2: 100% The respiratory care clinician is asked to titrate the FIO2 down from 1.0 to a safe level. Question 1. Estimate the FIO2 needed to obtain a PaO2 of 100 mmHg with an SaO2 of 0.97 (97%) The FIO2 to obtain a desired PaO2 is: Required FIO2 = (Initial FIO2 ÷ Initial PaO2) × Desired PaO2. Based on the initial oxygen concentration and initial and desired PaO2 this becomes: Required FIO2 = (1.0 ÷ 182 mmHg) × 100 mmHg = 0.55 or 55%.

Question 2. Suggest an approach to decreasing this patient’s FIO2 based on the calculation performed above. Based on the data provided, if the FIO2 is reduced to 0.55 (55%), the patient’s PaO2 should decrease to about 100 mmHg. However, initial FIO2 decreases from 1.0 should be limited to a maximum of 0.20 (20%) per step followed by patient assessment and SpO2 measurement. This patient’s FIO2 was decreased incrementally in a stepwise fashion, allowing 10 to 15 minutes for stabilization after each decrement in FIO2: Initial FIO2: 1.0

Initial PaO2: 182 mmHg

Initial SpO2: 100%

Step 1: decrease FIO2 to 0.80.



Resultant SpO2: 99%

Step 2: decrease FIO2 to 0.60.



Resultant SpO2: 98%

Step 3: decrease FIO2 to 0.55.

Resultant PaO2: 95 mmHg

Resultant SpO2: 97%

This patient’s FIO2 has been safely and successfully decreased from 1.0 to 0.55, resulting in a satisfactory PaO2 and oxygen saturation. The patient’s FIO2 can now be further decreased an additional 0.10 (10%) to 0.45, which should result in an acceptable PaO2 of about 78 mmHg with an SpO2 of about 95%. The goal is FIO2 ≤ 0.50 to 0.60 with PaO2 ≥ 60 mmHg and/or SpO2 ≥ 92%.

When titrating oxygen concentration, once the desired arterial oxygen level has been reached, monitoring should be continued. Oxygen levels are titrated up and down as needed with adjustments in FIO2 of 0.05 to 0.10 (5% to 10%) to maintain PaO2 in the range of 60 to 80 mmHg, SaO2 90% to 97%, and/or SpO2 ≥ 92%. The higher the FIO2, the lower the concentration of nitrogen within the alveoli; therefore, some clinicians titrate the SaO2 to 90% to 94% in all patients in order to minimize the risk of atelectasis. A lower oxygen saturation (e.g., SaO2 88%) may be acceptable for patients requiring very high oxygen concentrations (e.g., FIO2 ≥ 0.80) for an extended time. O2 concentration should be returned to 100% in emergencies and for performance of certain procedures (e.g., airway suctioning).

PEEP/CPAP Mechanical ventilation often incorporates PEEP or CPAP to help restore or maintain

lung volumes and prevent or treat atelectasis. PEEP/CPAP can be highly effective in improving oxygenation in patients with acute hypoxemic respiratory failure (e.g., ARDS, severe pneumonia, and pulmonary edema). Low levels of PEEP (e.g., 3 to 5 cm H2O; called “physiologic PEEP”) are thought to protect against the small decreases in functional residual capacity (FRC) that may occur following endotracheal intubation due to loss of normal glottic function. Small amounts of applied PEEP can also compensate for patient-trigger difficulties caused by autoPEEP. PEEP has also been used in the presence of flail chest to stabilize the chest wall. Initial ventilator settings for most patients include the application of 5 to 8 cm H2O PEEP. PEEP prevents end-alveolar collapse and may reduce the incidence of ventilator-associated pneumonia (VAP) and ventilator-associated lung injury (VALI).10 PEEP can cause pulmonary barotrauma or VALI by increasing alveolar pressures and causing alveolar overdistention.11 PEEP increases mean airway pressure, which may reduce venous return and compromise cardiac output and blood pressure. PEEP should be used cautiously in patients with hypotension or hypovolemia. Increased intrathoracic pressures due to PEEP may reduce cerebral venous outflow; PEEP should be used with care in patients with elevated intracranial pressures (ICP). Patients with obstructive lung disease (e.g., COPD, acute asthma) may have an already elevated FRC. Except in cases to balance autoPEEP to enable ventilator triggering, PEEP should be used with caution in these patients. Other relative contraindications to PEEP include unilateral or focal lung disease, pulmonary embolism, and bronchopleural fistula.10 PEEP may have unintended consequences in patients undergoing prone ventilation (e.g., regional lung over distention).10 PEEP may also increase Pplateau, and care must be used to maintain Pplateau < 30 cm H2O. Untreated tension pneumothorax is an absolute contraindication to PEEP.

Methods Many approaches to the application of PEEP have been advanced to include minimum PEEP, optimal PEEP for oxygen delivery, and compliance-titrated PEEP. The ARDSNet protocol suggests use of PEEP tables, which many clinicians find effective and easy to use. Others have advocated PEEP titration using pressure– volume curves as part of a lung-protective strategy. Extrinsic or applied PEEP is also

sometimes used to balance autoPEEP in certain circumstances. Each of these methods is described below.

Minimum PEEP PEEP can be effective in improving oxygenation in patients with hypoxemic respiratory failure. Minimum PEEP is simply the least PEEP needed to achieve adequate arterial oxygenation at a safe oxygen concentration. PEEP is incrementally increased (2 to 5 cm H2O) followed by patient assessment. The lowest PEEP level that results in a PaO2 ≥ 60 mmHg and/or SaO2 ≥ 90% with FIO2 ≤ 0.50 to 0.60 is maintained. Minimum PEEP is easy to apply and results in the lowest PEEP level associated with satisfactory oxygenation. Minimum PEEP may avoid the adverse consequences sometimes associated with the application of high PEEP levels.

Optimal PEEP for Oxygen Delivery Optimal or best PEEP can be defined as the PEEP that maximizes oxygen delivery to the tissues. Oxygen delivery (ḊO2) is simply arterial oxygen content (CaO2) times cardiac output (Q̇T) as described above. Ventilation-perfusion (V̇/Q̇) mismatch, right to left shunt, diffusion limitation, and hypoventilation may reduce arterial oxygenation and CaO2. Specific factors that affect CaO2 include PaO2, SaO2, and hemoglobin level. FIO2 and PEEP/CPAP may improve PaO2 and SaO2. Cardiac output may be affected by cardiac disease or hypovolemia. PEEP provided to maximize ḊO2 is increased in a stepwise fashion followed by measurement of variables associated with oxygenation and cardiac output. PEEP continues to be increased until one or more variables associated with cardiac output (Q̇T) and tissue oxygen delivery decreases. The optimal PEEP is the PEEP level just below that at which the decline occurred. Typical measures that have been used to assess tissue oxygen delivery to determine best or optimal PEEP include: Cardiac output (Q̇T): normal values 5 L/min (range 4 to 8 L/min) Cardiac index (CI = Q̇T/BSA): normal values 2.5 to 4 L/min/m2 Mixed venous oxygen tension (Pv̄O2): normal values 40 mmHg (range 35 to 40 mmHg) Mixed venous oxygen saturation (Sv̄O2): normal values 75% (70% to 75%) Arterial-venous oxygen content difference (CaO2 – Cv̄O2): normal values 5 vol%

(3.5 to 5.0 vol%) Calculated oxygen delivery (ḊO2: normal value 1000 mL/min Arterial blood pressure (ABP): normal values 120/80 mmHg (range 90 to 140/60 to 90 mmHg) Except for CaO2 – Cv̄O2, best or optimal PEEP (based on oxygen delivery) has been exceeded when these values (above) decline following an incremental increase in PEEP. CaO2 – Cv̄O2 increases when best or optimal PEEP has been exceeded. PEEP is returned to the level just below the level at which measures related to ḊO2 decline, and that value is considered the best or optimal PEEP. Titration of PEEP to optimize tissue oxygen delivery has theoretic appeal for patients with hypoxemic respiratory failure (e.g., ARDS) and may improve arterial oxygenation. Measures reflecting ḊO2 can be time consuming and in some cases difficult to obtain. For example, mixed venous oxygen levels and invasive measures of cardiac output require a pulmonary artery catheter (although newer, less-invasive techniques to measure cardiac output are available). Titration of PEEP to optimize ḊO2 has not been shown to clearly improve other important patient outcomes (e.g., time to extubation, duration of ICU stay, or mortality) and cannot be recommended for routine application in most patients.11,12 Other high PEEP strategies employed in patients with ARDS may improve mortality in patients with moderate to severe ARDS but worsen it in patients with mild ARDS.11 High PEEP strategies probably work best in ARDS patients with a large volume of recruitable lung.

PEEP–FIO2 Tables The use of PEEP–FIO2 tables to adjust PEEP was first described in the landmark ARDSNet study, which demonstrated improvement in mortality in ARDS patients ventilated with lower tidal volumes.13 In that study, the oxygenation goals were PaO2 55 to 80 mmHg or SpO2 88% to 95%. The tables provide higher and lower PEEP options; clinicians can choose based on the patient’s condition. For example, patients expected to require higher PEEP for lung recruitment may benefit from the higher PEEP option if they are hemodynamically stable and have no barotrauma. The lower PEEP/higher FIO2 option maintains PEEP in the range of 5 to 10 cm H2O for FIO2 of 0.30 to 0.60, while the higher PEEP option allows PEEP values in the

range of 5 to 18 cm H2O for FIO2 of 0.30 to 0.50. Both tables allow PEEP levels of up to 24 cm H2O on 100% oxygen. Allowable combinations of FIO2 and PEEP to achieve these goals are found in Table 7-4. Additional information can be found at the ARDSNet website. TABLE 7-4 ARDSNet PEEP–FIO2 Tables

Data from National Institutes of Health (NIH) National Heart, Lung, and Blood Institute (NHLBI) ARDS Clinical Network Mechanical Ventilation Protocol summary. Available at www.ardsnet.org/files/ventilator_protocol_2008-07.pdf

Compliance-Titrated PEEP With acute hypoxemic respiratory failure patients often have reductions in pulmonary compliance and functional residual capacity (FRC). With such patients, lung compliance and FRC tend to increase as PEEP increases. Compliance-titrated PEEP seeks to identify the PEEP level at which compliance is optimized. Compliance-titrated PEEP generally begins at a modest PEEP level (e.g., 5 cm H2O), followed by measurement of static total compliance (CST) where: CST = VT ÷ (Pplateau – PEEP). Following initial measurement of CST, PEEP is increased by 2 cm H20 and CST measurement is repeated. PEEP continues to be increased in an incremental stepwise fashion until a decrease in compliance is observed. At that point, PEEP is lowered to the previous value that represents the best or optimal PEEP based on compliance. With nonuniform lung disease, regional overdistention can occur below the compliance-titrated PEEP level. PEEP increases mean airway and intrathoracic pressures, which may reduce venous return and cardiac output; cardiac output may be affected at PEEP levels below the optimal PEEP. Clinical Focus 7-2 provides an example of compliance-titrated PEEP.

CLINICAL FOCUS 7-2 Compliance-Titrated PEEP A patient with acute hypoxemic respiratory failure is receiving mechanical ventilation in the assist/control volume ventilation mode. Initial ventilator settings include: Mode: assist/control volume ventilation (aka VC-CMV) Tidal volume: 8 mL/kg IBW Set rate: 14 breaths/minute FIO2: 1.0 PEEP: + 5 cm H2O The respiratory care clinician decides to provide compliance-titrated “best”

PEEP for this patient and the following information is collected:

Description Question 1. Calculate the patient’s static total compliance (CST) at times 4 and 5. CST = VT ÷ (Pplateau – PEEP) 1. Answer for time #4 compliance: CST = VT ÷ (Pplateau – PEEP) = 500 mL ÷ (29 cm H2O – 12 cm H2O) = 29 mL/cm H2O 2. Answer for time #5 compliance: CST = VT ÷ (Pplateau – PEEP) = 500 mL ÷ (34 cm H2O – 14 cm H2O) = 25 mL/cm H2O Question 2. What is the PEEP level that results in the best static total compliance? The best compliance value was obtained at a PEEP of 12 cm H2O:

Question 3. What PEEP level is most appropriate for this patient? Compliance-titrated best PEEP is 12 cm H2O. The resultant Pplateau is 29 cm H2O, which is acceptable. Suggested PEEP for this patient is 10 to 12 cm H2O while maintaining Pplateau < 30 H2O (slightly higher Pplateau may be acceptable in patients with decreased thoracic compliance).

Pressure–Volume Curves Static pressure–volume curves provide a visual representation of changes in pressure and volume as the lung is inflated in a stepwise fashion. To generate a static pressure–volume curve, the clinician increases volume in increments of approximately 100 mL measuring Pplateau following each increase. The pressures and corresponding volumes are then plotted graphically (Figure 7-6). Often the result provides an easy to identify lower inflection point (LIP), which represents the point when lung compliance improves due to alveolar recruitment. As incremental volume continues to be added, the curve tends to rise in a linear fashion until an upper inflection point (UIP) is reached, which represents the point at which the lung overdistention begins. PEEP is then set at approximately 2 cm above the LIP and tidal volume is adjusted to ensure that the UIP is not exceeded. Some patients, however, do not exhibit a LIP and interobserver variability can be significant. A lung

recruitment maneuver may be done prior to assessing LIP for the purposes of titrating PEEP (see below). Figure 7-6 illustrates a static pressure–volume curve with lower inflection point (LIP, aka p-flex) and upper inflection point (UIP) illustrated.

FIGURE 7-6 Static Pressure–Volume Curve Showing Upper and Lower Infection Points.

Development of a static pressure–volume curve is labor intensive, time consuming, and can be difficult. As an alternative, slow-flow (< 6 L/min) pressure– volume curves can be generated by most ventilator graphics packages to identify patients’ lower inflection points and PEEP is set accordingly (e.g., LIP + 2 cm H2O). Figure 7-7 illustrates a slow-flow pressure–volume curve for identifying LIP for the purposes of setting PEEP.

FIGURE 7-7 Slow-Flow Pressure–Volume Curve. Respiratory gas flow is approximately 6 L/min.

Decremental PEEP Trials Some authors suggest that the best method for identifying optimal PEEP with ARDS is a decremental PEEP trial performed following a lung recruitment maneuver.14 To begin a decremental PEEP trial, a recruitment maneuver is first performed, such as the one described in Box 7-3. Immediately following a successful recruitment maneuver, the patient’s ventilatory mode is adjusted to volume control with tidal volume in the range of 4 to 6 mL/kg IBW and an inspiratory time in the range of 0.6 to 0.8 seconds. Respiratory rate is set at a value that provides the desired minute volume without causing autoPEEP.

BOX 7-3 Lung Recruitment Maneuver A variety of lung recruitment maneuvers have been suggested for ARDS to recruit closed alveoli and improve oxygenation. Recruitment maneuvers require that the patient be apneic and hemodynamically stable. Recruitment maneuvers should be performed early during the course of the disease, ideally soon after the initiation of mechanical ventilation. Recruitment maneuvers may improve oxygenation but have not been shown to improve patient outcomes. Overaggressive maneuvers may also be harmful. One method suggested for lung recruitment includes the following steps: 1. Assess the patient to ensure hemodynamic stability. 2. Apnea is required, and sedation may be necessary. 3. Adjust the ventilator to provide pressure-control ventilation (PCV) with the following settings: a. FIO2 of 1.0 b. PEEP of 20 to 25 cm H2O c. PCV adjusted to 15 cm H2O above set PEEP (e.g., PIP 35 to 40 cm H2O) d. Respiratory rate of 15 to breaths/min e. I:E ratio of 1:1 or 1:2 4. Maintain settings for 2 to 3 minutes while observing patient response (heart rate, cardiac monitor, blood pressure, and SpO2). Discontinue recruitment maneuver immediately if signs of distress appear (SpO2 < 85%; HR > 140 beats/min or < 60 beats/min; MAP < 60 mmHg or a decrease more than 20 mmHg). 5. Follow the recruitment maneuver immediately with a decremental PEEP trial. If the lung recruitment maneuver is not successful in opening the lung, the maneuver can be repeated not sooner than 30 minutes following patient stabilization using incrementally higher PEEP levels (e.g., +5 cm H2O). At no point should peak inspiratory pressure (PIP) during a recruitment maneuver exceed 50 cm H2O. HR: heart rate; MAP: mean arterial blood pressure. Data from Kacmarek RM, Stoller JK, Heuer AJ. Initiating and adjusting invasive ventilatory support. In: Kacmarek RM, Stroller JK, Heuer AJ, Chatburn RL, Kallet RH, eds. Egan’s Fundamentals of Respiratory Care. 11th ed. St. Louis, MO: Elsevier; 2017:1078–1110.

The decremental PEEP trial may begin with PEEP set at 20 to 25 cm H2O (assuming those values were adequate to maintain the lung open during the recruitment maneuver).14 The initial PEEP level chosen should be sufficient to keep the lung open based on recruitment maneuver results and may be higher in some cases. Static total compliance (CST) is then measured and recorded (see compliance-titrated PEEP, above). The PEEP level is then decreased by 2 cm H2O and measurement of CST is repeated in 1 to 2 minutes (or as soon as compliance has stabilized). This process is repeated until the best PEEP based on CST is identified. Generally, compliance improves with each decrease in PEEP until alveolar derecruitment and atelectasis occur, at which point CST declines. The PEEP level immediately preceding the CST decline is the best PEEP based on compliance using this method. The lung recruitment maneuver is repeated because derecruitment has occurred during the last CST measurement. Following the recruitment maneuver, the applied PEEP level is adjusted to 2 to 3 cm H2O above the best compliance PEEP to ensure optimal tissue oxygen delivery.14

PEEP and AutoPEEP Intentionally applied PEEP is sometimes referred to as extrinsic PEEP. Intrinsic PEEP or autoPEEP is PEEP caused by incomplete gas expiration prior to the initiation of the next breath provided by the ventilator. AutoPEEP is most common in patients with obstructive lung disease; however, it may develop in any patient when inadequate expiratory time is provided. Common causes for the development of autoPEEP include inappropriate ventilator settings, high minute ventilation, expiratory flow limitation, and expiratory resistance.10 Minute ventilation (V̇E) is a function of tidal volume (VT) and respiratory rate (f). Large tidal volumes require adequate time to be exhaled while rapid respiratory rates reduce expiratory time. Bronchospasm, inflammation, or airway remodeling can cause expiratory flow limitation, which leads to hyperinflation.10 Expiratory flow limitation is common with COPD, acute asthma, and other forms of obstructive lung disease; these patients require adequate expiratory time or dynamic hyperinflation may occur. Resistance to expiratory gas flow can occur due to the artificial airway (e.g., partially obstructed or kinked endotracheal tubes) or airway obstruction (e.g., thick secretions, tumor). Resistance to expiratory gas flow will slow the rate of lung

emptying and may cause autoPEEP. Inappropriate ventilator settings that may cause autoPEEP include large tidal volumes, low peak inspiratory flows, increased inspiratory time, and inadequate expiratory time. AutoPEEP can be detected by physical assessment and observation of flow–time curves provided by the ventilator’s graphics package. Breath sounds in which inspiratory airflow occurs before expiratory airflow ceases suggest the presence of autoPEEP.10 Observation of the expiratory flow–time curves in which expiratory gas flow does not cease prior to the initiation of inspiration indicate autoPEEP. AutoPEEP can be measured directly (in the absence of patient inspiratory efforts) by applying an expiratory pause (e.g., 2 to 3 seconds) to allow airway pressure to equilibrate with alveolar pressure.15 Static autoPEEP is calculated by subtracting the extrinsic PEEP from the observed end-expiratory pressure observed during the expiratory pause.15 AutoPEEP can be difficult to measure accurately in spontaneously breathing patients and those with acute severe asthma due to airway closure.10 Dynamic autoPEEP can be quantified in spontaneously breathing patients by observing the esophageal pressure change from the onset of the inspiratory effort to the point of zero flow as observed on the flow–time curve.15 Steps to correct autoPEEP should focus on identifying and correcting the underlying cause. Ventilator adjustments to correct or prevent autoPEEP include altering peak flow, inspiratory time, tidal volume, and respiratory rate to ensure adequate expiratory time and I:E ratio. Resistance to expiratory gas flow may be corrected by using larger endotracheal tubes and correcting (if possible) airway obstruction or mechanical factors (e.g., PEEP or expiratory valves) that are causing increased resistance. Bronchodilator and steroid administration may be helpful in the presence of expiratory flow limitation (e.g., asthma, COPD). AutoPEEP may cause triggering asynchrony and this can sometimes be corrected by the application of extrinsic PEEP of not more than 50% to 80% of the measured autoPEEP value. The use of extrinsic PEEP to correct autoPEEP should be reserved for those cases where correction of the underlying cause has been unsuccessful, and the presence of autoPEEP is causing triggering difficulty.

Application of PEEP PEEP is commonly applied to improve oxygenation of ventilated patients in acute

respiratory failure (e.g., ARDS). Extrinsic PEEP is also sometimes used to correct triggering difficulty due to autoPEEP.

Minimum PEEP We suggest that most patients receive 5 cm H2O of PEEP or CPAP to maintain lung volumes and prevent atelectasis. Higher PEEP/CPAP is generally indicated for hypoxemia that is less responsive to oxygen therapy (e.g., PaO2 < 60 mmHg, SaO2 < 90% and FIO2 > 0.60). Minimal PEEP to increase PaO2 and oxygen saturation to acceptable levels while reducing FIO2 to < 0.50 to 0.60 is a good general strategy for many patients.

ARDS The principal causes of VALI in ARDS are thought to be alveolar overdistention and cyclic atelectasis. An open lung strategy may reduce the risk of VALI in ARDS patients. An open lung strategy that combines low tidal volume ventilation with a recruitment maneuver followed by titration of PEEP to maximize alveolar recruitment and minimize cyclic atelectasis has been suggested.11 Acceptable plateau pressures (< 28 to 30 cm H2O) are maintained to prevent alveolar overdistention. The lack of convincing evidence that an open lung strategy is beneficial and does not cause harm suggests that this approach should not be used as an initial strategy for most patients.11 While some clinical trials suggest that open lung ventilation may improve mortality and other important clinical outcomes, others have reported higher mortality with an open lung ventilation strategy.11 Open lung strategies should probably be limited to patients with severe ARDS that does not respond to a conventional approach using low tidal volumes, Pplateau < 28 to 30 cm H2O, and more conservative levels of PEEP. Use of ARDSNet-suggested PEEP tables is probably a good initial approach for setting PEEP for most ARDS patients. Patients with severe ARDS, however, may require a high PEEP strategy. High PEEP can be effective in improving oxygenation in patients with recruitable lung. High PEEP may open collapsed alveoli and decrease alveolar overdistention because of the larger number of alveoli being ventilated. There is some evidence that a high PEEP strategy can improve oxygenation, increase ventilator-free days, and lower ICU mortality, although these

results have not been consistently confirmed by later studies.11 There is also evidence that a high PEEP strategy can be harmful in patients with mild ARDS.11 It may be that a high PEEP strategy is beneficial in patients with severe ARDS with sufficient recruitable lung, but harmful in patients with little recruitable lung.11 High PEEP should probably be avoided as an initial strategy. That said, a high PEEP strategy may be beneficial in patients with severe ARDS if they have sufficient recruitable lung.11 Box 7-4 illustrates a high PEEP strategy.

BOX 7-4 High PEEP Strategy High PEEP may be necessary in patients with severe ARDS when more conventional approaches are ineffective. The clinician should assess whether (or not) high PEEP is effective in improving oxygenation as certain patients may have limited recruitable lung (i.e., they are PEEP non-responders). A high PEEP strategy may employ the following combinations of FIO2 and PEEP to achieve PaO2 60 to 80 mmHg and SaO2 90% to 95% at an FIO2 ≤ 0.50 to 0.60. FIO2

PEEP (cm H2O)

0.30

12 to 14

0.40

14 to 16

0.50

16 to 18

0.50 to 0.80

20

0.80

22

0.90

22

1.0

22 to 24

Data from Browen RG, Lanken PH, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med. 2004;351(4):327–336. doi: 10.1056/NEJMoa032193.

PEEP may cause barotrauma or VALI by increasing alveolar pressures. PEEP may also decrease venous return and reduce cardiac output. The optimal PEEP strategy for patients with ARDS has not been identified.10,11 It is also of interest to note that lung ultrasound can be used to visualize the effects of PEEP on lung aeration in patients with ARDS, and this may prove to be of clinical value in PEEP

titration in the future.11

AutoPEEP AutoPEEP should be quickly identified and treated. Ventilator adjustments, bronchodilator, and steroid administration, and correction of any mechanical factors that are contributing to autoPEEP should be performed. In cases of persistent triggering difficulty, modest levels of extrinsic PEEP (e.g., 50% to 80% of measured autoPEEP) may be applied. A simple approach is to incrementally increase extrinsic PEEP by 1 cm H2O until the patient is able to adequately trigger the ventilator. In no cases should intrinsic PEEP exceed 80% of the autoPEEP value.

Recruitment Maneuvers Various recruitment maneuvers have been suggested to open collapsed alveoli and improve oxygenation in patients with ARDS. A common sustained-inflation maneuver known as “30 for 30” or “40 for 40” applies 30 cm H2O of PEEP for 30 seconds or 40 cm H2O of PEEP for 40 seconds. Another common method combines PCV with the peak pressures of 35 to 50 cm H2O, inspiratory times of 1 to 2 seconds and PEEP set at 20 to 30 cm H2O applied for a period of 1 to 3 minutes. A decremental PEEP study is performed immediately following the maneuver to identify the PEEP level necessary to maintain lung recruitment (see decremental PEEP above). Sigh breaths may also be considered a type of recruitment maneuver that may be beneficial in patients undergoing prone ventilation or with extrapulmonary causes of ARDS, although there is conflicting evidence that sigh breaths are beneficial.11 Recruitment maneuvers are most likely to be effective in patients with reduced FRC, and there is evidence that recruitment maneuvers improve oxygenation and ventilatory mechanics and reduce intrapulmonary shunt. They may be effective in postoperative patients with significant atelectasis and in certain patients with ARDS. There is currently little evidence that recruitment maneuvers improve important patient outcomes in ARDS (e.g., time to extubation, mortality).16 There is wide variability in the approaches that have been used and it is uncertain if any specific approach is most effective. Recruitment maneuvers can significantly increase peak inspiratory pressure, mean airway pressure, and intrathoracic pressure. Because recruitment maneuvers

increase lung volumes, barotrauma may occur (e.g., pneumothorax). Increased intrathoracic pressures may reduce venous return and compromise cardiac output and blood pressure. Cardiac arrhythmias may develop up to and including cardiac arrest. Recruitment maneuvers require patients to be sedated to apnea and risks of the procedure must be balanced against possible benefit. Chapter 9 provides additional information regarding recruitment maneuvers. RC Insight When performing a recruitment maneuver carefully monitor the patient’s heart rate, blood pressure, and cardiac monitor for development of arrhythmias.

Prone Positioning Pulmonary blood flow varies with position because of gravity. Traditionally, mechanical ventilation is provided to patients lying in the supine position, which increases blood flow to the posterior portions of the lung. Prone positioning will increase blood flow to the anterior portions of the lung, which may be beneficial in improving oxygenation in ARDS patients. With ARDS patients in the supine position, alveolar collapse is greater in posterior regions of the lung. Prone positioning will cause previously dependent portions of the lung to open and they will continue to receive most of the blood flow as now nondependent alveoli reopen.16 Prone positioning is thought to improve oxygenation by placing the heart in a dependent position (the heart lies just behind the sternum), reducing the volume of dependent lung, increasing FRC, improving V̇/Q̇, and reducing shunt.16 Prone positioning has been shown to improve oxygenation and may have a mortality benefit for those with severe ARDS.16 Prone positioning has not been shown to reduce ICU length of stay, although it may increase the number of ventilator-free days.16 ARDS patients should receive a lung protective strategy including the use of small tidal volumes, limited plateau pressures, and the appropriate application of PEEP. Most ARDS patients can be effectively ventilated in the supine position. Prone positioning may be considered for patients with severe ARDS (e.g., PaO2/FIO2 < 150 with FIO2 ≥ 0.60 and PEEP ≥ 5 cm H2O) and those with refractory hypoxemia (which can be defined as a PaO2 rise < 5 mmHg following an increase in FIO2 ≥ 0.10)

unresponsive to a more conventional ventilatory approach.16 Prone ventilation should probably be initiated within the first 36 hours and maintained 18 to 20 consecutive hours.16 Prone positioning may be stopped following patient improvement or for acute emergencies or specific procedures.16 Contraindications to prone positioning include shock, hemorrhage, multiple fractures or trauma, spinal instability, pregnancy, increased intracranial pressure, or recent tracheal surgery or sternotomy.16 Prone positioning should be used with caution (if at all) in patients with severe burns, recent lung transplant, chest tubes with air leaks, major abdominal surgery, recent pacemaker insertion, or recent treatment for deep vein thrombosis (DVT).16 Prone positioning can be difficult and labor intensive to accomplish in the ICU. Enteral feeding can be problematic during prone positioning (e.g., vomiting) and should be approached cautiously.16 Care should also be taken to avoid accidental extubation or dislodging vascular catheters or drainage tubes.16 Electrocardiogram (ECG) monitoring leads can be placed on the posterior thorax and hemodynamic monitoring should continue.16 Increased sedation is required and some patients may require neuromuscular blockade.16 Rescue alternatives to prone positioning in ARDS include the use of ECMO or pulmonary vasodilators.16

Bronchial Hygiene Bronchial hygiene techniques that may improve oxygenation in ventilated patients include suctioning and airway care, provision of adequate humidification, and administration of bronchodilators and inhaled anti-inflammatory agents. There is no strong evidence for the effectiveness of nonpharmacologic airway clearance therapies (except in cystic fibrosis) to improve oxygenation, reduce time on the ventilator, reduce time in the ICU, or treat atelectasis and lung consolidation. Evidence for the effectiveness of bronchodilators or mucosal active medications to improve airway clearance and prevent complications such as atelectasis is also lacking. That said, absence of evidence is not the same as evidence of absence (in terms of benefit), and decision making should be made based on individual patient needs, response to therapy, and potential for harm. Careful attention to appropriate humidification, airway suctioning, monitoring and correcting endotracheal tube position, and monitoring and adjusting airway cuff

pressures is required. In cases where airway obstruction is suspected, bronchodilators and inhaled anti-inflammatory agents should be employed. Endotracheal tubes may cause reflex bronchoconstriction and we suggest routine aerosol bronchodilator administration for most invasively ventilated patients. Early mobilization of ventilated patient may be helpful in improving oxygenation, as well as decreasing the consequences of ICU-acquired weakness.14 This may include turning, sitting up in bed, sitting in a chair, and walking with support. The head of the bed should be elevated > 30 degrees in ventilated patients to reduce the incidence of ventilator-associated pneumonia.14 In summary, various methods have been used to improve oxygenation in ventilated patients including adjustment of FIO2, optimal PEEP techniques (e.g., minimum PEEP, compliance-titrated PEEP, decremental PEEP, and PEEP based on ḊO2), recruitment maneuvers, and prone positioning. Bronchial hygiene techniques that may improve oxygenation include bronchodilator and steroid/anti-inflammatory medications, suctioning and airway care, attention to proper humidification, and bronchopulmonary hygiene. Specific modes of ventilation may sometimes improve oxygenation in certain patients; these include pressure-control inverse-ratio ventilation (PCIRV), airway pressure-release ventilation (APRV), and high-frequency oscillatory ventilation (HFOV). For most patients, providing the least PEEP to achieve adequate arterial oxygenation at a safe FIO2 is a sound approach. PEEP tables are also a good place to start for patients with ARDS. High PEEP, open lung ventilation, recruitment maneuvers, prone positioning, PCIRV, and rescue HFOV should be reserved for patients with severe ARDS that is refractory to a more conventional ventilatory approach.11

Ventilation The primary purpose of mechanical ventilatory support is to augment or replace normal ventilation. Components of ventilation include tidal volume, respiratory rate, and minute ventilation. Ventilation directly affects carbon dioxide removal, and measurement of the arterial carbon dioxide tension (PaCO2) allows the respiratory care clinician to precisely assess the effectiveness of the ventilatory support provided and provides a guide for making needed ventilator adjustments.

Tidal Volume, Rate, and Minute Ventilation Ventilation can be subdivided into tidal volume (VT), respiratory rate (f), and minute ventilation (V̇E), where V̇E = f × VT. Ventilatory volumes and respiratory rate can be easily measured at the bedside using a handheld respirometer or with the ventilator’s built-in monitoring system. Normal adult values for each of these variables are: f = 12 breath/min (normal range 12 to 20 breaths/min); f < 30 (but ≥ 10 breaths/min) is associated with adequate spontaneous breathing for adults in the ICU. VT = 500 mL (normal range 400 to 700 mL [about 7 mL/kg IBW]); VT > 5 mL/kg is associated with adequate spontaneous breathing. V̇E = 6 L/min (normal range 5 to 10 L/min [about 100 mL/kg IBW]); V̇E < 10 L/min but ≥ 5 L/min is associated with adequate spontaneous breathing; higher values are associated with distress. Tachypnea, bradypnea, rapid, shallow breathing, and other abnormal breathing patterns commonly seen in adult ICU patients are described in Box 7-5.

BOX 7-5 Ventilatory Pattern Alterations in ICU Patients Alterations in spontaneous breathing are common in ICU patients and include: ∎ Tachypnea: f > 20 breaths/min (adults) although rates of 20 to 30 breaths/min are common in the ICU; f > 30 breaths/min is cause for concern. • Causes of tachypnea include anxiety, pain, hypoxemia, acute pulmonary disease, cardiac insufficiency, and metabolic acidosis. • f > 35 breaths/min with severe distress, air hunger, diaphoresis, and

∎

∎

accessory muscle use may signal an impending respiratory arrest. Bradypnea in spontaneously breathing adults: f < 8 to 10 breaths/min. • Causes include excessive sedation, anesthesia, opioid drug overdose, excessive alcohol consumption, head trauma, increased intracranial pressure, neurologic disease, hypothermia, or cardiogenic shock. Abnormal ventilatory patterns include: • Rapid shallow breathing: in adults, this typically corresponds to VT < 300 mL and f > 30 breath/min. Rapid, shallow breathing is not synonymous with hyperventilation. Most patients experiencing rapid shallow breathing are in fact hypoventilating. • Biot’s breathing: rapid shallow breathing with periods of apnea sometimes seen with stroke or trauma. • Cheyne-Stokes breathing: cyclical increases and decreases in tidal volume with periods of apnea sometimes seen with cardiac or neurologic disease, sedation, or acid-base disturbances. • Kussmaul breathing: increased depth of breathing associated with diabetic ketoacidosis. • Obstructive sleep apnea (OSA): caused by repetitive collapse of the soft tissue of the upper airway during sleep resulting in frequent apneas, hypopneas, and respiratory effort–related sleep arousals. OSA may be seen in patients receiving inappropriate levels of support via noninvasive ventilation (NIV) and prior to endotracheal intubation and following extubation.

Alveolar Ventilation Alveolar ventilation per minute (V̇A) determines the effectiveness of ventilation and removal of carbon dioxide; V̇A is determined by VT, f, and dead space volume (VD). The volume of gas in the conducting airways that does not participate in gas exchange is VD anatomic, while alveoli which are ventilated but not perfused make up the VD alveolar. VD anatomic plus VD alveolar is the physiologic dead space (VD phys

). Thus, alveolar ventilation (V̇A) is: V̇A = (VT – VD phys) × f.

Normal VD phys can be estimated at approximately 1 mL/lb IBW or 2.2 mL/kg IBW.

Normal VD phys for a 150 lb (IBW) person would be about 150 mL. Thus, normal adult V̇A is about 4.2 L/min (range: 4 to 5 L/min): V̇A = (VT – VD phys) × f = (500 mL – 150 mL) × 12 breaths/min = 4200 mL/min = 4.2 L/min Dead space to tidal volume ratio (VD/VT) is sometimes measured at the bedside: VD/VT = (PaCO2 – PēCO2) ÷ PaCO2, where PaCO2 is arterial carbon dioxide tension (normally 40 mmHg; range: 35 to 45 mmHg) and PēCO2 is mean exhaled CO2 tension (normally 28 mmHg; range: 24 to 32 mmHg). PēCO2 should not be confused with end-tidal CO2 (i.e. PET CO2, which is normally about 35-40 mmHg and sometimes used as a surrogate for PaCO2). Normal VD/VT is 0.30 (range: 0.20 to 0.40) although patients receiving invasive mechanical ventilation with positive pressure may have a higher VD/VT (e.g., ≥ 0.50). Some newer ventilators (e.g., the Dräger XL ventilator) are equipped with integrated CO2 and volume measurement capabilities, which may allow for accurate calculation of VD/VT in ventilated patients without requiring a separate device to measure PēCO2. Possible causes of increased VDphys include emphysema (which can result in obliteration of pulmonary capillaries) and pulmonary embolus (with complete occlusion of the pulmonary vessel). Additional large-bore ventilator tubing placed between the patient “Y” and the endotracheal or tracheostomy tube connection adds additional rebreathed gas volume known as mechanical dead space. Alterations in mechanical ventilatory support that increase V̇A include increased VT, increased f, and decreased mechanical dead space (if present). Ventilator changes that decrease V̇A include decreased VT, decreased f, and the addition of mechanical dead space.

Alveolar Ventilation and PaCO2 The relationship between alveolar ventilation (V̇A) and PaCO2 is defined by the following equation: V̇A = (0.863 × V̇CO2) ÷ PaCO2,

where: V̇A is alveolar ventilation in L/min (normally 4 to 5 L/min). V̇CO2 is carbon dioxide production in mL/min (normally about 200 mL/min, although this varies with activity, metabolic rate, and diet). PaCO2 is the partial pressure of arterial carbon dioxide in mmHg (normally 40 mmHg [range 35 to 45 mmHg]). 0.863 is a conversion factor. The above equation can be rearranged as follows: PaCO2 = (0.863 × V̇CO2) ÷ V̇A. Inserting normal values, this becomes: V̇A= (0.863 × 200) ÷ 4.3 = 40 mmHg. Assuming V̇CO2 is constant, this can be further simplified to:

This should make it clear that PaCO2 and V̇A are inversely proportional and as: V̇A increases → PaCO2 decreases. V̇A decreases → PaCO2 increases. This allows the following definitions: Normal ventilation: PaCO2 of 40 mmHg (range 35 to 45 mmHg) Hyperventilation: PaCO2 < 35 mmHg Hypoventilation: PaCO2 > 45 mmHg Thus, PaCO2 is the single best clinical indicator of alveolar ventilation and provides the best measure of the effectiveness of ventilatory support provided during mechanical ventilation. It is important to note, however, that changes in carbon dioxide production (V̇CO2) may alter PaCO2. Causes of increased V̇CO2 include fever, agitation, increased level of activity, “fighting the ventilator,” overfeeding, and

hypermetabolism seen with sepsis, burns, and trauma.14,17 Decreased V̇CO2 may occur with relaxation, sleep, sedation, general anesthesia, administration of paralytic drugs, cooling, or slowed metabolic rate.14,17 The normal response to increased V̇CO2 is increased V̇A; PaCO2 will increase if the patient is unable to compensate for increased carbon dioxide production by increasing alveolar ventilation.

PaCO2 during Mechanical Ventilation A major goal of mechanical ventilation is to provide ventilatory support resulting in satisfactory alveolar ventilation as assessed by measurement of PaCO2. For most patients, the goal is to normalize PaCO2 in the range of 35 to 45 mmHg. In the absence of a metabolic acid-base disorder, a normal PaCO2 should result in a normal arterial pH of 7.35 to 7.45. An exception to the goal of normalizing PaCO2 in the range of 35 to 45 mmHg are COPD patients whose “normal” baseline state is chronic ventilatory failure (aka chronic hypercapnic respiratory failure). Such patients are chronically hypercapnic resulting in a normal or near-normal pH due to renal compensation. With acute exacerbation of their COPD, these patients may develop acute ventilatory failure superimposed on chronic ventilatory failure characterized by a further elevated PaCO2 and acidotic pH (e.g., < 7.35). The goal of ventilatory support for these patients is to return their PaCO2 to their baseline levels. In such cases, mechanical ventilation resulting in a PaCO2 of 50 to 60 mmHg will often return the pH to near the baseline value; pH in 7.30 to 7.35 is a reasonable target for such patients.14

Intentional Hyperventilation Low arterial carbon dioxide tension produces cerebral vasoconstriction and reduces intracranial pressure (ICP). Certain patients with dangerously elevated ICP may be briefly hyperventilated to achieve a PaCO2 between 26 and 30 mmHg to cause cerebral vasoconstriction and reduce ICP. This is a short-term strategy to prevent the brain from herniating and the beneficial effects start to decrease after 6 to 12 hours. Patients that may benefit from this strategy include those with very high ICP concurrent with cerebral edema, intracranial hemorrhage, or bacterial meningitis. Such a strategy is not recommended as a part of initial ventilator setup (unless life-

threatening brain herniation is feared) or for patients with stroke or traumatic brain injury, as it may reduce local cerebral perfusion.

Permissive Hypercapnia Permissive hypercapnia refers to a ventilatory strategy that decreases VT and associated delivery pressures to reduce alveolar pressures and minimize alveolar overdistention. With permissive hypercapnia, PaCO2 rises and pH falls, resulting in a respiratory acidosis. The respiratory rate is increased to minimize the degree of acidosis while avoiding the introduction of autoPEEP.11 Permissive hypercapnia may improve outcomes in certain patients with severe ARDS. Permissive hypercapnia can also be a useful approach in the presence of severe bronchospasm with acute asthma exacerbation or exacerbation of COPD. Most patients will tolerate a PaCO2 in the range of 45 to 65 mmHg with pH in the range of 7.25 to 7.35 well.18 There is no established upper limit for PaCO2 or lower limit for pH when pursuing a permissive hypercapnia strategy.18 Ventilator changes that allow PaCO2 to rise should be made slowly and incrementally, limiting increases to a rate of 10 mmHg per hour or less.18 Use of sodium bicarbonate to correct pH ≤ 7.20 to 7.25 should be considered.18 Permissive hypercapnia should be avoided in patients with increased intracranial pressure (ICP), head trauma, cerebral edema, brain lesions, or seizure disorders.18

Ventilator Adjustments to Alter PaCO2 Ventilator adjustments that will decrease PaCO2 include increased VT, increased f, or decreased mechanical VD (if present). Ventilator adjustments that will increase PaCO2 include decreased VT, decreased f, or the addition of mechanical VD. Changes in alveolar ventilation (V̇A) required to obtain a desired PaCO2 can easily be calculated (assuming no change in V̇CO2):14,17 Initial PaCO2 × Initial V̇A = Desired PaCO2 × Desired V̇A This can be rearranged to calculate the alveolar ventilation required to make a desired change in PaCO2: Desired V̇A = (Initial PaCO2 × Initial V̇A) ÷ Desired PaCO2

For example, if a patient receiving mechanical ventilation has a V̇A of 3.5 L/min, resulting in a PaCO2 of 50 mmHg, the V̇A needed to lower the patient’s PaCO2 to 40 mmHg would be 4.375 L/min: Desired V̇A = (Initial PaCO2 × Initial V̇A) ÷ Desired PaCO2 = (50 × 3.5) ÷ 40 = 4.375 L Thus, if the patient’s alveolar ventilation was increased from 3.5 L/min to 4.375 L/min, the PaCO2 would to decrease from 50 mmHg to 40 mmHg. Recall that alveolar ventilation is simply tidal volume minus dead space times respiratory rate: V̇A = (VT – VD phys) × f Substituting tidal volume, dead space, and respiratory rate into our predictive equation, we have: Desired V̇A = (Initial PaCO2 × Initial V̇A) ÷ Desired PaCO2 Desired ([VT – VD phys] × f) = Initial (PaCO2 × ([VT – VD phys] × f) ÷ Desired PaCO2 This equation has the potential to accurately predict the effect of changes in tidal volume, respiratory rate, or physiologic dead space on PaCO2 (assuming no change in V̇CO2). The equation is cumbersome to use and requires accurate input of all the variables. As an alternative, some clinicians substitute minute ventilation as follows: Desired V̇E = (Initial V̇E × Initial PaCO2) ÷ Desired PaCO2 This equation uses minute ventilation alone to predict changes in PaCO2 and requires that V̇CO2 and VD remain unchanged. For example, if a patient’s initial minute ventilation and PaCO2 were 8 L/min and 25 mmHg respectively, the equation suggests that if the minute ventilation is reduced to 5 L/min the PaCO2 will rise to 40 mmHg: Desired V̇E = (Initial V̇E × Initial PaCO2) ÷ Desired PaCO2 Desired V̇E = (8 L/min × 25 mmHg) ÷ 40 mmHg = 5 L/min

This equation provides a rough estimate of the effect changes in V̇E on PaCO2 and assumes VD and V̇CO2 are constant.

Rate Changes Effect on PaCO2 Tidal volume for patients receiving mechanical ventilatory support generally is initiated at 6 to 8 mL/kg IBW and titrated up or down to ensure Pplateau < 28 to 30 cm H2O. This leaves ventilator rate adjustments as the primary tool for altering the patient’s PaCO2. In apneic patients it is very easy to predict the effect of a specific rate adjustment on the patient’s PaCO2 (assuming VT and VD have not changed). Recall that alveolar ventilation is simply tidal volume minus dead space times respiratory rate: V̇A = (VT – VD phys) × f Substituting tidal volume, dead space, and respiratory rate into our earlier predictive equation, we have: Desired V̇A = (Initial PaCO2 × Initial V̇A) ÷ Desired PaCO2. Desired ([VT – VD phys] × f) = Initial (PaCO2 × ([VT – VD phys] × f) ÷ Desired PaCO2 Assuming no change in VT or VD phys, this becomes: Desired f = (Initial PaCO2 × f) ÷ Desired PaCO2. If an apneic patient receiving mechanical ventilation has a respiratory rate of 12 breaths/min, resulting in a PaCO2 of 50 mmHg, the rate needed to lower the patient’s PaCO2 to 40 mmHg would be 15 breaths/min: Desired f = (Initial PaCO2 × Initial f) ÷ Desired PaCO2 = (50 × 12) ÷ 40 = 15 breaths/min

Tidal Volume and PaCO2 Alterations in tidal volume will affect alveolar ventilation and PaCO2. With apnea during time-triggered volume ventilation, the respiratory care clinician can easily adjust VT to obtain a desired PaCO2 using a modification of our predictive equation:

Desired VT = (Initial PaCO2 × Initial VT) ÷ Desired PaCO2 Assuming respiratory rate and dead space remain constant, if an apneic patient receiving mechanical ventilation has a VT of 400 mL resulting in a PaCO2 of 50 mmHg, the VT needed to lower the patient’s PaCO2 to 40 mmHg would be 500 mL: Desired VT = (Initial PaCO2 × Initial VT) ÷ Desired PaCO2 = (50 × 400) ÷ 40 = 500 mL. This predictive equation requires that V̇CO2 and VD be constant. V̇CO2 may vary with changes in metabolic rate, although these changes are less likely within the time interval typically used to adjust VT and obtain followup ABGs. Dead space, however, may change with changes in VT. For example, during positive-pressure ventilation, an increase in VT will often be accompanied by increased airway pressure. This increased airway pressure may increase inspiratory mechanical bronchodilation. Put another way, the conducting airways may increase in diameter due to the positive pressure resulting in a small increase in anatomic dead space. The reverse may occur with decreases in VT during positive-pressure ventilation. Tidal volume adjustments will also affect peak inspiratory pressure and Pplateau. For most patients, VT should be maintained in an appropriate range (e.g., 6 to 8 m/kg IBW), and any adjustments made should not cause Pplateau to increase beyond 28 to 30 cm H2O.

Control Mode Volume Ventilation (Time-Triggered VC-CMV) For apneic patients in whom the respiratory care clinician has control over the patient’s tidal volume, respiratory rate, and minute ventilation (e.g., time-triggered volume ventilation), it is very easy to predict the ventilator changes required to achieve a desired PaCO2 using one of the methods described above. To decrease PaCO2, the clinician may increase the respiratory rate or increase VT using the formulas provided. Typically, the change is made followed by an arterial blood gas (ABG) in 20 or 30 minutes to confirm that the desired PaCO2 has been reached. It is generally a safe assumption that there will be little or no change in V̇CO2 or VD within that time interval. To increase PaCO2, the clinician simply decreases VT or f as described followed by an ABG in 20 to 30 minutes.

The addition of mechanical dead space volume provides another method to alter PaCO2 during mechanical ventilation in the control mode. Large-bore tubing may be added between the ventilator connection and the patient “Y” in order to increase rebreathed volume and PaCO2. Dead space tubing is typically added in increments 6 inches in length, each of which adds 50 to 70 mL of mechanical dead space.14,17 While the application of mechanical dead space provides an additional method to alter PaCO2, the results are less predictable. This method should not be used in patients able to trigger the ventilator or modes that incorporate spontaneous breathing. The effect of mechanical dead space increases with small tidal volumes. The removal of VD should decrease PaCO2, and the effect can be significant when smaller tidal volumes are being employed. It also should be noted that heat moisture exchange (HME) humidifiers increase mechanical dead space, and the amount added varies by brand. Most patients receiving mechanical ventilatory support are breathing spontaneously and have some control of their respiratory rate as the case with assist/control ventilation. Other modes of ventilation such as PSV, PAV, and NAVA provide the patient a great deal of control over their respiratory rate, tidal volume, and inspiratory time. While this is good for patient–ventilator synchrony, it makes ventilator adjustments to achieve a desired PaCO2 much less precise.

Assist/Control Ventilation Assist/control ventilation may be employed as assist/control volume ventilation (VCCMV) or assist/control pressure-control ventilation (PC-CMV). With assist/control ventilation, a backup respiratory rate is set by the clinician; however, the patient may trigger the ventilator as often as desired above that minimum rate threshold. With properly set trigger sensitivity, each patient’s inspiratory effort results in a mandatory breath. Should the patient cease inspiratory efforts, the respiratory rate will fall to the set minimum. Typical backup rate settings are 10 to 12 breaths/min or 2 to 4 breaths/min less than the patient’s resting trigger rate. In traditional assist/control volume ventilation, the mandatory breath delivers a set tidal volume, and the clinician determines the peak flow, flow waveform, and inspiratory time. The respiratory rate and expiratory time are determined by the patient. Should the patient cease triggering the ventilator, a minimum guaranteed

minute ventilation will be provided. Normally, the backup rate is set to assure a minimum minute ventilation should the patient become apneic. With assist/control PCV, the clinician determines the inspiratory pressure and inspiratory time, while patient effort (assuming appropriate trigger sensitivity) determines the respiratory rate. Tidal volume is determined by the inspiratory pressure, inspiratory time, and patient effort. Inspiratory pressure for mandatory breaths will be constant, but VT will vary with the patient’s pulmonary mechanics (compliance and resistance) and inspiratory effort. There are also dual and adaptive control modes that allow for patient-triggered breaths to set the rate and provide a volume guarantee (on average for adaptive targeting) using pressure control (e.g., PRVC, available with the Maquet Servo-i and Servo-u). Should the patient cease triggering the ventilator, a minimum guaranteed backup ventilation rate will provided. With controlled ventilation, the clinician can set the respiratory rate and tidal volume or inspiratory pressure to achieve the desired level of ventilatory support. With assist/control ventilation, patients set their own respiratory rate and can trigger mandatory breaths as often as needed or desired. PaCO2 is determined by the assist rate, which is set by the patient. Patients may increase or decrease their respiratory rates, based on their physiologic needs. Should apnea occur due to sedation or other reasons, the minimum backup rate is provided. In most cases, the patient’s respiratory center will dictate a trigger rate resulting in an appropriate level of alveolar ventilation, PaCO2, and pH. Some patients, however, will trigger the ventilator too rapidly, resulting in alveolar hyperventilation, decreased PaCO2, and respiratory alkalosis. Common causes of rapid ventilator triggering include pain, anxiety, hypoxemia, respiratory distress, bronchospasm, airway secretions, inappropriate ventilator settings, and metabolic acidosis. Sepsis and hepatic encephalopathy are additional conditions that may result in hyperventilation. Rapid trigger rates can result in reduced expiratory time, poor I:E ratio, increased mean airway pressure, and the development of autoPEEP. Patient–ventilator asynchrony may result, increasing the WOB and causing the patient to fight the ventilator. The respiratory care clinician should promptly identify and correct causes of rapid triggering. Anxiety can sometimes be relieved by reassuring the patient. Pain assessment tools should be employed, and appropriate pain management protocols

utilized.19 Hypoxemia should be recognized and immediately addressed by adjustments in FIO2 and PEEP and correction of treatable causes (e.g., bronchospasm, airway secretions). Causes of metabolic acidosis should be identified and treated. Inappropriate ventilator settings should be corrected promptly. This may include adjustment of peak inspiratory flow, inspiratory time, tidal volume, inspiratory pressure, trigger sensitivity (e.g., autotriggering), or mode of ventilation. An alternative to assist/control ventilation is SIMV with pressure support. SIMV with pressure support allows the patient to continue to spontaneously breathe in between mandatory breaths, but the volume for spontaneous breaths will be reduced and alveolar hyperventilation less likely. SIMV with pressure support should also reduce mean airway pressure as compared to continuous mandatory ventilation. Sedation may improve patient–ventilator synchrony and reduce inappropriate trigger rates. Sedation protocols should be employed that include intermittent sedation with daily interruption. Administration of neuromuscular-blocking agents will allow for complete control of the patient’s ventilation; however, these should not be employed except as a last resort (see below).

IMV/SIMV and PaCO2 SIMV intersperses mandatory breaths and spontaneous breathing. SIMV may be employed to deliver volume- or pressure-control mandatory breaths. Spontaneous breaths may be provided with pressure augmentation (pressure support or automatic tube compensation [ATC]) and PEEP/CPAP may be added. With volume SIMV (V-SIMV), tidal volume is typically initiated in the range of 6 to 8 mL/kg IBW with the mandatory respiratory rate sufficient to provide full ventilatory support (e.g., 12 to 14 breath/min). Care is taken to ensure Pplateau < 28 to 30 cm H2O. PEEP/CPAP is initially set at 5 cm H2O and adjusted in combination with FIO2 to meet oxygenation goals. Pressure support is provided in the range of 5 to 10 cm H2O to balance the imposed WOB of the endotracheal or tracheostomy tube. Pressure support is often adjusted to assure the patient’s spontaneous tidal volumes are at or above the patient’s estimated dead space (1 mL/lb IBW). Patients may take as many or as few spontaneous breaths in between mandatory breaths as desired. Factors that affect alveolar ventilation and PaCO2 with V-SIMV include:

Mandatory VT Mandatory rate (f) Spontaneous VT Spontaneous f Pressure-support level In general, as the mandatory rate is decreased, patients will tend to increase their level of spontaneous breathing and the effect on PaCO2 is difficult to predict. As mandatory rate increases, PaCO2 tends to decrease. As the PSV increases, patients’ spontaneous VT tends to increase, and this should reduce WOB and may reduce PaCO2. With V-SIMV, once appropriate VT, rate, and PSV values have been determined, SIMV rate is simply titrated up and down to meet the patient’s ventilatory needs. As with other forms of volume-control ventilation, SIMV trigger sensitivity must be appropriate and mandatory breath peak flow, flow waveform, and inspiratory time must be adjusted to avoid patient–ventilator asynchrony. Pressure-control SIMV (P-SIMV) is initiated in a similar fashion as V-SIMV. The primary difference is that inspiratory pressure and inspiratory time are set by the clinician, and mandatory breath tidal volume varies with the patient’s pulmonary mechanics and patient effort. Generally, P-SIMV is initiated at the pressure-control level necessary to obtain VT in the range of 6 to 8 mL/kg IBW with the mandatory respiratory rate sufficient to provide full ventilatory support (e.g., 12 to 14 breath/min). PSV and PEEP/CPAP are set in a similar fashion to V-SIMV. The primary advantage of P-SIMV is that inspiratory pressures are consistent and will not change with changes in the patient’s pulmonary mechanics or inspiratory effort. This ensures that alveolar pressures and Pplateau will remain in a safe range (e.g., Pplateau < 28 to 30 cm H2O) assuming appropriate pressure-control values are set by the clinician. As with all pressure-control modes, mandatory breath VT will vary with changes in the patient’s pulmonary mechanics and inspiratory effort. As with V-SIMV, P-SIMV mixes mandatory breaths with spontaneous breathing and the effect of ventilator changes on PaCO2 are difficult to predict. Trigger sensitivity, inspiratory pressure, and inspiratory time must be adjusted to meet the patient’s needs and avoid patient–ventilator asynchrony. Once appropriate initial ventilator settings have been determined, P-SIMV mandatory rate is simply titrated up and down to meet changes in the patient’s ventilatory needs.

PSV and PaCO2 Pressure support may be used as the primary mode of ventilatory support. When used as the primary mode of ventilation, the PSV level is generally adjusted to achieve a tidal volume in the range of 4 to 8 mL/kg IBW at a patient-triggered respiratory rate of ≤ 25 breaths/min. Pressure support allows the patient to trigger and cycle each breath and the patient has control of his or her respiratory rate, inspiratory and expiratory times, and I:E ratio. Tidal volume is determined by inspiratory pressure and patient effort. PSV should provide good patient–ventilator interaction and reduce the likelihood of patient–ventilator asynchrony. Because the patient sets the respiratory rate, the clinician has little control over the PaCO2. Assuming an intact, properly functioning respiratory control center, the result should be an appropriate PaCO2 and pH. The patient can then vary his or her respiratory rate as their physiologic needs change. Assuming a patient with an intact and properly functioning respiratory control center, problems associated with PSV are primarily related to inappropriate ventilator settings. Slow rise times or inappropriate expiratory cycle criteria can result in increased WOB and patient–ventilator asynchrony. Care should also be taken to set an appropriate inspiratory pressure level that results in adequate gas flow and volume that meets the patient’s inspiratory needs. PSV does not allow for the setting of a backup control rate and PSV should not be used in patients who experience periods of apnea or who have irregular breathing patterns. If PSV is employed as the primary mode of ventilatory support, care should be taken to ensure that an appropriate backup apnea ventilation mode has been set.

Acid-Base Balance Patients in respiratory failure often experience acid-base disorders and the patient’s ventilatory status can have a significant impact on acid-base balance as described by the simplified form of the Henderson-Hasselbalch equation:

and

Where pKa is the –log (Ka) = 6.1, HCO3– is the bicarbonate ion concentration (mEq/L), H2CO3 is the carbonic acid concentration, PCO2 is the partial pressure of carbon dioxide in mmHg, and 0.03 is the solubility constant for CO2 in plasma (H2CO3 = PCO2 × 0.03). Normal arterial blood pH is 7.40 with a range of 7.35 to 7.45, while normal PaCO2 is 40 mmHg (range 35 to 45 mmHg) and normal bicarbonate concentration (HCO3–) is 24 mEq/L (range 22 to 28 mEq/L). Because mechanical ventilatory support has the potential to significantly alter patients’ alveolar ventilation and PaCO2, the respiratory care clinician must understand the relationship between PaCO2 and pH when making ventilator adjustments. Increases in VT, f, and V̇E generally result in decreased PaCO2 while decreases in these values generally result in increased PaCO2. Acute increases in PaCO2 will cause a corresponding decrease in pH while acute decreases in PaCO2 will increase pH. The effects of acute changes in PaCO2 on pH and HCO3– are as follows: For every 10-mmHg increase in PaCO2 (acutely), the pH decreases approximately 0.08 units; so for every 1-mmHg increase, the pH decreases 0.008 units.

For every 10-mmHg increase in PaCO2 (acutely) HCO3– will increase about 1 mEq/L. This small increase in HCO3– is due to increased CO2 and does not represent renal compensation; every 1-mmHg of increase will increase HCO3– about 0.1 mEq/L. For example, a sudden rise in PaCO2 from 40 to 60 mmHg due to a change in the level of mechanical ventilatory support provided would cause the pH to decrease from 7.40 to 7.24; HCO3– would increase from 24 mEq/L to 25 mEq/L (assuming normal initial values). With respect to sudden decreases in PaCO2, the relationships between PaCO2, pH, and HCO3– are as follows: For every 10-mmHg decrease in PaCO2 (acutely), pH increases approximately 0.08 units. For every 10-mmHg decrease in PaCO2 (acutely), HCO3– decreases about 2 mEq/L. For example, a sudden decrease in PaCO2 from 40 to 30 mmHg due to an increase in the level of ventilatory support provided, would cause the pH to increase from 7.40 to 7.48; HCO3– would decrease from 24 mEq/L to 22 mEq/L (assuming normal initial values). RC Insight For acute increases in PaCO2, every 1-mmHg increase in PaCO2 will decrease pH by 0.008; for acute decreases in PaCO2, every 1-mmHg decrease in PaCO2 will increase in pH by 0.008.

Chronic alterations in the level of ventilation and PaCO2 will also affect acid-base balance. A chronic increase in PaCO2 of 10 mmHg will cause plasma HCO3– to increase about 4 to 5 mEq/L due to renal compensation, which takes 3 to 5 days to complete. With chronic decreases in PaCO2 of 10 mmHg, HCO3– will decrease about 4 to 5 mEq/L due to renal compensation. With chronic alterations in the level of ventilation and PaCO2, pH will often return to near-normal due to renal compensation; this process generally takes at least 3 to 5 days to complete. Clinically, patients may be inappropriately over- or underventilated (as compared to their baseline status) following ventilator initiation, and this will immediately affect

their pH. If overventilation continues for a period of days, renal compensation will ensue, and the result will be an artificially created compensated respiratory alkalosis. When ventilator discontinuance is attempted, patients may continue to try and spontaneously hyperventilate to maintain their pH. If underventilation occurs for a period of days, renal compensation will also occur, resulting in an artificially created compensated respiratory acidosis. When ventilator discontinuance is attempted, these patients may continue to spontaneously hypoventilate in order to maintain their pH. The goal for mechanical ventilatory support should be to rapidly achieve a normal or near-normal PaCO2 and pH for that patient. Table 7-5 lists normal arterial blood gas values. TABLE 7-5 Normal Arterial Blood Gas Values Analyte (units)

Description

Normal (range)

pH

–log [H+]

7.40 (7.35 to 7.45)

Paco2 (mmHg)

Arterial carbon dioxide tension

40 (35 to 45)

Pao2 (mmHg)

Arterial oxygen tension

95 (80 to 100)

Sao2 (%)a

Arterial oxygen saturation

97.5 (95 to 98)

CoHb (%)a

Carboxyhemoglobin

0.5 to 1.5

MetHb (%)a

Methemoglobin

0.0 to 1.5

Hb (g/dL)a

Hemoglobin

15 (men: 13.5 to 16.5; women: 12 to 15)

CaO2 (mL/dL or vol%)a

Arterial oxygen content

19.8 (17 to 21)

Plasma HCO3– (mEq/L)b

Plasma bicarbonate

24 (22 to 28)c

B.E./B.D. (mEq/L)b

Base excess or deficit

0 (±2)

TCO2 (mmol/L or mEq/L)b,d

Total CO2

25 (22 to 30)

aRequires hemoximetry for measurement (e.g., co-oximetry). bCalculated values, usually based on algorithms incorporated into the blood gas analyzer. cClinical range for plasma bicarbonate varies by reference source; HCO – range of 21 to 27 mEq/L has been 3

suggested [Emmett, M. Simple and mixed acid-base disorders. In: Sterns RH, Forman JP, eds., UpToDate; 2013]. Others have suggested a normal HCO3– range of 22 to 26 mEq/L and 22 to 28 mEq/L [Post TW, Burton RD. Approach to the patient with metabolic acidosis. UpToDate; 2013].

d

Total CO2 range based on the Siggard-Andersen nomogram would be 23 to 27 mmol/L (arterial blood) and 24 to 29 mmol/L (venous blood).

Respiratory Acidosis Most patients receiving mechanical ventilatory support continue to breathe spontaneously, and their level of spontaneous ventilation can be affected by multiple factors. Patients’ respiratory drive may be decreased due to respiratory or metabolic alkalosis, CNS depressants (sedatives, tranquilizers, and opioids), neurologic disease, electrolyte disorders, decreased metabolic rate, or pain. Chronic elevations in PaCO2 as seen with chronic CO2 retention may depress the respiratory drive to breathe. Neuromuscular disease or ventilatory muscle fatigue may decrease patients’ ability to spontaneously ventilate. Causes of increased ventilatory workload include decreased compliance; increased resistance; or increased ventilatory demand due to hypoxia, metabolic acidosis, fear and anxiety, pain, increased CO2 production, or pulmonary disease. Mechanical ventilatory support allows the clinician to provide a sufficient level of ventilation to correct inadequate spontaneous breathing. However, prompt ventilator liberation will require that issues related to decreased respiratory drive, neuromuscular disease, or increased ventilatory workload be addressed.

Respiratory Alkalosis Some spontaneously breathing patients may have an increased respiratory drive while receiving mechanical ventilatory support. Causes of increased respiratory drive include hypoxemia, metabolic acidosis, increased CO2 production, lung receptor stimulation, pain, anxiety, and decreased blood pressure. Increased respiratory drive may cause patients receiving assist/control ventilation (e.g., PC-CMV or VC-CMV) to trigger the ventilator at excessively high rates resulting in an inappropriate respiratory alkalosis. Increased respiratory drive may also contribute to the patient– ventilator asynchrony and increased WOB and make ventilator weaning and discontinuance problematic. Issues causing increased respiratory drive should be identified and addressed promptly.

Metabolic Acidosis Common causes of metabolic acidosis seen in the ICU include lactic acidosis (acute severe hypoxia, cardiac arrest, cardiac failure, hypovolemia, sepsis, and shock), ketoacidosis (uncontrolled diabetes mellitus), and kidney failure. Other causes include ingestion of acids, diarrhea, pancreatic fistula, and intravenous hyperalimentation. Hyperventilation is the normal physiologic response to metabolic acidosis. Hyperventilation decreases PaCO2 and raises pH. Normal respiratory compensation for metabolic acidosis will decrease PaCO2 about 1.2 mmHg for each 1-mEq/L decrease in HCO3–. A quick estimate of the expected respiratory compensation for metabolic acidosis is simply the last two digits of the pH. For example, if pH is 7.20 due to metabolic acidosis, the expected respiratory compensation would be a PaCO2 of 20 mmHg. Patients in respiratory failure often are unable to spontaneously hyperventilate on their own in compensation for metabolic acidosis. When receiving mechanical ventilatory support in the assist/control mode, these patients will tend to rapidly trigger the ventilator, lowering PaCO2 and increasing in pH. Rapid triggering may cause patient–ventilator asynchrony, patient discomfort, and result in the patient fighting the ventilator. A common but inappropriate clinician response to this condition is to sedate the patient, sometimes heavily. While this may slow the patient’s trigger rate, PaCO2 will rise, worsening the metabolic acidosis. In such cases, identification and treatment of the underlying cause is best, while assuring that there are not significant swings in pH caused by inappropriate manipulation of the ventilator settings. RC Insight Normal respiratory compensation for metabolic acidosis results in a decrease in PaCO2 of about 1.2 mmHg for each 1-mEq/L decrease in HCO3–.

Metabolic Alkalosis Common causes of metabolic alkalosis seen in the ICU include vomiting, nasogastric (NG) tube suction, renal loss of hydrogen ions, hypokalemia,

hypovolemia, and sodium bicarbonate administration. Normal respiratory compensation for metabolic alkalosis typically results in an increase in PaCO2 of about 0.7 mmHg for each 1-mEq/L increase in HCO3–. A quick estimate of the expected respiratory compensation for a metabolic alkalosis is simply the last two digits of the pH. For example, if the pH is 7.55 expected respiratory compensation would be a PaCO2 of about 55 mmHg. Compensation for a metabolic alkalosis may be reduced since hypercapnia often creates a drive to increase the respiratory rate and/or tidal volume in most patients. In ventilated patients, a metabolic alkalosis will tend to decrease patients’ respiratory drive, which may result in hypoventilation in modes that require patients to contribute significantly to their minute ventilation. Metabolic alkalosis may also be problematic in terms of ventilator weaning and discontinuance. Treatment of metabolic alkalosis should be aimed at the cause. The most common clinical causes of a metabolic alkalosis are hypokalemia and volume depletion. In cases of severe metabolic alkalosis, where kidney function is compromised and dialysis is not an option, administration of ammonium chloride or an infusion of dilute hydrochloric acid solution may be considered. In summary, ventilation can have a significant impact on acid-base balance, and the respiratory care clinician must take this into account when considering adjustments in the level of ventilatory support provided. Identification and treatment of underlying causes of acid-base disorders should be performed. The clinician should also be aware that respiratory and metabolic disorders often coexist in critically ill patients.

Cardiac and Cardiovascular Support Oxygen delivery is dependent on adequate cardiac output, blood pressure, and tissue perfusion. Heart failure, acute myocardial infarction, shock, sepsis, and blood loss will reduce tissue oxygen delivery. Heart failure can be left sided, right sided, or both. Cor pulmonale is a form of right-sided heart failure associated with chronic lung disease. Heart failure can be characterized as ischemic (e.g., acute myocardial infarction [MI]), nonischemic (e.g., idiopathic cardiomyopathy), or valvular (e.g., mitral regurgitation). Left-ventricular myocardial dysfunction is the most common cause of heart failure seen in the ICU. This type of heart failure is heart failure due to systolic (pump) failure (HFrEF, or heart failure with reduced ejection fraction). Chronic heart failure is often caused by untreated or suboptimally treated hypertension where the heart fails to relax during diastole and results in heart failure with preserved ejection fraction (HFpEF). Treatment of heart failure is dependent on the cause and may include diuretics to treat fluid retention and the use of pharmacologic agents to improve cardiac function. Acute decompensated heart failure is a potentially life-threatening problem, requiring careful assessment and monitoring. Treatment of acute decompensated heart failure may include noninvasive ventilatory support, diuretic therapy, and assessment for vasodilator administration. Invasive mechanical ventilatory support with PEEP may be required. In some patients, heart failure may cause acute pulmonary edema, resulting in respiratory failure with severe hypoxemia. There are three broad types of acute coronary syndromes and myocardial infarction (MI) based on ECG findings: ST segment elevation MI (STEMI), non-ST segment elevation MI (NSTEMI), and unstable angina; treatment protocols for each should be employed. Shock generally is caused by circulatory failure and results in systemic hypotension, decreased oxygen delivery, and tissue hypoxia. Types of shock include cardiogenic, hypovolemic, obstructive, and distributive shock. There are three common types of distributive shock: septic shock, neurogenic shock, and anaphylactic shock. As shock progresses, patients may experience dyspnea, restlessness, diaphoresis, and cool, clammy skin. Hypotension, oliguria, and metabolic acidosis may then lead to tissue hypoxia, organ damage, multiorgan system failure, and death. Table 7-6 provides normal values for hemodynamic

measurements. TABLE 7-6 Adult Hemodynamic Measurements Parameter

Normal (Range)

Abnormal Values

Heart Rate (HR)

80 (60–100) beats/min

> 100 – Tachycardia < 60 – Bradycardia

Arterial Blood Pressure (ABP) Systolic Blood Pressure Diastolic Blood Pressure Mean Arterial Blood Pressure (MAP)

120 (90–140) mmHg 80 (60–90) mmHg 90 (80–100) mmHg

> 140/90 – Hypertension < 90/60 – Hypotension MAP < 100 – elevated MAP > 80 – decreased MAP > 65 with adequate tissue perfusion may be an acceptable goal for most patients in the ICU

Central Venous Pressure (CVP)

4–8 mmHg

> 6 – fluid overload, right ventricular failure, pulmonary hypertension, valvular stenosis, pulmonary embolus, cardiac tamponade, pneumothorax, positive pressure ventilation, PEEP, left ventricular failure < 2 – hypovolemia, blood loss, shock, peripheral vasodilation, cardiovascular collapse

Pulmonary Artery Pressure (PAP)

25/10 (20–35)/(5–15) mmHg

> 35/15 – pulmonary hypertension, left ventricular failure, fluid overload < 20/5 – pulmonary hypotension, hypovolemia, cardiovascular collapse

Mean Pulmonary Artery Pressure (MPAP)

15 (10–20) mmHg

> 20 – same as ↑ PAP above < 10 – same as ↓ PAP above

Pulmonary Capillary Wedge Pressure (PCWP)

6–12 (< 18) mmHg

> 18 – left ventricular failure, fluid overload > 20 – interstitial edema may occur > 25 – alveolar filling may occur > 30 – frank pulmonary edema may occur < 5 – hypovolemia, shock, cardiovascular collapse

Pulmonary Vascular Resistance (PVR)

110–250 dynes/sec/cm5

> 250 – pulmonary hypertension, severe atelectasis, lung over distension, hypoxemia, ↑ pH, ↓ PaCO2, vasopressors, emboli, emphysema, interstitial fibrosis, pneumothorax < 110 – pulmonary vasodilators, nitric oxide, oxygen, calcium blockers

Cardiac Output (Q̇ T or C.O.)

5 (4–8) L/min

> 8 – elevated, dependent on patient size (see cardiac index) < 4 – decreased, dependent on size (see

cardiac index) Cardiac Index (C.I.)

2.5–4.0 L/min/m²

> 4 – Stress, septic shock, fever, hypervolemia, drugs (dobutamine, dopamine, epinephrine, isoproterenol, digitalis, etc.) < 2.5 – left ventricular failure, myocardial infarction, pulmonary embolus, high levels of positive pressure ventilation, PEEP, pneumothorax, blood loss, hypovolemia

System Vascular Resistance (SVR)

800–1200 dynes/sec/cm2

> 1400 – cardiogenic shock, systemic hypertension, volume depletion/hypovolemia, vasoconstrictors (dopamine, norepinephrine, epinephrine, others), hypovolemia, late septic shock < 900 – distributive shock (e.g. sepsis), acidosis, vasodilators (nitroglycerin, nitroprusside, morphine, others), early septic shock. PV̄O2 < 27 mmHg and SV̄O2 < 50% associated with lactic acidosis

Mixed Venous Oxygen PV̄O2 CV̄O2 SV̄O2

35–40 mmHg 15 Vol% 75% (70%–77%)

Increased mixed venous oxygen values (e.g. SV̄O2 > 77%) may be caused by peripheral shunt (e.g.; sepsis), left-to-right cardiac shunt, marked elevation is cardiac output, cyanide poisoning, hypothermia, wedged PA catheter when syringe sample is drawn. Decreased mixed venous oxygen values may be caused by decreased CaO2, decreased C.O., increased CV̄O2 An acceptable goal in critically ill patients may be in SV̄O2 of 60% to 75% or ≥ 70% in sepsis

C(a-v)O2

3.5–5 vol%

Increased C(a-v)O2 may be caused by increased CaO2 or decreased CV̄O2 Decreased C(a-v)O2 may be caused by decreased CaO2 or increased CV̄O2

Hemodynamic monitoring may be accomplished by use of a central venous catheter or pulmonary artery catheter. Often noninvasive hemodynamic monitoring is performed by assessing arterial waveform analysis via an arterial line. A conservative approach to fluid management may help reduce pulmonary edema. A conservative approach to fluid management should not be at the expense of maintaining adequate systemic blood pressure. Hemodynamic changes seen with cardiac and cardiovascular disorders often seen in the ICU are described in Table 77.

TABLE 7-7 Hemodynamic Changes with Common Cardiopulmonary Disorders

Description ↑, increase; ↓, decrease; BP, blood pressure; CO, cardiac output; CVP, central venous pressure; N, normal; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance.

Positive-pressure ventilation increases mean airway and intrathoracic pressures, reduces venous return, and may compromise cardiac output. Steps to reduce the harmful cardiovascular side effects of positive-pressure ventilation include decreasing peak and mean airway pressures. Ventilator adjustments to reduce airway pressures include decreasing tidal volume, limiting inspiratory pressure, reducing rate, increasing expiratory time, improving I:E ratio, altering inspiratory flow waveform, reducing PEEP/CPAP, and use of modes that incorporate spontaneous breathing (e.g., SIMV).

Use of Sedation and Neuromuscular Blockade Pain, anxiety, fever, and fighting the ventilator will increase the WOB and oxygen consumption. Proper sedation and pain management can improve patient–ventilator synchrony and patient comfort and reduce oxygen consumption. Frequent pain assessment should be performed to document the severity, response to medication, and development of side effects.19 The use of pain scales (e.g., Critical Care Pain Observation Tool [CPOT]) will allow the clinician to quantify pain and assess the effectiveness of treatment. Sedation protocols and the use of sedation scales (e.g., Richmond Agitation–Sedation Scale) should be employed, including routinely waking patients each day.19 Intravenous administration of opiates generally is preferred for the treatment of pain in critically ill patients. Side effects of opioids include respiratory drive depression, hypotension, and the release of histamine. Gradual weaning of opioids has been suggested to avoid withdrawal symptoms. Neuromuscular-blocking agents paralyze skeletal muscle and are sometimes used in the ICU to achieve controlled mechanical ventilation. Neuromuscular blockade can eliminate patient–ventilator asynchrony, and some have speculated that it may benefit patients with severe ARDS during the initial phases of mechanical ventilation.11 The use of neuromuscular-blocking agents should be reserved for patients with persistent ventilatory asynchrony or severe oxygenation problems and for relatively short periods of time. Neuromuscular-blocking agents have no sedative or analgesic properties and must be used in combination with appropriate sedation and treatment of pain. As patients are unable to spontaneously breathe, a ventilator malfunction or disconnect can be catastrophic. Neuromuscular-blocking agents can also cause allergic reactions, cardiovascular side effects, prolonged paralysis, and ICU-acquired muscle weakness. Because of issues regarding safety and possible adverse effects, the use of neuromuscular-blocking agents is inappropriate for most patients. Exceptions may include the ventilation of patients with acute, severe asthma and patients who cannot be otherwise successfully ventilated.

Summary Following ventilator initiation, patients should be assessed for the adequacy of oxygenation, ventilation, and acid-base balance. Proper ventilator function and appropriate patient–ventilator interaction should be reviewed, and adjustments made to reduce or eliminate patient–ventilator asynchrony, reduce the WOB, ensure patient safety and comfort, and minimize harmful side effects. Support provided should promote prompt liberation from the ventilator. Alteration of ventilatory pressures, flows, volumes, and inspiratory time may be helpful to improve patient– ventilator synchrony. Ventilator adjustments may be necessary to improve oxygenation, adjust the level of ventilation provided, and insure adequate acid-base balance. Techniques to improve oxygenation include adjustment of FIO2 and PEEP. Other techniques which may be helpful in some patients include prone positioning, recruitment maneuvers, and use of alternative modes of ventilation (e.g., PCIRV, APRV, and HFOV). Provision of adequate humidification, suctioning and airway care, and administration of bronchodilator therapy may be helpful. Early mobilization of patients may also improve outcomes. Alteration of the level of ventilation provided may be required based on arterial blood gas assessment. Ventilator adjustments may include changes in tidal volume, respiratory rate, minute ventilation, or mode. The clinician should always consider the effect of PaCO2 on pH when considering ventilator adjustments. Care should also be taken to minimize possible harmful cardiovascular side effects associated with positive-pressure ventilation. Pain, anxiety, fever, and fighting the ventilator will increase the WOB and oxygen consumption. Proper sedation and pain management can improve patient–ventilator synchrony and comfort and reduce oxygen consumption.

Key Points An immediate assessment should be completed following initiation of mechanical ventilation. Initial assessment should include: physical assessment of the patient, assessment of ventilator settings and patient–ventilator interaction, cardiovascular assessment, oximetry, and measurement of arterial blood gases. Initiation of mechanical ventilation may lead to respiratory problems, which may include right mainstem intubation, misplaced endotracheal tube, cuff leak or malfunction, large air leak, inappropriate ventilator settings, or ventilator malfunction or disconnect. During assist/control volume ventilation, inspiratory peak flow should meet or exceed the patient’s ventilatory needs. Inadequate flow will increase the work of breathing (WOB) while excessive flow may result in immediate and persistent tachypnea. Patient–ventilator interaction refers to patient–ventilator synchrony, comfort, and work of breathing during ventilator-assisted breaths. A sustained increase in ventilatory workload can lead to ventilatory muscle fatigue and structural injury. Muscle fatigue requires a minimum of 24 hours for recovery. When set appropriately, ventilator mode and settings should reduce WOB while avoiding ventilatory muscle atrophy. Several modes may be selected to reduce inspiratory effort without eliminating respiratory muscle use. Patient-ventilator asynchrony occurs when the patient’s respiratory efforts do not coordinate with the ventilator’s set respiratory efforts. Asynchrony may be detected through physical assessment and observation of ventilator graphics. Patient–ventilator asynchrony is associated with adverse outcomes including increased WOB, hypoxemia, inadequate or ineffective ventilation, hemodynamic compromise, increased risk of complications, and prolonged ventilator dependency. Patient-triggered breaths may be pressure triggered or flow triggered. Trigger sensitivity should be adjusted so that trigger work is minimal without autocycling. The pressure trigger is typically set –0.5 to –1.5 cm H2O below the baseline expiratory pressure; flow trigger is typically set 1 to 2 L/min below the baseline or bias flow. Trigger asynchrony occurs when the patient’s inspiratory effort does not match the beginning of the ventilator-supported breath. Trigger work is the amount of patient’s WOB required to trigger the machine breath; inappropriate trigger sensitivity settings and autoPEEP can increase

trigger work. There are five types of trigger asynchrony: missed triggering, trigger delay, double triggering, reverse triggering and autotriggering. Missed triggering is when the patient’s inspiratory effort does not trigger the ventilator breath. Trigger delay occurs when there is a delay between the time the patient initiates inspiration and when the machine actually delivers the breath. Double triggering occurs when the ventilator cycles into expiration while the patient is still making an inspiratory effort, resulting in double triggering and two consecutive breaths before the patient exhales. Autotriggering occurs when the ventilator initiates inspiration without a corresponding patient effort due to inappropriate trigger sensitivity settings. Reverse triggering may occur during controlled ventilation in which a timetriggered ventilator breath stimulates the diaphragm, resulting in diaphragmatic contraction which then triggers the next breath. Flow asynchrony occurs when the inspiratory gas flow from the ventilator does not match the patient’s inspiratory flow demand. Cycle asynchrony occurs when there is poor coordination between the patient’s respiratory drive and the ventilator. Mode asynchrony occurs when the mode selected does not match the patient’s spontaneous ventilatory efforts. Tissue oxygenation is determined by inspired oxygen concentration, alveolar ventilation, ventilation–perfusion relationships, diffusion across the alveolar– capillary membrane, arterial oxygen content, cardiac output, and peripheral perfusion. Appropriate oxygenation values for most patients are PaO2 60 to 80 mmHg and SaO2 90% to 95% with FIO2 ≤ 0.50 to 0.60. Improved oxygenation can be achieved by adjusting FIO2, PEEP, and CPAP. Other methods for improving oxygenation include recruitment techniques, open lung ventilation, and prone positioning. FIO2 should be rapidly titrated down from 1.0 to avoid oxygen toxicity and related complications. Complications of high FIO2 include absorption atelectasis, cellular injury, accentuation of hypercapnia, airway injury, parenchymal injury, potentiation by bleomycin, and retinopathy of prematurity in premature infants. PEEP or CPAP is used to prevent or treat atelectasis by opening collapsed alveoli and reducing alveolar overdistention. PEEP may help to reduce the incidence of ventilator-associated pneumonia (VAP) and ventilator-associated lung injury (VALI); PEEP may cause pulmonary barotrauma, reduced venous return, or negatively affect cardiac output and blood pressure.

Methods for PEEP application include minimum PEEP, optimal PEEP, and compliance-titrated PEEP. Minimum PEEP is the least PEEP needed to achieve adequate arterial oxygenation at a safe oxygen concentration. Optimal or best PEEP can be defined as the PEEP that maximizes oxygen delivery to the tissues. Compliance-titrated PEEP is the best PEEP based on static total compliance (CST). A decremental PEEP trial is a method used to identify optimal PEEP for patients with ARDS following a lung recruitment maneuver. Intrinsic PEEP or autoPEEP occurs when gas is not completely exhaled before beginning the next inspiratory phase. Static autoPEEP is calculated by subtracting the extrinsic PEEP from the endexpiratory pressure observed during the expiratory pause. Dynamic autoPEEP can be assessed in spontaneously breathing patients by observing the flow–time curve. High PEEP can be effective in improving oxygenation in patients with severe ARDS with recruitable lung but harmful to patients with mild ARDS who have little recruitable lung. Various recruitment maneuvers have been suggested to improve oxygenation in patients with ARDS or those with reduced functional residual capacity (FRC), which include a “30 for 30” or “40 for 40” maneuver, sigh breaths, or a variation of pressure-control ventilation. It is important to monitor the patient’s heart rate, blood pressure, and cardiac monitor while performing a recruitment maneuver. Prone positioning may improve oxygenation for patients with severe ARDS. Contraindications to prone positioning include shock, hemorrhage, multiple fractures or trauma, spinal instability, pregnancy, increased intracranial pressure, or recent tracheal surgery or sternotomy. Bronchial hygiene techniques may improve oxygenation for ventilated patients. Techniques include suctioning and airway care, provision of adequate humidification, and administration of bronchodilators and inhaled antiinflammatory agents. Early mobilization of ventilated patient may improve oxygenation and decrease consequences of ICU-acquired weakness. PaCO2 is the single best clinical indicator of alveolar ventilation and allows for accurate evaluation of adequate ventilation. Arterial blood gases are typically drawn 20 to 30 minutes following a parameter change to confirm appropriate settings. Patients with dangerously elevated intracranial pressure (ICP) may be hyperventilated for a short period of time to lower PaCO2 and ICP.

Permissive hypercapnia is a ventilatory strategy that reduces delivered volumes and pressures to reduce alveolar pressure and overdistension. This strategy may be useful for patients with severe ARDS, severe bronchospasm with acute asthma exacerbation, or exacerbation of COPD. A decrease in PaCO2 may be achieved by increasing tidal volume or frequency, and decreasing mechanical dead space (if present). An increase in PaCO2 may be achieved by decreasing tidal volume or frequency and adding or increasing mechanical dead space. Tidal volume is initially set to 6 to 8 mL/kg IBW and titrated up or down to ensure Pplateau ≤ 30 cm H2O. Patients in respiratory failure often experience acid-base disorders; the patient’s ventilatory status can have a significant impact on acid-base balance. Acute increases in PaCO2 will cause a corresponding decrease in pH while acute decreases in PaCO2 will increase pH. Each time there is an acute change and PaCO2 increases by 1 mmHg, pH will decrease by 0.008, and each time there is an acute change and PaCO2 decreases by 1 mmHg, pH will increase by 0.008. Appropriate pain management and sedation protocols should be employed in ventilated patients. Cardiac and cardiovascular problems may impair tissue oxygen delivery. Neuromuscular blockade should be reserved for patients with persistent ventilatory asynchrony or severe oxygenation problems and for relatively short periods of time. Ventilator failure or accidental disconnection can be catastrophic in patients undergoing neuromuscular blockade.

References 1. Chatburn RL, El-Khatib M, Mireles-Cabodevila E. A taxonomy for mechanical ventilation: 10 fundamental maxims. Respir Care. 2014;59(11):1747–1763. doi:10.4187/respcare.03057. 2. Chatburn RL, Volsko TA, Hess DR, et al. Mechanical ventilators: classification and principles of operation. In: Hess DR, MacIntyre NR, Galvin WF, Mishoe SC, eds. Respiratory Care: Principles and Practice. 3rd ed. Burlington, MA: Jones & Bartlett Learning; 2016: 462–492. 3. Hyzy RC. Physiologic and pathophysiologic consequences of mechanical ventilation. In: Parsons PE, Finlay G, eds. UpToDate; April 2018. 4. Blanch L, Villagra A, Sales B, et al. Asynchronies during mechanical ventilation are associated with mortality. Intens Care Med. 2015;41:633–641. 5. Kacmarek RM, Stoller JK, Heuer AJ. Patient-ventilator interactions. In: Kacmarek RM, Stroller JK, Heuer AJ, eds. Egan’s Fundamentals of Respiratory Care. 11th ed. St. Louis, MO: Elsevier; 2017: 1058–1077. 6. Akoumianaki E, Lyazidi A, Rey N, et al. Mechanical ventilation-induced reverse-triggered breaths: a frequently unrecognized form of neuromechanical coupling. Chest. 2013;143:927–938. 7. Marini JJ, Capps JS, Culver BH. The inspiratory work of breathing during assisted mechanical ventilation. Chest. 1985;87:612–618. 8. Malhotra A, Schwartzstein RM. Oxygen toxicity. In: Manaker S, Finlay G, eds. UpToDate; May 2018. 9. Mechem CC. Pulse oximetry. In: Parsons PE, Finlay G, eds. UpToDate; December 2017. 10. Sagana R, Hyzy RC. Positive end-expiratory pressure (PEEP). In: Pearson PE, Finlay G, eds. UpToDate; 2017. 11. Siegel MD, Hyzy RC. Mechanical ventilation of adults in acute respiratory distress syndrome. In: Parsons PE, Finlay G, eds. UpToDate; November 2017. 12. Rosen IM, Manaker S. Oxygen delivery and consumption. In: Parsons PE, Finlay G, eds. UpToDate; June 2017. 13. Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301–1308. 14. Kacmarek RM, Stoller JK, Heuer AJ. Initiating and adjusting invasive ventilatory support. In: Kacmarek RM, Stroller JK, Heuer AJ, Chatburn RL, Kallet RH, eds. Egan’s Fundamentals of Respiratory Care. 11th ed. St. Louis, MO: Elsevier; 2017: 1078–1110. 15. Blanch L, Bernabe F, Lucangelo U. Measurement of air trapping, intrinsic positive end-expiratory pressure, and dynamic hyperinflation in mechanically ventilated patients. Respir Care. 2005;50(1):110–123. 16. Malhotra A, Kacmarek RM. Prone ventilation for adult patients with acute respiratory distress syndrome. In: Parsons PE, Finlay G, eds. UpToDate; April 2018. 17. Shelledy DC, Peters JI. Initiating and adjusting ventilatory support (Chapter 44). In: Wilkins RL, Stoller JK, Kacmarek RM. Egan’s Fundamentals of Respiratory Care. 9th ed. St. Louis, MO: Elsevier; 2009:1045– 1090. 18. Hyzy RC, Hidalgo J. Permissive hypercapnia during mechanical ventilation in adults. In: Parsons PE, Finlay G, eds. UpToDate; February 2018. 19. Panharipande P, McGrane S. Pain control in the critically ill adult patient. In: Parsons PE, O’Connor MF, Finlay G, Nussmeier NA, eds. UpToDate; September 2018.

CHAPTER

8

Critical Care Patient Assessment and Monitoring: Part I: Assessment J. Brady Scott, Joe Hylton, Jon C. Inkrott, and David C. Shelledy

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction History and Physical Assessment Medical Record Review History Patient and/or Family Interview Physical Assessment Assessment of Mental Status Neurologic Examination Pain Monitoring Ancillary Use of Equipment Chest Tubes, Drainage, and Management Urine Output Monitoring Bedside Assessment in the ICU Blood Gases Arterial sampling Arterial Line Insertion and Sampling Venous Blood Gases Sample Analysis Arterial Blood Gas Interpretation Laboratory Studies Hemoglobin and Hematocrit Complete Blood Count Clinical Chemistry Imaging in the ICU Portable Chest Radiographs Ultrasound Imaging Pulmonary Function Testing Bedside Tests of Spontaneous Breathing Electrocardiogram

OBJECTIVES

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Describe the components of the critical care patient history and physical examination. Explain the importance of the assessment of mental status in the intensive care unit (ICU). Review the neurologic examination as it applies to the critical care patient. Describe monitoring in the ICU. Explain the importance of the observation of ancillary equipment. Describe chest tube drainage and management. Explain the importance of urine output monitoring. Describe the indications for arterial blood gas analysis and indwelling arterial line placement. Contrast the different arterial puncture sites (radial, brachial, and femoral artery). Interpret the results of arterial and venous blood gas studies. List the components of the complete blood count. Interpret the results of the white blood cell count report. Describe other laboratory studies often performed in the ICU. Explain why recognition of diabetes is important in the ICU. Describe tests used to monitor kidney function. Explain the use of portable chest x-rays and ultrasound imaging in critical care. Describe the use of bedside tests of spontaneous breathing in the ICU. Recognize common cardiac arrhythmias on ECG. Overview the assessment of patients with acute myocardial infarction and heart failure.

KEY TERMS anion gap anteroposterior (AP) ascites asynchrony barrel chest basophils bicarbonate blood urea nitrogen (BUN) bowel sounds bradypnea brain natriuretic peptide (BNP) cardiac output (CO) chest radiographs chest tubes chief complaint comatose crackles cyanosis diabetes dull percussion notes electrocardiogram (ECG) electrolytes eosinophils family history fine crackles head, eye, ear, nose, throat (HEENT) hematocrit hemoglobin (Hb) hepatomegly history of present illness (HPI) hypercapnia hyperresonant

hypothermia hypoxemia lymphocytes maximal expiratory pressure (MEP) maximal inspiratory pressure (MIP) modified Allen test monocytes neutrophils obtunded occupational history peak flow percussion notes peritoneal fluid pH physical assessment plasma bicarbonate pleural friction rub pneumothorax portable chest x-rays posterior-anterior (PA) images red blood cell (RBC) count serum creatinine splenomegaly stuporous tachypnea tumor tympanic

Introduction Chapters 8 and 9 review the essential components of critical care patient assessment, support, and monitoring. Chapter 8 focuses on patient assessment, while Chapter 9 addresses critical care monitoring, airway care, and other supportive care provided to patients receiving mechanical ventilatory support. The respiratory care clinician must be able to properly assess, monitor, and care for critically ill patients. Because we believe that patient assessment provides the foundation for the proper care of critically ill patients, this chapter will expand on the basics of critical care patient assessment. Careful patient assessment and monitoring will help ensure the proper diagnosis, treatment, and care of the critically ill patient, as well as recognition of new problems and conditions that may jeopardize the patient’s recovery.1

History and Physical Assessment Critical care patient assessment begins with the review of the medical record, patient history, and physical examination. Obtaining a patient history in the ICU can be difficult, particularly in patients with mental status changes. In such cases, valuable historical information can often be found in the medical record or obtained by interviewing family members, caregivers, or other individuals familiar with the patient. Physical assessment in the ICU incorporates inspection, auscultation, palpation, and percussion, as well as review of reports of prior history and physical examinations found in the medical record. Key aspects of the medical record review, history, and physical examination are reviewed below.

Medical Record Review Medical records have evolved over time into a tool used by interprofessional teams in the acute care setting to monitor and evaluate patient care. The medical record serves as the central location for patient information and provides a means of communication between disciplines. Medical records are legal documents and information within may be used during legal proceedings. Further, they are used by payers (Medicare, Medicaid, and third party) to determine healthcare reimbursement. Thus, documentation in the medical record should be accurate, clearly written, and timely.2 Whenever possible, the critical care clinician should review the medical record before patient contact. There, information regarding the reason for admission, physician’s orders, results of prior history and physical examinations, consultation notes, and diagnostic test results can be found. Special reports such as operative/procedural reports, progress notes, and monitoring flow sheets should also be reviewed. Admission information found in the medical record includes the patient’s name, gender, admission date/time, attending physician, admitting diagnosis, and other demographic information. A review of physician’s orders can provide an overview of the treatment the patient has received, diagnostic tests that have been ordered, and planned procedures or operations. This information will often guide the clinician as he or she prepares for the initial encounter with the patient.2

The results of prior history and physical examinations found in the medical record can be extremely helpful. Consultation reports and progress notes from nurses, physicians, and other providers may also provide valuable information. These notes serve as one form of communication between different members of the multidisciplinary team and may include recommendations, treatment plans, and/or assessment findings specific to the individual provider’s clinical focus. The results of diagnostic studies provide objective measures that often help complete the clinical picture.2 Critical care monitoring flowsheets found in the medical record can be especially helpful, allowing for recognition of trends and changes in heart rate, blood pressure, respirations, oximetry (SpO2), temperature, intake and output, and body weight. Many critical care flowsheets include the results of arterial blood gas analysis, other laboratory testing, and hemodynamic variables (e.g., central venous pressure [CVP], mean arterial pressure [MAP], cardiac output [CO]). The results of neurological assessment (e.g., level of consciousness, pupil size and reaction, coma score) and pain management variables (e.g., pain scales, sedation scales) may be included. Medications, blood products, and enteral or parenteral nutrition are often documented on the flowsheets. The results of physical assessments are also often noted on the flowsheets. These may include breath sounds, heart sounds, abdominal exam, bowel sounds, skin assessment [color, edema, temperature], and urine color and volume. Isolation procedures in use, code status, artificial airway information, and respiratory care received (e.g., FIO2, ventilator settings) may also be recorded on the critical care monitoring flowsheets. Reviewing this information prior to contact with the patient readies the clinician for the patient encounter.2 Items that should be reviewed in the ICU patient’s medical record are summarized in Box 8-1.

BOX 8-1 Medical Record Review for the ICU Patient Whenever possible, the medical record should be reviewed prior to the ICU patient encounter. Pertinent items that may be found in the medical record include: ∎ Patient data/demographics (name, age, gender, and race/ethnicity) ∎ Admission date and time and admitting diagnosis and/or problem list

∎

Current physician’s orders • General care • Antibiotic and antimicrobial drugs • Cardiac drugs (inotropes, antiarrhythmic agents, antianginal medications) • Antihypertensive agents • Antithrombotics • Medications to treat hypotension (e.g., vasopressors) • IV therapy • Diuretics • Systemic steroids • Analgesics, sedatives, tranquilizers, hypnotics, neuromuscular-blocking agents • Nutrition, diet, and any restrictions (e.g., enteral or parenteral nutrition, salt restriction) • Orders for diagnostic testing (laboratory, imaging, pulmonary, cardiac, neurologic, other) • Orders for procedures or operations ∎ Respiratory care orders • Oxygen therapy (device and liter flow or FIO2)

• • • • • • • • ∎ ∎ ∎

Bronchodilators (medication, dosage, frequency, and method of delivery) Anti-inflammatory agents (e.g., steroids, antiasthmatic agents) Other aerosol therapy (humidity therapy, sputum induction, antibiotics, other) Lung expansion therapy (e.g., incentive spirometry, intermittent positive pressure breathing ([IPPB] therapy, other) Cough and deep breathing Bronchial hygiene therapy (e.g., chest physiotherapy, positive expiratory pressure (PEP) therapy, high-frequency chest wall oscillation, other) Suctioning and airway care Ventilatory support (invasive or noninvasive mechanical ventilation, ventilator settings, FIO2, PEEP/CPAP)

Results of history and physical examination(s) Reports of consultations (e.g., pulmonary, cardiology, renal, neurology, or psychiatric consults) Cardiopulmonary laboratory studies • Arterial blood gas (ABG) studies and oximetry

Pulmonary function testing (PFT) or pulmonary stress testing Cardiac stress testing Electrocardiogram (ECG) Sleep laboratory ∎ Laboratory study results • Sputum cultures, cytology • Blood chemistry (electrolytes, blood urea nitrogen [BUN], creatinine, serum enzymes, glucose) • Hematology (complete blood count [CBC], other) • Microbiology • Urinalysis • Histology and cytology • Skin testing ∎ Imaging reports • Chest x-rays • Computed tomography (CT) scan • Magnetic resonance imaging (MRI) • Ultrasound studies • Other advanced imaging studies (echocardiography, positron emission tomography [PET] scanning, nuclear medicine procedures, vascular ultrasound) ∎ Progress notes/SOAP notes ∎ Reports of procedures and operations • Surgeries (heart, lung, abdominal, head, other) • Bronchoscopy • Cardiac catheterization laboratory ∎ Flowsheets • Vital signs • Cardiac and hemodynamic monitoring • Ventilator/ventilatory support monitoring flow sheets ∎ Respiratory care notes ∎ Patient education provided

• • • •

History

Components of the standard patient history include chief complaint (CC), history of present illness (HPI), past medical history (PMH), social history, family history, and occupational history (Box 8-2). Patients in the ICU are often unable to provide a complete medical history. In such cases, information may be obtained from the patient’s family or others familiar with the patient, as well as the medical record.1 Box 8-2 summarizes respiratory care–related items found in the medical history.

BOX 8-2 Components of the Medical History In the intensive care setting, it is often difficult to obtain a complete medical history directly from the patient. A recent medical history, however, may often be found in the medical record. Information may also be obtained from the patient’s family, caregivers, or others familiar with the patient’s condition. A summary of the information to be included in a complete medical history follows. Chief Complaint. Respiratory-related complaints include cough, sputum production, hemoptysis, wheezing, chest tightness, and chest pain. Symptoms of respiratory failure and hypoxemia sometimes include shortness of breath, respiratory distress, restlessness, anxiety, lightheadedness, headache, nausea, dizziness, fatigue, agitation, confusion, disorientation, listlessness, tingling, and loss of coordination. History of Present Illness (HPI). Nature of the complaint, onset, duration, frequency, severity, location, progression, and any treatment given. Past Medical History (PMH). The past medical history should include the patient’s general state of health, childhood illnesses (e.g., neonatal disorders, congenital cardiovascular disorders, asthma, cystic fibrosis, pneumonia, epiglottitis, croup), and adult illnesses (e.g., pulmonary disease, heart disease, cancer, hepatitis, diabetes, and high blood pressure). Other important PMH information includes: ∎ Immunizations ∎ Allergies ∎ Medications ∎ Diagnostic, laboratory, and imaging studies ∎ Accidents and injuries (e.g., thoracic trauma, broken bones, head trauma) ∎ Hospitalizations (dates, hospital, diagnosis, and procedures) ∎ Operations (surgery) ∎ Pregnancy ∎ Cardiac disease (heart failure, angina, myocardial infarction [MI], cor

pulmonale, other) ∎ Pulmonary disease (e.g., pneumonia, tuberculosis, asthma, bronchitis, emphysema, COPD, bronchiectasis, exposure to respiratory infections [influenza, tuberculosis, other]) ∎ Respiratory care received (oxygen, history of intubation, history of mechanical ventilation, use of metered dose inhalers [MDI] or aerosolized medication) ∎ Psychiatric illnesses or mood disorders (e.g., anxiety, depression, other) ∎ Limitations to function or disabilities Personal and Social History. The personal and social history includes personal status, habits (e.g., diet and nutrition, alcohol, tobacco or illicit drug use), ability to provide self-care, sexual history, housing, environment, military record, religious and cultural preferences, and access to care. Family History. The family history should include family diseases, relatives’ causes and age at death, and family support available. Occupational History. The occupational history should include occupation; work environment; hours worked; work history; exposure to chemicals, dust, or fumes; protective devices worn at work; and military record. Occupational lung disease can be caused by inhalation of inorganic dusts (e.g., silicates, carbon, and metals), organic dusts (e.g., bacteria, fungi) or chemicals, gases, fumes, vapors, or aerosols. Occupational asthma is associated with exposure to a number of different substances including animal, plant, and vegetable products; chemicals; drugs; wood dust; and metals. The pneumoconiosis (i.e., dustcaused pulmonary disease) include asbestosis, coal workers pneumoconiosis, silica-induced interstitial lung disease, and berylliosis.

Patient and/or Family Interview The purpose of the patient interview is to collect subjective data (e.g., symptoms) from the patient. As noted, many critically ill patients are unable to provide a patient history, and other sources must be considered (medical record, family member/caregiver interviews). In cases where an interview is possible, the respiratory care clinician should ask questions regarding the patient’s overall condition, problem(s), and symptoms. A successful patient interview includes the following features1: 1. Establishing patient/family/caregiver rapport

2. Gathering information about the patient’s condition, chief complaint, and symptoms including a chronology of events and the patient’s (or others’) impression of the patient’s health 3. Obtaining feedback regarding the patient’s (or family members’/caregivers’) understanding 4. Demonstrating professionalism, compassion, and assurance that appropriate care and support will be provided An effective patient interview requires good communication and listening skills. The clinician should avoid the use of medical jargon; communications should be clear, direct, and appropriate for an individual at an eighth-grade education level. Although not always possible in the ICU, the environment for a patient interview should be well lit and optimized for privacy, patient comfort, and reduction of environmental noise and other distractions.1 The clinician should be aware that language barriers and differences in culture, beliefs, religion, and values may affect the patient interview. The patient’s emotional status (fear, stress, anxiety, anger) may also cause communication difficulties. Important elements of the medical history are described below.

Chief Complaint The chief complaint is a concise statement by the patient (or family member/caregiver) that explains the reason(s) medical attention was sought. The respiratory care clinician may ask simple questions such as, “Why did you come to the emergency room?” or “What medical problem brought you in to see your doctor?” Identifying the chief complaint is often the first step in determining the principal diagnosis. Common respiratory-related chief complaints include shortness of breath, chest tightness/pain, fever, hemoptysis, and cough. Critically ill patients may report anxiety, headache, respiratory distress, or other symptoms of respiratory failure. Family members or caregivers may report that the patient was anxious, restless, confused, or showed other signs of altered mental status. RC Insight The chief complaint is subjective. It is the main symptom experienced by the patient, explained in his or her own words.

Clinical Focus 8-1 provides an example of a patient with a chief complaint of

shortness of breath.

CLINICAL FOCUS 8-1 Patient Assessment: Shortness of Breath A 56-year-old man comes to the emergency department (ED) by personal vehicle, accompanied by his wife, after 1 week of cough with increasing sputum production and shortness of breath. The medical history is significant for chronic obstructive pulmonary disease (COPD) and a history of tobacco smoking of 25 pack-years, although the patient has not smoked in over 5 years. The patient has a history of chronic cough with some sputum production. There is no significant social history of illicit drug use or alcohol abuse, and he has not traveled outside of the United States in the preceding month. He works in the information technology field as a programmer and, to his knowledge, has had no significant occupational exposure to hazardous material. On arrival at the ED, his oral temperature is 101.8°F, and he states he is here because “my symptoms are getting worse.” He complains that his cough has been increasing in frequency and severity, and he has become increasingly short of breath. The patient has no known drug allergies and has been taking over-the-counter remedies to treat his week-long symptoms. On auscultation, his breath sounds are decreased in their intensity in the posterior lung fields and crackles are noted bilaterally, although more prominently on the left side. The patient is sitting up in bed due to dyspnea and his oxygen saturation (via pulse oximetry) while breathing room air is 71%. His respiratory rate is 30 breaths/min, and his heart rate is 120 bpm with sinus tachycardia noted on the monitor. Question 1. What could be causing this man’s symptoms? Answer: The patient has a history of tobacco use and a confirmed diagnosis of COPD. Considering the prior diagnosis, the patient may be experiencing an acute exacerbation of COPD. The patient’s oral temperature is 101.8°F, which is consistent with infection and most COPD exacerbations are due to respiratory infection. Breath sounds are noted as crackles, which are sometimes associated with congestive heart failure and pulmonary edema, although no cardiac history has been noted. The severity of the patient’s hypoxemia is of great concern and should be treated immediately. Question 2. Which diagnostic and laboratory tests are needed? Answer: An arterial blood gas study is indicated to further assess the degree of hypoxemia as well as evaluate the patient’s ventilatory and acid-base status. The

sample can be obtained after the patient has been placed on supplemental oxygen and enough time for stabilization has occurred (about 20 minutes). A portable chest x-ray should be obtained to evaluate lung fields for pneumonia, acute heart failure, or pneumothorax. A CBC with differential, electrolytes, and point-of-care testing for influenza may be helpful. Tests of kidney function (BUN and creatinine) and cardiac function (ECG, cardiac troponin) may also be helpful. Prior pulmonary function testing results should be reviewed, if available, to determine the degree of airflow obstruction. Pulmonary function testing should not be performed, however, during acute exacerbation. Other imaging studies may also be indicated to rule out conditions such as pulmonary embolism. Initial treatment may include oxygen therapy, bronchodilator administration, systemic glucocorticoids, antibiotics, and supportive care. Patients with likely influenza infection may also receive antiviral therapy. ICU admission and mechanical ventilatory support should be considered in patients with severe dyspnea, ventilatory muscle fatigue, increased work of breathing, and respiratory acidosis. If needed, mechanical ventilatory support may begin with noninvasive ventilation (NIV). Invasive ventilation may be considered in patients who do not do well with NIV.

History of Present Illness The history of present illness (HPI) describes the symptoms, chronology of events, and impact of the current health problem. A comprehensive HPI is comprised of eight elements to describe a symptom: location, duration, quality, severity, timing, context, associated signs and symptoms, and modifying factors.1 A pulmonary history should include questions regarding cough, sputum production, hemoptysis, wheezing, chest tightness, chest pain, and dyspnea. Current medications and current respiratory care should be noted. Smoking history and any history of alcohol or illicit drug use should also be noted.1 Clinical Focus 8-2 provides an example of the patient with chest pain.

CLINICAL FOCUS 8-2 Patient Assessment: Chest Pain A 63-year-old woman visiting a family member in the hospital collapsed in the hallway. The code blue team arrived to find her profoundly short of breath and complaining of severe chest and back pain. The woman described her chest pain as “heavy,” stating “it feels like someone

is sitting on my chest”! She is diaphoretic, tachycardic, tachypneic, and pale. She is also complaining of being light-headed and nauseous. Question 1. What could be causing this woman’s symptoms? Answer: Acute coronary syndrome (myocardial infarction or unstable angina) should be considered due to her complaint of chest pain, shortness of breath, and nausea. Other life-threatening causes for acute chest pain include aortic dissection, pulmonary embolus, pericardial tapenade, tension pneumothorax, and esophageal rupture. Question 2. What diagnostic tests are indicated? Answer: A 12-lead electrocardiogram, chest x-ray, and vital signs are indicated at this time. Laboratory tests such as CBC, blood glucose, and cardiac biomarkers (cardiac troponin) should be obtained. Elevations in cardiac troponin occur within a few hours following acute myocardial infarction. The CBC white blood count (WBC) may be elevated with inflammatory or infectious disease. Initial results: CBC: Normal WBC count. Normal red blood cell (RBC) and platelet counts Chest x-ray: Normal ECG: ST-segment elevation and tachycardia Cardiac troponin: Elevated above normal reference range Interpretation: Likely myocardial infarction as evidenced by elevated troponin and ECG findings of an abnormal ST segment (elevation), which is suggestive of myocardial ischemia or infarction.

Past Medical History The past medical history (PMH) provides an overview of the patient’s health history, including past illnesses, trauma, surgical procedures, hospitalizations, and ICU admissions. The PMH should note any childhood respiratory or cardiac disease, such as respiratory distress syndrome (RDS) of the neonate, meconium aspiration, congenital cardiac or cardiovascular disease, or pediatric respiratory disease (e.g., asthma, cystic fibrosis, pneumonia, croup, epiglottitis, pertussis, respiratory syncytial virus [RSV]). Adult cardiac or pulmonary disease should be noted, including history of pneumonia, asthma, chronic obstructive pulmonary disease (COPD), upper respiratory tract infection, influenza, pulmonary embolus, heart failure, or myocardial

infarction. Chronic illness, such as diabetes, high blood pressure, or neuromuscular disease should be noted, as well as any history of cancer, stroke, kidney disease, liver disease, or anemia. Allergies, medications, and immunizations should also be noted.1 A history of intubation and/or mechanical ventilation is important to note, as well as any respiratory care received (e.g., oxygen therapy, ventilatory support, inhaled medications).

Social History The social history may include information about the patient’s marital status, education, social support systems, home conditions, sexual activity, habits, military record, religious/cultural beliefs, and access to health care. Smoking history and use of alcohol and/or illicit drugs should be noted, as this may indicate whether one of these factors has influenced the health of the patient.1

Family History The family history of a patient may identify familial links (e.g., grandparents, parents, siblings) to hereditary diseases (e.g., hypertension, diabetes, cancer, heart disease, cystic fibrosis, and alpha-1 antitrypsin deficiency).1

Occupational History Some lung diseases are associated with specific occupations (e.g., asbestosis, silicosis, occupational asthma). When an occupational exposure is noted, it is important to clarify details of that patient’s actual role at work, and to what degree he or she was exposed to the material in question. The clinician should note the patient’s current occupation, previous jobs, working conditions, occupational exposure to dust or toxins, and military service. It should also be noted if disease severity is better or worse at home or at work, or on weekends or workdays.1 Components of the pulmonary history are described in Box 8-3.

BOX 8-3 Components of the Pulmonary History Cough. In spontaneously breathing patients seen in the ICU, the presence, cough effectiveness, onset, duration, nature, pattern, and severity should be assessed. Cough onset may be sudden or gradual, and the duration may be

acute (< 3 weeks), subacute (3–8 weeks), or chronic (> 8 weeks). The nature of the cough may be described as dry, moist, wet, hacking, hoarse, barking, whooping, bubbling, productive, or nonproductive. The pattern of the cough may be occasional, regular, or paroxysmal; related to time of day, weather, activities, talking, deep breaths; or change over time. Cough severity may be tiring and result in headache, chest muscle pain, or sleep disruption. Associated symptoms may include dyspnea, chest pain, headache, or choking. Efforts to treat at home often include medications, expectorants, cough suppressants, humidifiers, or inhalers. Cough may be further characterized as effective or ineffective, strong or weak, and productive or nonproductive. The most common cause of acute cough is acute respiratory tract infection (e.g., acute bronchitis). Other causes of acute cough include pneumonia, pulmonary embolus, and acute exacerbation of COPD. Upper airway and laryngeal disorders (e.g., croup, postextubation stridor) are associated with a hoarse, brassy, or barking cough. Subacute cough may be caused by postnasal drip, postinfectious cough, and pertussis. Chronic cough is often associated with smokers or those with postnasal drip. Chronic bronchitis is defined by chronic cough that produces a tablespoon or more of sputum that occurs on most days for as much as 3 months for 2 consecutive years (in the absence of other pulmonary disease). Asthma and gastrointestinal reflux disease (GERD) are common causes of chronic cough. Cough may also be a complication of certain medications (e.g., ACE inhibitors). Other causes of chronic cough include bronchiectasis, lung cancer, foreign body aspiration, interstitial lung disease, lung abscess, pertussis, nonasthmatic eosinophilic bronchitis, and chronic idiopathic cough. Patients who are intubated or have tracheostomy tubes in place often have an intact cough mechanism, and assessment of the effectiveness of these patients’ cough efforts should be noted. Tracheal suctioning should stimulate a cough, and absence of a cough reflex upon the introduction of a tracheal suction catheter suggests a central nervous system (CNS) or neurologic problem (e.g., brain death). Antitussive medications (e.g., codeine, morphine [Roxanol], gabapentin [Neurontin]) may inhibit the cough reflex. Sputum Production. The amount (milliliters [mL], tablespoons, teaspoons), frequency of sputum production (daily, mornings, Mondays, upon suctioning, etc.), sputum color (colorless, cream, white, green, yellow, brown, frothy pink, brick red, rust), consistency (purulent, viscous, tenacious, watery, saliva), and odor (foul-smelling, sweet-smelling) should be noted. Purulent sputum is associated with infection and inflammation (e.g., pneumonia, bronchitis). Green sputum is sometimes seen from draining sinuses. Brown or off-white brownish sputum is associated with long-standing infection (e.g., chronic bronchitis). Frothy white or pink sputum is associated with pulmonary edema. Inflammation from chronic asthma can also produce discolored sputum. Bloody or blood-tinged sputum, as well as the presence of mucous plugs should be noted. Bronchogenic carcinoma, tuberculosis, chronic bronchitis, and abscess may cause the sputum to be blood-streaked. Spontaneously breathing patients can be encouraged to cough and spit sputum into a clear plastic collection cup. Sputum volume and characteristics can also be observed following endotracheal or tracheal suctioning procedures. Hemoptysis. The amount (slight, blood-tinged sputum vs. frank hemoptysis) and color (bright red, brown) of expectorated blood should be noted. Common causes of hemoptysis include acute bronchitis, chronic bronchitis, bronchiectasis, cystic fibrosis, lung abscess, tuberculosis, pneumonia, neoplasms, and pulmonary embolism. Causes of massive hemoptysis include blunt or penetrating chest injury, other trauma, infection, cancer, and clotting disorders. Massive hemoptysis can also occur with other pulmonary diseases, aspirin overdose, crack cocaine use, and following bronchoscopy, lung surgery, or tracheal aspiration. Large amounts of expectorated blood may also be seen with gastrointestinal bleeding. Wheezing, Chest Tightness. The onset, duration, and frequency of wheezing, as well as associated events, should be noted. Asthma may cause recurrent wheezing, chest tightness, difficulty in breathing, or cough that may worsen at night. In addition to asthma, there are a large number of disease states or conditions that may cause wheezing. These include upper airway obstruction, COPD, bronchiectasis, cystic fibrosis, bronchiolitis, aspiration, heart failure, noncardiogenic pulmonary edema, and pulmonary embolus. Endotracheal intubation may cause reflex bronchoconstriction.

Chest Pain. The nature, location, duration, and associated activities or events should be noted. Chest pain may be substernal, pleuritic, or musculoskeletal. Substernal chest pain may be caused by coronary artery disease, cardiac ischemia, myocardial infarction, other heart disease, and cocaine abuse. Pleurisy, pneumonia, pulmonary embolus, pneumothorax, and pleuropericarditis may cause pleuritic chest pain. Rib fractures, chest trauma, thoracic or cardiac surgery, or injury to the chest muscles may cause musculoskeletal pain. Chest pain following cardiopulmonary resuscitation with chest compression is common. Breathlessness (Dyspnea). The onset, position, symptoms, and level of activity associated with dyspnea (severe exertion, exercise, stairs, walking, at rest) should be noted. Common causes of dyspnea include acute asthma exacerbation, COPD exacerbation, interstitial lung disease, myocardial dysfunction, obesity, and deconditioning. Various dyspnea scales are available to quantify shortness of breath (e.g., Borg scale, visual analog scale [VAS]). Respiratory distress with severe dyspnea is a common finding with acute respiratory failure. Respiratory distress with dyspnea in ventilated patients may be caused by inappropriate ventilator settings, hypoxemia, fighting the ventilator due to fear and anxiety, hypercapnia or metabolic acidosis, and the development of pneumothorax. Smoking History. Obtaining smoking history in the ICU may not be practical. Being aware of the patient’s smoking history, however, may be helpful. Use of cigarettes, cigars, or pipes; frequency and amount (pack-years for cigarettes); and attempts to quit are included in a complete smoking history. Current Medications. Medications used prior to ICU admission should be noted. These may include respiratory-related medications (bronchodilators, anti-inflammatory agents, other), antibiotics, cardiac drugs, antihypertensives, antithrombotics, diuretics, steroids, analgesics, opioids, or other medications. If the patient is unable to communicate, this information can sometimes be obtained from the medical record, patient family members, or other caregivers. Current Respiratory Care. Use of respiratory care prior to ICU admission should be noted. For example, home use of oxygen, ventilatory support, continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP), bronchodilators and antiasthmatic medications, or bronchial hygiene and airway care (chest physiotherapy, PEP therapy, flutter, artificial airways, humidifiers, nebulizers, etc.) should be noted.

Physical Assessment Major components of the physical examination include inspection, palpation, percussion, and auscultation. Physical assessment findings are reviewed along with the patient history and diagnostic tests in confirming the diagnosis and creating care and monitoring plans. A complete physical examination is performed using an organized and systematic approach by body system, which includes the assessment of:3 General appearance Vital signs Skin Head, eyes, ears, nose, and throat (HEENT) Neck Back and spine Heart and blood vessels

Thorax and lungs Abdomen/gastrointestinal Extremities Musculoskeletal Neurologic

General Appearance The first step in physical assessment of the patient in the ICU is to note the patient’s general appearance. Gender, ethnicity, age, height and weight, and overall state of health should be noted. For example, the patient’s general appearance may provide clues regarding nutritional status and whether the patient is underweight, overweight, or obese. The respiratory care clinician should note whether the patient is awake, alert, and responsive. The clinician may also note whether the patient is relaxed and resting quietly or anxious, restless, disoriented, confused, or unresponsive. Changes in mental status may be caused by hypoxia. For the ventilated patient, the clinician should note the type of airway employed, type of ventilator in use, and patency of the airway and ventilator circuit. Key ventilator displays include the peak airway pressure, exhaled tidal volume, and respiratory rate. For example, a sudden increase in peak airway pressure in patients receiving volume-targeted ventilation can be due to secretions, bronchospasm, pneumothorax, “fighting the ventilator,” or bronchial intubation. Progressive deterioration in pulmonary compliance (e.g., worsening pneumonia, development of pulmonary edema, atelectasis) will sometimes cause a more gradual increase in peak airway pressure in patients receiving volume-targeted ventilation. Peak airway pressure may fall suddenly due to a patient disconnect or large leak in the system. A quick assessment of monitoring equipment will include observing the patient’s heart rate and rhythm, as well as pulse oximetry values (SpO2). It is best to assure that the patient is adequately oxygenated and ventilated prior to continuing with more routine physical assessment techniques. The patient’s position should be noted. For example, spontaneously breathing patients in respiratory distress may exhibit orthopnea and be unable to comfortably lie supine. Other signs of respiratory distress should be noted, which include tachypnea, hyperventilation, intercostal retractions, and use of the accessory muscles. Loss of consciousness, somnolence, convulsions, and coma are findings

associated with very severe hypoxia, as well as other neurologic disorders. In addition to any mechanical ventilators that may be in use, the respiratory care clinician should note other ancillary equipment or supplies in use, such as oxygen therapy equipment, suctioning and airway care equipment, monitoring devices, intravenous lines, infusion pumps, chest drainage systems, and urinary catheter collection bags.

Vital Signs Vitals signs routinely monitored in patients admitted to the ICU include pulse, respirations, blood pressure, and temperature. Most ICU patients also receive continuous cardiac monitoring and continuous measurement of SpO2. Monitoring of vital signs, including cardiac rhythm, heart rate, and SpO2, may alert the clinician to a change in patients’ condition and may suggest the need for further evaluation or testing.3–5 The heart rate (HR) is typically assessed by palpating the patient’s pulse, but can also be determined by auscultation, pulse oximetry, or telemetry monitoring. Normal resting adult heart rate is 60 to 100 bpm; bradycardia and tachycardia are defined as HR < 60 and HR > 100 bpm, respectively. Children’s heart rates vary with age. For example, normal heart rates for infants range from 110 to 150 bpm, while 2-year-olds have a normal heart rate range of 80 to 130 bpm. Clinicians should note the characteristics of the pulse including rate (rapid, normal, or slow), rhythm (regular or irregular), strength (weak vs. strong), and amplitude (bounding, full, normal, diminished, or absent).3 Common causes of tachycardia seen in the ICU include hypoxia, anemia, blood loss, hypovolemia, hypotension, shock, heart disease, uncontrolled pain, anxiety, and fever. Drugs and medications that increase heart rate include sympathomimetic medications, anticholinergic medications (xanthenes, nicotine), and cocaine. Ventilated patients with inappropriate ventilator settings who are struggling to breathe and/or “fighting the ventilator” will often exhibit an increased heart rate. Cardiac arrhythmias sometimes observed on cardiac monitors in the ICU include sinus tachycardia, supraventricular tachycardia, and ventricular tachycardia. Common causes of bradycardia seen in the ICU include severe hypoxia, severe acidosis, cardiac disease, and heart block. Vagal stimulation and administration of

beta blockers may also cause bradycardia. Respiratory rate (f) can be assessed in spontaneously breathing patients by counting respirations during the pulse check session. Mechanical ventilators and various ICU monitoring systems also display measures of respiratory rate. Normal adult resting spontaneous respiratory rate is 12 to 20 breaths/min; bradypnea and tachypnea are defined as f < 12 and f > 20 respectively. Tachypnea is a normal physiologic response to hypoxemia, and thus any cause of hypoxemia may result in increased respiratory rate. Tachypnea and hyperventilation are also normal physiologic responses to metabolic acidosis. Severe pain, anxiety, or panic attacks may also cause tachypnea. Many patients with acute respiratory failure exhibit rapid shallow breathing. Very high or very low spontaneous respiratory rates (f > 30 to 35 breaths/min or f < 8 breaths/min) may signal the need for mechanical ventilatory support. Slowed or irregular breathing with periods of apnea are also suggestive of the need for mechanical ventilatory support. Bradypnea may be caused by overdose of CNS depressants (e.g., opiates, benzodiazepines, barbiturates), neurologic disease, or severe hypoxia. Children’s respiratory rates normally range from about 18 to 30 breaths/min, depending on age. Infants’ respiratory rates normally range from about 30 to 40 breaths/min.3 Blood pressure (BP) is measured invasively by an indwelling arterial line or noninvasively using an automatic or manual blood pressure cuff. Arterial blood pressure is determined by the force of ventricular contraction, blood volume, blood viscosity, systemic vascular resistance, and elasticity of arterial vessel walls. The relationship between blood pressure, cardiac output (CO), and systemic vascular resistance (SVR) is described below: BP = CO × SVR Normal adult blood pressure is 120/80 mmHg (range 90 to 140/60 to 90 mmHg).3 Many critical care monitoring systems calculate mean arterial pressure (MAP). Normal adult MAP is 80 to 100 mmHg, which can be estimated as follows: MAP = 1/3 (systolic pressure – diastolic pressure) + diastolic pressure Hypotension (BP < 90/60 mmHg) may be caused by decreased cardiac output, low circulating blood volume, or peripheral vasodilation. Common causes of

hypotension seen in the ICU include septic shock, trauma, acute blood loss, massive pulmonary embolism, and heart disease. Increased mean airway pressure due to mechanical ventilation with positive pressure may reduce venous return to the heart, decrease cardiac output, and cause systemic hypotension. Hypertension has classically been defined as sustained systolic pressures ≥ 140 mmHg or sustained diastolic pressures ≥ 90 mmHg in adults; however, newer American Heart Association/American College of Cardiology guidelines has lowered this to > 130/80 mmHg. Smoking, obesity, race, heredity, alcohol abuse, sedentary lifestyle, hyperlipidemia, vitamin D deficiency, depression, stress, and excessive salt intake are all risk factors for the development of chronic hypertension. In the acute care setting, patients with hypertensive emergencies are sometimes seen. In such cases, diastolic pressures ≥ 120 mmHg may be caused by head trauma, stroke, or hypertensive encephalopathy. Hypertensive emergencies are also sometimes seen with acute heart failure, myocardial infarction, aortic dissection, acute kidney disease, recent vascular surgery, or pregnancy. Sympathetic nervous system hyperactivity due to withdrawal of antihypertensive medications, ingestion of sympathomimetic drugs, or autonomic dysfunction associated with neuromuscular disease or acute spinal cord injury may also cause acute, severe hypertension. The term hypertensive urgency is used to describe severe hypertension in the absence of other symptoms. Body temperature is commonly measured orally, rectally, or by a tympanic sensor. Normally, body temperature fluctuates throughout the day and with activity levels. Normal oral temperature is approximately 37°C (98.6°F). Temperature may be elevated due to environmental conditions, damage to normal thermoregulatory response, or elevation in the body’s set point for temperature. An estimated 50% of fevers in the ICU are caused by infection, often viral, but can occur in bacterial, fungal, and parasitic infections. In general, a fever is when core temperature is > 38.3°C (101.0°F), although some clinicians use a threshold of 100.5°F as a “lowgrade fever.”6 Temperatures > 40.6°C (105°F) are considered medical emergencies.3,6 Common causes of fever seen in the ICU include bacteremia, sepsis, surgical site infection, ventilator-associated pneumonia (VAP), sinusitis, and decubitus skin ulcers and intravascular catheter-related infection. Other infectious causes of fever seen in the ICU include urinary tract infection, endocarditis,

empyema, abdominal abscess, and meningitis. However, not all fevers in the ICU indicate infection. Drugs, severe neurologic injury, and postsurgical wound inflammation are common noninfectious causes. Increased body temperature increases oxygen consumption, and this may further impair tissue oxygenation in the critically ill patient. Elderly patients with infection may have an impaired ability to develop fever and this should be considered when assessing these patients. Hyperthermia is an elevated temperature that may be caused by heavy exertion in a hot, humid environment. Malignant hyperthermia is a rare condition that may be precipitated by exposure to inhalational anesthetics or succinylcholine. Hypothermia may be caused by exposure to a very cold environment, such as winter conditions or cold-water immersion (near-drowning). Hypothermia is also sometimes seen in patients with spinal cord injuries with autonomic dysreflexia, severe infections and sepsis, kidney dialysis patients, and patients with liver cirrhosis. Therapeutic hypothermia is commonly employed in patients undergoing cardiopulmonary bypass (e.g., heart surgery, aortic surgery) to reduce potential tissue damage. Postoperative patients are usually warmed to at least 34°C before transfer to the ICU. Therapeutic hypothermia may also be useful in certain patients following cardiac arrest to reduce the risk of neurologic injury. Table 8-1 summarizes normal adult vital signs. TABLE 8-1 Adult Vital Signs Vital Sign

Values (range)

Heart rate (bpm) Normal Tachycardia Bradycardia

80 (60 to 100) > 100 < 60

Respiratory rate (breaths/min) Normal Tachypnea Bradypnea

12 (12 to 20) > 20 < 12

Blood pressure (mmHg) Normal Hypertension (sustained increases)

120/80 (90 to 140/60 to 90) ≥ 140 systolic or ≥ 90 diastolic

Hypotension Temperature (°F or °C)1 Normal (oral) Normal (rectal) Fever (oral) Fever (rectal) Hypothermia

< 90/60 98.6°F (97 to 99.5) or 37°C (36.5 to 37.5) 99.6°F (98.7 to 100.5) or 37.6°C (37.1 to 38.1) > 99.5°F or > 37.5°C > 100.5°F or > 38°C Abnormally decreased temperature

1

Normal body temperature varies throughout the day and night and with activity level. The values cited for fever assume normal baseline temperature.

Skin The inspection of patient’s skin is performed to assess skin color, temperature, sweating (diaphoresis), edema, and for the presence of skin rash, infection, or injury. While skin color varies with skin pigmentation, the gingiva (gums) and nail beds of the fingers and toes should be pink. Cyanosis may indicate hypoxemia, although this finding is variable and dependent on the hemoglobin (Hb) level. Pale, cold, clammy skin may be associated with hypotension or shock. Skin color may also be affected by skin rash, allergic reactions, carbon monoxide poisoning, methemoglobinemia, cyanide poisoning, and severe hypercarbia. For example, carbon monoxide poisoning may produce a bright cherry-red skin color, while cyanide poisoning may cause the skin to appear red due to increased venous oxygen concentration caused by impaired tissue oxygen uptake. Liver disease may cause jaundice (yellowing of skin), and elevated skin temperatures may cause erythema (reddening of the skin) due to vasodilation. Edema may indicate fluid overload, heart failure, low albumin, and/or sepsis.7 Scars may indicate previous surgery or injury that may be useful to corroborate the medical history.3 Noninvasive ventilation (NIV) is applied using an oronasal mask or full-face mask interface, which places pressure on the skin of the face and nose. This can result in facial skin breakdown, and skin ulceration from excessive pressures sometimes used to avoid leaks around the mask. Steps to avoid skin breakdown during NIV include use of a properly fitted mask interface, avoidance of overtightening the straps securing the mask, and rotation between oronasal masks and full facemasks. In addition, the respiratory care clinician should perform frequent skin assessment when using NIV.

Head, Eyes, Ears, Nose, and Throat (HEENT) Examination

Examination of the head and neck can provide important information about the patient’s condition. For example, facial expression may reveal level of consciousness (e.g., alert and awake vs. lethargic or obtunded), mood (e.g., relaxed vs. anxious or agitated), and mental status (e.g., oriented to person, place, time, and situation). Facial grimacing, frowning, or expressions of distress may indicate that the patient is in pain. Nasal flaring is associated with increased work of breathing, especially in infants and children. Jugular vein distension may indicate fluid overload or heart failure. Inspiratory contractions of the accessory muscles of the neck generally indicates increased work of breathing and respiratory distress. Central cyanosis is identified by observation of a bluish hue in the lips and adjacent oral tissue and is associated with severe hypoxemia. Pursed-lip breathing is sometimes seen in spontaneously breathing COPD patients in an attempt to diminish air trapping. Sweating (sometimes indicating respiratory distress) may be most easily noticed on assessment of the head and neck.3 Examination of the eyes, pupils, and eyelids also provides clues regarding the patient’s condition. Abnormal pupillary reflexes may be present with CNS disease, head trauma, brain death, and after the administration of certain medications (e.g., atropine). Brain death can cause pupils to be dilated and fixed, whereas pinpoint (miotic) pupils may be caused by opiate drug intoxication. Ptosis refers to drooping of the eyelids, which may be caused by a number of conditions including myasthenia gravis, botulism, and botulinum toxin cosmetic treatments. The HEENT exam can also help identify upper airway problems. For example, angioedema caused by an allergic reaction may result in swelling of the lips, tongue, pharynx, or larynx.3 Signs of upper airway obstruction (e.g., choking, gagging, stridor, change in voice, nasal flaring, altered/absent airflow) due to trauma, epiglottis, croup, foreign body aspiration, abscess, or tumor may also be detected in spontaneously breathing patients during the HEENT examination. As noted above, frequent skin assessment of the nose and face should occur during NIV in order to avoid facial skin breakdown and ulceration from excessive mask pressures.

Back and Spine Respiratory care clinicians should note the presence or absence of scoliosis (lateral spine curvature), kyphosis (anteroposterior [AP] spine curvature), or

kyphoscoliosis (combined lateral and anteroposterior spine curvature). Each of these are associated with reduced thoracic compliance and restrictive pulmonary disease.3

Cardiac Examination The cardiac examination begins with observation of the precordium for the presence of scars, lesions/rashes, or discoloration that may indicate prior surgeries or disease. Upon auscultation, normal heart sounds correlate with the opening and closing of heart valves during systole/diastole. The two “normal” heart sounds are S1 (lub) and S2 (dub). Additional heart sounds, S3 and S4, are associated with diastolic filling and blood striking the left ventricle, and may be caused by left ventricular dysfunction. Heart murmurs are sounds that are caused by turbulent blood flow due to mitral valve regurgitation, mitral valve stenosis, or aortic valve stenosis.3 Box 8-4 describes normal and abnormal heart sounds.

BOX 8-4 Normal and Abnormal Heart Sounds Heart Sounds The S1 and S2 “lub-dub” heart sounds are normal. The S3 heart sound is usually abnormal while the S4 heart sound is always abnormal. S1 “Lub” ∎

S1 marks the beginning of systole or ventricular contraction.

∎

This is the sound that is created when the mitral and the tricuspid valves close. S1 is best heard at the apex of the heart or along the left sternal border and is normally a single sound.

∎

S2 “Dub” ∎ ∎ ∎

S2 marks the beginning of diastole or ventricular filling that directly follows ventricular ejection. S2 is the heart sound created when the pressures between the atrium and ventricle change to allow the aortic and pulmonic (semilunar) valves to close. S2 is loudest and best heard at the base of the heart. S3

∎ ∎ ∎ ∎

S3 is heard in early diastole, just following S2 during the rapid ventricular filling phase. S3 can be a normal finding in healthy athletic young people but is rarely normal after the age of 40. S3 is most often a sign of a distended or floppy left ventricle and indicates some level of systolic dysfunction. S3 is commonly heard in patients with congestive heart failure.

∎

Timing of the S3 follows directly after S2 and before S1.

∎

The S3 is sometimes described as the “Kentucky gallop” where S1 = Ken; S2 = tuk; S3 = y.

∎

“Lub-du-bub” is the typical sound heard with S3. S4

∎

S4 is heard in late diastole, just prior to S1.

∎

S1 is caused by atrial contraction or atrial kick.

∎

S4 is also a low-pitched sound and is best heard with the bell of the stethoscope at the apex of the heart. S4 is never a normal finding and is caused by a still left ventricle.

∎ ∎ ∎

The mnemonic commonly utilized to describe an S4 is “Ten-ne-see” where S4 is the “Ten” syllable. “Dub-lub-dub” is the typical sound heard with S4.

Heart Murmurs Heart murmurs are “whooshing” sounds caused by turbulent blood flow from mitral valve regurgitation, aortic valve stenosis, and mitral valve stenosis, or due to an abnormal opening in a heart chamber. A “thrill” is a tremor or vibration felt upon palpation of the chest wall. ∎ Grade 1: Very faint murmur only appreciated by an expert in optimum conditions ∎ Grade 2: Faint murmur recognized by nonexpert in optimum conditions ∎ Grade 3: Loud murmur without an accompanying thrill ∎ Grade 4: Loud murmur with an accompanying thrill ∎ Grade 5: Loud murmur heard with stethoscope partially off the chest ∎ Grade 6: Loud murmur heard with stethoscope off the chest

Abdominal Examination Abdominal shape and contour, skin color, distension, scars, pulsation, and the presence of subcutaneous blood should be noted. Jaundice may be due to liver disease. Abdominal distension can be caused by abdominal gas, hepatomegaly, splenomegaly, tumor, and peritoneal fluid (ascites). Ascites can be caused by portal hypertension, lymph obstruction, infection, decreased plasma oncotic pressure, and inflammation.3 Abdominal auscultation is performed to evaluate bowel sounds and intestinal motility. Bowel sounds may be described as hyperactive, hypoactive, and absent. Hypoactive and absent bowel sounds suggest a decrease or absence of peristalsis. Clinically, decreased or absent bowel sounds may be caused by bowel obstruction, inadequate blood supply, or paralytic ileus.3 Abdominal palpation can be used to assess organ size, location of masses, and abdominal pain. Abdominal percussion can be performed to evaluate for the presence of excessive gas, pain, or air in the peritoneal cavity caused by trauma or perforation. In healthy patients, the abdomen is soft and nonrigid. The term “guarding” refers to tensing of the abdominal muscles that may occur during palpation and may be due to tenderness, pain, or inflammation. Abdominal rigidity, even in the absence of palpation, is worrisome and may indicate more severe abdominal issues, such as diffuse peritonitis.3

Extremities The upper and lower extremities should be inspected for skin color, temperature, and skin condition; presence of edema; capillary refill; and signs of digital clubbing. Warm, moderately moist extremities generally indicate good peripheral perfusion and oxygenation. Cold, clammy extremities are associated with poor peripheral perfusion. As noted, cyanosis is a variable finding which may indicate hypoxemia. Edema is associated with kidney failure, heart disease, liver disease, and lymph drainage issues.3,7 Pedal edema (edema of the feet and ankles), and edema of the legs and arms are common findings with left-sided heart failure and may occur in patients with multisystem organ failure. Edema of the lower legs and ankles is also commonly seen in patients with advanced lung disease and cor pulmonale (rightsided heart failure secondary to lung disease). The degree of edema is graded using

a scale that indicates how quickly the edematous area refills after being pressed by the assessing clinician.3 When the depression in the skin left by pressing on the edematous area does not refill immediately, pitting edema is present (Box 8-5).

BOX 8-5 Pitting Edema Edema is swelling of the soft tissues due to excess fluid accumulation. Common causes include heart failure, kidney failure, liver disease, or obstruction from venous or lymph drainage. Edema may be generalized or present only in the dependent portions of the body such as the legs and ankles. Pitting edema is present when depression in the skin left by pressing on the edematous area does not refill immediately. Pitting edema may be graded using the following descriptors. Grade

Description

Absent

Normal skin response following application and removal of pressure (e.g., indentation does not persist)

+

Mild pitting edema present in feet and ankles

++

Moderate pitting edema present in feet, ankles, and lower legs (also may be present in hands or lower arms)

+++

Severe generalized pitting edema including feet, ankles, legs, arms, and face

Digital clubbing is associated with various diseases of numerous organ systems, but most commonly associated with chronic pulmonary diseases. Clubbing is frequently seen in patients with interstitial lung disease, and less commonly in patients with cystic fibrosis, bronchiectasis, bronchogenic cancer, lung abscess, or chronic cardiovascular disease

Thorax and Lung Examination Examination of the thorax and lungs begins with inspection of the chest. If possible, place the patient in an upright position to allow for better observation of the anterior, lateral, and posterior aspects of the thorax. Observation of chest wall motion may provide information regarding the regularity and depth of breathing. Reduced chest wall motion may indicate reduced tidal volume, as is sometimes seen in patients with

COPD. Reduced chest wall motion on one side may suggest a unilateral problem (e.g., bronchial intubation, pneumothorax, unilateral atelectasis or pneumonia, pneumonectomy). Pneumothorax may be classified as spontaneous, traumatic, or tension. Pneumothorax can give the appearance of apparent unilateral hyperinflation with increased space between the ribs on one side. Patients receiving mechanical ventilatory support with positive pressure sometimes develop a tension pneumothorax. With tension pneumothorax, the trachea and mediastinum may be pushed towards the opposite side. The rate and pattern of breathing should be noted, as uneven breathing patterns such as Cheyne-Stokes respiration, in which tidal breathing increases to a crescendo followed by a period of apnea, may indicate a serious condition, such as cerebral vascular disease or heart failure. Another abnormal respiratory pattern, Biot’s respiration, is characterized by tidal breathing interrupted by regular and irregular periods of apnea. This type of pattern can be seen in meningitis or injuries to the pons. Kussmaul breathing, characterized by increased rate and depth of breathing, is sometimes seen with diabetic ketoacidosis. Rapid shallow breathing is common in patients with respiratory failure, while abnormally slowed breathing (bradypnea) may occur following head trauma, neurologic disease, or administration of CNS depressants. Whenever an abnormal breathing pattern is recognized, the respiratory care clinician should further investigate possible causes.3 Retractions are present when the tissue between the ribs, above the clavicles, and below the xiphoid moves inward during inspiration. Retractions are caused by significant negative pleural pressures on inspiration due to upper airway obstruction, decreased lung compliance, or flow starvation in mechanically ventilated patients. With flail chest, multiple rib fractures are present, and the chest wall sinks in on inspiration. Normally, the chest wall and abdomen should rise together during the inspiratory portion of the breathing cycle.3 When the upper abdomen moves inward during inspiration instead of the normal outward movement, abdominal paradox is present. This finding suggests paralysis or fatigue of the diaphragm, and respiratory failure may ensue. Observation of chest wall motion and ventilatory efforts in patients receiving mechanical ventilation should be performed to assess for patient–ventilator synchrony and ease of ventilator triggering for patient-triggered breaths.

Inspection of the chest may also reveal chest wall deformity, chest trauma, surgical scars (e.g., thoracotomy, cardiac surgery), or radiation markers. An abnormal increase in chest wall anterior–posterior (AP) diameter may be caused by pulmonary hyperinflation due to airway obstruction. The term barrel chest is used to describe a significant increase in AP diameter sometimes seen in patients with chronic obstructive lung disease (e.g., COPD, cystic fibrosis).

Palpation Palpation of the chest wall can be used to assess for the presence of subcutaneous emphysema, tactile fremitus, the position of the trachea, and to determine the degree and symmetry of chest expansion. Subcutaneous emphysema (air under the skin) produces a “crackly” feeling when palpating the neck and face. Subcutaneous emphysema may be caused by pneumothorax or pneumomediastinum. Tactile rhonchi are rumbling or gurgling vibrations felt over the chest caused by the presence of secretions in a large airway. Tactile rhonchi in intubated patients may disappear following suctioning. Tactile vocal fremitus can sometimes be assessed in cooperative, nonintubated patients by placing the lateral edge of one’s hand against the patient’s chest and having the patient repeatedly speak the number “99” as the examiner moves his or her hand from side to side and down the chest wall. A marked increase in vibration over a given area is associated with consolidation, while reduced or absent vocal fremitus may occur over pleural effusion or pneumothorax. A shift of the trachea from midline (tracheal deviation) can be assessed by placing the examiner’s index finger in the suprasternal notch. Significant unilateral atelectasis may shift the mediastinum and trachea towards the affected side while a tension pneumothorax may shift the mediastinum and trachea towards the opposite side. Chest wall motion can be assessed by palpation. Normally, chest wall motion should be equal and synchronous bilaterally. In the presence of unilateral disease, such as large pleural effusion, pneumothorax, and lobar consolidation, chest wall motion may be reduced on the affected side. All of these findings suggest the need for further diagnostic testing, such as chest x-ray or bedside chest ultrasonography.3

Percussion

Percussion of the chest wall provides information about the ratio of lung tissue to air. During percussion, the examiner taps the chest with their fingertips. A normal or resonant percussion note suggests normal lung tissue underneath the percussion point. Hyperresonant or tympanic percussion notes suggest an increased air-tolung tissue ratio, which may occur with emphysema or pneumothorax. Dull percussion notes may be caused by lung tissue consolidation, significant atelectasis, pleural effusion, or empyema.3 Figure 8-1 illustrates the technique for intermediate chest percussion.

FIGURE 8-1 Chest Percussion. Chest percussion is used to assess the ratio of air to lung tissue via transmission of sound waves created by striking the patient’s chest wall with one’s fingertip as illustrated above. A resonant percussion note suggests normal lung tissue underlying the percussion point. Hyperresonant percussion notes (aka tympanic) suggest increased air in the chest as may occur with hyperinflation (e.g., asthma or emphysema) or pneumothorax. A dull percussion note may be caused by pleural effusion, empyema, atelectasis, consolidation, or percussion over liver, heart, or kidneys. © Jones & Bartlett Learning. Courtesy of MIEMSS.

Auscultation Chest auscultation can identify normal and abnormal lung sounds and help ensure

patients are being adequately ventilated. Breath sounds assessment is an integral part of patient care monitoring in patients receiving mechanical ventilatory support. Chest auscultation can be especially helpful in ventilator patients to identify accidental bronchial intubation, development of pneumothorax, identify the need for suctioning, and assess for the development or progression of atelectasis, pulmonary edema or pneumonia. Ideally, auscultation of the chest will include anterior, posterior, and lateral breath sounds moving the diaphragm of the stethoscope from side to side from apices to bases in a systematic fashion (Figure 8-2).3 Often, in ICU setting, an abbreviated breath sounds assessment may be required. A brief review of common breath sounds terminology follows.

FIGURE 8-2 Chest Auscultation. For anterior chest auscultation, always move from side to side (e.g., 1 to 2, 3 to 4, 5 to 6, and so forth) in order to compare breath sounds on the left versus the right side. The respiratory care clinician should listen to inspiratory and expiratory breath sounds; posterior breath sounds should also be assessed, although this may be more difficult in the ICU setting.

Description Breath sounds may be normal or adventitious. Tracheal breath sounds are normally heard over the trachea and are loud, coarse, and high pitched. Bronchial breath sounds are normally heard over the large central airways and are also loud and course. Bronchovesicular breath sounds are normally heard over medium-sized airways, located between (and below) the scapulae posteriorly and around (and below) the sternum anteriorly, and are a combination of bronchial and vesicular sounds. Vesicular breath sounds are soft, low-pitched breath sounds normally heard over the periphery of the chest.3 Adventitious breath sounds are abnormal sounds that may be characterized as continuous or discontinuous. Wheezing is a continuous sound heard as the caliber of the small airways decrease and is associated with bronchospasm or other airflow limitation. Wheezing may be heard on inspiration, expiration, or both. In asthma, wheezing may be due to bronchospasm, secretions, and mucosal edema. While bilateral wheezing is strongly associated with asthma, it may also be present in COPD and in other conditions (e.g., “cardiac asthma” due to congestive heart failure). It should be recognized that with severe airway obstruction, wheezing may be absent because of severely decreased airflow, and this is an ominous finding in patients with acute, severe asthma exacerbation. Unilateral wheezing sometimes occurs in the presence of tumor, foreign body, or mucous plug.3 Rhonchi are continuous, low-pitched musical sounds similar to snoring and are sometimes heard in the presence of secretions in large airways. Rhonchi often clear following effective coughing or suctioning.3 It should be noted that the terms rhonchus and rhonchi are singular and plural, respectively. Crackles are discontinuous adventitious breath sounds that range from course to fine. Coarse crackles are associated with secretions (e.g., chronic bronchitis) and the opening/closing of medium and large airways. Fine crackles have a sound like Velcro strips being pulled apart and are generally heard over the lung periphery, particularly in the bases of the lungs. Fine crackles may be associated with the opening and closing of alveoli and are sometimes heard in the presence of interstitial

fibrosis, congestive heart failure, or pneumonia. Diminished breath sounds are associated with reduced airflow. Diminished breath sounds are softer and may be clear and equal bilaterally, as in severe COPD, where airflow is significantly reduced. Absent breath sounds suggest no airflow as may occur with consolidation, atelectasis, or pneumothorax. Pleural friction rubs are continuous, low-pitched sounds heard during expansion and contraction of the lung when the pleura are inflamed. Stridor is a high-pitched musical sound heard over the upper airways and associated with upper airway obstruction (e.g., croup, postextubation laryngeal edema). E-A egophony refers to a technique in which the patient repeats the vowel “E” as the clinician moves the stethoscope from side to side across the chest. A change in the sound heard through the stethoscope from “E” to “A” may be caused by lung consolidation or pleural effusion. Another technique known as whispered pectoriloquy refers to a distinct increase in transmission of vocal sounds associated with early pneumonia, atelectasis, or pulmonary infarction and is noted by asking the patient to repeat the number “99” as the clinician moves the stethoscope from side to side across the chest. It is important to note that opinions often differ between clinicians regarding nomenclature and significance of specific breath sounds. Because of this, it is important to interpret breath sounds in light of other clinical and diagnostic findings. Table 8-2 summarizes breath sounds associated with specific clinical conditions.3 TABLE 8-2 Breath Sounds Associated with Specific Clinical Conditions Breath Sounds

Clinical Conditions

Vesicular

Normal over most of the chest except over major airways.

Tracheal or bronchial

Harsh, loud sounds. Normal if found over a large airway. Indicative of consolidation if heard elsewhere.

Bronchovesicular

Normal over or near large airways. Associated with consolidation if heard elsewhere.

Diminished or absent

Associated with hypoventilation of that portion of the lung, severe COPD, pneumothorax, pleural effusion, atelectasis, and bronchial intubation.

Wheezing (high pitched)

Wheezes are associated with partial obstruction of small airways, such as occurs with bronchospasm as in asthma. Sometimes heard with tumor, foreign body, aspiration, or other irritation.

Rhonchi (low pitched)

Rhonchus (singular) and rhonchi (plural) are older terms, not currently recommended for use due to confusion regarding the terms. The terms, however, are still used among some clinicians to describe low-pitched, continuous sounds associated with secretions in the larger airways. These low-pitched sounds associated with secretions in a bronchus or larger airway may clear following cough.

Crackles (rales)

Discontinuous “popping” sounds associated with the opening and closing of alveoli during breathing. Inspiratory crackles are sometimes heard in the bases in patients with pulmonary edema, atelectasis, pneumonia, bronchiectasis, and interstitial lung disease.

E-A egophony

An audible A sound when the patient says E. Associated with consolidation.

Pleural friction rub

Loud, dry, creaky, course, leathery sound associated with pleural irritation and inflammation.

Assessment of Mental Status Many patients in the ICU setting have compromised neurologic function. Seizures, strokes, traumatic brain injury, and administration of sedative or narcotic drugs may affect neurologic function, levels of consciousness, and mental status. Mental status assessment includes sensorium (sensory components of brain and nervous system), level of consciousness (LOC), and orientation. Reviewing prior medical records, discussing the patient’s mental status (or changes in the mental status) with family members, and questioning other providers involved in the patient’s care can help in understanding of the patient’s current status and any changes. On assessment, one should note if the patient is awake, alert, and oriented to person (his or her name or others in the room, family), place (where he or she is), time (what year it is), and event (what is happening at this time). The clinician may observe the patient interacting with other healthcare professionals as well as his or her environment. These brief observations may provide insight to the patient’s mental and/or neurologic status. The patient may be described as awake, alert, and responsive, sleepy, sleeping, lethargic, stuporous, semi-comatose, or comatose.3 Confused patients may not understand directions or be confused as to place, time, people, and events. Delirious patients may experience hallucinations, but more commonly hypoactive delirium occurs in which the patient appears quiet but confused or otherwise noninteractive. Lethargic patients appear sleepy but are arousable. Obtunded patients are difficult to arouse but do respond appropriately when aroused. Stuporous patients cannot be completely awakened when attempts

are made to stimulate them. Semi-comatose patients only respond to painful stimuli while comatose patients are unconscious, not responding to stimuli. An assessment by the clinician of an awake, relaxed, and oriented patient versus one who is confused, anxious, disoriented, or obtunded could reflect the adequacy of the patient’s oxygenation, ventilation, and circulation. The brain is highly sensitive to hypoxia, which may cause restlessness, anxiety, overconfidence, impaired judgement, confusion, and disorientation. Severe hypoxia may cause somnolence, loss of consciousness, convulsions, or coma.3 To summarize, hypoxia may affect cognition, level of consciousness, and neurologic function. A decreasing level of consciousness is a significant finding, suggesting neurological impairment. Patients with neurologic insult, whether it be a result of trauma, narcotic or sedative drugs, hypoxia, or circulatory problems (e.g., shock, hypotension), may exhibit neurologic problems and decreased LOC. Patients may receive sedative or narcotic drugs to treat anxiety, restlessness, or pain, making neurologic assessment more difficult. The Glasgow Coma Scale (GCS) is commonly used to assess changes in patients’ level of consciousness.8 First published in 1974, the scale uses a numeric scoring method to document eye-opening response, verbal response, and integrated motor response.8,9 Scores range from a low of 3 points, which suggests deep coma or brain death, to a maximum total of 15, which indicates full consciousness. Other scoring systems to assess patients’ sedation and agitation are the Ramsay Sedation Scale and the Richmond Agitation-Sedation Scale. Chapter 2 provides additional information regarding assessment of patients’ cognitive and neurologic status. Chapter 2 Boxes 2-12 and 2-13 (see page 69) provide illustrations of the Glasgow Coma Score, Ramsey Sedation Scale, and Richmond Agitation-Sedation Scale. RC Insight “If less than eight, intubate” refers to a Glasgow Coma Score (GCS) of less than 8 points. If a patient’s GCS is less than 8, neurologic impairment is present and endotracheal intubation to secure and maintain the airway should be considered.

Upon entering the room, the respiratory care clinician should observe the patient’s overall appearance. Is the patient alert, awake, and responsive? Is the patient anxious, restless, or disoriented? Does the patient appear to be confused about his

or her surroundings (person, place, time, and events)? Is the patient able to respond to verbal questions or commands? While not always feasible in critically ill, compromised patients (and certainly not in an emergent situation), a mental status examination may include assessment of the patient’s attitude, body language, eye contact, orientation, motor behavior, speech and language, mood and affect, thought process and content, and perception (Box 8-6).3,9

BOX 8-6 Assessment of Mental Status In conscious and cooperative patients, the clinician can often assess aspects of cognitive functioning and neurologic status during the patient interview. In the ICU setting, information may be available in the patient’s medical record or from the patient’s family. Key points regarding the mental status examination are listed below. Level of Consciousness ∎ Note if the patient is confused, delirious, lethargic, obtunded, stuporous, semicomatose, or comatose. ∎ The Glasgow Coma Scale assesses eye opening, verbal response, and motor response. A high score of 15 points corresponds with patients who are fully conscious while a low score of 3 points corresponds with brain death. ∎ The Ramsey Sedation Scale ranges from a score of 1 (agitated, anxious, and restless) to a score of 6 (unarousable). A desirable score would be a score of 2 (cooperative, oriented, tranquil). ∎ The Richmond Agitation-Sedation Scale ranges from + 4 (combative) to –5 (unarousable). An ideal score would be 0 (alert and calm). Attitude ∎ Attitude can sometimes be inferred from the patient’s facial expressions and interaction with the clinician. ∎ Ideally, patients will be cooperative, interact in an appropriate fashion, and appear to be interested in the interaction with the clinician. ∎ Descriptors of patient attitude or affect include open, apathetic, hostile, defensive, easily distractive, secretive, vigilant, suspicious, focused, argumentative, evasive, and intense. ∎ Personality changes are not uncommon with critical illness. Body Language, Facial Expression, and Eye Contact ∎ Body language and use of eye contact may provide clues as to the patient’s feelings, the presence of pain and anxiety, and willingness to cooperate,

although body language and eye contact may be culturally determined. ∎ Grimacing, restlessness, slow, cautious body movements, increased or rigid muscle tension, or touching or rubbing the pain site are all associated with pain. Orientation ∎ The four aspects to patient orientation are: person, place, time, and event. Motor Behavior ∎ Motor behavior can be described as normal, hyperactive, fidgety, catatonic, dystonia, tremors, dyskinesia, or tics. ∎ It is often impractical to have ICU patients walk to observe gait, although this information is useful. Speech and Language ∎ Speech can be affected by neurologic and psychiatric disorders. Mood and Affect ∎ Mood refers to sustained feelings. ∎ Affect refers to the patient’s transient state of emotion (e.g., mad, sad, glad, or afraid). ∎ Fear and anger are common responses to critical illness. ∎ Patients may become irritable, depressed, or anxious. Thought Process and Content ∎ Thought process refers to the form and flow of thinking. ∎ The patient’s thought content describes what the patient is thinking about. Terms used to describe thought content include normal, delusional, obsessive, paranoia, depersonalization, and suicidal or homicidal ideation. ∎ Clinicians should be on the alert for suicidal ideation. ∎ Insight includes awareness of, or ability to understand his or her illness. For example, denial is a common defense mechanism when faced with a lifethreatening illness. ∎ Judgment includes the ability to identify consequences for his or her actions. Perception ∎ Perception can be distorted by neurologic or psychiatric disease. ∎ Problems of perception include hallucinations, illusions, and problems with structural perception. ∎ Hallucinations are visual, auditory, tactile, olfactory, or gustatory a patient experiences that are not shared by a competent observer. • Visual hallucinations are more common with delirium, such as may be experienced during narcotic or alcohol withdrawal.

•

ICU delirium and hallucinations may occur with frequent or continuous sedative use, specifically in those patients requiring prolonged mechanical ventilation.7, 8

Neurologic Examination The neurologic examination may identify cognitive, sensory, motor, or coordination deficits. For example, muscle weakness or paralysis that can impair ventilation may be caused by: Neuromuscular disease (e.g., Guillain-Barré syndrome, myasthenia gravis, multiple sclerosis [MS], amyotrophic lateral sclerosis [ALS]) Infectious disease (e.g., poliomyelitis, West Nile virus, postpolio syndrome, botulism, tetanus) Trauma (e.g., head trauma, spinal cord injury) Vascular disease (e.g., stroke, subdural or epidermal bleeding) Neurologic disease (e.g., ALS, MS, stroke, myopathies) may also cause swallowing dysfunction which, in turn, may predispose patients to aspiration and pneumonia. A complete neurologic examination includes mental status (as described above), the cranial nerves, motor examination (e.g., muscle strength, tone), examination of reflexes, cerebellar examination, sensory examination (touch, pain), and peripheral nerves. The cranial nerves lead to the head, neck, and trunk; control the muscles of the face; and are involved with sensory input. Neurologic symptoms sometimes related to cranial nerve disease include vision loss, double vision, tinnitus (ringing in the ears), hearing loss, vertigo, difficulty swallowing, difficulty speaking, and facial asymmetry/pain. Cranial nerve problems may also cause abnormal pupils, facial weakness/paralysis, tongue deviation, and laryngeal paralysis. Reflex assessment includes the pupillary reflexes, muscle stretch receptors (tendon reflexes), Babinski sign, and assessment of muscle tendon reflexes. Normally, the pupils will contract when light is directed onto the retina. Oculomotor or optic nerve damage may inhibit a proper pupillary response to light. In the presence of increased intracranial pressures (ICP), pupils may be fixed and dilated unilaterally.

When evaluating pupillary reflexes, it is important to note the recent use of opioids, anticholinergic drugs, and other illicit drugs, as they may cause abnormal responses. For example, patients that have recently received atropine (an anticholinergic drug) may have bilateral pupil dilation. LSD may also cause bilateral pupil dilation.3 Ideally, a complete neurologic exam will also include assessment of the patient’s posture, balance, gait, and coordination, as well as a sensory examination, although a complete examination is often not possible in the ICU setting. General neurologic symptoms include headache, memory loss, episodes of altered perception, and insomnia. Neurologic disease may also cause loss of balance, changes in level of consciousness, and seizures. Cerebral hemorrhage, head trauma, and bacterial meningitis resulting in hematoma provide other examples of neurologic disease.3 Stroke may be caused by cerebral venous blood clots or vessel dissection.

Pain Monitoring Many patients experience pain, which may be acute or chronic and localized or generalized.1,2 Pain is somatic if the source is from the skin, soft tissue, muscles, ligament, or tendons. Visceral pain may be caused by inflammation, injury, or ischemia associated with the body cavities.1,2 In the ICU, pain may be due to trauma, surgery, or medical procedures. Patients may have multiple invasive lines and catheters inserted and are often subject to unpleasant or painful procedures such as intubation, suctioning, arterial or venous puncture, thoracentesis, tracheostomy, or bronchoscopy. Airway care and mechanical ventilatory support may be a source of pain and hoarseness and sore throat are common complaints following extubation. In addition to causing psychological distress, pain may contribute to ventilator asynchrony in patients receiving mechanical ventilatory support. Inadequate pain control in the ICU may result in hypermetabolism, increased oxygen consumption, and fighting the ventilator in these patients. Chest pain may be characterized as substernal, pleuritic, or musculoskeletal chest pain.1,2 Chest pain may be caused by ischemic heart disease (i.e., angina), pneumonia, pleurisy, rib fractures, pneumothorax, or tumor. Substernal chest pain may be caused by coronary artery disease and cardiac ischemia, myocardial infarction, pericarditis, or heart valve disease. Substernal chest pain with dyspnea and diaphoresis may be caused by the effects of cocaine abuse. Chest pain that

responds to nitroglycerin is probably due to angina, whereas chest discomfort that responds to antacids suggests gastroesophageal reflux disease (GERD). Pleuritic chest pain may be caused by pleurisy, pneumonia, pulmonary embolus, pleuropericarditis, and pneumothorax. Musculoskeletal chest pain may be caused by rib fractures, chest trauma, thoracic surgery, or injury to the muscles of the chest. Life-threatening causes of chest pain include myocardial infarction, pulmonary embolus, tension pneumothorax, aortic dissection, and esophageal rupture (which may occur following endoscopy, trauma, or severe vomiting). Abdominal pain may be caused by gastric or intestinal disease, gastritis, GERD, appendicitis, diverticulitis, colitis, intestinal obstruction, irritable bowel syndrome, and inflammatory bowel disease. Other causes of abdominal pain include pancreatitis, cholecystitis, peritoneal inflammation, abdominal wall disorders, certain poisonings, metabolic disorders, neurologic problems, and referred pain from the heart, lungs, or esophagus. Acute, intense abdominal pain with hemodynamic instability represents a medical emergency. Causes of acute, intense abdominal pain include dissection of an abdominal aortic aneurysm, abdominal sepsis, intestinal ischemia, adrenal crisis, ketoacidosis, trauma, and organ perforation or rupture. Pain assessment may include the use of pain scales or questionnaires.1 If the patient is awake and alert, the patient may be asked to rate his or her pain on a scale of 0 to 10, where 0 indicates no pain and 10 indicates the worst possible pain. In patients who are unable to communicate, the physical signs of pain should be noted, which include grimacing, writhing, tachycardia, hypertension, tachypnea, diaphoresis, and (possibly) the elevation of hair follicles of the skin (piloerection). Pain is often underestimated in critically ill patients, and clinicians should seek to identify and treat pain when present. A number of valid and reliable pain assessment instruments have been developed for use with critically ill patients. These include the Behavioral Pain Scale (BPS) and the Critical-Care Pain Observation Tool (CPOT). For conscious patients using a rating scale, the goal is a pain rating of less than 3 out of 10 points. Intravenous (IV) administration of opiates generally is preferred for treatment of pain in critically ill patients. These medications include morphine, hydromorphone (Dilaudid), or fentanyl (Duragesic). Intravenous opiates can be delivered by bolus injection for moderate pain, or continuous infusion for moderate to severe pain that is poorly controlled by bolus injection. As an alternative, patient-

controlled analgesia may be employed for patients who are conscious and cooperative. Morphine and hydromorphone have a longer duration of action than fentanyl and may be preferred for intermittent bolus use. Fentanyl provides the most rapid onset of analgesia and may be preferred in patients with bronchospasm because it causes less histamine release. Fentanyl or hydromorphone are also generally recommended in place of morphine in patients with renal failure or hemodynamic instability. Given its rapid onset and potential for respiratory depression, IV fentanyl generally is reserved for intubated patients or procedural sedation with close vital sign monitoring. Side effects of opioids include nausea and vomiting, depressed consciousness, and the potential for causing hallucinations. Opiates may also cause respiratory drive depression, hypotension, and release of histamine. Histamine release is greatest with morphine and least with fentanyl. Other side effects of opioids include urinary retention and hypomotility of the gastrointestinal (GI) tract. Withdrawal signs and symptoms of opiates include drug craving, anxiety, sweating, tachycardia, tachypnea, vomiting, fever, and seizures. Withdrawal symptoms may occur in patients who have received moderate to high doses of opioids for as little as 1 week. Gradual weaning of opiates has been suggested to avoid withdrawal symptoms. Nonopioid analgesics that may be considered include acetaminophen, and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen. Complications of NSAIDs include increased risk of cardiovascular thrombotic events and gastritis, bleeding, ulcers, and GI perforation. Chapter 2 provides additional information regarding assessment of pain in the ICU. Box 2-16 (see page 72) provides an example of the Critical Care Pain Observation Tool (CPOT).

Ancillary Use of Equipment Respiratory care clinicians should be mindful of the presence of specific patient care supplies, equipment, and monitors in use that provide further clues regarding the patient’s clinical condition and care. Cardiac monitors, oximeters, capnography equipment, suction equipment, artificial airways, mechanical ventilators (in use or on standby), mechanical circulatory support devices, dialysis equipment, isolation supplies, chest drainage systems, infusion pumps, urinary catheter and drainage bags, cooling blankets, and restraints all provide information about the patient’s

condition and care.3

Chest Tubes, Drainage, and Management Intercostal chest drainage tubes are sometimes inserted into the pleural space (aka tube thoracotomy) to treat conditions such as a pneumothorax, hemothorax, and pleural effusion. Chest tube insertion allows for the removal of air and fluid from the pleural space and the restoration of negative pleural pressures. Chest tubes are generally about 20 inches long, with four to six holes or eyelets that serve as drainage ports at the distal (patient) end and an opening for connection to the chest drainage system at the proximal end. Chest tubes contain a radiopaque line that can be visualized on chest x-ray. The side holes of a chest tube can also be seen on a chest x-ray.10,30 Chest tubes vary in shape (straight or angled) and external diameter size (6 to 40 French [Fr]). In general, clinicians should choose the smallest diameter tube that will adequately drain the pleural space. Smaller diameter tubes (8–14 Fr) may be sufficient for the removal of air associated with a small, spontaneous pneumothorax. Larger diameter tubes (32 Fr) may be needed for the removal of blood or purulent fluid from the pleural space. The site of chest tube insertion will vary dependent on the type of drainage needed. As air tends to collect in nondependent regions of the lung, tube insertion location for air removal (i.e. pneumothorax) may be different than for fluid collection (i.e. pleural effusion). For example, in the presence of pneumothorax, the chest tube may be placed in the fourth or fifth intercostal space at the anterior or midaxillary line.10,11 When fluid is in the pleural space, the chest tube may be placed lower in the chest. Bedside ultrasound may be helpful in the proper placement of chest tubes.11 Malposition, misplacement, or dislodgment of chest tubes may occur. Lateral and frontal chest x-rays are sometimes needed to verify and properly position chest tubes, although bedside ultrasound imaging should be used to aid in chest tube placement.10,11 Other problems sometimes encountered include chest tube obstruction or kinking and air leak. For example, a bronchopleural fistula can cause an air leak and may require a surgical or endoscopic intervention. Tube drainage ports inadvertently positioned outside of the pleural space may cause excessive air leaks. Other possible complications of chest tubes include infection, subcutaneous emphysema, and re-expansion pulmonary edema.

Modern chest tube drainage systems utilize three chambers: a collection chamber, a water seal chamber, and a suction chamber, as described below. One- and twobottle drainage systems have been employed in the past.11

Collection Chamber The tubing from the patient connects to the drainage unit collection chamber and drainage from the chest flows directly into the collection chamber, typically on the right side of the collection system as you face the system. The collection chamber is made of transparent material with calibration markings to allow for observation of the amount, color, and consistency of the drainage fluid. Excessive fluid volume and cloudy or bloody drainage fluid should be evaluated.

Water Seal Chamber For three chamber drainage systems, the middle chamber is the water seal chamber. When this chamber is filled with sterile water 2 cm in depth, a 2-cm H2O water seal is created. The water seal acts as a one-way valve. This “valve” allows gas to exit the pleural space via the chest tube on exhalation while preventing air from entering the pleural space during inspiration. To maintain this seal, the clinician must keep the chest drainage system upright and maintain the water level in the water seal. Bubbling in the water seal chamber suggests an air leak. The clinician should always monitor the system for air leaks and (if present) note any increase or decrease in the volume of the leak. Newer chest drainage systems replace the traditional water seal with a mechanical one-way valve, although these units may include a fluid-based air leak detection system.

Suction Control Chamber In a three-chamber system, the chamber on the left side of the unit is usually the suction control chamber. Traditional chest drainage units regulate the amount of suction by the height of a water column in the suction control chamber. A suction pressure of –20 cm H2O is generally recommended. To achieve this, the suction control chamber is filled to the desired height with sterile water (e.g., 20 cm H2O) and suction tubing is connected from the suction control chamber to a suction source. The suction source is then adjusted to produce gentle bubbling in the suction control

chamber. Increasing suction at the suction source will increase airflow through the system but will have minimal effect on the amount of suction applied to the pleural space. Excessive suction may cause loud bubbling (which can disturb patients and caregivers) and may hasten evaporation of water from the suction control chamber (which can reduce the suction applied to the patient as the level of water decreases).11 Dry suction control systems are available on newer chest drainage units. Dry suction control systems are easier to set up and there is no fluid to evaporate. Suction may be adjusted in the range of –10 to –40 cm H2O, although a setting of –20 cm H2O will suffice for most patients.11 Not all patients require suction. For example, chest tubes placed for evacuation of pleural air due to spontaneous air leaks (e.g., pneumothorax) may not require suction and the tube is placed on water seal alone. In any case, the least amount of suction required should be applied. The drainage system should be positioned below the level of the patient’s chest, typically at or near floor level. If the chest tube is placed for a pleural effusion, the amount of drainage can be controlled by intermittently clamping the chest tube. This may be desirable in some patients because rapid removal of large volumes of fluid (> 1000 to 1500 mL) may lead to re-expansion pulmonary edema. As noted, the system should be monitored to ensure proper water levels in the suction control chamber and the water seal chamber and the water seal chamber should be observed for the presence of air leaks. Avoid disturbing the chest tube drainage system and ensure that the drainage tubing does not become kinked. Chest tubes are occasionally clamped prior to tube removal in order to assess whether the patient continues to require drainage and tube suction. Following removal of the chest tube, a sterile occlusive petrolatum gauze dressing should be placed immediately over the site to prevent air entry.

Urine Output Monitoring Urine output provides an indirect measure of renal function and fluid balance. In the ICU, many patients have indwelling urinary catheters attached to a calibrated urine collection drainage bag. Monitoring urine output can be helpful in identifying acute kidney injury. Monitoring urine output can also be useful to assess fluid resuscitation. Normal adult urine output is 0.5 mL/kg/hour or about 60 mL/hour (1500 mL/day; range 800 to 2000 mL/24 h). Generally speaking, fluid intake should be about twice

urine output. In addition to urination, water is lost through the skin, respiratory tract, and stool, which explains why fluid intake typically exceeds urine output. Polyuria (excessive urine production) may be caused by diabetes mellitus, diabetes insipidus, nervous disorders, excessive fluid intake, and diuretics (e.g., caffeine, digitalis, furosemide [Lasix]). Oliguria (reduced urine output; < 500 mL/24 h) may be caused by acute nephritis, hypotension, hypovolemia, and renal failure. As noted above, many patients in the ICU have urinary catheters and collection bags in place, which simplify the monitoring of urine output. Critically ill patients sometimes experience acute kidney insufficiency (AKI). AKI is defined as an acute decline in the glomerular filtration rate (GFR; the rate at which blood flows through the kidneys). Urine output is often used as an indicator to identify early renal insult but also may be used to determine adequate volume resuscitation in the treatment of shock. Severe AKI in critically ill patients is typically part of a triad that includes AKI, shock, and respiratory failure requiring positivepressure mechanical ventilation.12 AKI also appears as an independent factor associated with increased mortality in critically ill patients with sepsis, pneumonia, and following cardiac surgery.13,14 Inflammatory mediators associated with the development of ventilator-induced lung injury (VILI) are thought to also have a role in the pathogenesis of AKI, which in some cases might appropriately be called ventilator-induced kidney injury (VIKI).15 Following intubation and initiation of mechanical ventilation, factors that may contribute to the development of AKI include sedation and hypotension. Patients often receive sedative agents to facilitate placement of the endotracheal tube for invasive mechanical ventilation. These sedative agents may have vasodilatory effects that can lead to hypotension and reduced kidney perfusion.15 In addition, positive-pressure mechanical ventilation increases intrathoracic pressure, which may decrease venous return, decrease ventricular filling (preload), and decrease cardiac output. The resultant hypotension may decrease renal perfusion and urine output. Careful monitoring of the urine output may improve detection of AKI, help avoid fluid overload, and improve patient outcomes.

Bedside Assessment in the ICU The respiratory care clinician should perform an abbreviated physical assessment

routinely in the ICU at the patient’s bedside as a part of providing basic respiratory care in the ICU and when monitoring the patient–ventilator system. Key aspects of the ICU bedside assessment will include observation of variables associated with adequate oxygenation and ventilation. An abbreviated assessment performed in the ICU should include: Review of the patient’s medical record. The initial or admitting diagnosis, other medical problems listed, physicians’ orders, laboratory data, chest radiographs and other imaging reports, blood gas reports, progress notes, respiratory care flowsheets, nursing flowsheets, and related comments should be reviewed. Observation of the patient and the patient’s environment. Ancillary equipment and supplies in use should be noted, as described above. Initial physical assessment should include the patient’s general appearance, level of consciousness, extremities, respiratory rate and pattern, cardiac rhythm and rate displayed on the cardiac monitor, blood pressure, and other monitoring data displayed (e.g., SpO2, ventilatory waveforms). The chest physical examination should include inspection, auscultation, palpation, and percussion. Auscultation should be performed to ensure adequate bilateral ventilation. Palpation techniques may be employed to assess for the presence of equal and bilateral chest expansion, accessory muscle use, tracheal shift, or unilateral apparent hyperinflation. Chest percussion may help identify the presence of pneumothorax, bronchial intubation, or pleural effusion. Ventilated patients should be assessed for ventilatory volumes, pressures, and flows, and observed for the presence of patient–ventilator asynchrony.

Blood Gases Arterial blood gas studies are used to assess patients’ acid-base balance, ventilatory status, and oxygenation status. Arterial blood gas analysis can identify physiologic disturbances and evaluate response to therapeutic interventions. In the critical care environment, arterial blood samples can be obtained by arterial puncture or by use of indwelling arterial catheters.16

Arterial Sampling Respiratory care clinicians should understand the indications, contraindications, and hazards of the arterial sampling procedures. The clinician must also understand sampling techniques and errors that may interfere with the proper interpretation of the results. Indications for arterial blood gas and pH analysis include the need to:16 Evaluate the patient’s oxygenation status. Evaluate the patient’s ventilatory status. Evaluate the patient’s acid-base balance. Monitor severity and progression of disease processes. Measure the response to therapeutic interventions. Arterial blood gas samples may be obtained from the radial (most common), brachial, femoral, dorsalis pedis, or axillary artery. When the decision has been made to obtain an arterial blood gas sample, it is important for the clinician to use a puncture site that is safe and accessible.16,17 The lack of palpable pulses, wounds, and intravenous catheter dressings, absence of collateral circulation (for radial artery puncture), and overlying skin infection can make specific sites difficult or inappropriate to use.

Radial Arterial Puncture The radial artery sampling site is the most common choice for obtaining an arterial blood sample (Figure 8-3). The “thumb side” forearm location is easily accessible, easy to palpate, and easy to stabilize.18,19 In general, the ulnar artery provides adequate collateral circulation to the hand, which makes this site relatively safe.

FIGURE 8-3 Radial Arterial Puncture. (A) Assessment of collateral ulnar blood flow by use of the modified Allen test, in which the clinician first locates the radial and ulnar arteries. The patient clenches his or her fist as the clinician applies pressure to both the radial and ulnar arteries. The patient then relaxes the hand, which should appear blanched. The pressure on the ulnar artery is then released while maintaining pressure on the radial artery. Flushing of the hand and restoration of normal color within 10 seconds should occur, indicating good collateral (i.e., ulnar) blood flow. Pressure on the radial artery is then also released. (B) The location of the radial artery is illustrated in relation to the radius bone, and flexor carpi radialis and abductor pollicis longus muscles. (C) Palpation of the radial artery is illustrated. (D) Technique for radial artery puncture.

Equipment used to perform a radial arterial puncture may vary between institutions. Some facilities purchase preassembled kits that contain all of the necessary supplies; others may have clinicians assemble the needed supplies. While performing an arterial puncture, the clinician should use the smallest needle practical. Commonly, a 23-gauge, 1-inch needle is used for the arterial puncture, although smaller needles may sometimes be used (e.g., 25 gauge × 1 inch). The needle radius must be large enough to allow blood flow to fill the syringe, yet small enough to reduce the likelihood of vessel damage. Arterial blood gas syringes are heparinized to prevent blood clotting. Manufacturers vary in regard to the amount and type of heparin used in prepackaged, preheparinized plastic blood gas syringes.16 In general, 2 to 3 mL of blood is needed for analysis; this usually is enough to meet the requirements of the blood gas analyzer and to allow for retesting, if needed.

Brachial Artery A secondary site for arterial puncture is the brachial artery. Brachial artery punctures are generally safe, reliable, and fairly painless.20 The major drawback to using the brachial artery for blood gas punctures is the lack of collateral circulation and higher risk if the artery is damaged. Also, the clinician performing the procedure should be aware of the close proximity of the brachial artery and median nerve. During the puncture, the needle could touch the nerve, causing the patient to experience a sudden, sharp, neuropathic pain.

Femoral Artery The femoral artery site is sometimes used in hypotensive patients and when the radial and brachial pulses are not easily palpable (e.g., during cardiac resuscitation). The femoral artery is used less frequently for arterial punctures, as many clinicians

have limited experience in the procedure. When possible, the procedure should be performed by the clinician most familiar with the technique. Femoral artery punctures can be technically challenging because the patient is required to be in a supine position; in addition, the femoral artery may be difficult to locate and lies in close proximity to the femoral vein and nerve. The close proximity to the femoral vein makes it possible to inadvertently obtain a venous sample. As with all arterial samples, care should be taken to ensure venous blood has not been inadvertently obtained, as inappropriate medical decisions may be made by erroneous reporting analysis results of venous instead of arterial samples.16

Complications of Arterial Punctures While most arterial punctures can be performed safely, the procedure is not without risks. Complications of arterial punctures include vessel laceration, vessel spasm, excessive bleeding, infection, and vessel obstruction. Vessel laceration may occur due to needle manipulation and can be avoided with proper technique. Vessel spasm can occur, which may result in transient decline of blood flow to the distal tissues. Collateral blood flow may offset the decline in blood flow when the radial artery is used. Bleeding risks can be mitigated by identifying patients at risk prior to the procedure. Patients receiving anticoagulant medications (e.g., heparin, warfarin [Coumadin]) or tissue plasminogen activator (tPA), and/or those with bleeding disorders (e.g., hemophilia) may be more likely to develop a hematoma or bleed following arterial puncture. Proper postprocedure care of the puncture site (holding pressure over the site) is necessary to avoid excessive bleeding. Infection is a potential problem associated with arterial puncture. Vessels may also become obstructed from the loosening of arteriosclerotic plaques that may be attached to the walls of the artery. Clinicians should consider the need for arterial blood gas analysis in light of the risks of the procedure.16 The modified Allen test is commonly performed just prior to the radial artery puncture procedure in order to assess the presence of collateral circulation (Figure 8-3A). There is little data to suggest that it is a reliable method to properly identify potential complications associated with cessation of radial arterial blood flow. This is probably because evaluating hand perfusion by assessing blanching and flushing is subjective. Critically ill patients may be unable to participate because of their overall

condition. The individual clinician is challenged to assess the results of the modified Allen test. If there is a question about the status of collateral circulation to the hand, it may be necessary to look for an alternative site to perform the puncture.16

Arterial Line Insertion and Sampling Arterial catheters (indwelling) provide the medical team with valuable information, which may include continuous monitoring of arterial blood pressure and providing a route for repeated blood gas sampling.

Indications for Radial Artery Cannulation The main indications seen in the intensive care unit for radial artery cannulation are continuous blood pressure monitoring and the need for frequent blood gas sampling and analysis.16 Frequent blood gas sampling and analysis may be needed for critically ill patients receiving mechanical ventilation who require close monitoring of their oxygenation and ventilatory status (e.g., acute respiratory distress syndrome [ARDS], severe pneumonia, sepsis). Continuous blood pressure monitoring can be especially helpful in patients with hemodynamic instability (hypo/hypertension).16 The radial artery is commonly used for placement of indwelling arterial catheters. This location is easily accessed, palpated, and the catheter easily stabilized. The ulnar artery typically provides adequate collateral circulation should radial artery occlusion occur.16,21,22 Although complication rates are low, radial arterial lines are not without risks.21 Complications include blood loss, permanent ischemic damage, pseudoaneurysm formation, and infection.16,21 Because of this, arterial lines should be placed in the nondominant hand when possible.22 The medical team should continuously monitor the hand and fingers to ensure adequate perfusion. It may be necessary to remove the cannula if infection is suspected.16,21 Arterial line sampling is simple, and the three-way stopcock closest to the cannulation site is used to draw the sample. In order to draw an arterial sample, a waste syringe is first inserted into the three-way stopcock sample outlet port. The clinician must close the stopcock, that is, turn it OFF to the flush solution. The clinician withdraws the mixture of saline and diluted blood (waste) that fills the tubing and arterial catheter. This step eliminates any flush solution from the line between the cannulation site and the stopcock output port, assuring the sample contains only

arterial blood. After the waste is withdrawn (approximately 3 to 5 mL, or until blood enters the syringe, depending on length of tubing between stopcock and site), the stopcock is closed and the waste syringe is removed. The clinician next withdraws the undiluted arterial blood sample from the system. A heparinized blood gas syringe is then attached to the output port, and the stopcock is closed to the flush solution. About 2 to 3 mL of arterial blood is then drawn into the syringe. The stopcock is then closed, and the syringe is removed. The clinician should remove any bubbles in the sample and immediately cap the syringe. The tubing and stopcock output port is flushed to prevent blood clotting and bacterial colonization.16 Ongoing assessment and care of radial artery catheters is necessary. This ensures patient comfort, safety, and the accuracy of the blood pressure readings. The patient’s hand should be routinely assessed for signs of adequate perfusion. Clinicians should note appropriate skin temperature, color, and capillary refill during the assessment. The insertion site should be inspected for redness or drainage, which may indicate infection. Sterile techniques should be used if dressing changes are required.16 When radial arterial catheter system blood pressure readings fail to read accurately, it may be necessary to troubleshoot the system. Inaccurate readings can be due to human or monitoring system error. Clinicians should begin by inspection of the insertion site to assure the catheter is still inserted properly. Also, evaluate and ensure that pressure tubing is intact. Check all of the connections and tubing; if no problems are noted with the equipment, it may be necessary to remove the arterial catheter and replace it using an alternative site. Radial artery catheters should be discontinued as soon as clinically permissible. Removal may also be necessary because of infection or lack of perfusion of the distal extremity.16,21 Figure 8-4 illustrates a typical radial arterial line system for patient monitoring and blood gas sampling.

FIGURE 8-4 Radial Arterial Line for Arterial Blood Gas Sampling and Blood Pressure Monitoring. PHOTOS: Courtesy of Jonathan Scott.

Description

Venous Blood Gases Central venous and mixed venous blood gas studies can provide information useful in evaluation of oxygen delivery to the tissues.23 Central venous blood samples are drawn from a central venous catheter, whereas mixed venous blood samples are obtained from the distal port of a pulmonary artery catheter (aka Swan-Ganz catheter). Mixed venous blood gas analysis provides the oxygen tension (Pv̄O2), saturation (Sv̄O2), and oxygen content (Cv̄O2) of the blood returning from all parts of the body.24 Mixed venous blood gas studies also allow for the calculation of additional indices of oxygenation, such as arterial–venous oxygen content difference (CaO2 – Cv̄O2) and oxygen extraction ratio (O2 ER = [CaO2 – Cv̄O2] ÷ CaO2). Placement of a pulmonary artery catheter should not be performed for the sole purpose of obtaining mixed venous blood samples, as the procedure is not without complications.23,25 However, in addition to providing samples for mixed venous blood gas studies, pulmonary artery catheters allow for the direct measurement of central venous pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure, which can be used to estimate left ventricular end-diastolic pressure (i.e., preload). Measurement of Pv̄O2 and Sv̄O2 can be helpful in assessing a patient’s tissue oxygenation. Causes of decreased Pv̄O2 and Sv̄O2 include decreases in oxygen delivery (ḊO2) or increases in oxygen consumption (V̇O2). In the ICU, common causes of decreased ḊO2 include decreased arterial oxygen content (CaO2) and decreased cardiac output. Increased metabolic rate (e.g., fever) will increase V̇O2 and decrease Pv̄O2 and Sv̄O2. Pv̄O2 and Sv̄O2 values may be abnormally high with reduced tissue oxygen uptake (e.g., cyanide poisoning), sepsis (e.g., peripheral shunt), left-to-right cardiac shunt (e.g., ventricular septal defect), or marked elevations in cardiac output. Because of cost and complications, as well as availability of newer noninvasive and minimally invasive measures of hemodynamic parameters (e.g., bedside echocardiography, lithium dilution cardiac output, pulse contour analysis), the use of pulmonary artery catheters has declined in recent

years. Central venous blood gases are obtained from a central venous catheter blood sample, which provides an alternative to pulmonary artery catheterization that can also provide valuable information. Central venous oxygen tension and saturation reflect peripheral tissue oxygen delivery and V̇O2; values decrease with decreased ḊO2 or increased V̇O2. The use of central venous blood gases (in place of mixed venous blood gases) has become common in many intensive care units. Central venous pH and PCO2 values are similar to mixed venous values. Pulmonary artery blood includes blood from the superior vena cava (normally 70% saturated with oxygen), inferior vena cava (normally 80% saturated with oxygen), and coronary sinus (normally 56% saturated with oxygen). When blood is drawn from the right atrium (e.g., central venous sampling) it may mostly reflect the saturation of oxygen from the superior vena cava. This is significant because central venous oxygen saturation can be 16% higher than mixed venous saturation. Thus, central venous O2 may overestimate mixed venous O2.24,26 Peripheral venous blood gases can be used to assess acid-base balance (e.g., pH) and systemic carbon dioxide in patients where arterial blood gases are unavailable. Central venous and peripheral venous pH is highly correlated (usually ± 0.03), even with severe sepsis or septic shock. If the peripheral venous PCO2 is low (e.g., PCO2 < 45 to 50 mmHg), hypercapnea is unlikely.16

Sample Analysis Modern blood gas analyzers directly measure oxygen tension (PO2 via the Clark electrode), carbon dioxide tension (PCO2 via the Severinghaus electrode), and pH (via the Sanz electrode).16 Multiwavelength blood oximeters (e.g., co-oximeters) can also measure oxygen saturation (SaO2), hemoglobin (Hb), methemoglobin (MetHb), and carboxyhemoglobin (CoHb).16 Oxygen content (CaO2) may also be calculated based on Hb and SaO2 values. Calculated plasma bicarbonate (HCO3–) and base deficit or excess (BD or BE) are also routinely reported. In addition to traditional blood gas parameters, currently available blood gas analyzers allow for the measurement of electrolytes (i.e., potassium [K+], sodium [Na+], calcium [Ca2+], chloride [Cl–]), glucose, lactate, creatinine, and bilirubin.16

Good clinical decisions require accurate blood gas results. Critical care clinicians must be aware that errors can cause blood gas results to be inaccurate or misleading. Errors in blood gas analysis can occur as preanalytic, analytic, or postanalytic errors. Preanalytic errors refer to those happening before the blood sample is analyzed and usually relate to the methods used to obtain the sample or handling the sample prior to analysis. Common preanalytic errors include unintentional collection of venous blood, bubbles in the sample, excess liquid heparin in the sample, improper labeling of the sample, and failure to correctly record patients’ inspired oxygen concentration or ventilator settings. Analytic errors are those errors occurring during sample analysis, such as improper calibration or malfunction of the blood gas analyzer. Postanalytic errors are those occurring during documentation, reporting of errors, or the inappropriate action (or inaction) taken by the clinician when he or she receives the results.16

Arterial Blood Gas Interpretation Arterial blood gas studies can be extremely helpful in the assessment of the critically ill patient. For example, patients with acute respiratory failure may have hypoxemia alone or hypoxemia with hypercapnia. Hypoxemic respiratory failure is best identified by reviewing the patient’s PaO2, SaO2, and CaO2. Acute hypercapnic respiratory failure (aka acute ventilatory failure) is identified by the presence of an elevated PaCO2 with a corresponding decrease in arterial pH. Chronic hypercapnic respiratory failure (aka chronic ventilatory failure) is identified by the presence of a chronically elevated PaCO2 with a normal or near-normal arterial pH due to metabolic (i.e., renal) compensation. Hypoventilation or hyperventilation is identified by the presence of an abnormally elevated or decreased PaCO2. Assessment of the arterial pH, HCO3–, base excess (BE) or base deficit (BD), and PaCO2 will allow the respiratory care clinician to identify respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis, and mixed acid-base states, as well as the degree of compensation (if any) that is present.27 Chapter 2 (Respiratory Failure) provides a more in-depth discussion of the assessment of oxygenation, ventilation, and acidbase balance.

RC Insight When interpreting an arterial blood gas, consider the oxygen delivery device, liter flow rate, and FIO2 being used. If mechanical ventilation is being utilized, consider ventilatory parameters such as VT, f, FIO2, airway pressures (PIP, PEEP/CPAP), and minute ventilation.

Laboratory Studies Important laboratory studies for the assessment of critically ill patients include hemoglobin and hematocrit, complete blood count (red blood cell [RBC] count, white blood cell count, differential, platelets), clinical chemistry (electrolytes, anion gap), blood glucose, kidney function tests (e.g., blood urea nitrogen [BUN], serum creatinine) and cardiac markers (e.g., cardiac troponin, creatine kinase, and creatine kinase-muscle/brain [CK-MB]). Each of these tests is reviewed briefly below.

Hemoglobin and Hematocrit Hemoglobin is the iron-containing protein found inside of red blood cells that has the primary function of oxygen transport. Hemoglobin (Hb) values are reported in grams per deciliter (g/dL), and 1 g of normal hemoglobin has the capacity to carry 1.34 mL of oxygen. Normal Hb is 14 to 16 g/dL (males) and 13 to 15 g/dL (females). Hematocrit (HCT) is a measure of the volume of packed red blood cells as a percentage of the blood. In males, normal HCT is 40% to 50%; in females, it is 37% to 47%. Anemia is defined as a reduction in the amount of Hb, HCT, or number of circulating RBCs.28 Causes of anemia include blood loss, excessive RBC destruction, and decreased RBC formation. Trauma, surgery, gastrointestinal tract bleeds (e.g., esophageal varices, gastric ulcers, rectal bleeding), and bleeding secondary to inadequate blood clotting (e.g., platelet disorders or anticoagulant drugs) are common causes of blood loss seen in the ICU. Decreased RBC production may be caused by iron deficiency, bone marrow disorders or suppression, thyroid hormone deficiency, or chronic inflammatory disease. Sicklecell disease or malaria will cause abnormal RBC destruction. Anemic hypoxia is defined as decreased CaO2 due to low hemoglobin or Hb dysfunction (e.g., carbon monoxide poisoning, methemoglobinemia). Polycythemia is an abnormally elevated RBC count and should be suspected if Hb > 16.5 g/dL or HCT > 48% in women and Hb > 18.5 g/dL or HCT > 52% in men. Primary polycythemia is a genetic disorder, while secondary polycythemia is often a response to chronic hypoxemia, typically caused by any form of chronic hypoxia, including that related to chronic pulmonary disease, living at high altitude, or chronic exposure to carbon monoxide.

Complete Blood Count The complete blood count (CBC) provides information about the quantity and quality of erythrocytes, leukocytes (white blood cells), and thrombocytes (platelets) in the blood.28,29

Red Blood Cell Count Red blood cells (RBCs) are evaluated by their shape, size, and content of hemoglobin. A normal RBC is a biconcave, nonnucleated disc that ranges from 6 to 8 microns in diameter. The RBC count is a measure of the amount of RBCs in a sample in millions of cells per microliter (× 106/µL). A low RBC count may be found in anemic patients or those with significant blood loss; a high RBC count is found in polycythemic patients.28 RBCs are further differentiated by measurement of mean cell volume (MCV), mean cell hemoglobin (MCH), mean cell hemoglobin content (MCHC), and red blood cell distribution width (RDW). For example, MCV, MCH, and MCHC values may all be low in the presence of iron deficiency anemia or thalassemia, an inherited blood disorder. MCV and MCH may be increased with megaloblastic or pernicious anemia, which may be caused by vitamin B12 deficiency or folate deficiency.

White Blood Cell Count and Differential Assessment of leukocytes (WBCs) includes the count and cell type (WBC differential).28 WBCs are primarily involved in providing protection against bacterial, parasitic, fungal, and viral infection. A normal WBC count is 4500 to 10,000 WBCs per microliter (mcL or µL) of blood. An elevated WBC count is called leukocytosis and a low WBC count is leukopenia. WBC count may be abnormal due to infection or malignancy. There are five different WBCs, each with a different role in immunity: neutrophils, lymphocytes, monocytes, eosinophils, and basophils.28 WBC purpose, normal values, and causes of abnormal values are described in Box 8-7.

BOX 8-7 Types of White Blood Cells There are five types of white blood cells, each with a different purpose as described below:

∎

Neutrophils • Purpose: Fightbacterial infections • Normal values: 50% to 70% of the total blood differential • When elevated: Bacterial infections, chronic myelogenous leukemia, acute stress, trauma, eclampsia, gout, rheumatoid arthritis, rheumatic fever, thyroiditis • When low: Acute malignancies, overwhelming infections, aplastic anemia, chemotherapy, influenza, radiation therapy or exposure, viral infection ∎ Lymphocytes • Purpose: Fight viral infections • Normal values: 20% to 40% of total blood differential • When elevated: Viral infections, chronic bacterial infections, hepatitis, mononucleosis, lymphocytic leukemia, multiple myeloma • When low: Sepsis, steroid use, overwhelming infections, chemotherapy, HIV infection, leukemia, radiation therapy or exposure ∎ Monocytes • Purpose: Fight fungal and tubercular infections • Normal values: 2% to 10% of total blood differential • When elevated: Fungal infections, tuberculosis, chronic inflammatory disease, leukemia, parasitic infection, viral infection • When low: Acute malignancies, overwhelming infections ∎ Eosinophils • Purpose: Fight parasitic infections; allergic reactions • Normal values: 2% to 4% of the total blood differential • When elevated: Allergic reactions, asthma, eczema, hay fever, parasitic infections, chronic eosinophilic malignancies, Addison disease, cancer, chronic myelogenous leukemia, collagen vascular disease • When low: Infection, alcohol intoxication, overproduction of cortisol ∎ Basophils • Purpose: Allergic reactions • Normal values: 0% to 1% of total blood differential • When elevated: Allergic reaction, chronic myeloid malignancies, collagen vascular disease, myeloproliferative disease, varicella infection, following splenectomy • When low: Acute infection, cancer, severe injury

Platelets Platelets (aka thrombocytes) are small, anucleated blood cells produced in the bone marrow that play a major role in clot formation (coagulation). The normal platelet count is 150,000 to 400,000 per µL; thrombocytopenia and thrombocytosis represent low and high values for the platelet count, respectively. Thrombocytopenia can result in bleeding that can be very difficult to control. There are many causes of thrombocytopenia including infection (viral, HIV, sepsis), chronic liver disease, hypersplenism (i.e., an overactive spleen), pregnancy, immune thrombocytopenia, congenital platelet disorders, malaria, certain medications (e.g., sulfonamides, rifampin [Rifadin], vancomycin [Vancocin], antiepileptic agents), nutrient deficiencies, cancer, and bone marrow disorders. Other causes of thrombocytopenia include aplastic anemia, leukemia, lymphoma, genetic disease syndromes, chemotherapy, radiation therapy, auto immune disease, and disseminated intravascular coagulation (DIC). Thrombocytosis can increase clotting activity, which can lead to conditions such as pulmonary embolus, myocardial infarction, and transient ischemic attacks. Causes of thrombocytosis include infection, postsurgical status, malignancy, postsplenectomy, trauma, acute blood loss, essential thrombocytosis, and iron deficiency. Coagulation is a complex biochemical process that involves platelets and clotting factor proteins that result in the formation of a clot (thrombus). In addition to the platelet count, there are two other studies commonly used to assess coagulation status, prothrombin time (PT) and the activated partial prothromboplastin time (aPTT). The PT monitors factor activity in the extrinsic and common pathways involved in clot formation. It is often used to monitor coagulation when patients are receiving warfarin therapy. The results are generally expressed as a time. The aPTT monitors factor activity in the intrinsic and common pathways involved in clot formation. It is often used to monitor patients that are receiving heparin. In the absence of anticoagulant therapy, abnormal PT and aPTT values imply abnormal coagulation due to conditions such as liver disease, blood disorders, toxic ingestion of a substance, or DIC. Hemophilia is caused by a rare genetic clotting factor deficiency. When abnormal PT or aPTT values are present, specific clotting factor assays can used to confirm the causative condition.28

Clinical Chemistry Clinical chemistry involves the analysis of body fluids for diagnostic and therapeutic purposes. Common clinical chemistry tests include measurement of serum electrolytes, glucose, enzymes (e.g., aspartate transaminase [AST], alanine transaminase [ALT], alkaline phosphatase [ALP]), cardiac markers (e.g., troponin, CK–MB, brain natriuretic peptide [BNP]), renal function tests (e.g., creatinine, BUN), and liver function tests (e.g., total serum protein, albumin, globulin, bilirubin). A basic metabolic panel consists of measurement of glucose, calcium, sodium, potassium, chloride, CO2, creatinine, and BUN. A comprehensive metabolic panel adds the measurement of ALP, ALT, AST, bilirubin, albumin, and total protein.28

Electrolytes Electrolytes are free ions (e.g., charged particles of acids, bases, or salts) found in body fluids. The major electrolytes in the plasma are potassium (K+), sodium (Na+), chloride (Cl–), and bicarbonate (HCO3–). Other important electrolytes include calcium (Ca2+), magnesium (Mg2+), and phosphorus (HPO4–2, PO4–3).28 Potassium (K+) is a major intracellular cation (ion with a positive charge) that plays a role in the transmission of nerve impulses. Normal values for K+ in the plasma are 3.5 to 5 mEq/L. K+ has a major role in acid-base balance and muscle contraction, including the heart and ventilatory muscles. The loss of extracellular potassium will cause K+ to be pulled from within the cells in exchange for hydrogen ions, lowering the plasma hydrogen ion concentration and raising the pH. Hypokalemia refers to reduction in serum potassium that may be caused by K+ loss in the urine or body fluids, decreased K+ intake, or a potassium shift from extracellular to intracellular K+. A decrease in serum K+ will cause the kidneys to conserve K+ in exchange for H+ excretion. The result is a hypokalemic alkalosis. Significantly decreased serum K+ can be life-threatening and should be corrected as soon as possible. Specific causes of hypokalemia include inadequate K+ intake in the diet, administration of loop or thiazide diuretics (e.g., furosemide or hydrochlorothiazide [Aquazide H, HydroDIURIL]), gastrointestinal tract loss (e.g., diarrhea, vomiting), excessive sweating, and K+ loss during dialysis or plasmapheresis. Certain potassium-sparing diuretics (e.g., aldosterone inhibitors) may cause an abnormal increase in K+ (hyperkalemia). Levels of K+ > 6.0 mEq/L are associated with cardiac arrhythmias,

and levels that exceed 10 mEq/L can cause ventricular fibrillation.16,28 Chloride (Cl–) is a major extracellular anion (ion with a negative charge). Normal values for Cl– in the plasma are 98 to 105 mEq/L. Cl– is helpful in the maintenance of electrolyte balance, osmotic pressure, and hydration. Decreased plasma Cl– (hypochloremia) levels may be the result of prolonged vomiting or kidney disease. Chloride will also decrease as serum HCO3- increases to compensate for acid-base disturbances such as respiratory acidosis. A decrease in Cl– in the renal tubules may also cause additional K+ loss, further contributing to an alkalosis. The net result is a hypochloremic alkalosis (a type of metabolic alkalosis). Ammonium chloride can be used to treat patients with hypochloremic metabolic alkalosis. While low plasma Cl– levels are associated with metabolic alkalosis, elevated Cl– is associated with metabolic acidosis (i.e., hyperchloremic acidosis). Possible causes of a hyperchloremic acidosis include the loss of gastrointestinal HCO3–, renal tubular failure to reabsorb HCO3–, ingestion or administration of ammonium chloride, excessive infusion of normal saline, and intravenous nutrition (e.g., hyperalimentation).16,28 Plasma bicarbonate (HCO3–) is the major body anion responsible for maintaining acid-base balance. The pH of the body is determined by the ratio of HCO3– to carbonic acid (H2CO3). Metabolic acidosis occurs when there is a decrease in plasma HCO3–. Causes of HCO3– loss include diarrhea, renal tubular loss, and loss via pancreatic fistula. Low plasma HCO3– also occurs in the presence of lactic acid (i.e., lactic acidosis), ketoacidosis, renal failure (i.e., failure to excrete dietary acids), and ingestion of acids (e.g., salicylate [aspirin] overdose). Elevated plasma HCO3– occurs from the loss of acid through vomiting or nasogastric (NG) drainage (e.g., NG suction) or the urine (e.g., diuretics). Other causes of increased HCO3– include hypochloremia (↓Cl–), hypokalemia (↓K+), hypovolemia (low blood volume), and ingestion or administration of NaHCO3.16,28

Anion Gap The anion gap (AG) is calculated by subtracting the routinely measured cations from the routinely measured anions (AG = anions – cations). Routinely measured electrolytes include sodium (Na+), potassium (K+), chloride (Cl–), and bicarbonate (HCO3–). Other important electrolytes include calcium (Ca2+), magnesium (Mg2+), and

phosphorus (PO4), which may not be routinely measured in the standard basic metabolic panel. Physiologically, the values for plasma anions and cations must balance in order to maintain electrical neutrality (aka electroneutrality). Although the actual sum of charges for body anions and cations should be zero, for clinical assessment of acid-base balance, the anion gap can be calculated as: Anion gap (mEq/L) = [Na+] – ([Cl–] + [HCO3–]) For the purposes of the calculation, potassium (K+) and other sometimes unmeasured anions and cations are ignored. An example of the calculated anion gap using normal values for sodium, chloride, and bicarbonate would be: Anion gap (mEq/L) = [Na+] – ([Cl–] + [HCO3–]) Anion gap (mEq/L) = 140 – (105 + 24) = 11 mEq/L Laboratory values for a “normal” anion gap vary from one laboratory to another and are dependent on the methods used for electrolyte measurement. The “textbook” normal range for the anion gap has been reported at 8 to 16 mEq/L; in general, the values from modern clinical laboratories suggest a normal anion gap is < 11 mEq/L. Anion gap calculation is useful in identifying types of metabolic acidosis. For example, a metabolic acidosis due to lactic acid formation, toxic alcohol metabolites, salicylate ingestion, and ketone bodies causes an elevated anion gap. Acidosis in the presence of a normal anion gap could be from diarrhea, pancreatic fistula, and ingestion of substances such as ammonium chloride.16,28 RC Insight In the presence of a metabolic acidosis, calculating the anion gap can help to determine if the acidosis is due to a gain in acids or a loss of HCO3–.

Box 8-8 provides causes of elevated anion gap and normal anion gap metabolic acidosis.

BOX 8-8 Causes of Elevated Anion Gap and Normal Anion Gap Metabolic

Acidosis ∎

∎

Increased anion gap acidosisa • Lactic acidosis (e.g., acute, severe hypoxia, shock, tissue hypoperfusion) • Ketoacidosisb (e.g., diabetes mellitus [diabetic ketoacidosis], fasting, starvation, alcoholic ketoacidosis) • Most patients with renal failurec (retention of hydrogen ions, sulfate ions, phosphate, and urate ions) • Salicylate (aspirin) overdose • Ingestion of methanol (methyl alcohol [wood alcohol], antifreeze, solvents) • Ingestion of ethylene glycol (automotive radiator antifreeze, brake fluid) • Ingestion of large quantities of propylene glycol (newer automotive antifreeze, airport deicers, cosmetic products) • Ingestion of toluene (a solvent used in paint thinners and for other industrial uses); metabolic acidosis is an early finding seen with impaired kidney function • Accumulation of pyroglutamic acid (5-oxoproline) associated with genetic glutathione synthetase deficiency or acquired glutathione depletion Normal anion gap acidosis • Diarrhea (loss of HCO3–)

• • • • • • • • • •

Pancreatic fistula (loss of HCO3–) Distal (type 1) renal tubular acidosisc, d Proximal (type 2) renal tubular acidosis (failure to reabsorb HCO3–) Hypoaldosteronism (type 4 renal tubular acidosis)c,d Posttreatment ketoacidosisb Ureteral diversion (e.g., ileal loop) performed as part of surgery to remove the bladder Ingestion or administration of ammonium chloride (sometimes used to treat severe metabolic alkalosis) Administration of carbonic anhydrase inhibitors (e.g., acetazolamide [Diamox], a diuretic sometimes used to treat metabolic alkalosis) Intravenous hyperalimentation Ingestion of toluene (late finding or with good kidney function)

aLow albumin may cause a decrease in anion gap (AG). To adjust for this, some suggest calculation of

“corrected anion gap” = AG + 2.5 × (4 – measured albumin). If the corrected AG > 16 mEq/L, increased anion gap acidosis is present; if corrected AG< 16 mEq/L, normal anion gap acidosis is present. bDuring the treatment phase of diabetic ketoacidosis, the anion gap may return to normal. cWith renal failure, some patients may have a normal anion gap though most do not.

dType 1 renal tubular acidosis (RTA) or hypoaldosteronism (type 4 RTA) generally present with a normal

anion gap.

Blood Glucose and Diabetes Diabetes tests are used in the diagnosis and monitoring of the major forms of diabetes (e.g., type 1 and type 2 diabetes) and include measurement of hemoglobin A1C, fasting plasma glucose levels, and the oral glucose tolerance test. Hemoglobin A1C measurement is used to determine if the hemoglobin has been exposed to elevated glucose levels (above normal) during the lifespan of a RBC (about 120 days).28 Normal fasting (no food for 8 h) blood plasma glucose levels range from 74 to 99 mg/dL. In the primary care setting, elevated fasting blood glucose levels between 100 to 125 mg/dL are associated with prediabetes, and levels > 126 mg/dL are consistent with diabetes. Most adult ICU patients, however, experience elevated blood glucose values > 110 mg/dL at some point during the course of their illness, irrespective of the presence of diabetes mellitus. In addition to diabetes, causes of increased plasma glucose levels seen in the ICU include the stress of critical illness, metabolic disturbances, certain medications (e.g., corticosteroids, sympathomimetics), and IV therapy with glucose solutions. Insulin therapy should probably be considered for critically ill patients when blood glucose > 180 mg/dL. Diabetic ketoacidosis (DKA) may be seen in critically ill patients, most commonly in those with newly diagnosed type 1 diabetes or in patients who have not received their regular insulin therapy. It may also occur in patients with pancreatic failure or type 2 diabetes with severely reduced pancreatic function. DKA is a potentially lifethreatening form of increased anion gap metabolic acidosis, and generally is accompanied by neurologic symptoms, hyperglycemia, dehydration, and electrolyte disturbances. DKA usually occurs rapidly (< 24 h), and clinical manifestations may include nausea and vomiting, abdominal pain, and compensatory hyperventilation. Precipitating factors for DKA include sepsis, pneumonia, myocardial infarction, pancreatitis, certain medications (e.g., corticosteroids), urinary tract infections, and gastroenteritis. Treatment includes supportive care, administration of insulin, and IV fluids. Hyperosmolar hyperglycemic state (HHS) is another possible complication of

diabetes, particularly in patients with inadequate insulin treatment or those who are noncompliant. HHS typically develops gradually over a period of days; symptoms may include dehydration, extreme thirst, excessive urination, and sudden weight loss. Plasma glucose can reach very high levels with HHS, and electrolyte disturbances are generally present. Neurologic symptoms due to extreme elevations in blood glucose levels may include lethargy, stupor, coma, and seizures. Treatment of HHS generally is supportive and includes IV fluids and insulin.

Kidney Function Tests Two measures of kidney function are BUN and serum creatinine; elevated levels may be present in patients with reduced GFR and impaired kidney function. BUN is not specific to kidney disease and can be elevated when kidney filtration is low due to dehydration, shock, or tissue breakdown associated with trauma or hemorrhage, as well as in patients on high-protein diets, corticosteroids, and certain antibiotics (e.g., tetracyclines). Creatinine, on the other hand, is more specific to kidney disease but can also be elevated in the presence of severe muscle tissue breakdown, as in rhabdomyolysis.28 Normal adult values for BUN are 3 to 20 mg/day; normal adult serum creatinine values are 0.5 to 1.2 mg/dL (males) and 0.4 to 1.1 mg/dL (females). Normal BUN-tocreatinine ratios are about 10:1, and values greater than 20:1 may be seen with decreased renal perfusion. While elevated BUN and creatinine values are present with renal failure, they are not sensitive to early renal impairment. Other tests, such as urine protein tests for microalbumin, can signal early disease. The creatinine clearance test is another sensitive test for renal function, particularly glomerular filtration, but can be technically difficult. Kidney impairment can lead to significant metabolic disturbances, including metabolic acidosis.28

Cardiac Markers Laboratory studies are useful in the early detection and confirmation of heart muscle damage after myocardial infarction (MI). Cardiac troponin (cTn) is a protein found in the heart muscle. When damage to the heart tissue occurs, cTn elevates in blood. Cardiac troponin levels reveal the amount of damage that has occurred to the heart

due to decreased or blocked blood flow to the tissue. The amount of cTn detected in the circulating blood corresponds directly with the amount of tissue damage. It is important to note that cTn levels may not rise immediately after an acute MI. Because of this, cTn levels are drawn at intervals spaced out over several hours when there is suspicion of acute MI. In the past, other studies such as creatine kinase-muscle/brain (CK–MB), serum enzymes, and myoglobin were used, but lack the sensitivity/specificity of cTn.28 Beta-type natriuretic peptides, such as brain natriuretic peptides (BNP) and NTproBNP, may be useful in some settings where patients present with shortness of breath and heart failure is suspected.28,29 BNP levels generally are elevated in the presence of heart failure, and BNP levels may be measured to evaluate for the presence and severity of heart failure. The BNP may help to differentiate congestive heart failure (CHF) from other conditions, such as lung disease, that cause shortness of breath, but BNP levels can be affected by other comorbidities, such as renal failure, atrial fibrillation, and obesity. However, a BNP of less than 100 pg/mL makes the diagnosis of CHF unlikely. The overall value of BNP is still in debate, but it can provide additional information that may help lead to diagnosis. Newer biomarkers that also may become useful in evaluating heart failure include sST2, Gal-3, and GDF-15.28,29

Imaging in the ICU The respiratory care clinician must be familiar with the imaging techniques sometimes performed on critically ill patients including conventional radiography, computed tomography (CT) scans, magnetic resonance imaging (MRI), nuclear medicine techniques (e.g., positron emission tomography [PET] scans), multimodal fusion imaging, diagnostic arteriography, interventional radiography, and the use of diagnostic ultrasound. While many of these techniques require that the patient be transported to an imaging center, portable chest x-rays are commonly performed in the ICU and the use of bedside ultrasound has become widespread.

Portable Chest Radiographs Portable chest radiographs (chest x-rays) commonly are obtained in the critical care environment. The resultant images help clinicians identify anatomical structures; verify the position of lines, tubes and catheters; and perform assessment of abnormal conditions.30 Portable chest images obtained in the ICU are particularly useful for verification of proper endotracheal tube placement and identification of pneumothorax, if present. Chest x-rays obtained in the ICU are often taken with the patient in the bed using a portable x-ray machine resulting in an anterior posterior (AP) view.30 Unlike CT scans or MRIs, portable chest x-rays are quick and easy to obtain and do not require patient transport to radiology or other central imaging centers. The images are useful in the identification of major abnormalities such as pneumonia, pneumothorax, ARDS, pleural effusion, atelectasis, and inadvertent bronchial intubation. Portable chest x-rays do have certain limitations. Portable AP chest x-rays are often not as clear as posteroanterior (PA) images obtained in the radiology department. AP images are often somewhat distorted, coarse in appearance, and lower in resolution, and the patient may be twisted or rotated, resulting in distortion of anatomic structures. With AP images, the scapula may also partially obscure visualization of the underlying lung fields, and a good inspiratory effort may be lacking.30 AP images of the heart are larger than on the PA view, and in the ICU, there are often many artifacts present such as monitoring leads, catheters, tubes,

and intravascular lines. With an AP view of a pleural effusion, pleural fluid may be spread out, depending on the patient’s position. In spite of these problems associated with the portable chest x-ray, it remains an essential tool for the evaluation of very sick patients seen in the ICU.30

Ultrasound Imaging Ultrasound imaging has become increasingly useful in the critical care environment. Ultrasound imaging involves the use of sound waves to generate images. Because ultrasound imaging does not use ionizing radiation, it has a very low risk profile. Commonly, ultrasound is used for fetal imaging, cardiac imaging (e.g., echocardiography), and vascular imaging (e.g., vascular ultrasound). Portable, bedside ultrasound imaging (aka critical care ultrasonography) has become increasingly useful in the ICU environment. Ultrasound imaging can be used to help place invasive lines, such as arterial or central venous lines. Point-of-care chest ultrasound can help detect and evaluate pneumothorax, pleural effusion, pneumonia, and pulmonary edema. Bedside cardiac ultrasound imaging may also be useful in the classification of shock states (e.g., hypovolemic vs. obstructive vs. cardiogenic vs. distributive shock). In addition, ultrasound can be used to assist with bedside procedures and evaluate for the presence of venous thromboembolic disease.

Pulmonary Function Testing In the intensive care unit, a number of bedside measures are sometimes employed to assess patients’ pulmonary function.31–33 These include measurement of spontaneous tidal volume, minute ventilation, and respiratory rate, measures of pulmonary mechanics and vital capacity, as well as measures of forced expiratory gas flow.

Bedside Tests of Spontaneous Breathing Bedside assessment of spontaneous breathing is commonly performed for patient evaluation for liberation from mechanical ventilation, assessment for ventilatory failure due to neuromuscular disease (e.g., amyotrophic lateral sclerosis [ALS], Guillain-Barré syndrome), or for screening prior to surgery. Monitoring systems incorporated into mechanical ventilators or portable volume and flow-sensing devices (spirometers and respirometers) are commonly used for assessment of spontaneous breathing at the bedside.

Tidal Volume, Minute Ventilation, and Respiratory Rate Disease states, critical illness, and patient positioning can affect patients’ spontaneous tidal volume, minute ventilation (aka minute volume), respiratory rate, and pattern of breathing. Patients generally adopt a breathing pattern that minimizes ventilatory work. For example, patients with increased airway resistance may breathe slowly to reduce the work expended to overcome airway resistance. Patients with decreased lung compliance may reduce their tidal volume to reduce the work of breathing and increase respiratory rate in an attempt to maintain minute ventilation; this may result in rapid shallow breathing. Most intensive care ventilators have built-in systems to measure and monitor tidal volume, minute ventilation, and respiratory rate. Spontaneous breathing trials (SBT) are commonly performed on ventilated patients to determine if the patient is ready for ventilator discontinuance. SBTs may be performed by adjusting the ventilator settings to allow spontaneous breathing or via the use of a hand-held respirometer.32,33 Figure 8-5 illustrates a hand-held respirometer for bedside use, a pressure differential tachometer for respiratory flow measurement, and a modern

ventilator display, which may be customized to display tidal volume, minute ventilation, respiratory rate, and other variables.

FIGURE 8-5 Volume and Flow Monitoring Devices. (A) Wright Respirometer for measurement of tidal volume and minute volume. (B) Hans Rudolph Pneumotachometers for measurement of respiratory gas flow. (C) Puritan Bennet 980 ventilator monitoring displays. (A)Courtesy of nSpire Health Inc.; (B) Courtesy of Hans Rudolph,Inc.; (C) © 2019 Medtronic. All rights reserved. Used with the permissions of Medtronic.

Rapid Shallow Breathing Index (RSBI) Rapid shallow breathing is a common manifestation of acute respiratory failure. Causes include decreased lung compliance (acute lung injury, fibrosis, pulmonary edema, pneumonia, atelectasis) and severe respiratory distress.32,34 Generally speaking, adult respiratory rates > 30 breaths/min with tidal volumes < 300 mL are associated with the need for mechanical ventilatory support. The rapid shallow breathing index (RSBI) is sometimes used to evaluate mechanically ventilated patients for the adequacy of spontaneous breathing and weaning readiness.32,34 RSBI is calculated as spontaneous respiratory rate divided by spontaneous tidal volume (f/VT). For example, a normal respiratory rate of 12 breaths/min divided by a normal tidal volume of 0.5 L (500 mL) would result in a RSBI of 24 (RSBI = f/VT = 12/0.50 = 24). A respiratory rate of 30 breaths/min divided by a tidal volume of 0.30 L (300 mL) would result in an RSBI calculation of 100 (RSBI = f/VT = 30/0.30 = 100). RSBI < 105 has been associated with adequate spontaneous breathing and high chance of successful liberation from mechanical ventilation; RSBI of > 105 has been associated with inadequate spontaneous breathing and failure of ventilator weaning.32,34 This index was most predictive in patients intubated for less than a week and younger than 65 years of age.

Respiratory Mechanics (MIP, MEP) Respiratory muscle strength is affected by nutrition, acute/chronic illness, and conditioning. Serious illness can promote a hypermetabolic state and malnutrition is a complication of critical illness. Providing enteral or parenteral nutrition with an appropriate mix of amino acids, carbohydrates, fat, minerals, and vitamins tailored to meet the patient’s needs is an important aspect of the care of critically ill patients. Critical illness can produce sepsis, fever, shivering, agitation, and seizures, all of which increase metabolic rate. Neuromuscular disease, generalized weakness, and poor general health can also affect ventilatory muscle strength and endurance. Critical illness can impair ventilatory muscle strength resulting in reductions in

ventilation and CO2 elimination; impaired cough may affect respiratory mucous clearance.32,35 Maximal inspiratory pressure (MIP), also called negative inspiratory force (NIF), provides a measure of inspiratory muscle strength. Normal MIP ranges from –90 to – 125 cm H2O.36,37 MIP more negative (i.e. lower) than –20 to –30 cm H2O is associated with adequate inspiratory muscle strength, allowing for adequate spontaneous breathing. MIP less negative (i.e. higher) than –20 to –30 cm H2O is associated with the need for mechanical ventilatory support.32,38 Lung compliance, airway resistance, and metabolic demand should be considered during MIP assessment.39–42 For example, reductions in lung compliance may require increased ventilatory muscle strength in order to maintain adequate spontaneous breathing. MIP measurement is performed by instructing the patient to completely breathe out to residual volume, and then inhale as aggressively as possible against a closed valve system incorporating a pressure manometer (Figure 8-6). The pressure manometer will indicate the generated maximum inspiratory pressure.

FIGURE 8-6 Pressure Manometer and T-piece Configured for Measurement of MIP.

Maximal expiratory pressure (MEP) provides a measurement of expiratory (abdominal) muscle strength. A normal MEP ranges from +150 cm H2O to +230 cm H2O.32,36 A MEP of ≥ 60 cm H2O is associated with the ability to effectively cough and

clear secretions.32,38 Pressure manometers are also used to measure a patient’s ability to generate a MEP. This maneuver requires the patient to maximally inhale to total lung capacity, and then exhale as aggressively as possible against a closed valve system, allowing the manometer to register the maximally generated pressure. Newer mechanical ventilators often incorporate software options for the measurement of respiratory mechanics. For example, the Puritan Bennet 840 respiratory mechanics option allows for the measurement of MIP/NIF, occlusion pressure (P0.1), vital capacity (VC), and inspiratory and expiratory gas flow rates.42 Figure 8-6 provides an example of a bedside device used for the measurement of MIP and MEP.

Airway Occlusion Pressure The airway occlusion pressure (P0.1) is the airway pressure generated during the first 0.1 second (100 msec) of an inspiratory effort performed against a completely occluded airway.32,42 P0.1 provides a measure of the ventilatory drive to breathe and may be useful in predicting readiness for weaning from mechanical ventilation. Normal P0.1 is < 2 cm H2O; P0.1 > 6 cm H2O suggests the need for continuing mechanical ventilatory support. P0.1/MIP has been shown to have greater predictive power for ventilator discontinuance than P0.1 alone.

Vital Capacity Normal breathing is a dynamic process, varying as individuals sit, stand, eat, drink, and engage in other daily activities. Normal individuals also take a deep breath, or sigh, approximately every 6 to 10 minutes, or at least 10 sighs breaths/hour.32 Sigh breaths are usually 2 to 3 times the tidal volume. Periodic sigh breaths have been shown to reverse atelectasis that can occur in the presence of constant shallow tidal breathing (< 7 mL/kg).32,36,43,44 The ability to generate an intermittent deep breath to keep the lungs open, cough to clear the airway, and maintain pulmonary function is vital to normal lung function.32,43,44 Generating a deep breath requires adequate inspiratory muscle strength; an adequate cough requires sufficient abdominal muscle strength to exhale forcefully. Inspiratory capacity (IC) is the maximum volume of air an individual can inhale following a passive exhalation, and averages ~50 mL/kg IBW.32 Spontaneously breathing patients in the ICU are often encouraged to cough

and breathe deeply in order to maintain lung function. Incentive spirometry may be employed, with the goal of taking 10 to 15 deep breaths per hour while awake, although evidence of effectiveness in preventing postoperative pulmonary complications is limited. We suggest that intermittent deep-breathing exercises (volume targeted ≥ 1/3 of predicted IC = 1/3 × 50 mL/kg IBW), directed cough, early mobilization, and optimal pain management be employed in spontaneously breathing patients who are at risk for the development of complications following abdominal or thoracic surgery. RC Insight Deep-breathing goals to prevent the development of postoperative atelectasis can be estimated as follows: Volume goal = 1/3 × 50 mL/kg IBW

Vital capacity (VC) is the maximum volume of gas a person can exhale, following a maximal inspiration. Normal adult VC is ~60 to 70 mL/kg IBW.32 VC < 70 mL/kg IBW may reflect an acute or chronic restrictive lung defect (e.g., ARDS, pneumonia, neuromuscular disease, and interstitial lung disease). VC < 30 mL/kg IBW is associated with a decreased ability to cough effectively, and an increased potential for development of atelectasis.32,40 VC < 15 to 20 mL/kg IBW is associated with impending or actual ventilatory failure. When VC measurement is performed using pulmonary function equipment (e.g., pulmonary function screening spirometer, pulmonary laboratory spirometry), gender, age, and height are used to calculate predicted values. VC can be measured as slow vital capacity (SVC) or forced vital capacity (FVC). SVC is sometimes compared to FVC when obstructive lung disease is present because FVC maneuvers may cause air trapping (i.e., SVC > FVC). SVC is commonly measured in the ICU to assess patients’ spontaneous breathing. For example, mechanical ventilation may be initiated in adult patients with neuromuscular disease (e.g., Guillain-Barré) when VC declines to < 1.0 L. Patients unable to cough and breathe deeply are at risk for developing atelectasis, pneumonia, and respiratory failure.32,45

Peak Flow Peak expiratory flow (PEF or PEFR) is the maximum expiratory flow rate achieved

during a maximum forced expiratory maneuver, when starting from a point of maximal inspiration. Ideally, three maneuvers are performed, with the best measurement reported. The PEF is recorded in liters per second (L/sec) or liters per minute (L/min). PEF can be measured with a simple portable peak flow meter, using a portable screening spirometer, or in the pulmonary function lab, with sophisticated equipment. The PEF measurement at the bedside can assist in determining the severity of airway obstruction, as well as assessing a patient’s response to therapy. Normal PEF values in healthy young adults range from about 8 to 10 L/sec, depending on the patient’s age, height, and gender. Monitoring PEF over time can be a useful assessment tool, especially for patients with asthma. For example, a patient with asthma who has PEF values of 80% to 100% of predicted (or personal best) is considered to be in the “green zone,” suggesting that the patient’s asthma is under good control. PEF 50% to 79% of predicted (or personal best) are in the “yellow zone,” suggesting caution should be exercised and additional medication may be required. PEF < 50% of predicted (or personal best) is in the “red zone,” corresponding with severe airway obstruction. PEF values in the “red zone” represent a medical emergency requiring immediate attention. Increasing PEF following treatment (e.g., bronchodilator therapy, corticosteroids) suggests improvement. With acute asthma exacerbation resulting in emergency department visits or hospitalization, PEF monitoring is often performed in order to monitor the patient’s condition and response to therapy. PEF values can be highly variable and patient effort, understanding, and cooperation may affect the results.32,33 PEF measurement may not be practical in many critically ill patients seen in the ICU.

FVC and FEV1 Measurement of forced vital capacity (FVC) is easily performed in noncritically ill patients at the bedside in the acute care setting using a portable screening spirometer. FVC measurement in the ICU may be impractical for some patients, because the maneuver requires good patient cooperation and sufficient patient effort for the results to be useful. To perform the maneuver, the patient must make a maximal inspiratory effort followed by a rapid, forced exhalation for at least 6 seconds. As with PEF measurement, three acceptable maneuvers should be

completed, with the best maneuver reported. Predicted values are calculated based on the patient’s age, height, gender, and ethnicity. Measured values are compared to predicted values by the calculation of “percent predicted.” Normal FVC can be approximately estimated at about 70 mL/kg of IBW.32,33 Forced expiratory volume in 1 second (FEV1) is the volume of air that can be forcefully exhaled during the first second of an FVC maneuver. Normal FEV1 is 80% to 100% of predicted.33 FEV1 may be reduced with obstructive or restrictive lung disease. FEV1 is reduced in patients with COPD and acute asthma due to decreased expiratory flow rates. Patients with acute or chronic restrictive lung disease often have decreased FVC and decreased FEV1. Patients experiencing respiratory muscle weakness frequently cannot exhale forcefully, which may also reduce FEV1. Because FEV1 may be reduced due to obstructive or restrictive lung disease, patients with suspected obstructive lung disease require examination of the FEV1/FVC ratio. A healthy individual should be able to exhale 83% of their total FVC in 1 second, resulting in an FEV1/FVC ratio of 0.83. With a properly performed test, when the FEV1/FVC ratio is < 0.70 an obstructive lung defect is present. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) uses FEV1/FVC and FEV1 along with specific clinical symptoms to classify airflow limitation and COPD severity as follows:33,46 FEV1/FVC < 0.70 and FEV1 ≥ 80% predicted: mild COPD Patients with mild COPD may not experience clinical symptoms. FEV1/FVC < 0.70 and FEV1 < 80% but ≥ 50% predicted: moderate COPD Patients with moderate COPD may experience dyspnea upon exertion. FEV1/FVC < 0.70 and FEV1 < 50% but ≥ 30% predicted: severe COPD Worsening dyspnea may limit the patient’s activities of daily living (ADLs) and exacerbations may occur. FEV1/FVC < 0.70 and FEV1 < 30% predicted: very severe COPD Patient’s quality of life is markedly impaired and life-threatening exacerbations may occur. FEV1/FVC < 0.70 and FEV1 < 50% predicted with chronic respiratory failure is also considered to be very severe COPD. As noted, bedside measurement of FVC, FEV1, and calculation of the FEV1/FVC ratio is relatively easy in the acute care setting with alert, awake, and cooperative patients who are not experiencing severe respiratory distress. These measurements

can be especially helpful in assessment and monitoring of patients with acute asthma, as well as providing objective evidence of improvement following treatment. A significant response to a bronchodilator generally is considered to be an improvement in FEV1 or FVC of at least 12% and 200 mL over baseline values. Measurement of these parameters in the intensive care unit, however, may not be practical for many patients.

Electrocardiogram The electrocardiogram (ECG) is an essential diagnostic and monitoring tool in critical care.47 In fact, the need for continuous ECG monitoring is often reason enough alone to warrant critical care unit admission. The electrical activity of the heart can be displayed on a monitor or it may be printed on special paper that allows for detailed interpretation. Cardiac arrhythmias are abnormal rhythms associated with abnormal electrical activity. Arrhythmia management in cases where clinical symptoms are present, hemodynamic instability has occurred, or the patient is at risk for sudden cardiac death often includes pharmacologic therapy. An ECG helps clinicians understand the direction and strength of the electrical current that is generated during the depolarization and repolarization of the cells of the heart. The tracings noted on a monitor are made up of waves, segments, and intervals. The P wave denotes atrial depolarization. P waves are normally followed by the QRS complex, which denotes ventricular depolarization and contraction. QRS complexes are normally followed by T waves. T waves denote ventricular repolarization. Atrial repolarization happens during ventricular depolarization (during QRS complex), which explains why this is not seen on the ECG (Figure 8-7).47 Figure 8-8 illustrates a normal sinus rhythm (NSR).

FIGURE 8-7 A Normal ECG Tracing Showing Waves, Complexes, Intervals, and Segments.

Description

FIGURE 8-8 Normal Sinus Rhythm (NSR). From Garcia TB, Miller GT. Arrhythmia Recognition: The Art of Interpretation. Sudbury, MA: Jones & Bartlett Publishers; 2003, courtesy of Tomas B. Garcia, MD.

Description The PR segment and interval provide information about the conduction of the

heart’s electrical signal across the atria and the atrioventricular (AV) node. The PR segment connects the P wave to the QRS complex and is measured from the end of atrial depolarization to the beginning of ventricular repolarization. The PR interval is measured from the start of atrial depolarization to the beginning of ventricular depolarization. PR intervals are measured by time, with a normal PR interval being 0.12 to 0.20 seconds. An abnormal PR interval is > 0.20 seconds or < 0.12 seconds. PR intervals that are < 0.12 seconds can be caused by an ectopic pacemaker in the atria or atrioventricular (AV) junction. PR intervals > 0.20 seconds may indicate slowed electrical impulse through the AV node, bundle of His, or bundle branches.47 The QRS complex has a normal duration of 0.06 to 0.10 seconds. A QRS complex with a duration of ≥ 0.12 seconds may indicate a conduction disturbance or other conditions (e.g. electrolyte disturbances, Wolff-Parkinson-White syndrome). Toxic levels of certain antiarrhythmic drugs may also cause a wide QRS complex.47 The ST segment connects the end of the QRS complex to the beginning of the T wave. The normal duration of a ST segment is ≤ 0.20 seconds. This is the duration from the end of ventricular depolarization to the start of ventricular repolarization. ST segments that are elevated, depressed, or upsloping/horizontal/downsloping in shape are considered abnormal and may represent serious clinical conditions. ST segment elevation may suggest myocardial ischemia or infarction. ST segment depression may indicate ischemia, left ventricular hypertrophy, digitalis effect, or nontransmural myocardial infarction.47

Heart Rate and Rhythm When interpreting an ECG, the first step is to assess the heart rate. In normal healthy adults, the heart rate is normally 60 to 100 bpm. A heart rate of < 60 is termed bradycardia; a HR > 100 is termed tachycardia. An important clinical consideration is that the heart rate and the actual perfusing pulse rate may be different. In the setting of an arrhythmia, a clinician should verify the monitored heart rate by checking the patient’s pulse.47 After noting the heart rate, clinicians should assess the rhythm. The rhythm is the determination of the regularity or irregularity of the cardiac impulses that cause the heart to pump. The clinician should determine if the rhythm is regular, regular but interrupted, or irregular. The regularity of the atria is determined by P wave spacing.

Ventricular regularity is assessed by determining the distance between the QRS complexes. If the distances are equal across time, the rhythm may be considered regular. If the regularity is interrupted in a set pattern, the rhythm may be considered regularly irregular. If there is no pattern of irregularity, it may be considered irregularly irregular.47

Common Arrhythmias Sinus tachycardia is a regular rhythm and cardiac cycle with an elevated cardiac rate (100 to 150 bpm). Clinically, sinus tachycardia is often seen as a response to hypoxia, anxiety, uncontrolled pain, fever, cardiac and circulatory problems (e.g., hypovolemia, shock, heart disease, anemia), and certain drugs and medications (e.g., catecholamines, atropine, xanthenes, methamphetamines, cocaine). Sinus tachycardia may also be caused due to endotracheal suctioning, manipulation of tracheostomy tubes, or other procedures in the ICU. Supraventricular tachycardia (SVT) is a rapid rate that originates at or above the SA node. Atrial tachycardia occurs when an ectopic atrial focus other than the SA node results in a rapid rate of 100 to 250 bpm.47 Sinus bradycardia is a regular rhythm and cardiac cycle with a decreased cardiac rate (< 60 bpm). Sinus bradycardia may be caused by increased vagal tone (e.g., vasovagal reflex stimulated by suctioning, carotid sinus massage, Valsalva maneuver, vomiting, increased intracranial pressure [ICP]), hyperkalemia, hypothyroidism, hypothermia). Certain medications may also cause sinus bradycardia (e.g., digitalis, beta blockers, calcium channel blockers, antiarrhythmic agents). Sinus bradycardia is common in patients with acute inferior MI.47 Arrhythmias initiated in the atria include premature atrial contraction (PAC), atrial flutter, and atrial fibrillation. While most PACs are asymptomatic, symptoms can include palpitations, skipped beats, and in some cases, dizziness. PACs may be a warning for the development of more serious arrhythmias such as atrial tachycardia, atrial flutter, atrial fibrillation, or paroxysmal ventricular tachycardia. Atrial fibrillation is commonly associated with CHF. Treatment includes addressing the underlying cause and eliminating caffeine and alcohol from the diet. Symptoms of atrial flutter include palpitations, anxiety, weakness, shortness of breath, chest pain, and possible syncope. Treatment may include carotid sinus massage or Valsalva

maneuver, avoidance of stimulants, and administration of blood thinners to reduce the possibility of blood clots. Radiofrequency catheter ablation may be required in some patients. Atrial fibrillation is caused by multiple atrial ectopic pacemakers or sites of rapid reentry in the atria. Atrial rates may range from 350 to 600 fibrillations per minute with a ventricular rate of 160 to 180 bpm. Atrial fibrillation may be treated with medications, electrical cardioversion, or radiofrequency catheter ablation.47 Arrhythmias initiated at the AV junction include premature junctional complexes (PJCs), junctional or escape rhythms, and junctional tachycardia. A common cause of PJCs is digitalis toxicity; however, hypoxia, stimulants, increased parasympathetic tone, procainamide, quinidine, or sympathomimetic drugs may also cause PJCs. With PJCs, the rhythm is irregular and the cardiac rate is 40 to 60 bpm. Vagal stimulation, hypoxia, heart disease, or sinus node ischemia may cause junctional or escape rhythms. With junctional or escape rhythms, the rate is regular but slow, only 40 to 60 bpm. Treatment may include transcutaneous pacing, atropine, dopamine, or epinephrine. With junctional tachycardia, the rhythm is regular at a rate of 60 to 150 bpm. Digitalis toxicity may also cause junctional tachycardia. Other causes include heart disease, sympathetic stimulation, electrolyte imbalance, stress, the use of stimulants, or hyperventilation. If cardiac output is affected, beta blockers, calcium channel blockers, or adenosine may be prescribed. Carotid massage may be helpful to slow the heart rate, although cardioversion may be required for unstable patients.47 Figure 8-9 depicts atrial flutter and atrial fibrillation.

FIGURE 8-9 Atrial Arrhythmia Tracings. (A) Atrial flutter. (B) atrial fibrillation. (A) Reproduced from Garcia TB, Miller GT. Arrhythmia Recognition: The Art of Interpretation. Sudbury, MA: Jones & Bartlett Publishers; 2003, courtesy of Tomas B. Garcia, MD.

Description Arrhythmias initiated in the ventricles include premature ventricular contractions (PVCs), idioventricular rhythms (IVR), ventricular tachycardia (V-tach), ventricular fibrillation (V-fib), and a form of polymorphic ventricular tachycardia (torsades de pointes) as well as asystole (lack of any rhythm). PVCs are simply QRS complexes that are wide and bizarre in shape. Occasional PVCs generally are not a problem unless they cause symptoms. PVCs may be caused by heart disease, hypokalemia, and hypoxia. Other causes include hypomagnesium, stress, and anxiety. Treatment of PVCs should be focused on the cause. IVR is a regular ventricular escape beat at a rate of 20 to 40 bpm. The QRS is wide and bizarre with no P waves. Cardiac output will be decreased, and vascular collapse may occur. Treatment includes epinephrine, oxygen therapy,

and pacemaker insertion. CPR should be initiated in cases of severe hypotension. Ventricular fibrillation occurs when the heart has multiple ectopic pacemaker sites all firing at different times. The rhythm is chaotic, distinct QRS complexes, P waves, or T waves are absent, and there is no detectable rate. Cardiac output falls to zero and there is no palpable pulse. Ventricular fibrillation may be caused by cardiomyopathy, heart failure, myocarditis, hypovolemic shock, blunt or penetrating trauma, and valvular heart disease. Other causes of ventricular fibrillation include severe hypoxia, acid-base imbalance, electrolyte disturbances, drowning, drug overdose, and accidental electrical shock. Treatment includes electrical defibrillation, cardiopulmonary resuscitation (CPR), oxygen, ventilatory support, and medications. Torsades de pointes is a polymorphic form of ventricular tachycardia that may progress to ventricular fibrillation. Torsades de pointes may be caused by certain drugs (e.g., amiodarone [Cordarone], procainamide [Procanbid, Pronestyl], quinidine [Quinora]) or due to cardiomyopathy, heart failure, myocarditis, or valvular heart disease. Other causes include acid-base imbalance, electrolyte disturbances, and severe hypoxia. Treatment may include administration of magnesium, cardioversion, or defibrillation. Asystole is the absence of any cardiac electrical activity (i.e., cardiac death). The ECG tracing will be a flat line. Asystole may be caused by complete cardiac collapse, severe hypoxia, or other catastrophic system damage or failure. Treatment includes immediate application of CPR, chest compressions, epinephrine, oxygen, ventilatory support, and attention to causative factors.47 Figure 8-10 illustrates a variety of ventricular arrhythmias and asystole.

FIGURE 8-10 Ventricular Arrhythmias. (A) Premature ventricular contractions (PVCs); (B) Ventricular Tachycardia. (C) ventricular flutter. (D) Ventricular Fibrillation. (E) Asystole. From Garcia TB, Miller GT. Arrhythmia Recognition: The Art of Interpretation. Sudbury, MA: Jones & Bartlett Publishers; 2003, courtesy of Tomas B. Garcia, MD.

Description Description Description Atrioventricular blocks (AV block) are another group of cardiac arrhythmias that include first-degree AV block, second-degree Mobitz I AV block (aka Wenckebach), second-degree Mobitz II AV block, and third-degree or complete heart block. With first-degree AV block, the PR interval is increased, there generally are no symptoms, and treatment is targeted at the cause. Causes of first-degree AV block include ischemia and certain medications (e.g., digitalis, beta blockers, calcium channel blockers). With second-degree Mobitz I AV block, the PR interval may increase until a QRS complex is dropped; the rate is irregular. With second-degree Mobitz II AV block, there may be normal P waves with normal QRS complexes except for intermittent blocked P waves (Mobitz II) and the rhythm may be regular or irregular. A 2:1 second-degree AV block occurs when there are two P waves for every QRS complex. There are many causes for second-degree heart blocks, including acute MI, medications, hypoxia, ethanol poisoning, obstructive sleep apnea, cardiac tumors, valvular heart disease, or lesions in the conduction system. Treatment will be dependent upon the cause, however, may include transcutaneous pacemaker, oxygen therapy, or specific cardiac medications. Third-degree or complete heart

blocks occur when there is no relationship between P waves and QRS complexes and there is a dissociation between the atrial and ventricular rate of contraction. For example, the atrial rate of contraction may be 60 to 100, while the ventricular rate is 20 to 60. Causes of complete heart block include MI, certain medications, hypoxia, or conduction system lesions. Treatment should address the underlying cause and may include oxygen therapy, use of transcutaneous pacing, and specific medications (e.g., epinephrine, dopamine).47 Table 8-3 summarizes common cardiac arrhythmias. Figure 8-11 provides examples of first-, second-, and third-degree heart blocks.

FIGURE 8-11 Atrioventricular Blocks. (A) First degree AV block. (B) Second-degree AV block. (C) Third-degree AV block. Reproduced from Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description TABLE 8-3 Common Cardiac Arrhythmias

Description *If rate is < 60 beats per minute, it is called sinus bradycardia. If rate is > 100 beats per minute, it is sinus

tachycardia. †Narrow is defined as ⩽ 0.12 second and wide as > 0.12 second. ^This clinical severity is used as a general guide for clinicians in training, but the actual severity takes into account numerous factors of a patient’s illness and the clinical context and thus should be interpreted accordingly.

Myocardial Infarction MI occurs when heart muscle tissue is damaged or dies due to a lack of blood flow, often due to blockage of one of the coronary arteries by a blood clot. The site of the blockage will determine which areas of the heart are affected. Acute MI is identified based on symptoms and physical findings and confirmed by ECG changes and elevation of cardiac biomarkers. (e.g., elevated troponin-I or troponin-T). ECG changes with acute coronary syndrome allow for classification of patients with suspected MI:47 ST segment MI (STEMI) Non-ST segment elevation MI (NSTEMI)

Unstable angina (ST segment depression, inverted T waves, or transient ST segment elevation) Treatment of STEMI includes initial assessment, immediate administration of aspirin, oxygen therapy, ECG, and measurement of cardiac biomarkers, electrolytes, hemoglobin, and hematocrit. Patients are then evaluated for percutaneous coronary intervention (PCI) or IV fibrinolytic administration for myocardial reperfusion. Angina is treated with sublingual nitroglycerin and arrhythmias are managed appropriately. NSTEMI and unstable angina are similar conditions and initial treatment is similar to STEMI with the exception of fibrinolysis, which is not indicated in cases of NSTEMI.47Figure 8-12 provides an example of typical changes with myocardial ischemia and the evolution of MI. The management of acute myocardial infarction is discussed in Chapter 2.

FIGURE 8-12 Typical Changes with the Evolution of Myocardial Infarction. (A) ST segment elevation characteristic of myocardial ischemia. (B) ECG changes with evolution of MI. (A) Courtesy of AMC/R.C.B. Kreuger.

Description

Heart Failure Left ventricular failure refers to failure of the left side of the heart to adequately pump blood out to the body, whereas right-sided heart failure refers to failure of the right side of the heart to adequately pump blood to the lungs. An ECG should be obtained in patients with suspected heart failure to help identify the cause and detect any arrhythmias.47 For example, patients in heart failure may exhibit PVCs, episodes of ventricular tachycardia, or atrial fibrillation. AV heart block or other conduction

abnormalities may be present. ECG changes may help identify the presence of left or right ventricular hypertrophy. General treatment of patients with heart failure may include diuretics, salt restriction, avoidance of NSAIDs, and use of an angiotensinconverting enzyme (ACE) inhibitor or beta blocker.47 The management of heart failure is discussed in Chapter 2.

Key Points Careful patient assessment and monitoring will help ensure proper diagnosis, treatment, and care for critically ill patients as well as recognition of new problems and conditions that may jeopardize the patient’s recovery. The standard patient history includes chief complaint, history of present illness, past medical history, social history, family history, and occupational history. A prior history of intubation and/or mechanical ventilation is important to note. Physical assessment incorporates inspection, auscultation, palpation, percussion, and review of prior reports of history and physical examinations found in the medical record. Physical examination includes the assessment of vital signs, skin, HEENT, neck, back and spine, heart and blood vessels, thorax and lungs, abdomen, extremities, musculoskeletal, and neurologic status. Critical care monitoring flowsheets allow for recognition of changes in heart rate, blood pressure, respirations, oximetry, body temperature, intake and output, and body weight. With volume-targeted ventilation, a sudden increase in peak airway pressure can be due to secretions, bronchospasm, pneumothorax, bronchial intubation, or fighting the ventilator. In ventilated patients, a sudden fall in peak airway pressure may be due to a patient disconnect or large leak in the system. Signs of respiratory distress include tachypnea, hyperventilation, intercostal retractions, and use of accessory muscles. Loss of consciousness, somnolence, convulsions, and coma may be caused by very severe hypoxia or other neurologic disorders. Common causes of tachycardia include hypoxia, anemia, blood loss, hypovolemia, hypotension, shock, heart disease, uncontrolled pain, anxiety, and fever. Bradycardia may be caused by severe hypoxia, severe acidosis, cardiac disease, heart block, vagal stimulation, and administration of beta blockers. Tachypnea is a normal physiologic response to hypoxemia and many patients with acute respiratory failure exhibit rapid shallow breathing. Bradypnea may be caused by overdose of opiates, benzodiazepines, and barbiturates. Hypotension may be caused by decreased cardiac output, low circulating blood volume, peripheral vasodilation, shock, trauma, blood loss, sepsis, and heart disease. Hypertensive emergencies are sometimes associated with stroke, trauma, hypertensive encephalopathy, acute heart failure, myocardial infarction, aortic dissection, acute kidney disease, recent vascular surgery, or pregnancy. Approximately 50% of fevers in the intensive care unit are caused by infection,

which may be viral, bacterial, fungal, or parasitic. Common infectious causes of fever in the ICU include bacteremia, sepsis, surgical site infection, ventilator-associated pneumonia, intravascular catheterrelated infection, urinary tract infection, endocarditis, empyema, abdominal abscess, and meningitis. Therapeutic hypothermia is commonly employed in patients undergoing cardiopulmonary bypass, and in some cases, after cardiopulmonary arrest. Cyanosis is a variable finding dependent on hemoglobin level. Pale, cold, clammy skin may be associated with hypotension or shock. Facial grimacing, frowning, or expressions of distress may indicate that the patient is in pain. Jugular vein distention may indicate fluid overload or heart failure. Abnormal pupillary reflexes may be present with CNS disease, head trauma, brain death, and after administration of certain medications. Choking, gagging, stridor, change in voice, nasal flaring, and absent or altered airflow may be signs of upper airway obstruction; causes include epiglottitis, croup, foreign body aspiration, abscess or tumor, trauma, or angioedema. Scoliosis, kyphosis, or kyphoscoliosis may cause reduced thoracic compliance and chronic restrictive pulmonary disease. Heart murmurs may be caused by mitral valve regurgitation, mitral valve stenosis, or aortic valve stenosis. Abdominal distention may be caused by hepatomegaly, splenomegaly, tumor, bowel wall edema, bowel obstruction, and ascites. Pedal edema and edema of the legs and arms are common findings with leftsided heart failure. Digital clubbing is associated with chronic pulmonary disease and, occasionally, lung cancer. Pneumothorax may be spontaneous, traumatic, or tension. Tactile rhonchi are rumbling or gurgling vibrations felt over the chest caused by the presence of secretions in large airways. Tension pneumothorax may cause a shift in the trachea away from the affected side. Hyperresonant percussion notes may occur with emphysema or pneumothorax; dull percussion notes may occur with lung consolidation, significant atelectasis, pleural effusion, and empyema. Adventitious breath sounds include wheezing, crackles, and rhonchi. Many patients in the ICU have compromised neurologic function. The Glasgow Coma Scale is commonly used to assess changes in a patient’s level of consciousness. Muscle weakness or paralysis may be caused by neuromuscular disease, certain infectious disease (e.g., botulism, tetanus, polio), trauma (e.g., head

trauma, spinal cord injury), or vascular disease (e.g., stroke). Chest pain may be substernal, pleuritic, or musculoskeletal. Pain is often underestimated in critically ill patients, and clinicians should seek to identify and treat pain when present. Chest tubes are sometimes inserted to treat pneumothorax, hemothorax, and pleural effusion. Urine output provides an indirect measure of renal function and fluid balance. Arterial blood gases provide information about patients’ acid-base balance, ventilatory status, and oxygenation status. Arterial blood gases can be drawn from the radial, brachial, and femoral artery. The most common site is the radial artery. Indications for arterial line insertion are continuous blood pressure monitoring and frequent blood gas sampling. Central venous and mixed venous blood gas studies can provide useful information in evaluating oxygen delivery to the tissues. Complete blood counts are used to provide information about the quantity and quality of red blood cells, white blood cells, and platelets. Causes of anemia include blood loss, excessive red blood cell destruction, and decreased red blood cell formation. Secondary polycythemia is often a response to chronic hypoxemia. White blood cells are primarily involved in protection against bacterial, parasitic, fungal, and viral infection. Platelets play a major role in clot formation. Clinical chemistry tests include measurement of serum electrolytes, glucose, enzymes, renal function tests, and liver function tests. Anion gap calculation can be useful in identifying types of metabolic acidosis. Diabetes tests aid the diagnosis and monitoring of the major forms of diabetes. Blood urea nitrogen and creatinine provide tests of kidney function; both indicate the body’s ability to rid nitrogenous waste. Cardiac markers, like cardiac troponin, reveal information that pertains to the level of damage the heart has sustained after a myocardial infarction. The major electrolytes in the plasma are potassium, sodium, chloride, and bicarbonate. Portable chest x-rays provide valuable information about the anatomic structures of the chest; lines, tubes, and drains; and abnormal conditions, such as pneumothorax or inadvertent bronchial intubation. Ultrasound imaging can be useful in placing invasive lines and performing procedures like drainage of pleural fluid as well as identifying pneumothorax, pleural effusion, alveolar consolidation, and interstitial syndrome. Bedside tests of pulmonary function are sometimes performed in evaluation of patients for liberation from mechanical ventilation, assessment of ventilatory

failure due to neuromuscular disease, and for screening prior to surgery. Maximum inspiratory pressure and maximal expiratory pressure provide measurements of inspiratory muscle strength and expiratory muscle strength, respectively. The ability to generate an intermittent deep breath to keep the lungs open, cough to clear the airway, and prevent atelectasis is essential. Monitoring of the peak expiratory flow rate and/or forced expiratory volume in 1 second (FEV1) can be very valuable when monitoring patients with acute asthma exacerbation. Electrocardiograms use characteristics of the electrical current in the heart and to identify specific and clinically important arrhythmias or patterns of cardiac injury. Acute MI is identified based on symptoms and physical findings and confirmed by ECG changes and elevation of cardiac markers. Left ventricular failure occurs when the left side of the heart cannot adequately pump blood out to the body whereas right-sided heart failure refers to failure of the right side of the heart to adequately pump blood to the lungs.

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25. Maki DG, Kluger DM, Crnich CJ. The risk of bloodstream infection in adults with different intravascular devices: a systematic review of 200 published prospective studies. Mayo Clinic Proc. 2006;81(9):1159– 1171. 26. Jalonen J. Invasive haemodynamic monitoring: concepts and practical approaches. Ann Med. August 1997;29(4):313–318. 27. Theodore AC. Arterial blood gases. In: Basow DS, ed. UpToDate; 2013. 28. Flaws M, Radtke J, Castillo D. In: Shelledy DC, Peters JL, eds. Respiratory Care: Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016: 347–383. 29. Colucci WS, Chen Horng HH. Natriuretic peptide measurement in heart failure. In: Gottlieb SS, Jaffe A, Yeon SB, eds. UpToDate; 2017. 30. Vasquez LP, Shelledy DC, Peters JL. In: Shelledy DC, Peters JL, eds. Respiratory Care: Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016: 427–501. 31. West J. Mechanics of breathing. In J. West, ed. Respiratory Physiology: The Essentials. 8th ed. Philadelphia, PA: Williams & Wilkins; 2008: 95–122. 32. Shelledy DC. Assessment of ventilation. In: Shelledy DC, Peters JL, eds. Respiratory Care: Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016: 241–279. 33. Hirst KR, Walsh BK. Adult pulmonary function. In: Shelledy DC, Peters JL, eds. Respiratory Care: Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016: 503–542. 34. Patel KN, Ganatra KD, Bates JH, Young MP. Variation in the rapid shallow breathing index associated with common measurement techniques and conditions. Respir Care. 2009;54(11):1462–1466. 35. Cordova FC, Mullarkey J, Criner GJ. Neuromuscular dysfunction. In: Hess DR, MacIntyre NR, Galvin WF, Mishoe SC, eds. Respiratory Care Principles and Practice. 3rd ed. Burlington, MA: Jones & Bartlett Learning; 2016: 993–1032. 36. Beachey W. Mechanics of ventilation. In: Beachey W, ed. Respiratory Care Anatomy and Physiology. 3rd ed. St Louis, MO: Elsevier-Mosby; 2013: 44–82. 37. Hautmann H, Hefele S, Schotten K, Huber R. Maximal inspiratory mouth pressures (PIMAX) in healthy subjects—what is the lower limit of normal? Respir Med. 2000;94(7):689–693. 38. Epstein S. Weaning from mechanical ventilation: readiness testing. In: Parsons P, Finlay G, eds. UpToDate; 2013. 39. Beachey W. Pulmonary function measurements. In: Beachey W, ed. Respiratory Care Anatomy and Physiology. 3rd ed. St Louis, MO: Elsevier-Mosby; 2013: 95–109. 40. Mehta S. Neuromuscular disease causing acute respiratory failure. Respir Care. 2006;51(9):1016–1023. 41. Moxham J. Tests of respiratory muscle strength. In: Stoller J, Finlay G, eds. UpToDate; 2013. 42. Vines DL, Jendral K, Wilson K, Kaur R. Acute and critical care monitoring and assessment. In: Shelledy DC, Peters JL, eds. Respiratory Care: Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016: 557–591. 43. Levine M, Gilbert R, Auchincloss JH Jr. A comparison of the effects of sighs, large tidal volumes, and positive end expiratory pressure in assisted ventilation. Scand Journal of Resp Dis. 1972;53:101–108. 44. Branson RD, Campbell RS. Sighs: Wasted breath or a breath of fresh air? Respir Care. 1992;37:462–468. 45. Ruppel G. Ventilation. In: Wilkins R, Stoller J, Kacmarek R, eds. Egan’s Fundamentals of Respiratory Care. 9th ed. St. Louis, MO: Elsevier-Mosby; 2009: 215–236. 46. Pellegrino R, Viegi G, Brusasco V, et al. Interpretative strategies for lung function testing. Eur Respir J. 2005;26(5):948–968. 47. Siddal VJ, Shelledy DC. Cardiac Assessment and the electrocardiogram. In: Shelledy DC, Peters JL, eds. Respiratory Care: Patient Assessment and Care Plan Development. Burlington, MA: Jones & Bartlett Learning; 2016: 385–426.

CHAPTER

9

Critical Care Patient Assessment and Monitoring Part II: Monitoring and Care J. Brady Scott, Joe Hylton, Jon C. Inkrott, and David C. Shelledy

© Anna RubaK/ShutterStock, Inc.

OUTLINE Overview Introduction ICU Patient Assessment Monitoring Oxygenation Monitoring Ventilation Ventilatory Parameters and Mechanical Ventilation Respiratory Rate Tidal Volume and Minute Ventilation Measurement and Evaluation Alveolar Ventilation and Dead Space I:E Ratio Tests of Spontaneous Breathing Monitoring during Mechanical Ventilation Airway Pressures Compliance, Resistance, and Work of Breathing Ventilator Graphics Pressure, Flow, and Volume Curves Optimal PEEP and Recruitment Maneuvers Types of Recruitment Maneuvers Noninvasive monitoring Pulse Oximetry Capnometry, Capnography, and VD/VT Transcutaneous O2/CO2 Exhaled Nitric Oxide Cardiac and Hemodynamic Monitoring Electrocardiogram Monitoring Hemodynamic Monitoring Cardiopulmonary Calculations Mechanical Circulatory Assistance Other Assessment Parameters Assessment of Mental Status and Neurologic Function

Pain Monitoring Intracranial Pressure Monitoring Renal Function and Urine Output Monitoring Chest Tubes, Drainage, and Management Temperature Monitoring and Regulation in the ICU Nutritional Support Managing and Monitoring the Patient Airway Endotracheal Tube Characteristics Cuff Pressure and Volume Managing the Artificial Airway Tracheostomy Tubes Patient Care Bronchial Hygiene and Airway Care Patient–Ventilator System Monitoring Recognition and Treatment of Common Complications

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

17.

18. 19. 20.

Describe the purpose and importance of critical care monitoring for patients receiving mechanical ventilatory support. Explain the process for ICU patient assessment to include review of the medical record, observation of the patient and environment, physical assessment, and a complete patient–ventilator system check. Describe overview assessment and monitoring the patient’s oxygenation and ventilation status. Describe the importance of monitoring respiratory rate, tidal volume, minute ventilation (aka minute volume), and I:E ratio. Contrast the effects of ventilatory mode and monitored ventilatory parameters. Describe the assessment of physiologic dead space and alveolar ventilation in patients receiving mechanical ventilatory support. Describe and interpret tests of spontaneous breathing sometimes performed when patients are receiving mechanical ventilatory support. Explain the monitoring of airway pressures in ventilated patients and interpret the results. Explain the importance of monitoring compliance, resistance, and measures related to work of breathing. Review the assessment of pulmonary mechanics in patients receiving mechanical ventilation. Explain the use of ventilator graphics in the critical care unit and interpret the results. Describe methods to achieve optimal positive end-expiratory pressure (PEEP). Describe the use of recruitment maneuvers in patients receiving mechanical ventilatory support. Explain how to interpret information provided by noninvasive monitoring devices to include pulse oximetry, capnography, and transcutaneous oxygen and CO2 monitoring. Review ECG monitoring in the intensive care unit. Discuss hemodynamic monitoring in critical care to include arterial blood pressure, vasopressor and inotropic titration, fluid balance, central venous pressure, the use of pulmonary artery catheters, and the measurement of cardiac output and cardiac index. Explain the importance of each of the following in assessment and monitoring of the ICU patient: mental status and neurologic function, pain, intracranial pressure monitoring, renal function and urine output, chest tube drainage, temperature monitoring and regulation, and nutritional support. Explain the management and monitoring of the patient airway. Review other forms of critical respiratory care provided in the ICU to include support of oxygenation, ventilation, secretion management and airway care, and bronchial hygiene. Describe patient–system ventilator checks and recognize and treat common complications, including patient–ventilator asynchrony, airway problems, secretions and bronchospasm, pneumothorax, infection, and ventilator malfunction.

KEY TERMS

alveolar dead space anatomic dead space asynchrony cardiac output (CO) dead space fluid overload hypercapnia hyperresonance hypothermia inotropes intrapulmonary shunt laryngeal mask airway (LMA) maximal expiratory pressure (MEP) maximal inspiratory pressure (MIP) mechanical dead space nasopharyngeal airway oropharyngeal airway parenteral nutrition percussion notes physiologic dead space pneumothorax pulse oximetry recruitment maneuvers (RMs) respiratory system compliance (Crs) serum bicarbonate tracheostomy tube vasopressors ventilator-associated lung injury (VALI) ventilator-associated pneumonia (VAP) ventilator-induced lung injury (VILI)

Overview The respiratory care clinician must be able to properly assess, monitor, and care for critically ill patients. This chapter is devoted to critical care patient monitoring and care, with a focus on patients requiring mechanical ventilatory support; it will briefly review assessment of oxygenation and ventilation, discuss measures of lung function during mechanical ventilation, describe the use of ventilatory graphics in patient–ventilator system monitoring, and review monitoring and care of the patient airway. Noninvasive monitoring will be reviewed including oximetry, capnography, transcutaneous oxygen and carbon dioxide monitoring, and exhaled nitric oxide. Invasive monitoring will be described to include hemodynamic monitoring and monitoring of intracranial pressure. Troubleshooting the ventilator and patient care provided in the ICU will also be reviewed. Careful patient assessment and monitoring will help ensure the proper care of critically ill patients, as well as ensuring prompt recognition of conditions that may jeopardize recovery.1–4

Introduction Monitoring of the patient–ventilator system is primarily aimed at ensuring patients remain properly oxygenated and ventilated and that any complications of mechanical ventilation are promptly identified and addressed. Potential hazards and complications of mechanical ventilation include ventilator-associated lung injury (VALI), ventilator-associated pneumonia (VAP), inappropriate ventilator settings, airway problems, and ventilator system failure. Hemodynamic monitoring seeks to identify and treat problems with blood flow including alterations in cardiac output (CO) and blood pressure (i.e., hypotension, hypertension) and to maintain sufficient oxygen delivery to the tissues. Clinical and laboratory monitoring should also seek to identify organ system complications such as gastrointestinal bleeding, renal failure, and increased intracranial pressure. Other complications seen in the ICU environment, particularly in patients receiving mechanical ventilatory support, include generalized skeletal muscle weakness, delirium, psychological distress, pain, sleep deprivation, and traumatic stress. Critical care monitoring may be invasive or noninvasive.4,5 Examples of noninvasive monitoring techniques include pulse oximetry, capnography, transcutaneous oxygen and CO2 monitoring, and ECG. Arterial blood gas analysis requires obtaining an arterial blood sample. Forms of invasive hemodynamic monitoring include use of arterial lines for continuous blood pressure monitoring, measurement of central venous pressure, pulmonary artery catheterization, and measurement of cardiac output. Newer, “minimally invasive” techniques have been introduced for hemodynamic monitoring that include transpulmonary thermodilution and pulse-induced contour analysis to estimate cardiac output. Noninvasive techniques using bioreactance have been developed for calculation of stroke volume and cardiac output. Intracranial pressure monitoring may be helpful in patients with head trauma, cerebral hemorrhage, cerebral edema, brain tumors, and certain other conditions associated with increased intracranial pressure. Although monitoring technology has advanced considerably, the best monitor in the intensive care unit remains the well-trained healthcare provider.

ICU Patient Assessment The respiratory care clinician should perform an abbreviated physical assessment routinely in the ICU at the patient’s bedside as a part of providing basic respiratory care in the ICU and when monitoring the patient–ventilator system. Key aspects of the ICU bedside assessment will include observation of variables associated with adequate oxygenation and ventilation. Assessment of the ICU patient should include: Review of the patient’s medical record. In addition to the patient’s demographics and problem list (age, gender, admission date and time, initial or admitting diagnosis, other medical problems), the respiratory care clinician should review respiratory care orders and other physicians’ orders; laboratory test results; chest radiograph and other imaging reports; blood gas reports; progress notes; respiratory care and nursing critical care flowsheets; and related comments. Observation of the patient and the patient’s environment. The patient’s general appearance should be noted to include height and weight, level of consciousness, and apparent overall state of health. For ventilated patients, the type of ventilator and artificial airway in use should be noted. Key monitored parameters should also be quickly noted to include oxygen saturation by oximetry, ECG rhythm and rate, and an overview of ventilator function, if in use (e.g., peak airway pressure, exhaled tidal volume, ventilator waveforms). Ensure that the patient is being adequately oxygenated and ventilated before continuing the assessment process. Ancillary equipment and supplies in use should be noted, to include monitors, oximeters, suctioning equipment, mechanical circulatory support devices, dialysis equipment, isolation supplies, chest drainage systems, infusion pumps, urinary catheter and drainage bags, cooling blankets, and restraints. Initial physical assessment should include the patient’s general appearance, level of consciousness, perfusion of extremities, respiratory rate and pattern, cardiac rhythm and rate displayed on the cardiac monitor, and other monitoring data displayed (e.g., SpO2, ventilatory waveforms). The chest physical examination should include inspection, auscultation, palpation, and percussion. Auscultation should be performed to ensure adequate bilateral ventilation. Palpation techniques may be employed to assess for the presence of equal and bilateral chest expansion, accessory muscle use, tracheal shift, or unilateral apparent hyperinflation. Chest

percussion may help identify the presence of pneumothorax, pleural effusion, and lung consolidation or collapse. Administration of aerosolized medications, suctioning, and airway care may be performed at this time, and should precede a complete patient–ventilator system check. A complete patient–ventilator system check should be performed as part of routine assessment, and on a regular basis.

Monitoring Oxygenation The oxygenation process begins with observation of the patient’s inspired oxygen concentration (FIO2) and proceeds to oxygen transfer across the lung, oxygen loading of the arterial blood, and delivery of oxygenated blood to the peripheral tissues. Assessment of the patient’s oxygenation status includes being alert to the signs and symptoms of hypoxia. Routine monitoring of oxygenation in the ICU often involves the use of continuous pulse oximetry and intermittent arterial blood gas analysis. Transcutaneous oxygen tension monitoring provides a noninvasive estimate of PaO2, which may be particularly useful in newborn infants. Measures of oxygen transfer across the lung include alveolar to arterial oxygen gradient (PAO2 – PaO2), alveolar to arterial oxygen ratio (PaO2/PAO2), and the arterial oxygen tension to fraction of inspired oxygen ratio (PaO2/FIO2). Arterial oxygen content (CaO2) is dependent on arterial oxygen tension (PaO2), arterial oxygen saturation (SaO2), and hemoglobin (Hb) levels. Oxygen delivery (ḊO2) is determined by the cardiac output (Q̇T) and the arterial oxygen content (CaO2). Peripheral perfusion and tissue oxygen uptake may be affected by regional blood flow, as well as tissue utilization of oxygen. Measures that indirectly reflect tissue oxygen delivery and utilization include measurement of mixed venous oxygen tension, saturation, and content (Pv̄O2, Sv̄O2, Cv̄O2) and arterial–venous oxygen content difference (CaO2 – Cv̄o2). Chapter 2 (Respiratory Failure) provides additional information regarding assessment of oxygenation.

Monitoring Ventilation Observation of the patient’s rate and depth of breathing and ventilatory pattern provides an initial assessment of ventilation. Patients should be observed for the

presence of the signs of respiratory distress, increased work of breathing, diaphragmatic fatigue, intercostal retractions, and accessory muscle use. Monitoring of tidal volume, minute ventilation, and respiratory rate provides additional valuable information regarding patients’ ventilatory status. Patients receiving mechanical ventilation often have ventilatory graphic monitoring displays that allow for the assessment of ventilatory volumes and flows. Noninvasive measures of ventilation include measurement of end-tidal and mean exhaled carbon dioxide tension (PetCO2 and PĒCO2) and measurement of transcutaneous carbon dioxide tension (PtcCO2).4 Calculated values that reflect ventilation include dead space to tidal volume ratio (VA/VT) and alveolar ventilation (V̇A). Clinically speaking, the single best index of alveolar ventilation remains measurement of arterial carbon dioxide tension (PaCO2). Chapter 2 (Respiratory Failure) provides additional information regarding assessment of ventilation.

Ventilatory Parameters and Mechanical Ventilation Assessment and monitoring of patients receiving mechanical ventilatory support should include evaluation of respiratory rate, tidal volume, and minute ventilation, as well as review of ventilator graphics for ventilatory volumes, pressures, and flows. In spontaneously breathing patients, ventilatory parameters can be assessed using a simple hand-held respirometer. In ventilated patients, measurement of respiratory rate, tidal volume, and minute ventilation may be accomplished by the use of the ventilator’s monitoring system or the use of a separate hand-held respirometer.

Respiratory Rate Respiratory rate is the number of breaths (spontaneous breaths or mandatory breaths delivered by a mechanical ventilator) received by the patient over a 1-minute time interval. Normal adult spontaneous respiratory rate (f) is approximately 12 breaths/min with a range of 12 to 20 breaths/min; tachypnea is an elevated spontaneous respiratory rate (f > 20 breaths/min) while bradypnea is an abnormally slowed spontaneous respiratory rate (f < 10 to 12 breaths/min). Hypoxia, hypercapnia, metabolic acidosis, fever, pain, and/or anxiety may contribute to an increased spontaneous respiratory rate. Increasing levels of sedation, severe hypercapnia, and severe critical illness may cause unconsciousness, coma, and bradypnea. In ventilated patients, when assessing respiratory rate, the clinician must discriminate between the types of breaths delivered based on the ventilator mode in use. In the assist/control mode the patient may trigger the ventilator at a higher frequency than the backup set “machine rate.” Both of these values would be recorded as part of routine patient monitoring. For example, in the volume-targeted assist/control mode (aka volume-controlled continuous mandatory ventilation [VCCMV]), the ventilator tidal volume may be set at 500 mL and the backup rate may be set at 12 breaths/min. In this example, if the patient then triggered the ventilator at 15 breaths/min, the resulting total respiratory rate would be 15 breaths/min and each breath would be supported by the ventilator with a volume 500 mL. Should the patient become apneic for any reason (e.g., administration of a sedative), the respiratory rate will decrease to the set backup rate (i.e., f = 12 breaths/min) and the

tidal volume would remain 500 mL. In the volume-targeted or pressure-targeted synchronized intermittent mandatory ventilation (SIMV) modes, the patient is able to breathe spontaneously between mandatory breaths. These “spontaneous” breaths may (or may not) be supported with pressure support. For example, in the SIMV mode the machine rate may be set at 10 breaths/min, and the patient may take an additional 10 spontaneous breaths in between mandatory breaths. In this case, the machine rate would be 10, the spontaneous rate would be 10, and the total rate would be 20 breaths/min. With controlled ventilation (aka time-triggered CMV), every breath is a time-triggered mandatory breath and patient triggering is absent. In these cases, the set mandatory rate is the total respiratory rate.

Tidal Volume and Minute Ventilation Measurement and Evaluation In spontaneously breathing patients, exhaled tidal volume is the volume of gas passively exhaled following a normal inspiration. Normal adult spontaneous tidal volume is approximately 7 mL/kg of ideal body weight (IBW), with a normal range of about 400 to 700 mL/breath.6–8 Ideal body weight (IBW), sometimes called predicted body weight (PBW), may be calculated using several different formulas (e.g., Broca formula, Devine formula, Hamwi formula). ARDSNet uses the term predicted body weight where: Males PBW (kg) = 50 + 2.3 (height in inches – 60) Females PBW (kg) = 45.5 + 2.3 (height in inches – 60) In spontaneously breathing patients and in those receiving assist/control volume ventilation, minute ventilation (V̇E) is simply the tidal volume (VT) multiplied by the respiratory rate (f): V̇E = VT × f Normal minute ventilation in adult patients is approximately 6 L/min with a normal range of 5 to 10 L/min or about 80 to 100 mL/kg IBW/min. In spontaneously breathing patients, bedside measurement of tidal volume, minute ventilation, and respiratory rate may be performed using a handheld respirometer.

Compressible Volume In patients receiving mechanical ventilation, measurement of tidal volume, minute ventilation, and respiratory rate may be performed using a hand-held respirometer or the ventilator’s built-in monitoring system. Depending on the volume measurement method used, measured volumes may have to be adjusted for the ventilator’s compressible volume (also referred to as tubing compliance). Simply put, the ventilator circuit tends to expand during inspiration as pressure increases and contract during expiration as pressure is released. This compressible volume is not delivered to the patient, although it will be recorded by flow-sensing devices located at or near the exhalation valve of the ventilator circuit. The compressible volume for most ventilator circuits is about 1.5 to 2.5 mL/cm H2O and the actual tidal volume delivered to the patient will be reduced by this amount. For example, in the volumecontrol mode (VC-CMV or VC-SIMV), if the ventilator tidal volume is set at 500 mL, peak airway pressure is 25 cm H2O, baseline pressure is 5 cm H2O (i.e., PEEP = 5 cm H2O), and the compressible volume is 2.5 mL/cm H2O, the volume lost due to tubing compliance would be about 50 mL per breath, and the actual delivered tidal volume would be approximately 450 mL: VT delivered = VT set − ([peak pressure − baseline pressure] × compressible volume mL/cm H2O) VT delivered = 500 mL − ([25 cm H2O − 5 cm H2O] × 2.5 mL/cm H2O) VT delivered = 500 mL − (20 cm H2O × 2.5 mL/cm H2O) VT delivered = 500 mL − 50 mL = 450 mL Attention to the ventilator’s compressible volume is especially important when small tidal volumes are in use, as may be the case with infants, children, and certain adult patients. Most current critical care ventilators are able to measure and correct for the ventilator’s compressible volume, and manual calculation of volume lost due to tubing compliance is unnecessary when using ventilators with this capability.

Tidal Volume and Ventilatory Mode As with respiratory rate, assessment of tidal volume in ventilated patients must take

into consideration the mode of ventilation provided. During mechanical ventilation, the respiratory care clinician can set the ventilator rate, tidal volume (or pressure), inspiratory time (or flow), and ventilatory mode. Commonly used modes include assist/control (A/C), synchronized intermittent mandatory ventilation (SIMV), pressure-support ventilation (PSV), and pressure-control ventilation (PCV). Inspiration may be time or patient triggered, and the ventilator may be volume, time, or flow cycledd to expiration, depending on mode. With volume ventilation, tidal volume is constant for mandatory breaths even in the face of changes in compliance or resistance. With pressure-limited ventilation, tidal volume varies with changes in compliance or resistance and patient effort. During mechanical ventilation, the respiratory care clinician typically monitors the respiratory rate, tidal volume, and minute ventilation. The set “machine rate” is the minimum number of mandatory breaths that will be delivered by the ventilator every minute. These breaths may be volume targeted (volume control) or pressure targeted (pressure control). The total rate is the total number of breaths the patient receives per minute, which includes any breaths initiated by the patient in the assist/control mode (patient-triggered mandatory breaths) or spontaneous breaths in the SIMV mode. In volume-control continuous mandatory ventilation (VC-CMV), the tidal volume delivered by the ventilator is set by the operator and constant for each breath. Put another way, all breaths are mandatory and delivered by the ventilator at a preset volume. VC-CMV breaths may be time triggered (control mode) or patient triggered (assist mode). With pressure-controlled continuous mandatory ventilation (PC-CMV), all breaths are mandatory and delivered by the ventilator at a preset pressure. PCCMV breaths may also be time triggered (control mode) or patient triggered (assist mode). With PC-CMV, delivered tidal volume will vary with changes in compliance and resistance. The terms assist/control (A/C) and patient- or time-triggered CMV are generally interchangeable. With volume-controlled synchronized intermittent mandatory ventilation (VCSIMV), mandatory “machine” breaths deliver a preset tidal volume, while the tidal volume delivered during spontaneous breaths is determined by patient effort, which may be pressure supported (e.g., SIMV with pressure support). In such cases, the respiratory care clinician should measure the patient’s total minute ventilation,

spontaneous minute ventilation, and “machine” or “set” minute ventilation. Clinical Focus 9-1 provides examples of measured and calculated ventilatory parameters in patients receiving assist/control volume ventilation and SIMV with pressure support.

CLINICAL FOCUS 9-1 Assessment of Respiratory Rate, Tidal Volume, and Minute Ventilation during Mechanical Ventilation Respiratory rate, tidal volume, and minute ventilation should be assessed during mechanical ventilation of patients in the ICU, and their measurement depends (in part) on the mode of ventilation employed. Assist/Control Mode or Continuous Mandatory Ventilation Assist/control is a mode of mechanical ventilation in which the patient receives a preset tidal volume or pressure with each mandatory breath. If the patient makes no inspiratory effort, the breaths are delivered at a preset rate. If the patient makes an inspiratory effort, the ventilator is triggered, and a mandatory breath is delivered. These mandatory “machine” breaths are delivered at the same tidal volume (volume-control mode) or pressure (pressure-control mode) for each breath. In the assist/control mode, the inspiratory time or inspiratory flow rate for each breath may also be set by the clinician. Minute ventilation (V̇E) is simply tidal volume (VT) times rate (f): V̇E = VT × f With assist/control volume ventilation, if the patient triggers the ventilator at a rate faster than the preset ventilator backup rate, tidal volume will remain constant, but minute ventilation will increase. 1. Given a patient receiving assist/control volume ventilation in the ICU, with the following monitoring information collected, calculate the patient’s minute ventilation. Ventilator backup control rate: 12 breaths/min Tidal volume: 500 mL Patient-triggered (assist) rate: 16 breaths/min V̇E = VT × f = 500 mL × 16 = 8000 mL/min = 8 L/min 2. The above patient receives a bolus of intravenous morphine for pain and ceases spontaneous ventilatory efforts. Calculate the patient’s minute ventilation in the absence of spontaneous breathing. Ventilator backup control rate: 12 breaths/min Tidal volume: 500 mL

Patient-triggered (assist) rate: no spontaneous respiratory efforts V̇E = VT × f = 500 mL × 12 = 6000 mL/min = 6 L/min In this example, the ventilator backup rate of 12 breaths/min would ensure a minimum minute ventilation of 6 L/min. If the patient again begins to trigger the ventilator by making spontaneous breathing efforts (as may occur when the blood level of the narcotic medication diminishes), the total rate and minute ventilation would increase. Synchronized Intermittent Mandatory Ventilation (SIMV) SIMV combines aspects of assist/control ventilation and spontaneous breathing. Mandatory breaths are delivered using a preset tidal volume or pressure. The tidal volumes during spontaneous breathing vary and are usually less than the mandatory breath tidal volumes. Spontaneous breaths may be supported using pressure support. The pressure-support levels used are usually much less than the pressures used during mandatory breaths. The total respiratory rate is determined by the sum of the mandatory set rate and the spontaneous rate. The total minute ventilation is the sum of the “machine”-delivered minute ventilation and the patient’s spontaneous minute ventilation. Consider a patient in the ICU receiving volume-control SIMV (VC-SIMV) with the following monitoring information collected: SIMV rate: 12 breaths/min SIMV mandatory breath tidal volume: 500 mL Pressure-support (PSV) level = 5 cm H2O Total rate = 20 breaths/min Patient’s measured spontaneous rate: 8 breaths/min Total measured minute ventilation (V̇Etotal): 7 L/min 1. Calculate the patient’s spontaneous minute ventilation and tidal volume. With SIMV, the total minute ventilation (V̇Etotal) is the sum of the mandatory V̇E and the patient’s spontaneous V̇E and: V̇Emandatory = VTmandatory × fmandatory = 500 mL × 12 = 6000 mL/min = 6 L/min V̇Espont = V̇Etotal − V̇Emandatory = 7000 mL − 6000 mL = 1000 mL/min VTspont = V̇Espont ÷ fspont = 1000 mL ÷ 8 = 125 mL To summarize, the patient is currently receiving a total minute ventilation of 7 L/min. Of this total, 6 L/min is provided based on the SIMV rate and tidal volume and 1 L/min of the minute ventilation is generated by the patient’s spontaneous breathing. The patient is taking 8 breaths/min spontaneously with an average spontaneous tidal volume of only 125 mL.

Because the patient’s spontaneous tidal volume is very low, the respiratory care clinician decides to increase the level of pressure support to 10 cm H2O and the following information is now collected: SIMV rate: 12 breaths/min SIMV-delivered mandatory tidal volume: 500 mL Pressure-support (PSV) level = 10 cm H2O Total rate = 20 breaths/min Patient’s measured spontaneous rate: 8 breaths/min Total measured minute ventilation (V̇Etotal): 9 L/min 2. Calculate the patient’s spontaneous minute ventilation and tidal volume with the addition of a total of 10 cm H2O PSV. V̇Emandatory = VTmandatory × fmandatory = 500 mL × 12 = 6000 mL/min = 6 L/min V̇Espont = V̇Etotal − V̇Emandatory = 9000 mL − 6000 mL = 3000 mL/min VTspont = V̇Espont ÷ fspont = 3000 mL ÷ 8 = 375 mL To summarize, the patient is now receiving a total minute ventilation of 9 L/min. Of this total, 6 L/min is provided based on the SIMV rate and tidal volume and 3 L/min of the minute ventilation is generated by the patient’s spontaneous breathing. With the increase in PSV to 10 cm H2O, the patient is now taking 8 breaths/min spontaneously with an average spontaneous tidal volume of 375 mL.

Inspired versus Expired Tidal Volume During mechanical ventilation, inspired tidal volume is sometimes measured and compared to exhaled tidal volume. Normally, these values are almost identical, although a small difference between inspired and expired tidal volume may be present due to differences between oxygen consumption (V̇O2) and carbon dioxide production (V̇CO2). Normal resting oxygen consumption is about 250 mL/min, while normal resting carbon dioxide production is about 200 mL/min, creating a slight difference between inspired and expired tidal volume of 4 to 5 mL per breath in normal subjects. Occasionally, large differences are observed between inspired and expired tidal volume in patients receiving mechanical ventilation. These large differences are usually caused by leaks in the system, whereby inspired tidal volume is much greater than expired tidal volume. Common sources of leaks are around the cuff of an endotracheal (ET) or tracheostomy tube or gas leakage through chest

tubes. For example, an intubated ventilator patient may have an inspired tidal volume of 600 mL and an expired tidal volume of only 400 mL due to a large air leak. As noted, common sources of air leaks seen in ventilated patients include faulty endotracheal tube or tracheostomy tube cuffs and improperly inflated tube cuffs. If an endotracheal tube cuff does not seal the airway (i.e., cuff leak), inspired gas delivered to the endotracheal tube will exit the patient’s mouth and will not be measured by the ventilator’s volume-sensing system. Another source of differences between inspiratory and expiratory tidal volumes is a pneumothorax with chest tubes. Ventilator patients who experience a pneumothorax will often have chest tubes inserted into the pleural space to remove fluid and gas. If there is a tear in the lung tissue, gas delivered by the ventilator during inspiration may exit via the tear into the pleural space and then out the chest tubes. In such cases, inspired tidal volume will be greater than expired tidal volume. Modern chest drainage systems have three chambers: a collection chamber, a water seal chamber, and a pressure-regulating chamber. The collection chamber allows for pleural fluid to be collected and measured on a daily basis. With standard chest drainage systems, the water-seal chamber allows for air leaks to be detected by observing bubbling through the water-seal chamber during various parts of the respiratory cycle. The pressure-control chamber of drainage systems can be either a “wet system” (where the water level in the chamber controls the amount of negative pressure or a “dry system” (also called a “dry vac”) where a resistor controls the maximal amount of negative pressure applied by the system.

Ventilatory Requirements and Ventilatory Capacity Illness and disease states can cause variations in spontaneously breathing patients’ ventilatory capacity or ventilatory requirements, and in turn, tidal volume, respiratory rate, and minute ventilation. Disease states or conditions that may reduce ventilatory capacity include reduced ventilatory drive (e.g., sedative or narcotic medications, neurologic disease), impaired lung function (e.g., airway obstruction, bronchospasm, reduced lung compliance, increased airway resistance), or ventilatory muscle fatigue. A reduction in a ventilatory capacity may result in reduced spontaneous tidal volume and minute ventilation. Patients’ ventilatory requirements may be altered by ventilatory dead space, metabolic rate, oxygen consumption, and carbon dioxide

production.8 For example, increased metabolic rate (e.g., stress, fever, agitation), or increased dead space can increase patients’ ventilatory requirements resulting in increased spontaneous tidal volume and minute ventilation. As noted above, for most patients minute ventilations of 80 to 100 mL/kg/min are required to maintain normal PaCO2 and acid-base balance.4,9 Hyperventilation and hypoventilation are best assessed by measurement of PaCO2 (PaCO2 < 35 mmHg = hyperventilation; PaCO2 > 45 mmHg = hypoventilation). When using modes of mechanical ventilation that may provide partial ventilatory support (e.g., SIMV, PSV, proportional assist ventilation), patients’ spontaneous ventilatory capacity will determine the level of ventilatory support needed. The relationship between patient’s ventilatory requirements and ventilatory capacity will also determine the patient’s readiness for liberation from mechanical ventilation.

Alveolar Ventilation and Dead Space Alveolar ventilation is the volume of gas that reaches alveoli that are ventilated and perfused per breath (VA) and per minute (V̇A). Alveolar ventilation per minute (V̇ A) is simply tidal volume (VT) minus dead space (VD) times respiratory rate (f): V̇A = (VT – VD) × f Dead space ventilation is the portion of gas that does not participate in gas exchange (i.e., ventilation without perfusion). Types of dead space include anatomic dead space, alveolar dead space, physiologic dead space, and mechanical dead space. Anatomic dead space (VD anatomic) is the volume of gas in the conducting airways.8,10 Normal anatomic dead space is approximately 1 mL/lb of IBW or about 150 mL in a typical adult.8 Alveolar dead space (VD alveolar) is the volume of gas that reaches alveoli being ventilated, but not perfused.7,11 Physiologic dead space (VD physiologic) is the total functional dead space and is the sum of anatomic and alveolar dead space:7,11 VD physiologic = VD anatomic + VD alveolar In healthy individuals, VD physiologic and VD anatomic are approximately the same. Disease can increase alveolar dead space (e.g., emphysema) or decrease

alveolar perfusion (e.g., shock, pulmonary embolus).8 If alveolar dead space increases, then VD physiologic > VD anatomic.8 Mechanical dead space is simply the volume of rebreathed gas due to a mechanical device. Mechanical ventilator circuits that place additional large bore tubing between the ventilator “Y” and patient connection may introduce mechanical dead space. For example, heat-moisture exchangers (HMEs), closed suction systems, or additional tubing placed between a ventilator circuit “Y” and the endotracheal/tracheostomy tube connection may introduce mechanical dead space and cause rebreathing of exhaled gas. Increases in mechanical dead space may cause increases in PaCO2.8 The modified Bohr equation provides an easy method for measurement of VD physiologic at the bedside, provided arterial blood gas analysis (PaCO2) and measurement of mean exhaled carbon dioxide tension (PĒCO2) are available.7,11,12 This will allow for calculation of the dead space to tidal volume ratio (VD/VT), and in turn, calculation of VDphys, where: VD/VT = (PaCO2 – PĒCO2) ÷ PaCO2 VDphys = VD/VT × VT Normal VD/VT is about 0.30 (i.e., 30% dead space ventilation) with a range of 0.20 to 0.40. VD/VT in patients receiving positive-pressure ventilation is typically higher (e.g., VD/VT = 0.50) due to inspiratory mechanical bronchodilation. Disease states or conditions causing increased dead space may further increase VD/VT in patients receiving mechanical ventilatory support.8 As noted, V̇A is simply tidal volume (VT) minus physiologic dead space (VDphys) times respiratory rate (f). Inserting normal adult values, we have: V̇A = (VT – VD phys) × f = (500 mL – 150 mL) × 12 = 4200 mL/min = 4.2 L/min Clinically, the single best measure of V̇A is PaCO2 and the relationship betweenV̇A and PaCO2 is as follows: V̇A = (0.863 × V̇CO2) ÷ PaCO2

AND PaCO2 = (0.863 × V̇CO2) ÷ V̇A Inserting normal values, we have: V̇A = (0.863 × V̇CO2) ÷ PaCO2 = (0.863 × 195 mL/min) ÷ 40 ≈ 4.2 L/min Where: V̇A is alveolar ventilation in L/min. V̇CO2 is carbon dioxide production in mL/min (normally about 200 mL/min, although this varies with metabolic rate and diet). PaCO2 is the partial pressure of arterial carbon dioxide in mmHg. 0.863 is a conversion factor. Thus, an increase in V̇A will result in a decrease in PaCO2 while a decrease in V̇A will cause an increase in PaCO2. Increased V̇CO2, with no change in V̇A will result in an increased PaCO2: decreased V̇CO2 (with no change in V̇A) will cause a decrease in PaCO2. Chapter 2 provides additional guidance in terms of assessment of ventilation for patients in respiratory failure.

I:E Ratio The I:E ratio describes the relationship between inspiratory and expiratory time. Normal I:E ratios in healthy, spontaneously breathing subjects are approximately 1:2 to 1:3. An I:E ratio of 1:5 is considered decreased; inspiratory time must decrease or expiratory time must increase for this to occur. An I:E ratio of 1:1 is considered increased; inspiratory time must increase, or expiratory time must decrease for this ratio to occur. During spontaneous breathing, the patient’s I:E ratio can sometimes provide clinicians with useful information about pulmonary mechanics. For example, prolonged expiratory time during spontaneous breathing may point to increased airway resistance (asthma), airway obstruction (mucous, foreign body obstruction), or increased compliance (emphysema).13

I:E Ratio and Time-Triggered VC-CMV

During mechanical ventilation, the I:E ratio is determined by the mode of ventilation being employed, type of breath (e.g., mandatory versus spontaneous), and specific ventilator settings (e.g., tidal volume, respiratory rate, peak inspiratory flow) in use. With respect to terminology, it should be noted that to be consistent with other sources, we will describe relationships for I:E ratio based on the ratio vs length of E time. For example, an I:E ratio of 1:1 will be referred to as greater than an I:E ratio of 1:2, while an I:E ratio of 1:3 is less than 1:2. For time-triggered volume ventilation (aka time-triggered, volume-controlled continuous mandatory ventilation [VC-CMV]), the operator will set the delivered tidal volume, respiratory rate, and the inspiratory flow OR inspiratory time, depending on the specific ventilator in use. If the ventilator incorporates controls that allow the user to adjust inspiratory flow and tidal volume, then inspiratory time and I:E ratio will vary as flow and tidal volume are adjusted. Specifically, inspiratory time and I:E ratio will increase with increased tidal volume or decreased inspiratory flow (assuming no change in respiratory rate). For example, in the volume-control mode an increase in tidal volume from 500 mL to 600 mL at an inspiratory flow of 40 L/min (square wave) and rate of 12 breaths/min (5-second respiratory cycle time) will increase inspiratory time from 0.75 second to 0.90 second. Expiratory time would decrease from 4.25 seconds to 4.1 seconds and I:E ratio would increase from 1:5.7 to 1:4.6. With respect to changes in inspiratory flow, if tidal volume and rate remain at 500 mL and 12 breaths/min, respectively, and inspiratory flow is increased from 40 L/min to 60 L/min (square wave), inspiratory time will decrease from 0.75 second to 0.50 second. Expiratory time would increase from 4.25 seconds to 4.5 seconds and I:E ratio would decrease from 1:5.7 to 1:9. It should be noted that for most adult patients in the volume-control mode, inspiratory time and flow should be initially set in the range of 0.60 to 1.0 second with a peak flow from 40 to 80 L/min resulting in an I:E ratio of 1:2 or lower. For time-triggered VC-CMV, if the ventilator incorporates controls for inspiratory flow and tidal volume, inspiratory time and I:E ratio will decrease with decreased tidal volume or increased inspiratory flow (assuming no change in respiratory rate). Expiratory time will increase and I:E ratio decrease with reduced respiratory rate, while expiratory time will decrease and I:E ratio increase with increased respiratory rate.

In ventilators with an inspiratory time control (as opposed to an inspiratory peak flow control), the operator will set inspiratory time and expiratory time will be determined by the respiratory rate and set inspiratory time; changes in tidal volume when using the volume-control mode in these ventilators will not affect inspiratory time.

I:E Ratio and Patient- or Time-Triggered VC-CMV (Assist/Control) With assist/control (A/C) volume-targeted ventilation (also referred to as patienttriggered or time-triggered volume-controlled continuous mandatory ventilation [VCCMV]), the operator will set the delivered tidal volume, backup respiratory rate, ventilator trigger sensitivity, and the inspiratory flow OR inspiratory time, depending on the specific ventilator in use. In ventilators with controls for inspiratory flow and tidal volume, inspiratory time will be determined by the tidal volume and inspiratory flow settings in the same manner as controlled-volume ventilation. Respiratory rate will vary with the patient’s inspiratory efforts (i.e., assist breaths). As respiratory rate increases, expiratory time will decrease and I:E ratio will increase; as respiratory rate decreases, expiratory time will increase and I:E ratio will decrease. In ventilators with an inspiratory time control (as opposed to an inspiratory flow control), the operator will set inspiratory time and expiratory time will be determined by the A/C rate; changes in set tidal volume in these ventilators will not affect inspiratory time or I:E ratio, instead the inspiratory flow will now be altered.

Intermittent Mandatory Ventilation (IMV) and I:E Ratio With volume-controlled IMV (VC-IMV), inspiratory time for volume-targeted mandatory breaths is determined by the set tidal volume and the ventilator’s inspiratory flow OR inspiratory time setting, similar to VC-CMV. For spontaneous breaths, inspiratory time, expiratory time, and I:E ratio are largely determined by the patient’s spontaneous ventilatory pattern. The inspiratory time for spontaneous breaths, however, may increase with the addition of pressure support. It should be noted that most modern mechanical ventilators incorporate synchronized intermittent mandatory ventilation (SIMV) in which mandatory breaths can be time or patient triggered. Simply put, SIMV is a form of IMV and SIMV breaths can be pressure or

volume targeted.

Monitoring and Adjustment of I:E Ratio Many modern mechanical ventilators incorporate a monitoring display for I:E ratio and may also allow for display of spontaneous inspiratory time (TIspont), spontaneous percent inspiratory time (TI/TTOT), and spontaneous minute ventilation (V̇Espont). The I:E ratio should be monitored and adjusted (where possible) in patients receiving mechanical ventilation in order to optimize oxygenation and ventilation, ensure patient comfort, and minimize any harmful side effects associated with inappropriate ventilator settings. For example, increased inspiratory times during volumecontrolled or pressure-controlled ventilation will generally increase mean airway pressures; this may improve arterial oxygenation in certain patients. Increased mean airway pressures may reduce venous return and cardiac output in hemodynamically compromised patients. Inverse I:E ratio ventilation (e.g., pressure-controlled inverse ratio ventilation [PCIRV]) has been advocated in the past as a means to improve oxygenation in patients with severe acute respiratory distress syndrome (ARDS), although this has not been shown to be more effective than properly applied PEEP. Decreased expiratory time will reduce the time available for complete exhalation, and this may cause (or worsen) air trapping and inadvertent PEEP, particularly in patients with airway obstruction (e.g., chronic obstructive pulmonary disease [COPD] or acute asthma). Asthmatic patients receiving mechanical ventilation with inadequate expiratory time can experience air trapping, lung overinflation (pneumothorax), and hemodynamic compromise (↓ preload, ↓ cardiac output).8 Increased expiratory times may reduce air trapping and avoid inadvertent PEEP in these patients. Chapter 3 (Principles of Mechanical Ventilation) and Chapter 4 (Ventilators) further describe factors that affect I:E ratio and associated controls on the more common critical care ventilators. Chapter 7 provides guidance on patient–ventilator interaction and adjustment of ventilatory support.

Tests of Spontaneous Breathing Assessment of patients’ spontaneous breathing is commonly performed in the ICU for patients receiving mechanical ventilatory support and for those patients being

considered for the initiation of mechanical ventilation.8,14 In the ventilated patient, spontaneous breathing trials (SBTs) are often conducted for patient evaluation for liberation from mechanical ventilation. Patients at risk for the development of ventilatory failure requiring mechanical ventilatory support may also be evaluated using a bedside tests of spontaneous breathing (e.g., tidal volume, respiratory rate, minute ventilation), as well as tests of ventilatory muscle strength (e.g., maximum inspiratory pressure [MIP], and the ability to cough and deep breathe (e.g., vital capacity [VC], maximum expiratory pressure [MEP]). Monitoring patients with neuromuscular diseases such as amyotrophic lateral sclerosis (ALS), Guillain-Barré syndrome (GBS), and myasthenia gravis is sometimes performed for assessment of impending ventilatory failure. Bedside pulmonary function tests are also sometimes performed for screening prior to surgery (e.g., functional vital capacity [FVC], forced expiratory volume [FEV1.0]). Bedside measurement of peak expiratory flow rates (PEFR) may also be useful in the management of acute asthma exacerbation. Tests of spontaneous breathing that may be helpful in evaluating patients for ventilator weaning include measurement of patients’ spontaneous VT, f, and V̇E; MIP, MEP, and VC; rapid shallow breathing index (RSBI = f/VT); and assessment of respiratory drive (e.g., PO.1). Measures of ventilatory workload are also sometimes considered including lung compliance, airway resistance, and work of breathing. Many modern ICU ventilators incorporate volume- and flow-sensing systems to allow for assessment of spontaneous breathing in patients receiving mechanical ventilatory support. Portable bedside spirometers and respirometers are also commonly used for assessment of spontaneous breathing in ICU patients. Chapter 8 provides additional information regarding bedside pulmonary function testing in the critical care unit.

Monitoring During Mechanical Ventilation Careful monitoring of measures related to lung function and pulmonary mechanics during mechanical ventilation can be helpful to evaluate the patient’s progress, ensure optimal support, and to avoid complications and hazards. Airway pressures that should be monitored during mechanical ventilation include peak inspiratory pressure (PIP) and mean airway pressure (P̄AW), plateau pressures (Pplateau), PEEP, and autoPEEP. Monitoring for changes in system compliance (CST) or airway resistance (RAW) can also be helpful to identify problems or improvement. Assessment of the rapid shallow breathing index (RSBI) and assessment of the work of breathing (WOB) may also be helpful when evaluating patients’ readiness for ventilator liberation. Pulmonary mechanics include measurement of MIP, MEP, and VC; as noted above, measurement of these parameters may be helpful in assessing patients for the continuing need for mechanical ventilation. Each of these monitoring parameters are discussed below.

Airway Pressures Monitoring patients’ airway pressures during mechanical ventilatory support can alert the clinician to significant changes in the patient’s condition. For example, during volume ventilation a sudden increase in peak airway pressure with a corresponding rise in plateau pressure may signal the development of tension pneumothorax or ET tube migration into the right mainstem bronchus. A sudden fall in airway pressures may be caused by patient disconnect or patient–ventilator system leak. Gradual increases in peak airway pressure during volume ventilation may signal a decrease in the patient’s lung compliance, while decreases in peak airway pressure may signal an improvement. Key airway pressures that should be monitored are discussed below.

Peak and Mean Airway Pressure In patients receiving mechanical ventilatory support, peak inspiratory pressure (PIP) is simply the highest proximal airway pressure reached during inspiration (the terms PIP and peak airway pressure [Paw] may be used interchangeably). During volumecontrol continuous mandatory ventilation (VC-CMV) or volume-controlled

synchronized intermittent mandatory ventilation (VC-SIMV), PIP during mandatory volume breaths will vary with changes in lung compliance, thoracic compliance, airway resistance, or ventilator settings. For example, a decrease in compliance or increase in resistance will cause an increase in PIP during VC-CMV or with mandatory breaths during VC-SIMV. Changes in ventilator settings will also affect PIP. In the VC-CMV or VC-SIMV modes, increases in ventilator-set tidal volume or increases in ventilator-set inspiratory flow rate will increase PIP. During pressuresupport (PSV) or pressure-control ventilation (PCV), inspiratory pressure is set by the operator and PIP should not vary during PSV or PCV breaths. Mean airway pressure (P̄AW) is determined by PIP, inspiratory time (TI), expiratory time (TE), and PEEP. Time spent during inspiration (TI) may be expressed as a fraction of the total respiratory cycle time (Ttot). During constant flow volume ventilation (triangular pressure waveform, constant flow waveform), mean airway pressure can be calculated as follows: P̄AW = 0.5 (PIP – PEEP) × TI/Ttot During pressure ventilation with a rectangular pressure waveform (and decelerating ramp flow waveform), mean airway pressure can be calculated as follows: P̄AW = (PIP – PEEP) × TI/Ttot Mean airway pressure will increase with increases in PIP, increases in PEEP, or increases in inspiratory time with respect to total respiratory cycle time (TI/Ttot). Mean airway pressure will decrease with decreases in PIP, decreases in PEEP, or decreases in inspiratory time with respect to total respiratory cycle time (TI/Ttot). When using a volume-targeted mode such as VC-CMV (if set respiratory rate is held constant): P̄AW will increase with decreased set inspiratory flow (which will increase inspiratory time), increased set inspiratory time, or increased set tidal volume. P̄AW will decrease with increased set peak inspiratory flow (which will decrease inspiratory time), decreased set inspiratory time, or decreased set tidal volume. Critical care ventilators often calculate and display mean airway pressure.

Increasing P̄AW may be useful to improve arterial oxygen levels in patients receiving mechanical ventilation. Increased P̄AW will further reduce venous return during mechanical ventilation and may impair cardiac output.

Plateau Pressure Plateau pressure (Pplateau) is a static measurement, completed by performing an inspiratory hold (or plateau) maneuver at end inspiration of a volumecontrolled/volume-targeted mandatory breath. Typically, a 1-second inspiratory hold maneuver will allow for graphical identification of the plateau pressure. During the inspiratory hold maneuver, the ventilator exhalation valve is completely closed, and the ventilator delivers no gas flow during the terminal portion of the maneuver. Airway resistance [RAW] does not contribute to the observed Pplateau under conditions of no airflow. Since no additional gas flow is provided by the ventilator during the terminal portion of the maneuver, airway and alveolar pressures (Palv) should equilibrate. Thus, Pplateau should reflect Palv. In other words, Pplateau should reflect Palv at a point of no gas flow (i.e., without the effect of RAW). Decreases in lung compliance or thoracic compliance will increase Pplateau while improvements in Pplateau may reflect improvements in lung or thoracic compliance. It should be noted that accurate Pplateau measurement requires adequate time for airway and alveolar pressures to equilibrate (i.e., 0.5 to 2 sec) and no active patient breathing during the breath hold. Active breathing during an inspiratory hold maneuver may yield a falsely low or high plateau pressure. Figure 9-1 graphically demonstrates PIP and Pplateau during mechanical ventilation. It should be noted that during volume ventilation the difference between PIP and Pplateau provides a very useful and easily available measure that reflects changes in airway resistance (RAW) if the ventilator settings (i.e., tidal volume, inspiratory flowrate, and inspiratory flow pattern) have not otherwise been changed:

FIGURE 9-1 Pressure–, Flow–, and Volume–Time Curves during Volume Ventilation. Pressure, flow, and volume versus time curves during controlled (time-triggered) volume ventilation using a constant flow waveform with an inspiratory plateau. Note: There is a noticeable difference between PIP and plateau pressures due to elevated airway resistance.

Description PIP – Pplateau increases → increase in RAW PIP – Pplateau decreases → decrease in RAW RC Insights Spontaneous breathing may not allow for an accurate plateau pressure reading to be obtained.

Ventilator-induced lung injury (VILI) refers to acute lung injury caused by mechanical ventilation. Ventilator-associated lung injury (VALI) is the term more commonly used for injury that occurs during mechanical ventilation when a direct cause by the ventilator is not clearly proven. VALI is thought to be caused by alveolar overdistention and cyclic atelectasis. Alveolar overdistention may occur when the tidal volume delivered by the ventilator is large in comparison to the volume of aerated lung available. Atelectasis, consolidative pneumonia, and ARDS all reduce the aerated lung available to receive a given ventilator breath. Cyclic atelectasis occurs when alveoli are overdistended during inspiration and collapse during expiration.

Monitoring Pplateau is of special importance during mechanical ventilation to avoid the development of VALI. Excessive pressures that increase alveolar volume, or excessive volumes that create excessive pressure, can cause alveolar overdistension, promoting the development of VALI. Alveolar overdistention may be avoided by using smaller tidal volumes, maintaining a low Pplateau, and using pressure-limited ventilation. Monitoring Pplateau and implementing low tidal volume ventilatory approaches (e.g., 6 to 8 mL/kg IBW) are methods routinely used to keep Pplateau ≤ 30 cm H2O in patients with ARDS and others at risk for the development of VALI. Proper application of PEEP may reduce or eliminate cyclic atelectasis.

PEEP and AutoPEEP Positive end-expiratory pressure (PEEP) is commonly applied during mechanical ventilation. PEEP can prevent end-expiratory alveolar collapse, increase functional residual capacity (FRC), and improve arterial oxygenation. The PEEP provided intentionally by the clinician during mechanical ventilation is sometimes referred to as “applied PEEP” or “extrinsic PEEP.” Various methods to apply and adjust PEEP are discussed in Chapter 6 (Ventilator Initiation) and Chapter 7 (Patient Stabilization). During mechanical ventilation, incomplete emptying of the lungs may occur during the expiratory phase if insufficient expiratory time is not provided. This incomplete emptying of the lungs may result in increased end-expiratory lung volume and dynamic lung hyperinflation (i.e., air trapping). PEEP caused by incomplete exhalation is referred to as “intrinsic PEEP” or “autoPEEP.” AutoPEEP may cause alveolar overdistention, increase the likelihood of pulmonary barotrauma and ventilator-associated lung injury (VALI), increase patients’ ventilator trigger work, and raise intrathoracic pressures. Increased intrathoracic pressures may further reduce venous return, which may impede cardiac output and cause hypotension, particularly in patients who are hypovolemic. Assessment for the presence of autoPEEP during mechanical ventilation can be performed by use of an end-inspiratory pause for a brief period (0.5 to 2 seconds). AutoPEEP is simply the difference between the set (applied) PEEP and the pressure observed at the end of the expiratory pause where: Total PEEP = autoPEEP + set PEEP

In order to accurately measure autoPEEP, patients must be relaxed, breathing in synchrony with the ventilator and making no ventilatory efforts during the endexpiratory pause. AutoPEEP can be measured in spontaneously breathing using an esophageal balloon to determine esophageal pressures. It should also be noted that with severe asthma, use of an end-inspiratory pause may underestimate actual levels of autoPEEP.

Compliance, Resistance, and Work of Breathing Many modern intensive care ventilators incorporate systems designed to measure patients’ compliance, airway resistance, and ventilatory mechanics. These measures can provide important information regarding the patient’s condition, as well as signaling patient improvement or decline. Various estimates of work of breathing are also sometimes monitored in the ventilated patient; however, the clinician must be aware of the method used, as well as clinical implications of any data generated.

Compliance Changes in compliance will have an inversely proportional effect on ventilatory workload: When compliance decreases, ventilatory workload will increase; when compliance increases, ventilatory workload decreases. Compliance (C) is the change in volume for a given change in pressure, and simply defines how easily the lungs and thorax expand or “stretch,” or how easily the lung inflates during inspiration.11,12 Elastance represents the elastic resistance of the lungs and thorax to inflation; elastance is the inverse of compliance. It is important to note that elastance is different from elastic recoil. Elastic recoil refers to the tendency of the lung to deflate following inflation, due to collagen fibers in the lung parenchyma and alveolar surface tension.12 As compliance decreases, elastance increases. As compliance improves, or increases, elastance will decrease. Mathematically, compliance is the change in volume divided by the change in pressure:

Clinically, total lung compliance (CT) is often measured in intubated patients receiving mechanical ventilation. Normal CT ranges from 60 to 100 mL/cm H2O.11,15,16 Lung compliance is more difficult to measure in intubated or mechanically ventilated patients. Esophageal balloon pressure monitoring is sometimes used to provide an estimate of pleural pressures, which may allow for calculation of lung compliance (CL).8 Modern mechanical ventilators possess sophisticated flow and pressure sensors, which partner with microprocessor-controlled breathing valves. This coordination of mechanical breath control, flow, and pressure measurement allows breath-by-breath display of ventilatory volumes, pressures, and the calculation of pulmonary mechanics (e.g., respiratory system compliance [Crs] and airway resistance [RAW]). Dynamic compliance (Cdynamic) and static compliance (Cst) are most often measured in patients receiving mechanical ventilation. Dynamic compliance is calculated by dividing the delivered tidal volume by the peak inspiratory pressure adjusted for the baseline pressure (PEEP):

Dynamic compliance can be affected by changes in lung compliance, thoracic compliance, or airway resistance. Box 9-1 provides examples of conditions that affect compliance. Often, comparing dynamic and static compliance can provide valuable insight into a patient’s condition, or responses to changes in therapy. A decrease in dynamic compliance with no change in static compliance suggests increasing airway resistance.

BOX 9-1 Conditions That Affect Compliance Factors that affect lung compliance, thoracic compliance, and FRC are listed. Lung elasticity is inversely related to lung compliance. As compliance decreases elasticity increases (and vice versa). Lung compliance ∎ Decreases with atelectasis, pneumonia, pulmonary edema, ARDS, and

pulmonary fibrosis. ∎ Increases in COPD/emphysema. Thoracic compliance ∎ May decrease with thoracic cage deformities such as kyphoscoliosis or ankylosing spondylitis. ∎ Abdominal disorders such as ascites, obesity, and severe intra-abdominal hypertension can decrease compliance. FRC changes ∎ Disease states that affect lung elasticity will affect FRC (emphysema, ARDS). ∎ Emphysema will cause a loss of elasticity (i.e., decreased elasticity) and an increase in FRC and air trapping. ∎ ARDS causes increased elasticity and a decrease in FRC.

Static compliance (Cst) requires an inspiratory hold maneuver, to create a “no flow” state. Static compliance is calculated by dividing the delivered tidal volume by the plateau pressure adjusted for the baseline pressure.

Static compliance is a reflection of the ability of the lung and thorax to stretch together. Normal Cst is roughly 60 to 100 mL/cm H2O.4,8 Decreases in lung compliance, chest wall compliance, or both will decrease static compliance. Increases in lung compliance, thoracic compliance, or both will increase static compliance. Figure 9-2 demonstrates peak and plateau pressures and calculation of static compliance, dynamic compliance, and airway resistance.

FIGURE 9-2 Pressure–Time Curves during Volume-Control Mechanical Ventilation with an Inspiratory Pause.

Description

Airway Resistance The caliber of the airways significantly determines airway resistance (RAW). Changes in RAW have a direct effect on ventilatory workload. When RAW increases, ventilatory workload increases; when RAW decreases, ventilatory workload decreases. It is important to remember that ~80% of total RAW occurs in the upper and large lower airways, whereas ~20% of RAW is due to small airways (diameter 105 has been associated with weaning failure.9 Chapter 14 (Ventilator Discontinuance) provides additional guidance regarding the use of various weaning indices.

Pulmonary Mechanics: Maximum Inspiratory and Expiratory Pressure and Vital Capacity Assessment of pulmonary mechanics includes measurement of ventilatory volumes, pressures, and flows and may include calculation of compliance, resistance, and work of breathing. Measurement of pulmonary mechanics during mechanical ventilation can provide the respiratory care clinician with valuable data regarding lung function in order to determine the continuing need for mechanical ventilation, or to assess the potential for success in liberation from the ventilator. As noted above, MIP measurement (sometimes referred to as negative inspiratory force [NIF]) provides information regarding the patient’s inspiratory muscle strength and ability to take a deep breath. In ventilated patients, MIP measurement can be performed using a bedside pressure manometer; however, the patient must be disconnected from the ventilator to perform the maneuver. Newer critical care ventilators allow MIP measurement by use of an integrated MIP measurement system. In either case, the patient must be stable enough to tolerate a short disconnection from the ventilator or short period without ventilatory support. In addition, the patient should be able to follow instructions and perform the maneuver. Depending on gender and age, a normal MIP is between –90 to –125 cm H2O; MIP < –20 to –30 is sometimes considered acceptable as criteria for ventilator weaning.8,21 MEP measurement can also be performed on ventilated patients by disconnecting

the ventilator and using a bedside pressure manometer. As with MIP measurement, the patient must be stable enough to tolerate a brief period without ventilatory support. Patients may generate very high MEPs, and this maneuver should not be performed while the patient is connected to the mechanical ventilator. The MEP maneuver also requires the patient to be able to follow directions, be stable enough to tolerate ventilator disconnection, and possess the muscle coordination to perform the maneuver. MEP measurement provides information regarding the patient’s ability to generate an effective cough and clear secretions. Healthy adults may generate MEP values that are in the range of +150 to +230 cm H2O or higher. MEP < 40 cm H2O suggests the likelihood of a weak and ineffective cough.14 VC measurement can also be performed on ventilated patients by disconnecting the patient from the ventilator and using a bedside respirometer. As with MIP and MEP measurement, the patient must be stable enough to tolerate ventilator disconnection, be able to follow directions, and possess sufficient muscle coordination to perform the maneuver. Newer critical care ventilators may incorporate methods to measure VC through the ventilator’s monitoring system; however, the patient must be able to tolerate the procedure. VC measurement provides information on the patient’s ability to cough effectively, as well as intermittently deep breathe spontaneously to minimize or prevent development of atelectasis. Normal VC is ~ 70 mL/kg IBW; VC < 30 mL/kg IBW is associated with a weak cough and increased potential for development of atelectasis.8,22 VC values < 15 to 20 mL/kg IBW suggest the need for continuing mechanical ventilatory support.

Ventilator Graphics Graphics packages on modern critical care mechanical ventilators are commonplace. These packages can be basic (e.g., simple pressure, flow, and volume waveforms [Figure 9-1]), or very detailed (e.g., pressure, flow and volume curves/loops, volumetric capnography, esophageal pressure waveforms, transpulmonary pressure waveforms, trend functions). Ventilator graphics monitoring allows for confirmation of ventilator mode, ventilatory volumes, and airway pressures. Observation of ventilator graphics allows for the assessment and adjustment of ventilator sensitivity (i.e., trigger effort), evaluation of the adequacy of inspiratory gas flow during volume ventilation, adjustment of rise time and flow termination during pressure ventilation, evaluation and adjustment of inspiratory time and I:E ratio;, and observation of PEEP levels and detection of autoPEEP. Ventilator graphics monitoring can also be useful to identify lung overdistention requiring a reduction in tidal volume, guide adjustment of PEEP levels, and provide an assessment of the work of breathing. Ventilator graphics can be especially useful in identifying and correcting patient–ventilator asynchrony.

Pressure, Flow, and Volume Curves Examination of the pressure–time and flow–time curves during mechanical ventilation can allow for identification of breaths, method of breath initiation (e.g., patient triggered vs. time triggered), nature of gas flow during inspiration (e.g., constant flow, decreasing flow), cycle variable (e.g., pressure, volume, flow, or time cycled to expiration), control variable (e.g., volume control vs. pressure control), and breath sequence (e.g., continuous mandatory ventilation [CMV] vs. intermittent mandatory ventilation [IMV] vs. continuous spontaneous ventilation [CSV]). Examination of pressure–time curves, flow–time curves, and pressure–volume loops can also be useful for assessment of a patient’s trigger effort, adequacy of inspiratory flow rate settings, and patient–ventilator synchrony. Waveform representations of pressure, flow, or volume on the y-axis versus time on the x-axis are sometimes known as scalars while pressure versus volume or flow versus volume curves are known as loops.

Pressure–Time Curves

The pressure–time waveform display (aka pressure vs. time scalar) provided by most critical care ventilators provides visualization of the patient’s breathing during mechanical ventilatory support. When observing the ventilator’s graphics package display, initiation of inspiration (patient or time triggered) will be followed by a rise in airway pressure. PIP can be observed as the highest pressure reached during a mandatory breath. Depending on the selected ventilator mode and settings, the appearance of the airway pressure waveform will vary. For example, with constant flow (aka square-wave flow waveform) volume ventilation, pressure will rise throughout inspiration in a triangular fashion, reaching PIP at the end of the breath. During volume ventilation with a decreasing flow waveform (aka down-ramp or decelerating flow waveform) or with PSV or PCV, PIP is rapidly achieved and then sustained throughout inspiration (i.e., square pressure waveform). The speed at which airway pressure rises depends on multiple factors: gas flow rate, gas flow pattern, lung mechanics (RAW, Crs), resistance of the ventilator circuit and airway adjunct, and spontaneous patient efforts. To summarize, the pressure–time curve can be useful to identify: Mode of ventilation being employed. Examination of the pressure–time waveform can allow the respiratory care clinician to discriminate between different modes of ventilation (e.g., VC-CMV vs. VC-SIMV vs. PSV vs. PCV). Identification of the ventilator breath control variable (e.g., volume or pressure control). For example, during constant flow volume ventilation the airway pressure waveform is triangular ( ). During pressure ventilation (e.g., PCV) the ideal pressure waveform is rectangular ( ). Identification of cycle variable (i.e., inspiration stops). Examination of the pressure–time curve (in combination with flow–time or volume–time curves) is often is useful for discrimination between volume-cycled breaths, flow-cycled breaths (e.g., PSV), and time-cycled breaths (e.g., PCV). Trigger method for each breath received. Examination of the pressure waveform should allow for discrimination between patient-triggered [assist] breaths vs. time-triggered [control] breaths. In the assist/control or pressuresupport ventilation modes, an inspiratory effort by the patient should cause a “negative” deflection of the pressure waveform (i.e., deflection below baseline pressure) triggering the ventilator to deliver an assisted or supported breath, depending on the selected mode. If the breath is time triggered to inspiration, there will be no “negative” deflection prior to initiation of inspiration. Trigger effort. Trigger effort can be assessed by the size of the negative

deflection below baseline pressure of the pressure waveform prior to the initiation of an assisted or supported breath. A slight deflection (e.g., 0.5 to 1.5 cm H2O) indicates minimal patient trigger effort is required to initiate a breath. If a patient makes an inspiratory effort (as judged by negative deflection of the pressure waveform coinciding with the patient effort), which does not result in a patient-triggered ventilator breath, trigger sensitivity should be adjusted. Trigger sensitivity should be such that trigger effort is minimal, although trigger sensitivity should not be such that autotriggering occurs. Adequacy of set inspiratory flow. Examination of the pressure waveform can help identify whether the inspiratory flow rate provided by the ventilator is sufficient to meet or exceed the patient’s inspiratory demand. Spontaneously breathing patients will continue to make inspiratory efforts, even though a patient-triggered breath from the ventilator has been initiated. Inadequate inspiratory flows can be identified by a “concave” deflection of the inspiratory pressure waveform. I:E ratio. Examination of the pressure waveform and associated time spent during inspiration and expiration provides a visual cue regarding inspiratory time (TI), expiratory time (TE), respiratory cycle time (Ttot), I:E ratio, and the proportion of time spent during inspiration (TI/Ttot).

Peak Inspiratory Pressure PIP can easily be observed using a ventilator graphics package with display of the pressure–time curve. Volume-control ventilation delivers a preset tidal volume for mandatory (mechanical) breaths. During volume ventilation, PIP is the maximum pressure used by the ventilator to overcome RAW and Crs. PIP will increase during volume ventilation due to decreased lung compliance (acute lung injury, ARDS), decreased chest wall compliance (obesity, ascites, chest wall deformity), or increased airway resistance (secretions, bronchospasm); improvements in compliance or resistance will reduce PIP. During volume-controlled modes of ventilation, there are several ventilator adjustments that can be made to decrease PIP. These include decreasing tidal volume, decreasing inspiratory flow settings, increasing inspiratory time, or changing the inspiratory flow waveform from a square (constant flow) to decreasing (decelerating) flow waveform.

Inspiratory Plateau Pressure During volume ventilation, Pplateau is measured at the end of inspiration, while employing an end-inspiratory hold of approximately 1 second. As no gas flow occurs

during the end-inspiratory hold, airway resistance does not contribute to the observed plateau pressure. When properly performed, Pplateau pressure measurement reflects alveolar pressures. Accurate Pplateau measurement requires the absence of spontaneous breathing efforts during the inspiratory hold maneuver, as well as sufficient time for gas equilibration between the proximal airway and the alveoli. Figure 9-2 graphically demonstrates PIP and plateau pressure. During volume ventilation PIP is usually greater than Pplateau; the difference between PIP and Pplateau reflects airway resistance. If the patient makes an inspiratory effort during the inspiratory hold, Pplateau will be falsely low. If the patient exhales during an inspiratory hold, Pplateau will be falsely high. Decreases in lung and/or thoracic compliance will increase Pplateau, although changes in airway resistance will have minimal effects on Pplateau because there is no gas flow during the inspiratory hold. With increased airway resistance, PIP will increase without change in Pplateau and thus the PIP–Pplateau difference will also increase. Said another way, if PIP increases and Pplateau does not, RAW has increased, but if both PIP and Pplateau increase, lung and/or chest wall compliance has decreased. Patient–ventilator flow asynchrony can affect the pressure–time curve, as well as significantly increase patients’ work of breathing. For example, during assist-mode volume-control ventilation (VC-CMV), patients may continue to make inspiratory breathing efforts during the ventilator-supported breath. If the patient’s inspiratory flow demand exceeds the inspiratory flow rate set on the ventilator, a downward deflection (i.e., “scooping”) of the inspiratory pressure waveform may occur and WOB will increase. In such cases, increasing the peak flow set on the ventilator to greater than 60 L/min should reduce flow asynchrony; higher flows may be required in some patients. Other ventilator adjustments that may reduce flow asynchrony due to high patient inspiratory demand include reducing the ventilator’s inspiratory time to better match the patient’s inspiratory time or changing the ventilator’s inspiratory flow waveform (e.g., changing from a square wave flow pattern to a decelerating flow pattern with a high initial peak flow setting). Flow asynchrony can also occur during pressure ventilation. During pressure ventilation if flow is inadequate, adjustment of the rise time may be helpful. Figure 9-5 illustrates flow asynchrony during volume ventilation.

FIGURE 9-5 Flow Asynchrony During Volume Ventilation. Pressure, flow, and volume versus time graphics during volume-control ventilation (VCV) with a decelerating flow pattern are shown. The arrows depict the scooping of the pressure waveform due to the patient’s effort exceeding the peak inspiratory flow set on the ventilator. Note that the flow and volume waveform did not change since these are set parameters.

Description

Pressure-Control Ventilation and Pressure-Support Ventilation PCV and PSV are pressure-targeted (i.e., pressure-control) breaths. With PCV, breaths are patient or time triggered to inspiration (assist/control), pressure targeted, and time cycled to expiration. With PSV, breaths are patient triggered to inspiration, pressure-targeted and flow cycled to expiration. With PCV and PSV the inspiratory pressure waveform is usually square or rectangular (i.e., constant pressure), while the inspiratory flow waveform will be decelerating in shape (i.e., decreasing flow). This occurs due to pressure differences between the proximal airway and the alveoli. At the beginning of the PCV or PSV breath, there is a large pressure gradient between the proximal airway and the alveoli, creating a rapid inspiratory flow. As ventilator and alveolar pressures equalize during the inspiratory phase, the pressure gradient decreases, resulting in decreasing inspiratory flow. With PCV, when proximal airway and alveolar pressures are equal, there is no pressure gradient, and gas flow stops. At this point, the PIP and Pplateau are equal. When the clinician-set

inspiratory time ends, exhalation begins. With PSV, inspiration ends when the flow decreases to a preset value, usually around 5 L/min or 25% of the peak flow, depending on the specific ventilator in use. As noted, with PSV the inspiratory phase is patient triggered. During inspiration, the rise time setting controls the rise of inspiratory pressure. If inspiratory pressure and flow increase too quickly, this can cause an “overshoot,” creating a “dog-ear” or pressure spike on the left side of the pressure waveform. This can be corrected by decreasing the inspiratory rise time percentage, which will decrease peak flow, decrease the inspiratory pressure slope, and minimize pressure overshoot. Figure 9-6 demonstrates a rapid rise time and overshoot. If the inspiratory pressure increases too slowly, the pressure waveform may appear rounded, indicating rise time percentage should be increased. Increasing inspiratory rise time will accelerate the initial rise in pressure, minimizing the rounded appearance. Figure 9-7 demonstrates a slow rise time setting and rounding. If the inspiratory time is too long, the patient may try to exhale before the breath ends. This can create a “dog ear” on the right side of the pressure waveform, creating asynchrony and increasing work of breathing. Figure 9-8 demonstrates this phenomenon. Decreasing inspiratory time during a PCV breath or increasing the flow termination percentage on a PSV breath (in ventilators with adjustable flow termination) can alleviate this problem.

FIGURE 9-6 Rapid Rise Time. Pressure, flow, and volume versus time graphics during pressure-control ventilation (PCV) with a rapid rise time are shown. The arrow is depicting an inspiratory rise that is set too fast resulting in overshoot on the pressure waveform. Rise time or slope should be slowed down until overshoot is eliminated.

Description

FIGURE 9-7 Effect of Increasing Inspiratory Rise Time. Pressure, flow, and volume versus time graphics during

pressure-control ventilation (PCV) with a slow rise time are shown. Arrow A identifies the point where inspiratory flow has reached zero and the pressure set on the ventilator has equilibrated with the lung. Arrow B identifies the slope or rise time observed when using a pressure-limited mode. In this example, the rise time or slope is set too slow and should be set faster.

Description

FIGURE 9-8 Excessive Inspiratory Time Resulting in Patient Expiration and “Dog Ear.” Pressure, flow, and volume versus time graphics during pressure-control ventilation (PCV) showing cycle asynchrony, in which the ventilator’s inspiratory time does not match the patient. Arrow A is identifying the patient actively exhaling against the set pressure and results in an upward deflection on the right side of the curve. It is generally corrected by shortening the inspiratory time.

Description As noted, the inspiratory phase of a PSV breath is terminated when peak inspiratory gas flow decreases to a preset level. Newer ventilators offer a flow termination setting, allowing adjustment of the PSV breath’s cycle to expiration. This setting is often a percentage of the peak inspiratory flow rate. A higher set percentage of flow termination will shorten the PSV inspiratory time, and a lower set percentage of flow termination will lengthen the PSV inspiratory time. Leaks in the system during PSV may prolong inspiration; ventilators have a backup time cycle as a safety feature. It should also be noted that PSV breaths can be pressure cycled should the patient cough or forcefully exhale during a PSV inspiration. Figure 9-9 demonstrates the effects of changing flow termination to benefit patient needs.

FIGURE 9-9 Effects of Changing Pressure-Support Flow Termination Criteria. Flow-cycling criteria are adjustable with certain ventilators in the pressure-support mode. These pressure–time curves demonstrate the effects of late (left - 10%), middle (25%), and early (right - 50%) flow cycling on airway pressures and inspiratory time in the pressure-support mode. In the figures, breaths are patient triggered to inspiration, and inspiration is terminated when the flow-cycling criterion is met.

Description

Volume–Time Curves Visual confirmation of the patient’s actual inspired and exhaled tidal volume is provided by the volume–time curve. The volume waveform should begin and end at a baseline volume of zero. During assist/control volume-targeted ventilation (aka VCCMV), mandatory breaths should be delivered at the set volume. With volumetargeted SIMV, mandatory breaths should be delivered at the set volume while spontaneous breaths will vary depending on patient effort and level of pressure support provided. With pressure-targeted ventilation (e.g., PCV and PSV), tidal volume will vary with compliance, resistance, and patient effort. Occasionally during mechanical ventilation there may be a difference between inspired and expired tidal volume. When inspired tidal volume exceeds exhaled tidal volume, a leak may be present in the patient–ventilator system, or air trapping may be present. The patient–ventilator circuit must be closed, with minimal leaks, to effectively deliver positive-pressure breaths and promote breath synchrony. Leaks may be present at any place in the system where connections or seals should occur.

Common sites for leaks are the ventilator inhalation and/or exhalation ports, the heater interface, circuit connections within the inspiratory limb (nebulizer, iNO attachments, temperature probes), interfaces between the circuit Y and the endotracheal tube (closed suction catheters, ETCO2 adapters, HMEs), poor tracheal tube cuff seals, trachea-esophageal or bronchopleural fistulas, or leaking chest tube seals (pleural air leak). If a leak in the patient–ventilator system is difficult to locate, a hand-held respirometer can be used to measure delivered volume at differing points along the system. If tidal volume is effectively delivered to the circuit Y, but not to the expiratory limb, the leak exists somewhere within the patient (e.g., faulty ETT cuff, chest tubes). During spontaneous breathing (continuous spontaneous ventilation [CSV]) with or without continuous positive airway pressure (CPAP) and with modes of ventilation that include spontaneous breaths (e.g., IMV, SIMV), observation of the patient’s volume–time curve can provide a sense of the regularity, breath rate, and volume of spontaneous breaths. This should allow for the recognition of an irregular respiratory rate, periods of apnea, reduced tidal volume, or rapid shallow breathing.

Pressure–Volume Curves Pressure–volume curves can be useful when assessing interactions between the patient and the mechanical ventilator. Pressures (cm H2O) are expressed on the xaxis (horizontal) and volumes (mL) are expressed on the y-axis (vertical). Pressure– volume curves can be useful to assess trigger method (e.g., time trigger versus patient trigger), trigger effort, pulmonary overdistention, and inadequate ventilator inspiratory flow settings (i.e., flow asynchrony), as well as changes in airway resistance or system compliance. Trigger sensitivity should be adjusted to minimize the work required to trigger the ventilator without causing autocycling. Trigger work can be estimated by the volume of the curve to the left of the vertical axis. Figure 9-10 compares assisted mandatory volume breaths when using a flow versus pressure trigger to initiate inspiration. In this example (Figure 9-10), flow triggering is providing a lower imposed work of breathing than pressure triggering.

FIGURE 9-10 Flow and Pressure Curves. (A) Flow–time and pressure–-time curves with pressure trigger and flow trigger. (B) Pressure–volume curve during an assisted mechanical breath using a flow versus pressure trigger to initiate inspiration.

Description Pressure–volume curves can also be useful to assess adequacy of set inspiratory flow rates during mandatory breaths. During mandatory breaths, flow from the ventilator should meet or exceed patient inspiratory demand. If the patient’s inspiratory demand exceeds the ventilator’s set inspiratory flow, the pressure curve (x-axis) will shift to the left. The more significant the left shift, the greater the imposed work of breathing. Figure 9-11 demonstrates increased WOB from inadequate inspiratory flow resulting in a “figure eight” appearance of the curve.

FIGURE 9-11 Pressure–Volume Loop during Volume-Control Ventilation with Inadequate Inspiratory Flow.

Description With increased RAW, the pressure curve (x-axis) will balloon outward and to the right, because of the increased pressure required to overcome the RAW. Changes in respiratory system compliance (Crs) will change the slope of the pressure–volume loop. A decrease in Crs will shift the slope down, and to the right, while an increase in Crs will shift the slope up and to the left (Figure 9-12).

FIGURE 9-12 Pressure–Volume Curve for Normal Lungs and ARDS. Note the shift in the curve down and to the right associated with reductions in lung compliance with ARDS.

Description Horizontal flattening towards the end of inspiration on the pressure–volume curve is usually due to pulmonary overdistension. This should not be confused with the appearance of the curve in the presence of a very strong patient inspiratory effort, which will create a similar flattening of the curve. Figure 9-13 demonstrates alveolar overdistension as observed on a pressure–volume curve.

FIGURE 9-13 Pressure–Volume Curve Associated with Alveolar Overdistention.

Description

Flow-Time Curves The flow–time curve (aka flow–time scalar) provides a graphic display of the inspiratory and expiratory flow rate on the y-axis (vertical) and time on the x-axis (horizontal). For mandatory breaths, the most common flow patterns are a constant flow waveform (aka square wave, rectangular wave, or constant flow generator) or a decreasing flow waveform (aka down ramp, decelerating or descending ramp). In the volume-control mode, most modern ventilators allow the clinician to select the

inspiratory flow waveform, usually offering an option for a square wave (i.e., constant flow waveform) or down ramp (i.e., decreasing flow waveform). For pressure-targeted ventilation (e.g., PCV or PSV), the flow pattern is decreasing (or decelerating) flow; however, the decreasing flow is a function of the mode and characteristics of the patient. The shape of the flow waveform will vary depending on the inspiratory rise time setting and whether inspiration is time cycled (PCV) or flow cycled (PSV) to expiration. When inspiration is time cycled, the decreasing ramp flow waveform may descend to zero (i.e., no flow) if sufficient time is allowed for the pressures at the proximal airway and alveoli to equilibrate. When inspiration is flow cycled, the appearance of the decreasing flow waveform will vary depending on the flow termination criteria of the ventilator; however, flow will not decrease to zero at end inspiration. Some ventilators have an adjustable flow termination control while others are preset at 5 L/min or 25% of the peak flow. Figure 9-1 illustrates pressure, flow, and volume versus time curves during volume ventilation using a square wave flow pattern. Figure 9-14 illustrates pressure, flow, and volume versus time curves during PCV as inspiratory time varies.

FIGURE 9-14 Pressure, Flow, and Volume Versus Time Curves During PCV with a Short Inspiratory Time. In breath “A” inspiratory time is too short and inspiratory flow is not reaching zero before expiration begins. Inspiratory time for breath “B” is increased, allowing adequate time for the inspiratory flow to decrease to zero prior to the expiratory phase resulting in an increased tidal volume.

Description In the volume-control mode, the tidal volume and inspiratory flow rate OR inspiratory time are set by the clinician. For ventilators where the clinician sets the tidal volume and inspiratory time (e.g., Servo-i, Hamilton G5, Dräger Evita-4), the inspiratory flow rate is determined as follows: Inspiratory flow rate (L/min) = (VT [L] ÷ inspiratory time [sec]) × 60 For example, if the tidal volume is set at 500 mL (0.5 L) and the inspiratory time is set at 0.5 seconds, the inspiratory flow will be:

During volume ventilation, typical inspiratory time settings in adults range from about 0.6 to 1.0 seconds generally resulting in peak flows in the range of 40 to 80 L/min. Some patients may benefit from slightly longer inspiratory times (e.g., 0.8 to 1.2 sec). Other modern ventilators (e.g., Puritan Bennett 840, Puritan Bennett 980) offer an adjustable inspiratory peak flow rate, instead of an inspiratory time control. During volume ventilation, typical inspiratory peak flow settings in adults are range from 40 to 80 L/min. Set peak flow, tidal volume, and flow waveform will dictate inspiratory time. If tidal volume remains constant, decreasing the set inspiratory peak flow will heighten inspiratory time; increasing set inspiratory peak flow will decrease inspiratory time. When using ventilators with an adjustable inspiratory peak flow rate and tidal volume, changing the flow pattern from square wave to down ramp will increase inspiratory time. Changing the flow pattern from down ramp to a square wave in these ventilators will decrease inspiratory time. Generally speaking, increases in inspiratory flow rate will increase the gradient between PIP and Pplateau and RAW will increase; decreases in inspiratory flowrate tend to decrease measured RAW. In volume-control modes, changes in inspiratory flow rate, tidal volume, and the inspiratory flow pattern will also affect the shape of the pressure waveform. A down

ramp flow pattern will result in an inspiratory pressure waveform that is curvilinear in shape, while a square wave will result in a pressure waveform with a linear increase (i.e., ascending ramp). As noted above, if the peak flow setting is constant, changing from a square wave to a down ramp will increase inspiratory time while changing from a down ramp to a square wave will decrease inspiratory time.

PCV and PSV Flow Waveforms Because PCV and PSV are pressure-targeted modes of ventilation, the preset pressure is rapidly achieved and then maintained throughout the remaining portion of the inspiratory phase. The pressure waveform with these modes of ventilation tends to be square or rectangular (i.e., constant pressure waveform). The characteristic flow pattern will be a decreasing flow waveform. With pressuretargeted ventilation, changes in RAW or Crs do not result in changes in peak inspiratory pressure (PIP). Changes in RAW or Crs will affect tidal volume and inspiratory gas flow. Specifically, increases in RAW (secretions, bronchospasm) or decreases in Crs (atelectasis, pneumonia, ARDS) will cause a decrease in delivered tidal volume; improvements in RAW or Crs will increase delivered tidal volume. During PCV, inspiratory time is usually adjusted to allow pressure equilibration between the ventilator (i.e., proximal airway) and alveoli to occur before the end of the inspiratory time, at which point flow reaches zero. With inadequate inspiratory time in the PCV mode, flow may not decline to zero during inspiration; this will result in a smaller delivered tidal volume. In such cases, an increase in inspiratory time or an increase in preset pressure may be required to deliver the desired tidal volume (Figure 9-14). Figure 9-15 illustrates the effects of changes in RAW during PCV due to secretions in the airway.

FIGURE 9-15 Pressure, Flow, and Volume Versus Time Curves During PCV with Increased Airway Resistance Due to Secretions. Fluctuations in airway pressure and flow indicated by the squiggly variations are due to increased secretions in the airway (see arrows).

Description

AutoPEEP Detection Incomplete emptying of the lungs during mechanical ventilation may result in air trapping and unintentional or inadvertent PEEP (i.e., autoPEEP). AutoPEEP may be caused by insufficient expiratory time, or increased airway resistance. Observation of the flow waveform may allow for the prompt recognition of autoPEEP. Specifically, air trapping is present when the expiratory gas flow does not return to zero prior to beginning the next breath cycle. The clinician can perform an expiratory hold maneuver, to measure the level of autoPEEP that is present. Figure 9-16 illustrates the effect of autoPEEP on the flow–time curve.

FIGURE 9-16 Pressure, Flow, and Volume Versus Time Curves During PCV with Air Trapping/AutoPEEP. Arrow A identifies air trapping because inspiration is beginning before expiration is complete. The patient’s high respiratory rate with a set inspiratory time is noted resulting in air trapping/autoPEEP.

Description Clinicians should assess ventilator patients for the presence of autoPEEP, especially when the I:E ratio is increased (e.g., I:E ≥ 1:1) or if airway resistance is increased. Patients with obstructive lung disease (e.g., asthma, COPD) are at increased risk for development of autoPEEP, although appropriately increasing expiratory time can eliminate autoPEEP in most patients. During control-mode volume ventilation in ventilators with peak flow, tidal volume, and rate controls (e.g., Puritan Bennett 840 and Puritan Bennett 980), this may be achieved by increasing set inspiratory peak flow, decreasing set tidal volume, or decreasing the mandatory rate. During control-mode volume ventilation in ventilators with inspiratory time or inspiratory percentage time controls (e.g., Dräger Evita V500, Hamilton-G5, Servo-i, Servo-s), this may be achieved by decreasing the inspiratory time (or inspiratory percentage time) setting. Decreasing the respiratory rate with the same inspiratory time will also result in an increased expiratory time in this situation. Changes in set tidal volume will not affect inspiratory or expiratory time in ventilators where the inspiratory time or inspiratory time percentage is set.

Patients in the assist/control mode who are triggering inspiration at a rapid rate may develop autoPEEP due to inadequate expiratory time. These patients may benefit from identification and treatment of the cause for the rapid triggering rate. Common causes for a rapid assist rate include hypoxemia, hypercarbia, acidosis, pain and anxiety, and inappropriate ventilator settings. Correction of hypoxemia, hypercarbia, or acidosis, if present, should be accomplished (if possible). Ventilator settings for peak flow (or inspiratory time), tidal volume, and trigger sensitivity should be reviewed to eliminate patient–ventilator asynchrony. Sedation and/or analgesia for pain and anxiety may also prove beneficial by reducing the trigger rate, which will increase expiratory time and minimize or eliminate air trapping. If not addressed, autoPEEP can result in barotrauma from alveolar overdistension. AutoPEEP may also increase intrathoracic pressure, which may (in turn) increase pulmonary vascular resistance, decrease preload, decrease cardiac output, and decrease blood pressure. AutoPEEP can also interfere with patients’ ability to trigger a mechanical breath, creating patient–ventilator asynchrony and increased WOB.

Optimal PEEP and Recruitment Maneuvers Various methods have been used to achieve alveolar recruitment and improve oxygenation in ventilated patients including: Various optimal PEEP techniques Sustained inflation followed by a decremental PEEP study Stepwise recruitment, also known as incremental PEEP Compliance-titrated PEEP Inverse-ratio ventilation Airway pressure-release ventilation (APRV) High-frequency oscillatory ventilation (HFOV) Sigh breaths Prone positioning Pressure–volume curves may be useful in optimizing PEEP and in performing and assessing the results of recruitment maneuvers. Recruitment maneuvers (RMs) are techniques that briefly increase alveolar pressures to relatively high levels in order to open collapsed alveoli, increase resting lung volume (FRC), and improve oxygenation.23,24 Recruitment maneuvers increase transpulmonary pressures in order to reopen alveolar units that are not aerated or poorly aerated. The inspiratory pressure–volume curve represents system compliance as lung volume increases during lung inflation. In patients with acute restrictive lung disease (e.g., ARDS), resting expiratory lung volume (FRC) and lung compliance are reduced. PEEP increases resting end-expiratory lung volume or FRC. Increasing FRC from a level where alveoli are collapsed to a more inflated state produces a shift in the pressure–volume curve as lung volume and compliance improve. With ARDS, maintaining FRC above the point at which alveolar collapse occurs is thought to be necessary in preventing repetitive inflation and deflation of alveoli during the respiratory cycle. Shear force injury, which may occur with cyclic recruitment and derecruitment of alveoli, is thought to be an important factor in causing ventilatorinduced lung injury (VILI). With ARDS and reduced FRC, the pressure change to increase volume at the beginning of inspiration is high, and the pressure–volume curve is deflected to the right. Put another way, it takes more pressure initially to achieve a given volume due to reduced lung compliance. As the lung inflates, the pressure–volume relationship

improves, and an inflection point can be observed where the pressure–volume curve begins to ascend upward in a more linear fashion.25 The point where this occurs is known as the lower inflection point (LIP), also known as the Pflex value. Once past the LIP during lung inflation, less pressure is required to achieve a given volume because compliance is improved. During volume-targeted mechanical ventilation, the shape and position of the pressure–volume curve is affected by system compliance, airway resistance, and inspiratory flow rates. Because of this, static pressure–volume curves or slow-flow pressure–volume curves are sometimes obtained. The LIP observed on a slow flow (e.g., < 6 L/min) or static inspiratory pressure–volume curve has been suggested as a useful reference point for setting PEEP levels. PEEP may then be adjusted to approximately 2 cm H2O above the LIP. It is important to note that 10% to 20% of ARDS patients do not manifest in an observable LIP. Figure 9-17 illustrates the LIP on a slow-flow pressure–volume curve.

FIGURE 9-17 Inspiratory and Expiratory Pressure–Volume Curves. Open circles indicate inspiration, while closed

circles indicate expiration. The lower inflection point is indicated with an arrow.

Description The term “pulmonary hyperinflation” has been used in the past to describe methods to reverse intraoperative atelectasis and hypoxemia by applying inflation pressures of 30 to 40 cm H2O over a brief period (e.g., 15 seconds).25,26 The term “lung recruitment” was introduced to explain how PEEP improved pulmonary function by opening collapsed lung units.27 Open-lung ventilation refers to a strategy used with early-stage ARDS that incorporates small tidal volumes (4 to 8 mL/kg IBW) and lung RMs followed by the application of relatively high levels of PEEP to keep recruited lung units open.28

Types of Recruitment Maneuvers Mechanical ventilators have long incorporated the option to provide intermittent deep breaths (i.e., sigh breaths) in order to fully inflate the lungs at preset intervals and avoid the development of atelectasis. Sigh breaths were generally delivered 6 to 10 times per hour with volumes of 2 to 3 times the set VT.29,30 This intermittent hyperinflation of the lungs might be considered an early type of RM; studies of patients with ARDS have reported improved alveolar recruitment with the use of sighs.31 Currently, there are a number of different methods used to achieve lung recruitment and adjust PEEP to achieve and maintain alveolar recruitment.32–35 Of these, perhaps the most common method combines the use of pressure-controlled ventilation (PCV) with peak pressures of 35 to 50 cm H2O, inspiratory times of 1 to 2 seconds with PEEP set at 20 to 30 cm H2O applied for a period of 1 to 3 minutes.33 Immediately following the RM, a decremental PEEP study is performed to identify the PEEP level necessary to maintain lung recruitment.36,37 Other methods sometimes used to set PEEP levels include the use of the minimal PEEP needed to maintain lung volumes and achieve adequate oxygenation with an acceptable FIO2 (e.g., PEEP to achieve PaO2 ≥ 60 mmHg and SaO2 ≥ 0.90 with FIO2 ≤ 0.40 to 0.50), incremental increases in PEEP to optimize oxygen delivery, compliance-titrated PEEP, and the use of static or low-flow pressure–volume curves to determine LIP. It is important to note there is little evidence showing benefit in important patient

outcomes (e.g., time to extubation, mortality) as a result of RMs.34 It is also uncertain whether any one approach is superior, as there is no universally recognized, standardized technique. A common technique for lung recruitment is a sustained inflation, where a high pressure is held for a specified period of time, for example, 30 cm H2O of PEEP for 30 seconds or 40 cm H2O of PEEP for 40 seconds, commonly referred to as 30 for 30 or 40 for 40.35 Table 9-1 provides a description of an alternative method for lung recruitment. TABLE 9-1 Recruitment Maneuver 1.Assess the patient for oxygenation status, hemodynamic stability, and existing barotrauma or the potential for development of barotrauma. Barotrauma refers to alveolar rupture resulting in air leaks, which may lead to the development of pneumothorax, pneumomediastinum, and/or subcutaneous emphysema. 2.Sedate the patient to apnea to avoid patient–ventilator asynchrony. 3.Place the patient in the pressure-controlled continuous mandatory ventilation mode (PC-CMV). 4.Adjust PEEP to at least 20 cm H2O to avoid lung derecruitment. 5.Adjust the peak inspiratory pressure (PIP) to 35 cm H2O. 6.Assure pressure difference (ΔP) is ≤ 15 cm H2O. ΔP is simply peak inspiratory pressure minus PEEP (PIP – PEEP). For example, if PIP is 35 cm H2O and PEEP is 20 cm H2O, the pressure difference would be PIP – PEEP or 35 – 20 = 15 cm H2O. 7.Adjust inspiratory time to 1 to 2 seconds and rate to 15 to 20 breaths/min. 8.Apply the maneuver for approximately 1 to 3 minutes. 9.Monitor the patient for continuing hemodynamic stability and satisfactory oxygenation status. 10.Follow the RM with a decremental PEEP trial to adjust PEEP levels. 11.Repeat RMs may be required with increased pressures (e.g., PIP 40 to 45, PEEP 25 to 30 cm H2O; driving pressure 15 cm H2O) if initial response was unsatisfactory. 12.Recruitment maneuvers are associated with considerable risk and should not be performed in patients who are hemodynamically unstable or have barotrauma or the potential for the development of barotrauma.

Patient selection is key when considering RMs, as they are associated with considerable risk. RMs can have a dramatic impact on intrathoracic pressures and increase lung volumes. This could lead to hemodynamic instability, barotrauma, and

cardiac arrhythmias. Thus, RMs should not be applied to hemodynamically unstable patients or those with barotrauma or susceptible to the development of barotrauma (e.g., emphysema with blebs or bullae). The application of RMs also require that patients be sedated to apnea during the performance of the maneuver. RC Insights When performing a recruitment maneuver, carefully monitor the systemic blood pressure. Hypotension may occur due to the increase in intrathoracic pressure, at which point the RM should be immediately discontinued.

Patients with low FRC are more likely to respond positively to lung recruitment.27 Postoperative patients with significant atelectasis requiring mechanical ventilation and patients with ARDS are the most common patient populations where RMs are utilized. Ultimately, the practitioner must evaluate the RM benefit versus risk in each individual patient. As noted above, there is currently no high-level evidence that RMs improve outcomes in ARDS, although the periodic application of RMs has gained some acceptance among clinicians.33 Improvement in oxygenation, intrapulmonary shunt, and lung mechanics has been demonstrated with RMs, but these benefits may also be obtained with higher PEEP alone.38 Clinical Focus 9-2 describes the use of RMs and PEEP with ARDS.

CLINICAL FOCUS 9-2 PEEP and Recruitment Maneuvers in ARDS ARDS is a serious, potentially fatal disorder that interferes with oxygen getting from the alveoli into the pulmonary capillaries and, in turn, into the arterial blood. ARDS is caused by diffuse alveolar damage to the lungs from injury or disease. Common conditions associated with the development of ARDS include pneumonia, inhalation of toxic chemicals, aspiration of gastric contents, lung transplantation, septicemia, septic shock, or severe trauma. Other possible causes include massive transfusion and hematopoietic stem cell transplant. ARDS has also been associated with drug overdoses including cocaine, opioid drugs, tricylic antidepressants, and aspirin. The primary pathophysiologic disorder in ARDS is increased pulmonary capillary permeability resulting in leaky capillaries. This leads to profound oxygenation disturbances, often requiring mechanical ventilation with PEEP and high FIO2. The severity of ARDS is determined by the degree of hypoxemia

based on the PaO2/FIO2 ratio. Question 1. Given a patient with a diagnosis of ARDS receiving mechanical ventilation with an FIO2 of 0.60 and PEEP of 5 cm H2O resulting in a PaO2 of 60, what is this patient’s ARDS severity classification? ARDS severity is classified based on the PaO2/FIO2 ratio (on PEEP 5 cm H2O or more) where: PaO2/FIO2 ratio 201 to 300: mild PaO2/FIO2 ratio 101 to 200: moderate PaO2/FIO2 ratio ≤ 100: severe The patient’s PaO2/FIO2 ratio is 60 mmHg/0.60 = 100, which is classified as severe ARDS. Question 2. Given a patient with a diagnosis of ARDS requiring mechanical ventilation, what tidal volume should be set on the ventilator? The patient’s predicted body weight is 70 kg. Mechanical ventilation with reduced tidal volumes in the range of 4 to 8 mL/kg of predicted body weight and reduced inspiratory pressures ( 150 to 200 mmHg) Ambient light striking the sensor

Perform Pulse Oximetry The pulse oximeter sensor may be placed on fingers or toes. The forehead, nose, ears, and neck are alternative sites when movement, low peripheral perfusion, or skin/nail pigmentation prevent accurate readings. Assessment should be on the quality of the oximeter values and not simply the numbers. Heart rate displayed by the pulse oximeter should correlate with the cardiac monitor or a manual pulse. If the oximeter provides a pulsatile waveform, the waveform should be assessed for uniformity and consistency over time. Some modern pulse oximeters provide specific measurements for quality of the signal, such as pleth variability index (PVI), perfusion index (PI), and patient state index (PSI). Some newer pulse oximeters have the capability to perform co-oximetry, measuring carboxyhemoglobin (COHb), methemoglobin (metHb), and total hemoglobin (totHb).39

Interpret Results Interpretation of pulse oximetry results is completed once the sensor is placed, and a steady-state reading is achieved. As noted, the signal quality and correlation with the patient’s condition and other measures should be assessed. For example, poor perfusion may cause periodic loss of the signal or inability to read SpO2. Carbon monoxide poisoning and sickle cell anemia may result in falsely elevated or falsely normal SpO2 values. Severe anemia, fingernail polish, inherited forms of abnormal hemoglobin, intravenous (IV) administration of pigmented dyes, excessive movement, and venous pulsations may also cause falsely low SpO2 values. SpO2

may be falsely low or high in the presence of methemoglobin, sulfhemoglobinemia, sepsis, and septic shock. Normal ranges for heart rate and oxygen saturation vary with patient age, disease states, and critical illness. An SpO2 reading of 95% to 97% while breathing room air is normal. In critical illness, SpO2 ≥ 90% may be acceptable. Altitude can affect oxygen saturation readings; a patient in Vail, Colorado would have a lower normal SpO2 due to altitude. Patients with chronic lung disease (COPD) may live with a “normal for them” oxygen saturation in the range of 88% to 92%. The oxyhemoglobin dissociation curve must be considered when interpreting oxygen saturation levels. When the curve is in normal position, an arterial oxygen saturation of 96% to 98% corresponds to an arterial oxygen tension (PaO2) of 80 to 100 mmHg and a saturation of 90% corresponds to an arterial oxygen tension (PaO2) of about 60 mmHg (Figure 9-20). Arterial oxygen saturations from 91% to 95% correspond to PaO2 in the range of 60 to 79 mmHg, which may be considered mild hypoxemia. Saturations from 85% to 90% correspond to PaO2 in the range of 50 to 59 mmHg (moderate hypoxemia), while saturations from 75% to 84% correspond to PaO2 in the range of 40 to 49 mmHg (moderate to severe hypoxemia). Arterial oxygen saturations < 75% correspond to PaO2 < 40 mmHg, and represent very severe, life-threatening hypoxemia.

FIGURE 9-20 The Oxyhemoglobin (HbO2) Dissociation Curve. Normally a SaO2 of 96% to 98% corresponds to an arterial oxygen tension (PaO2) of 80 to 100 mmHg. SaO2 of 90% corresponds to a PaO2 of about 60 mmHg. SaO2 from 91% to 95% corresponds to PaO2 in the range of 60 to 79 mmHg, which may be considered mild hypoxemia. SaO2 85% to 90% corresponds to PaO2 in the range of 50 to 59 mmHg (moderate hypoxemia), while SaO2 from 75% to 84% corresponds to PaO2 in the range of 40 to 49 mmHg (moderate to severe hypoxemia). SaO2 < 75% corresponds to PaO2 < 40 mmHg, and represents very severe, life-threatening hypoxemia.

Description Hypothermia, alkalosis, hypocapnea, and decreased 2,3-DPG levels shift the oxyhemoglobin dissociation curve to the left, which indicates an increase in the affinity between oxygen and hemoglobin (Figure 9-21). With a left shift, a lower PaO2 may be required to achieve a given saturation. For example, with a left shift a PaO2 of 55 mmHg may be sufficient to achieve an oxygen saturation of 90%. Unfortunately, while a left shift makes it easier to load the hemoglobin with oxygen at the lung, it makes it more difficult for the hemoglobin to release the oxygen at the tissue level because O2 molecules are more tightly bound to hemoglobin.

Hyperthermia, acidosis, hypercarbia, and increased 2,3-DPG levels shift the curve to the right, which decreases the affinity between oxygen and hemoglobin. With a right shift, it is more difficult to load the hemoglobin with oxygen because of the reduced affinity; a given PaO2 will result in a lower arterial oxygen saturation. Clinically, it is best to try and normalize the patient’s temperature, pH, and PaCO2 and avoid extreme right or left shifts in the oxyhemoglobin dissociation curve.

FIGURE 9-21 Right and Left Shifts in the Oxyhemoglobin (HbO2) Dissociation Curve. The curve shifts to the right with an increase in PCO2, increase in temperature, decrease in pH, or increase in 2,3-DPG. A right shift reduces SaO2 at a given PaO2. The curve shifts to the left with a decrease in PCO2, decrease in temperature, increase in pH, or decrease in 2,3-DPG. A left shift increases SaO2 at a given PaO2. Extreme shifts due to severe acidosis (right shift) can impair oxygen loading at the lung; extreme alkalosis (left shift) can impair oxygen unloading at the tissues. Modified from Baum GL, Crapo JD, Celli BR, et al, eds. Textbook of Pulmonary Diseases. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1998.

Description

Capnometry, Capnography, and VD/VT Capnography provides a graphic display of carbon dioxide concentrations (percent or partial pressure) of the inspired and expired gases versus time. Capnometry refers to measurement and display of exhaled CO2 concentration in numerical values (e.g., end-tidal PCO2 [ETCO2 or PetCO2], mean exhaled PCO2 [PĒCO2]). Capnography provides a noninvasive measure of exhaled carbon dioxide (CO2), which can be helpful in detecting acute changes in ventilatory status (e.g., hyperventilation, hypoventilation, and apnea). Capnography can also be useful to detect changes in CO2 production (V̇CO2) or pulmonary blood flow (e.g., major pulmonary embolus, severe hypotension, cardiac arrest). Capnography (or other form of CO2 detection) should be used for verification of proper endotracheal tube placement, and it may be useful for assessing the effectiveness of resuscitation efforts following cardiac arrest. Carbon dioxide detection and monitoring devices detect CO2 via pH-sensitive media (colorimetric ETCO2) (Figure 9-22) or infrared absorption or mass spectrometry. Capnography displays the inspired and exhaled CO2 concentrations against time as a graphic waveform. Capnography devices will often also display respiratory rate, based on the waveform-time graph. End-tidal carbon dioxide (ETCO2) measurement provides the partial pressure of CO2 (PETCO2) in mmHg at the very end of exhalation. A normal exhaled CO2 waveform consists of three very important parts, or phases. Phase I represents initial exhalation of dead space gas, with no CO2 present. Phase II represents continuing exhalation, with a significant increase in CO2, from both terminal airways and alveoli. Phase III, or the plateau phase, represents exhalation of alveolar gas rich in CO2 (Figure 9-23). The very end of the plateau phase represents the ETCO2 measurement. Patients with no abnormal physiology should observe a gradient ≤ 2 to 5 mmHg between PaCO2 and PETCO2, with PETCO2 being the same or lower than PaCO2. Airway compromise, cardiopulmonary disease, and hypoperfusion states can significantly affect the PETCO2, when comparing to PaCO2. Deviations from the normal shape of the capnography waveform may also shed light on clinical complications or changes in physiology. Airway obstruction (Figure 9-24), hypo- or hyperventilation, rapid shallow breathing, apnea, ventilation/perfusion mismatches, airway leaks, ventilator disconnects, CPR compression quality, and return of spontaneous circulation

(ROSC) during CPR can be sometimes detected by capnography. Capnography in combination with pulse oximetry may also reduce sedation-related adverse events during procedural sedation and analgesia administered for ambulatory surgeries.

FIGURE 9-22 Colorimetric CO2 Sensor Used to Confirm Successful Endotracheal Intubation. Courtesy of Covidien. Used with permission.

FIGURE 9-23 Capnogram. The capnogram displays carbon dioxide tension (PCO2) or concentration (percentage CO2) versus time. Phase I represents the emptying of the upper airways (i.e., dead space) with no CO2 present. Phase II is characterized by an abrupt rise in CO2 as anatomic dead space is emptied and the terminal airways and alveoli begin emptying. Phase III represents the alveolar plateau. The end-tidal PCO2 (PETCO2) is the CO2 level at the end of exhalation; PETCO2 normally approximates alveolar CO2 (PACO2).

Description

FIGURE 9-24 Capnogram with Airflow Obstruction (e.g., asthma, COPD).

Description

Perform Capnography Exhaled CO2 can be measured quantitatively using infrared absorption or mass spectrometry technology. Most clinical devices use absorption of infrared light by CO2 to determine CO2 concentration or partial pressure. Qualitative CO2 detection incorporates specially treated litmus paper that changes color when exposed to CO2. These colorimetric CO2 detectors provide a qualitative measure of ETCO2 where purple indicates PCO2 < 3 mmHg, tan indicates PCO2 3 to 15 mmHg, and yellow indicates PCO2 > 15 mmHg. If exhaled CO2 measurement is performed using a colormetric CO2 detector (e.g., Nellcor Easy Cap, II), the detector is directly connected to the proximal airway (e.g., endotracheal tube 15-mm adapter) in spontaneously breathing intubated patients, and between the airway and the manual resuscitator bag connection or ventilator circuit in patients requiring ventilatory support. Care must be taken to place the device close to the airway and to minimize the effects of any mechanical dead space.

For capnography performed using an end-tidal CO2 (ETCO2) monitor, the sensor adapter is attached to the artificial airway, then to the bag-valve (BV) device or ventilator circuit. Proper adapter placement should minimize mechanical dead space. Capnography uses one of two sampling systems: mainstream or sidestream sensing technology. Figure 9-25 demonstrates mainstream and sidestream configurations.

FIGURE 9-25 Types of Capnometry. (A) Mainstream Capnometry. (B) Sidestream Capnometry.

Description Mainstream technology utilizes an airway adaptor that connects to the

endotracheal or tracheostomy tube. The infrared sensor attaches to the airway adaptor, passing light across the airstream through the adaptor to a photodetector. Advantages of mainstream technology are a real-time waveform, respiratory rate, and an ETCO2 reading. Mainstream systems also do not aspirate the gas sample and do not reduce delivered tidal volume. Mainstream devices do have disadvantages: the sensor weight can tug on the airway, potentially causing discomfort or airway dislodgement, or the airway adaptor can become coated with secretions, blood, or moisture, affecting the unit’s ability to effectively monitor CO2. Mainstream systems are also difficult to use in nonintubated patients. Sidestream technology also utilizes an airway adaptor that attaches to the airway; however, a small-bore sampling line is attached to the adaptor through which a gas sample is drawn into a measuring chamber attached or within the monitor itself. An advantage of sidestream technology is the lightweight airway adaptor. Like mainstream capnography, the monitor provides a display of the CO2 waveform, respiratory rate, and ETCO2 values. Sidestream systems can also be used with specially designed nasal cannula for CO2 monitoring in nonintubated patients. Disadvantages of sidestream devices include a delay in analysis of the waveform and reading (i.e., not real time) and the volume of gas being aspirated from the airway for analysis, which may reduce delivered tidal volume in ventilated patients. Sidestream systems typically require a water trap or filter placed proximal to the analysis chamber to remove accumulated moisture, although some systems incorporate water vapor-permeable tubing. Advantages and disadvantages of mainstream and sidestream capnometry are summarized below. Advantages of Mainstream Capnometry Sensor placed at the airway. Fast response time. Real-time readings. No gas sample flow required, which may reduce delivered tidal. Disadvantages of Mainstream Capnometry Secretions and/or humidity can obstruct sensor. Sensor may need to be heated to minimize condensation.

Sensor is bulky and heavy at the patient’s airway. Does not measure nitrous oxide (N2O). Difficult to adapt to nonintubated patients. Reusable sensor requires cleaning and sterilization. Adds dead space to the ventilator circuit. Advantages of Sidestream Capnometry No bulky sensor at the patient airway. Able to measure nitrous oxide (N2O). Disposable sampling line and sensor adapter. More easily used on nonintubated patients. Disadvantages of Sidestream Capnometry Secretions may block sample tubing. Water trap required. Slower response time. Delayed readings. Sample flow may reduce delivered tidal volume.

Interpret Results End-expiratory gas concentrations should represent alveolar gas. Thus, in healthy individuals end-tidal CO2 (PETCO2) should approximate alveolar CO2 (PACO2), which should in turn reflect arterial CO2 (PaCO2): PETCO2 ≈ PACO2 ≈ PaCO2 Normal PETCO2 is 35 to 40 or 45 mmHg, and the normal difference between PaCO2 and PETCO2 is 2 to 5 mmHg, or less. Colorimetric CO2 detection systems are commonly used to assess for proper endotracheal tube placement following intubation. For colormetric devices, six brisk color changes from purple to yellow (i.e., purple → yellow → purple × 6) indicate proper tube placement and adequate perfusion. If the color change is not a brisk for six complete breath cycles, misplacement of the endotracheal tube (e.g., esophageal intubation) may have occurred or perfusion may be absent (e.g., cardiac arrest). Because small amounts of CO2 may be present in the esophagus, at least five breaths with a consistent CO2 level should be present to assure proper tracheal

placement of an endotracheal tube. It also must be noted that patients in cardiac arrest may not produce exhaled CO2. If capnography is utilized, the waveform shape should be assessed along with the ETCO2 values. Alteration of one or all of the waveform phases may indicate an airway disconnect or dislodgement, airway obstruction, or leak in the patient– ventilator system. When comparing PaCO2 to PETCO2, a gradient > 2 to 5 mmHg may indicate a ventilation/perfusion mismatch (e.g., pulmonary embolus, atelectasis, hypoperfusion). Capnography can be utilized to calculate the tidal volume/dead space ratio (VD/VT) by providing the mean exhaled carbon dioxide tension (PĒCO2), where: VD/VT = (PaCO2 – PĒCO2) ÷ PaCO2 Normal values for PĒCO2 are 28 mmHg with a range of about 24 to 32 mmHg. The normal range for VD/VT is 0.20 to 0.40, or 20% to 40%. During mechanical ventilation, the VD/VT may be somewhat higher, in part due to the inspiratory mechanical dilation of the conducting airways that occurs during a positive-pressure breath. The VD/VT ratio can be multiplied by the VT to calculate physiologic dead space: VDphys = VT × VD/VT Alveolar dead space then can be calculated by subtracting physiologic dead space from VT as described earlier. Alveolar dead space may also be estimated directly using end-tidal carbon dioxide values (PETCO2): VDalv = [(PaCO2 – PETCO2) ÷ PaCO2] × VT For example, if PaCO2 = 40 mmHg, PETCO2 = 35 mmHg and VT = 500 mL, alveolar dead space would be: VDalv = [(40 – 35) ÷ 40] × 500 mL = 62.5 mL Capnography is beneficial during cardiopulmonary resuscitation (CPR) to assist in the evaluation of the effectiveness of external cardiac compressions. During CPR,

PETCO2 values of 10 to 20 mmHg corresponds to effective cardiac compressions, while readings ≤ 10 mmHg are suggestive of ineffective compression. Table 9-2 summarizes the indications, contraindications, hazards, and limitations of capnography and capnometry. Box 9-3 summarizes causes for alterations in endtidal carbon dioxide levels. It should also be noted that volume-based capnography and a rebreathing technique can be used to noninvasively measure cardiac output. TABLE 9-2 Indications, Contraindications, Hazards, and Limitations of Capnometry and Capnography Capnometry refers to the measurement and display of exhaled CO2 concentrations (percent of partial pressure) in numerical values, while capnography provides a graphic display of carbon dioxide concentrations of the inspired and expired gases versus time. Indications Monitor and evaluate exhaled CO2 (PETco2, PĒco2, CO2 waveform). PETco2 will generally rise with decreased alveolar ventilation, increased CO2 production (i.e., increased V̇CO2), and rebreathing exhaled gas (e.g., increased mechanical dead space), and may increase with leaks in the ventilator circuit resulting in hypoventilation. PETco2 will generally decrease with increased alveolar ventilation, decreased V̇CO2, ventilator disconnect, esophageal intubation, complete airway obstruction, and leaks around the endotracheal tube cuff. The capnogram waveform provides a visual display of CO2 concentration versus time. Assess adequacy of ventilation. The single best clinical index of alveolar ventilation is measurement of Paco2. PETco2 tends to reflect Paco2 values; however, PETco2 monitoring should not be used as a substitute for measurement of arterial blood gases, when needed. Within its limitations, capnography does allow for monitoring ventilatory status in patients with respiratory distress and in patients who are obtunded or unconscious. Capnography may also be used to monitor ventilation during procedural sedation during outpatient surgical procedures to detect adverse airway events or respiratory problems. Verify proper endotracheal tube placement. A normal capnogram waveform (phases I to III) with appropriate PETco2 (2% to 5% [purple on colorimetric devices] or > 15 mmHg) suggest proper endotracheal tube placement. PETco2 may also be elevated if the tip of the endotracheal tube is placed just above the vocal cords; however, values will tend to be erratic in such cases. It should also be noted that with antacid consumption or consumption of carbonated beverages may elevate esophageal CO2 levels slightly. With esophageal intubation, a flat line capnogram with PETco2 at or near zero will be present. It must be noted that complete cessation of pulmonary blood flow (e.g., cardiac arrest) may also cause a flat line capnogram with PETco2 at or near zero. Monitor/maintain proper endotracheal tube placement during transport. Endotracheal tubes are sometimes accidently dislodged or advanced during patient transport. Monitoring PETco2 can be helpful to ensure adequate ventilation during patient transport and detect accidental ETT misplacement. Any change in PETco2 during patient transport from one site to another should alert the clinician to reassess the position of the endotracheal tube. Assess the effectiveness of resuscitation efforts following cardiac arrest. PETco2 rapidly increases when the heart restarts (e.g., return of spontaneous circulation [ROSC]) following

cardiac arrest. Continued low PETco2 (≤ 10 mmHg) for more than 20 minutes following the institution of advanced cardiac life support (ACLS) is predictive of death. Avoid hypercapnia and hyperventilation following head trauma. Hypoventilation and resultant hypercapnia increases cerebral blood flow due to cerebral vasodilation, which can be detrimental following head trauma. Hyperventilation causes cerebral vasoconstriction and sustained hyperventilation (Paco2 ≤ 30 mmHg) is associated with worse outcomes in severely brain injured patients. Assess VD/VT and V̇/Q̇. Alveolar dead space (ventilation without perfusion) may increase due to COPD or pulmonary embolus with complete pulmonary capillary blockage. With increased alveolar dead space (i.e., increased V̇/Q̇, alveolar CO2 [PACO2]) and PETco2 will decrease. With decreased V̇/Q̇, PACO2 and PETco2 may increase slightly. PETco2 may also be used with a modification of the Bohr equation to estimate alveolar dead space (see text). Monitor the integrity of the ventilator circuit. With complete ventilator–patient circuit disconnect, PETco2 will fall to zero. Other circuit leaks may cause hypoventilation reflected in the capnogram waveform. Assess the PETco2 to arterial Paco2 difference (Paco2 – Petco2). Difference will increase with ventilator disconnection, apnea, esophageal intubation, moderate to severe hypoventilation, moderate to severe airway obstruction, increased physiologic dead space, and high rate low tidal volume ventilation. The difference will also increase with decreased blood flow to the lung (e.g., pulmonary embolus, decreased blood volume, cardiac arrest) and equipment problems (e.g., increased mechanical dead space, air leak and sampling system, air leak around endotracheal tube). Assess pulmonary blood flow. Decreased pulmonary blood flow may reduce PETco2, while complete secession of blood flow to the lung will cause PETco2 to fall to zero. Assess cardiac function. Low cardiac output reduces PETco2. With cardiac arrest, PETco2 will cease. Detect metabolic acidosis. Metabolic acidosis (e.g., diabetic ketoacidosis) will generally cause a compensatory increase in minute ventilation and reduction in PETco2. Determine CO2 elimination to assess metabolic rate ( V̇CO2) and/or alveolar ventilation (V̇A). Increased V̇CO2 production may increase PETco2. Increased V̇CO2 may be caused by fever, sepsis, increased metabolic rate, seizures, and overfeeding. Decreased V̇CO2 production may decrease PETco2. Decreased V̇CO may be caused by hypothermia, decreased metabolic rate, or correction of fever, sepsis, or seizures. 2

Decreased blood flow to the lung, cardiac arrest, pulmonary embolus, hemorrhage, or hypotension may reduce CO2 transport to the ventilated alveoli and reduce PETco2. Contraindications No specific contraindications, although capnography/capnometry should not be used as a substitute for arterial blood gas analysis. If properly applied, PETco2 is a good surrogate for Paco2 in healthy individuals, but most patients seen in the ICU have V̇/Q̇ abnormalities. Increased VD/VT, decreased pulmonary blood flow, pulmonary embolus, PEEP, and high rate Crapo JD, Celli BR low tidal volume ventilation will all cause an increase in the difference between arterial and end-tidal CO2. In addition, severe hypoventilation, apnea, ventilator disconnect, and cardiac arrest will cause PETco2 to fall to zero, even though Paco2 may be very high. Thus, capnometry or capnography should not be substituted for measurement of arterial blood gases and Paco2. Hazards and Complications Additional weight placed on the artificial airway. Increased mechanical dead space. Misapplication of the information provided.

Limitations ▪ Gas mixture may affect the capnogram (e.g., nitrous oxide, helium). ▪ Elevated respiratory rates may exceed device capabilities. ▪ Freon metered-dose inhaler (MDI) propellant may affect CO2 readings with mass spectrometers. ▪ Unreliable results due to secretions, condensate, and obstruction of the sampling chamber. ▪ Low cardiac output or cardiac arrest will invalidate results when assessing for proper endotracheal tube placement. ▪ Elevated esophageal CO2 due to in antacids or carbonated beverages may invalidate results when assessing for possible inadvertent esophageal intubation. ▪ Sidestream flow sampling rate may decrease tidal volume delivery in ventilated patients (especially in neonates and pediatrics). ▪ Leaks in the patient–ventilator system may result in inaccurate CO2 measurement. Data from Hess DR. Respiratory Monitoring. In: Hess DR, MacIntyre NR, Galvin WF, and Mishoe SC. Respiratory Care Principles and Practice. Jones & Bartlett Learning.

BOX 9-3 Alterations in End-Tidal CO2 (PETCO2) Levels Normally, PETCO2 generally reflects alveolar CO2 tension (PACO2), which in turn reflects PaCO2. With some important caveats, increased PETCO2 may be due to hypoventilation while decreased PETCO2 may be due to hyperventilation. It is important to note that with severe hypoventilation PETCO2 may be decreased and PETCO2 falls to zero with apnea. Deviations from normal graphic tracings may be useful to identify airway obstruction, rapid shallow breathing, ventilationperfusion mismatch, inadequacy of cardiopulmonary resuscitation efforts, or a large air leak. Measurement of PETCO2 during cardiopulmonary resuscitation (CPR) may be helpful in assessing chest compressions; PETCO2 of 10 to 20 mmHg suggest compressions are effective. Return of spontaneous circulation following CPR is associated with a significant increase in PETCO2. Causes of increased, decreased, and absent PETCO2 are listed. 1. PETCO2 will generally increase with: a. Decreased alveolar ventilation (↓ V̇A) due to: i. Decreased tidal volume ii. Decreased respiratory rate iii. Decreased minute ventilation b. Increased CO2 production (↑ V̇CO2) due to: i. ii. iii. iv.

Agitation Stress Shivering Fever

v. Sepsis vi. Seizures vii. Pain viii. Anxiety ix. Recovery from sedation or paralysis x. Fighting the ventilator 2. PETCO2 will generally decrease with: a. Increased alveolar ventilation due to: i. Increased tidal volume ii. Increased respiratory rate iii. Increased minute ventilation b. Very small tidal volumes approaching dead space volumes c. Rapid shallow breathing d. Decreased CO2 production (↓ V̇CO2) i. Sleep ii. Cooling, hypothermia iii. Relaxation e. Decreased lung perfusion i. Decreased cardiac output ii. Pulmonary embolus iii. Hypotension 3. PETCO2 may be absent with: a. b. c. d. e. f.

Apnea Cardiac arrest Complete airway obstruction Ventilator disconnect Ventilator malfunction Esophageal intubation

* ETCO2 may be reported as percentage CO2 or partial pressure (PETCO2). Normal ETCO2 is about 3.5% to 4.5% or about 35 to 40 (or 45) mmHg. Data from Hess DR. Respiratory Monitoring. In: Hess DR, MacIntyre NR, Galvin WF, and Mishoe SC. Respiratory Care Principles and Practice. Jones & Bartlett Learning.

Transcutaneous O2/CO2 Transcutaneous monitoring provides a noninvasive estimate of arterial oxygenation (PaO2) and carbon dioxide (PaCO2) using sensors placed on the skin surface. Transcutaneous monitors use heated electrodes to increase skin circulation. When properly applied in appropriate patients, the transcutaneous partial pressure of oxygen (PtcO2) and carbon dioxide (PtcCO2) should reflect arterial values. Transcutaneous monitoring has successfully been used in neonates, infants, children, and adults, although it is most commonly used in infants and neonates. Transcutaneous monitoring may also be used to determine the adequacy of tissue perfusion and monitoring reperfusion. A prerequisite for successful transcutaneous monitoring is adequate circulation and available skin sites for electrode placement. Transcutaneous monitoring should be avoided in the presence of increased skin thickness or edema or subcutaneous edema. Transcutaneous oxygen monitoring uses a Clark polarographic electrode integrated into a skin sensor, which is heated to 42° to 45°C. The heated sensor melts the lipid layer of the skin, and alters the stratum corneum, which causes hyperemia and increased skin permeability. The increased permeability greatly enhances oxygen diffusion between the tissues and skin surface. The monitor adjusts for factors such as barometric pressure, ambient temperature, and humidity. Sensors must be calibrated periodically. The sensor site must also be changed periodically, to avoid thermal injuries. Transcutaneous carbon dioxide monitoring uses a Severinghaus electrode integrated into a skin sensor, which is heated to 42°C. The heated sensor works similarly to the oxygen sensor, melting the lipid layer and altering the stratum corneum to increase skin permeability for CO2 diffusion. Again, care must be taken to periodically move the sensor site to avoid thermal injuries. PtcCO2 generally correlates well with PaCO2 and may be used in clinical settings where monitoring of ventilation is required. Arterial blood gas values for PaCO2 should be compared to PtcCO2 transcutaneous values taken at the same time in order to verify the correlation; arterial blood gases should also be obtained periodically, based on the patient’s condition. Modern transcutaneous monitors combine PtcCO2 and PtcO2 electrodes, for ease of

use and decreased occurrence of thermal injury from multiple transcutaneous sites. Some monitors combine a PtcCO2 and pulse oximetry (SpO2) into a single sensor, for ease of operation. These sensors can be adapted to clip to the ear, for a more central site that is richly perfused or placed on the chest, abdomen or a limb (Figure 9-26). Box 9-4 summarizes the indications, contraindications, hazards, complications and limitations of transcutaneous blood gas monitoring.

FIGURE 9-26 Transcutaneous Monitor Provides Noninvasive Monitoring for PtcCO2 and PtcO2. Courtesy of SenTec AG.

BOX 9-4 Indications, Contraindications, Hazards and Complications, and Limitations of Transcutaneous Blood Gas Monitoring Transcutaneous monitoring typically includes measurement of skin surface oxygen Ptc O2 and carbon dioxide (PtcCO2) tension to provide an estimate of arterial oxygenation (PaO2) and carbon dioxide (PaCO2). Transcutaneous monitoring is especially useful when arterial blood gases are not available or immediately accessible. Transcutaneous blood gas monitoring may be used for continuous monitoring during mechanical ventilation, as well as diagnostic assessment of functional shunts (e.g., persistent pulmonary hypertension of the newborn, persistent fetal circulation, and congenital heart disease). Indications ∎ Continuous monitoring of the adequacy of oxygenation and/or ventilation is needed. ∎ To assess response to diagnostic or therapeutic interventions on P O and/or tc 2 PtcCO2.

•

PtcCO2 values may guide weaning and extubation decisions.

∎

Transcutaneous oxygen index (PtcO2/FIO2) provides an early marker of hypoperfusion and mortality. • PtcO2/FIO2 < 200 requires prompt evaluation and intervention.

∎

To monitor tissue perfusion and revascularization in wound care and peripheral arterial occlusive disease. • PtcO2 provides an effective tool to monitor limb ischemia during wound care and hyperbaric oxygen therapy. • PtcO2 of at least 30 to 40 mmHg in the effected limb is needed to maintain adequate perfusion. • PtcO2 < 30 mmHg indicates poor perfusion to the limb.

• •

∎

PtcO2 < 10 mmHg is incompatible with the healing process.

PtcO2 ≥ 30 mmHg is thought to be needed for successful amputation stump healing. PtcCO2 correlates with serum bicarbonate levels (HCO3–); PtcCO2 can be used to monitor response to therapy in patients with diabetic ketoacidosis.

Contraindications

∎ ∎

No absolute contraindications. Relative contraindications include poor skin integrity and adhesive allergy.

Hazards and Complications ∎ Misinterpretation of results may lead to inappropriate treatment. ∎ P CO overestimates PaCO (some devices use a correction factor to adjust tc 2 2 for this difference). ∎ P O underestimates PaO (some devices use a correction factor to adjust for tc 2 2 this difference). ∎ Thermal injury at the sensor site. • Erythema, blisters, burns, skin tears. Limitations ∎ Setup may be labor intensive. ∎ Stabilization time (5 to 10 min) is required following electrode placement. ∎ Erroneous results due to improper calibration, trapped air bubbles, damaged membranes, or leaks in the fixation device. • Falsely elevated PtcO2 values (e.g., PaO2 > 100 mmHg, improper electrode placement, increased capillary blood flow due to patient movement), • Falsely decreased PtcO2 values (e.g., hypoperfusion, shock, acidosis, and vasoactive drug administration, increased thickness or edema of the skin or subcutaneous tissue, distal extremity sensor site vasoconstriction), • Falsely elevated PtcCO2 values (increased capillary blood flow caused by patient movement). • Falsely decreased PtcCO2 values (e.g., hypoperfusion, shock, acidosis, vasoactive drug administration, improper electrode placement, increased thickness or edema of the skin or subcutaneous tissue, distal extremity sensor site vasoconstriction). ∎ Arterial blood gases obtained at the same time as transcutaneous monitoring values should be used to validate monitor results. Data from American Association of Respiratory Care (AARC). AARC Clinical Practice Guideline: transcutaneous monitoring of carbon dioxide and oxygen: 2012. Respir Care. 2012; 57: 1955–1962.

Perform Transcutaneous Monitoring Transcutaneous monitoring requires skin site placement over an area that is well perfused. Skin integrity must be assessed, as well as any potential allergies to

adhesive. Ideally, the lateral trunk is used, but newer technology allows the ear lobe to be utilized. The areas may need to be prepped (shaved, cleaned) if hair is present, or the desired site is dirty. Often, contact gel is used between the skin and the sensor. Again, the sensor site must be changed periodically, to avoid thermal injury. The sensor may require periodic calibration.

Interpret Results Assessing the quality of the transcutaneous measurement is vital. Poor perfusion (hypothermia, sepsis, shock, vascular disease, and edema) can significantly affect the reliability of the transcutaneous measurement. Decreased skin perfusion can cause an increase in PtcCO2; edema can increase the diffusion distance, causing a false low PtcO2 measurement. Close attention to trending, along with patient considerations, is an important aspect of transcutaneous monitoring.

Exhaled Nitric Oxide Measurement of exhaled nitric oxide (NO) has been advanced as a test of airway inflammation.40 NO is a neurotransmitter that promotes pulmonary vascular and bronchial smooth muscle dilation. NO can be measured in exhaled gas and levels are elevated in asthmatics, although NO levels may return to normal following administration of corticosteroids. Other causes of increased exhaled and NO (FENO) include eosinophilic bronchitis, COPD exacerbation, viral upper respiratory tract infection, bronchiectasis, and atopy (a genetic predisposition to allergic hypersensitivity reaction).40 FENO may be reduced in smokers, pulmonary hypertension, bronchopulmonary dysplasia, and cystic fibrosis.40 Interpretation of FENO values in asthma is associated with specific cut points where FENO > 50 parts per billion (ppb) in adults (> 35 ppb in children) is associated with eosinophilic airway inflammation. Measurement of FENO may be of value in discriminating between eosinophilic and noneosinophilic asthma and provide guidance in patient management.

Cardiac and Hemodynamic Monitoring In addition to satisfactory arterial blood oxygen levels, oxygen delivery to the tissues requires an adequate cardiac output, as well sufficient peripheral tissue perfusion. Cardiac and hemodynamic monitoring helps ensure that critically ill patients have adequate cardiac function and hemodynamics, as well as providing for identification of important abnormalities such as cardiac arrhythmias, abnormal blood pressure, heart failure, systemic hypotension, and shock.

Electrocardiogram Monitoring The cardiac monitor provides an essential, noninvasive monitoring tool in the ICU for monitoring the electrical activity of the heart.41 In fact, the need for continuous ECG monitoring is often reason enough alone to warrant admission to the critical care unit. Routine observation of the cardiac monitor should include assessment of heart rate and rhythm, as well recognition of major arrhythmias. Normal adult heart rate is 60 to 100 beats per minute; heart rate < 60 bpm is bradycardia while heart rate > 100 bpm is tachycardia. Sinus tachycardia may be caused by hypoxia, anxiety, uncontrolled pain, fever, cardiac disease, circulatory problems, and certain medications. Endotracheal suctioning, manipulation of artificial airways, and other procedures performed in the ICU may cause tachycardia. Bradycardia may be caused by severe hypoxemia, certain medications, heart disease, and alterations in vagal tone. Airway suctioning is a fairly common cause of bradycardia in the ICU. Cardiac arrhythmias originating in the atria include premature atrial contractions (PACs), atrial flutter, and atrial fibrillation. Arrhythmias initiated at the atrioventricular (AV) junction include premature junctional complexes (PJCs) and junctional tachycardia. Arrhythmia initiated in the ventricles include premature ventricular contractions (PVCs), idioventricular rhythms, ventricular tachycardia, and ventricular fibrillation. AV blocks include first-degree AV block, second-degree Mobitz I AV block (aka Wenckebach), second-degree Mobitz II AV block, and third-degree or complete heart block. Asystole and ventricular fibrillation represent medical emergencies requiring immediate application of cardiopulmonary resuscitation (CPR) and advanced cardiac life support (ACLS). ECG changes characteristic of acute coronary syndrome and myocardial infarction

(MI) include ST segment elevation MI (STEMI), non-ST segment elevation MI (NSTEMI) and unstable angina associated with ST segment depression, inverted T waves, or transient ST segment elevation. Chapter 8 provides additional information regarding assessment of the ECG.

Hemodynamic Monitoring Hemodynamics describes the study of blood flow through the body. Blood moves from the right side of the heart, through the lungs to the left side of the heart, and then out to the systemic circulation. If something impedes blood flow, it will tend to increase the pressure proximal to this point. For example, excessive PEEP may overdistend the lungs and increase pulmonary artery and right atrial pressure. This may decrease venous return to the right heart and elevate central venous pressures, which may in turn lead to neck vein distention and peripheral edema. If blood return to the left heart is significantly reduced, cardiac output may decline, resulting in decreased systemic blood pressure. Hemodynamic-measures include systemic blood pressure, central venous pressure, right ventricular pressure, pulmonary artery pressure, pulmonary artery wedge pressure, and cardiac output. Figure 9-27 summarizes the hemodynamic cycle. Table 9-3 lists normal values for hemodynamic measurements.

FIGURE 9-27 Hemodynamic Cycle. CVP, central venous pressure; IVC, inferior vena cava; PAP, pulmonary artery pressure; PCWP, pulmonary venous wedge pressure; SBP; systolic blood pressure; SVC, superior vena cava.

Description TABLE 9-3 Normal Values for Hemodynamic Measurements Variable

Normal Range (units)

Systolic blood pressure

90 to 140 (mmHg)

Diastolic blood pressure

60 to 90 (mmHg)

Mean arterial pressure

80 to 100 (mmHg)

Central venous pressure

4 to 8 (mmHg)

Right ventricular systolic pressure

15 to 30 (mmHg)

Right ventricular end-diastolic pressure

0 to 8 (mmHg)

Mean pulmonary artery pressure

10 to 20 (mmHg)

Pulmonary artery wedge pressure

6 to 12 (mmHg)

Cardiac output

4 to 8 (L/min), varies with patient size

Cardiac Index

2.5 to 4.0 (L/min/m2)

Arterial Blood Pressure Monitoring The arterial systolic blood pressure (SBP) represents the peak pressure within the artery during systole (left ventricular contraction). Normal SBP is 90 to 140 mmHg. The diastolic blood pressure (DBP) is the lowest pressure in the artery during diastole (left ventricular filling). Normal DBP is 60 to 90 mmHg. The mean arterial pressure (MAP) is approximately equal to the diastolic pressure plus one-third of the pulse pressure and normally ranges from 80 to 100 mmHg. Pulse pressure is simply systolic pressure minus diastolic pressure.4 Arterial blood pressure can be measured noninvasively with a blood pressure cuff, or invasively using a fluid-filled arterial catheter connected to a pressurized transducer. Automated noninvasive blood pressure cuff monitoring systems are in common use in many ICUs. Indwelling arterial catheters can be placed and attached to a pressure transducer and monitoring system. The catheters are connected to the transducer by short, noncompliant tubing. This tubing is rigid enough to prevent inaccurate readings on the monitor. The transducer changes the pulsatile blood pressure signal within the artery to an electrical signal. Transducers must to be positioned at the level of the heart or the phlebostatic axis (the midaxillary line at the fourth intercostal space at the level of the right atrium). If the transducer is positioned below the heart, the blood pressure reported will be artificially high. If the transducer is positioned above the heart, the blood pressure reported will be artificially low. Mean arterial blood pressure is displayed on the monitor and is the most accurate,

since arterial lines may overestimate the systolic and underestimate the diastolic blood pressure.4 Figure 9-28 illustrates a normal arterial pressure waveform. The management of hypertension, hypotension, and shock are discussed in Chapter 2.

FIGURE 9-28 Normal Arterial Pressure Waveform. Courtesy of Hess DR, MacIntyre NR, Mishoe SC, Galvin WF and Adams AB.

Description

Titrate Vasopressors and Inotropes In the critical care unit clinicians are often faced with caring for patients with hemodynamic instability. Hypotension may be caused by bleeding or fluid loss (e.g., hypovolemia), reductions in cardiac output (e.g., MI, heart failure, cardiac arrhythmias), or inappropriate peripheral vasodilation (e.g., sepsis, anaphylaxis). Vasopressors cause vasoconstriction and can be used to increase mean arterial blood pressure. Adrenergic vasopressors activate alpha-1 (α1) adrenergic receptors located within vascular smooth muscle. Inotropes, on the other hand, increase myocardial contractility and cardiac output by beta-1 (β1) adrenergic receptor

stimulation. Many adrenergic drugs cause vasoconstriction (α1 activation), increased myocardial contractility (β1 activation), increased heart rate (β1 activation), and bronchodilation (β2 activation). Vasopressors are sometimes necessary to restore adequate tissue perfusion in patients with shock; however, they may be harmful in patients without adequate prior fluid resuscitation (e.g., hemorrhagic shock). Vasopressors are generally indicated when mean arterial pressure (MAP) is less than 65 mmHg resulting in inadequate organ perfusion. Vasopressors may also be indicated in patients with a substantial fall in MAP below baseline resulting in inadequate tissue perfusion. Hypovolemia, if present, should be corrected prior to administration of vasopressors. Commonly used adrenergic vasopressors and inotropic drugs include phenylephrine (Sudafed), norepinephrine, epinephrine, dopamine (Intropin), and dobutamine (Dobutrex). Of these, phenylephrine and norepinephrine are primarily alpha-1 receptor stimulants (i.e., vasoconstrictors), while epinephrine and dopamine have alpha-1 and beta-1 effects (i.e., vasopressor and inotropic effects). Dobutamine, on the other hand, is primarily an inotropic drug that increases cardiac output by stimulation of the beta-1 receptors in the heart. Dobutamine also activates beta-2 adrenergic receptors and causes vasodilation, which may result in hypotension in certain patients. With shock, selection of specific vasopressors is dependent on the type of shock present. For example, norepinephrine may be the initial vasopressor of choice with septic, cardiac, and hypovolemic shock. Epinephrine may be the initial drug of choice with anaphylactic shock while phenylephrine may be useful in patients with tachycardia. Dobutamine, on the other hand, may be the initial drug of choice in cardiogenic shock. Vasopressors and inotropic drugs should be administered through a central venous catheter; however, therapy may be started using a peripheral IV line until a central line can be placed. Volume replacement therapy is essential in patients requiring it, prior to administration of vasopressors, if possible. Titration of vasopressors and inotropes is somewhat complicated and beyond the scope of this chapter. For example, dobutamine stimulates beta-1 adrenergic receptors at lower doses and alpha-adrenergic receptors at higher doses. Norepinephrine may increase MAP but cause a reflex decrease in heart rate. Generally, dosage is titrated up to achieve an acceptable arterial blood pressure (MAP of > 65 mmHg) and adequate tissue perfusion.42 In addition to MAP,

improvements in urine output and neurologic status suggest improved peripheral perfusion. In cases where the initial drug is ineffective at maximal dosage, a second drug may be added.

Fluid Balance A patient’s volume status can be challenging to assess. In general, fluid volume changes can be estimated by changes in body weight. Fluid volume loss may cause a reduction in body weight, while volume gain is generally associated with increased body weight. Put another way, volume loss can be estimated by comparing the prefluid deficit body weight with body weight post fluid deficit, based on the degree of weight loss. Laboratory studies, such as urine sodium concentration, can also help assess the degree of volume depletion in a patient. The presence of low urine output may also indicate hypovolemia. Low blood pressure and low urine output may be caused by hypovolemia. Indications for intravenous volume replacement therapy (e.g., isotonic saline) include hypovolemia, and fluid replacement is an important component in treatment of undifferentiated hypotension and shock. Fluid resuscitation is often necessary to maintain blood pressure and cardiac output in cases where intravascular volume is inadequate (e.g., blood loss, hemorrhagic shock, septic shock); fluid resuscitation with isotonic saline (i.e., normal saline) is an essential component in the initial management of patients with traumatic shock. One approach is to administer IV fluid boluses of 500 mL to 1000 mL, which are then repeated until adequate blood pressure and tissue perfusion are achieved. Prehospital whole blood transfusions administered by paramedics in the field are now being tested in the treatment of trauma patients in a few locations. Hypervolemia may be caused by volume overload following excessive fluid or blood administration. In the setting of volume gain, peripheral edema may develop. Edema occurs from the movement of fluid from the vasculature to the interstitial space. With hypervolemia, this may be caused by high capillary hydrostatic pressures. In contrast to volume loss, volume gain can be estimated by pre-post gain in body weight, if the degree of weight gain is known.43 Fluid overload is most commonly treated with administration of an IV diuretic, such as furosemide (Lasix). Left-sided heart failure may be caused by hypertension, myocardial ischemia or

infarction, valvular heart disease, cardiomyopathy, cardiac arrhythmias, fluid overload, or kidney failure, as well as a number of other potential causes/contributing factors (e.g., diabetes, obesity, hyperthyroidism). Symptoms may include dyspnea, fatigue, and edema in the legs, ankles and feet due to fluid overload. Pulmonary edema may occur due to elevated pulmonary arterial pressures. In addition to addressing the underlying cause, medications to improve cardiac function (e.g., ACE inhibiters, angiotensin II receptor blockers, beta blockers, digoxin [Lanoxin]) and diuretics are often administered to treat fluid retention. Chapter 2 (Respiratory Failure) provides additional information regarding heart failure.

Central Venous Pressure Central venous pressure (CVP) is measured by a catheter with the tip positioned in the superior vena cava. The CVP reflects right atrial pressure and loosely correlates with intravascular volume status early in resuscitation. Normal CVP is 4 to 8 mmHg, which provides an estimate of the filling pressure of the right ventricle. CVP may be influenced by cardiopulmonary disease and positive-pressure breathing. Causes of increased CVP include right ventricular failure, pulmonary valvular stenosis, tricuspid valvular stenosis and regurgitation, pulmonary hypertension, pulmonary embolus, cardiac tamponade, and volume overload. Left ventricular failure results in increased pulmonary arterial pressures, which may be followed by increased CVP and right ventricular failure. Other possible causes for increased CVP include mechanical ventilation with positive pressure, PEEP, and pneumothorax. CVP may be abnormally decreased due to inadequate circulating blood volume (e.g., hypovolemia, blood loss, and shock), cardiovascular collapse, or technical errors (see below). The central venous line used to measure CVP can also be used for venous blood sampling, fluid administration, and medication administration.4 Some clinicians carefully examine the CVP pressure waveform and identify specific points (i.e., “a, x, c, v, and y” waves) associated with right heart function. The “a” wave represents atrial systole, the “c” wave represents tricuspid valve closure, while the “v” wave represents ventricular contraction. Complications associated with central venous lines include bleeding, pneumothorax, nerve injury, catheter malposition, and

bloodstream infections. Improper positioning of the transducer may lead to erroneous pressure measurements. For example, if the pressure transducer is placed below the level of the patient’s right atrium, pressures displayed may be artificially increased. If the transducer is placed above the level patient’s right atrium, pressures displayed may be artificially decreased. Figure 9-29 illustrates a normal central venous pressure waveform.

FIGURE 9-29 Normal Central Venous Pressure Waveform. The “a” wave is associated with atrial contraction. The “x” descent is the period following atrial emptying before the tricuspid valve closes (“c” wave). The “v” wave reflects ventricular contraction followed by the “y” descent as the right ventricle begins to fill during diastole. Courtesy of Hess DR, MacIntyre NR, Mishoe SC, Galvin WF and Adams AB.

Description

Pulmonary Artery Catheters Pulmonary artery (PA) catheters are sometimes placed in order to assess central venous (right atrial), right ventricular, pulmonary artery, and pulmonary capillary wedge pressures (PCWP).44 PA catheters can also be used to measure cardiac output and as a source for obtaining central venous blood samples. Specific indications for pulmonary artery catheterization include unexplained or unknown volume status in shock, severe cardiogenic shock, and known or suspected pulmonary artery hypertension. Pulmonary artery catheterization is also sometimes

performed in patients undergoing surgical procedures related to heart disease. Pulmonary artery catheter insertion may be helpful to assess the degree of pulmonary hypertension, cardiomyopathy, valvular disease, or vascular volume. With shock, assessment of PA pressures can help determine the type of shock present. Normal pulmonary artery systolic pressure (PASP) is 20 to 35 mmHg while normal pulmonary artery diastolic pressure (PADP) is 5 to 15 mmHg. Normal mean pulmonary artery pressure (MPAP) is 10 to 20 mmHg and normal pulmonary capillary wedge pressure (PCWP) is about 6 to 12 mmHg. Central venous blood gases may include the measurement of central venous oxygen content (Cv̄O2) and central venous oxygen tension (Pv̄O2) and allow for the calculation of the arterial venous oxygen content difference (CaO2 – Cv̄O2). PA catheters are inserted through the subclavian or external jugular vein and then guided to the right heart and then on to the pulmonary artery. The catheter continues to be advanced until the inflated balloon near the tip of the catheter can be wedged in the pulmonary artery (Figure 9-30). During placement, waveforms and pressures indicate the location of the catheter and help guide insertion (Figure 9-31). It is important that the catheter tip be positioned in the lung zone where pulmonary artery and venous pressures are greater than alveolar pressures (i.e., zone 3). This placement will allow the pulmonary capillary wedge pressure to reflect left atrial pressure.

FIGURE 9-30 Pulmonary Artery Catheter. The pulmonary artery catheter and its associated ports are used to

measure right atrial pressures (i.e., central venous pressures [CVP]), pulmonary artery pressures [PAP] (systolic, diastolic, and mean), and pulmonary capillary wedge pressure (PCWP). Cardiac output can be measured using the thermodilution technique based on temperature changes sensed at the thermistor tip following injection of saline.

Description

FIGURE 9-31 Pulmonary Artery Catheter Waveforms Seen During Catheter Insertion. During pulmonary catheter insertion, the catheter balloon is inflated, and the catheter is advanced to the right atrium (RA), right ventricle (RV), and pulmonary artery (PA) until the wedge position wave form is observed (PCWP). The catheter balloon is then deflated except when measurement of PCWP is needed. Modified from Longnecher D, Brown D, Newman M, Zapol W. Anesthesiology. New York, NY: McGraw-Hill. © 2007 The McGraw-Hill Companies, Inc. Used with permission of The McGraw-Hill Companies, Inc.

Description RC Insights CVP represents the right heart’s preload while PCWP represents the left heart’s preload.

Common causes for increased CVP, PAP, and PCWP include fluid overload, left ventricular failure, and cardiogenic shock. Hypovolemic shock will cause a decrease in CVP, PAP, and PCWP, while septic shock may cause a decrease in these pressures or these pressures may be within normal range. With ARDS, echocardiography or PCWP measurement may be used to verify that the pulmonary edema present is not entirely attributable to increased hydrostatic pressures. A PCWP < 18 mmHg is consistent with a diagnosis of ARDS, as opposed to congestive heart failure or fluid overload, in which PCWP will be elevated. It should be noted that ARDS and heart failure can occur in the same patient. Complications associated with pulmonary artery catheters include bleeding, pneumothorax, nerve injury, catheter malposition, arrhythmias, valve injury, ventricular injury, pulmonary infarction, and bloodstream infections. It is also important to always be sure that the catheter balloon is deflated except during measurement of PCWP. Because of cost and possible complications, routine use of pulmonary artery catheterization in the ICU has become much less common in recent years and many hemodynamic parameters can now be measured relatively noninvasively using bioimpedance, bioreactance, or ultrasound technology.

Cardiac Output/Index Cardiac output (Q̇T) provides a global measure of blood flow and is determined by stroke volume (SV) and heart rate (HR): Q̇T = HR × SV Stroke volume is determined by preload, afterload, and cardiac contractility. Preload is the filling pressure of the ventricles during diastole. Afterload is the resistance that the heart must pump against. Contractility is the strength with which the heart contracts during each beat. Normal adult cardiac output is 4 to 8 L/min, but this will vary based on the patient’s size. Cardiac index (CI) relates cardiac output to the patient’s body surface area (BSA) and allows comparison of smaller and larger sized patients where CI = Q̇T ÷ BSA. A normal CI is 2.5 to 4.0 L/min/m2.2,4 Measurement and monitoring of cardiac output is helpful in the management of hemodynamically unstable, critically ill patients. Measurement of cardiac output can guide fluid resuscitation and the use of inotropic medications. Measurement of

cardiac output in patients following severe traumatic injuries with blood loss, and those with sepsis can help guide treatment to optimize tissue oxygen delivery. Clinically, cardiac output may be measured using the thermodilution technique using a pulmonary artery catheter with a thermistor tip to sense temperature changes. With this technique, a bolus of saline is injected into a proximal port of the catheter and the temperature changes as the blood moves downstream and passes the thermistor at the tip of the catheter are recorded. Stroke volume is then calculated based on the volume under the temperature change curve and cardiac output calculated based on heart rate (Q̇T = HR × SV). Less-invasive methods to measure cardiac output include transpulmonary thermodilution, and lithium dilution cardiac output (LiDCO) analysis. Transpulmonary thermodilution calculates cardiac output using a method in which cold injectate is introduced via a central venous catheter and the resultant temperature change is quantified using a thermistor tipped arterial line in a large proximal artery, such as the femoral artery. Pulse contour analysis estimates stroke volume from the contour of the arterial pressure waveform. LiDCO is one form of pulse contour analysis for calculation of cardiac output; however, there are other pulse contour methods. Bioreactance/bioimpedance devices have been developed that measure the change in voltage across the thorax (i.e., phase shift), which occurs as the result of pulsatile blood flow through the aorta. For example, with the Cheetah system (Cheetah Medical, Newton Center, MA), four non-invasive sensor pads are applied to the thorax creating a “box” around the heart. A small electrical current is passed through the outer sensors and recorded by the inner sensors and the resultant signal change is used to calculate cardiac stroke volume. Echocardiography and the use of suprasternal Doppler provide two additional noninvasive methods for cardiac output estimation.

Cardiopulmonary Calculations A number of cardiopulmonary calculations may be completed that often provide insight into patients’ tissue oxygen delivery (ḊO2) and hemodynamic status. These include calculation of oxygen delivery to the tissues (ḊO2), oxygen tissue extraction ratio (O2 ER), and examination of mixed venous oxygen levels (Pv̄O2, Sv̄O2, Cv̄O2).

Other calculations provide information regarding oxygen transfer across the lung. These measures include the alveolar to arterial oxygen gradient (PAO2 – PaO2), alveolar to arterial oxygen ratio (PaO2/PAO2), and the arterial oxygen tension to oxygen concentration ratio (PaO2/FIO2). Box 9-5 summarizes important cardiopulmonary calculations. Chapter 2 (Respiratory Failure) provides additional information regarding the indices of oxygenation.

BOX 9-5 Cardiopulmonary Calculations Measures of Oxygen Transfer Across the Lung Alveolar versus Arterial Oxygen Levels A-a gradient or P (A-a) O2. A normal alveolar-arterial (A-a) oxygen difference for healthy young adults breathing room air is about 10 mmHg with a range of 5 to 15 mmHg. The A-a difference increases with age (normally) and with lung disease. Clinically, this can be used to understand if lung function is getting better or worse (when inspired oxygen levels are constant). A-a difference will vary as inspired oxygen varies. For example, while the normal A-a gradient while breathing room air is 10 mmHg, the normal A-a difference while breathing 100% oxygen increases to 80 to 120 mmHg. The A-a gradient is calculated by subtracting the PaO2 from the PAO2: A-a gradient = PAO2 – PaO2 PAO2 is calculated as: PAO2 = PIO2 – PACO2 (FIO2 + [1 – FIO2]/R) Where: PAO2 = Calculated alveolar oxygen tension (mmHg) PIO2 = Inspired oxygen tension (mmHg) = FIO2 (PB – PH2O) PACO2 = Alveolar carbon dioxide tension (mmHg) FIO2 = Fractional inspired oxygen concentration R = Respiratory quotient where R is V̇CO2/V̇O2 Clinically, PAO2 is calculated using the simplified alveolar air equation where: PAO2 = PIO2 – PaCO2/0.80 The a/A Ratio is calculated simply by dividing PaO2 by PAO2. Clinically, PaO2 is

obtained via an arterial blood gas study, while PAO2 is usually calculated using the alveolar air equation above. A normal a/A ratio while breathing room air is about 0.80 with a range of about 0.77 to 0.82. Unlike the A-a gradient, a/A ratio does not change significantly with increasing FIO2 and may be used to compare the patient’s condition as FIO2 changes. The P/F ratio is calculated simply by dividing PaO2 by FIO2. Normal PaO2/FIO2 is 380 to 500. PaO2/FIO2 ≤ 300 is one criterion for identification of ARDS, while severity of ARDS is then classified as mild, moderate, or severe based on PaO2/FIO2 values. Measures of Oxygen Delivery Mixed Venous Blood Gas Values Mixed venous blood gases are obtained from the analysis of a blood sample taken from the distal port of a pulmonary artery catheter (i.e., pulmonary artery). Normal mixed venous blood gas values are: ∎ Mixed venous oxygen tension (Pv̄O ): 35 to 40 mmHg. Pv̄O decreases with 2 2 decreased cardiac output, increased oxygen consumption, fever, hyperthermia, and arterial hypoxemia. Pv̄O2 increases increased cardiac output, decreased tissue oxygen consumption, skeletal muscle relaxation, hypothermia, and cyanide poisoning ∎ Mixed venous oxygen saturation (Sv̄O ): 70% to 75%. Sv̄O changes tend 2 2 to follow changes in Pv̄O2. ∎ Mixed venous oxygen content (Cv̄O ): 15 vol%. Cv̄O changes tend to 2 2 follow changes in Pv̄O2. Arterial Blood Gases, Mixed Venous Blood Gases, Oxygen Delivery, and Oxygen Extraction Ratio ∎ Oxygen delivery (V̇O ) is simply cardiac output times arterial oxygen 2 content: V̇O2 = Q̇T × CaO2 Arterial to venous oxygen content difference (CaO2 – Cv̄O2). Normal CaO2 – Cv̄O2 is 3.5 to 5 mL/dL. CaO2 – Cv̄O2 may increase with decreased cardiac output, increased tissue oxygen consumption, arterial hypoxemia, seizures, shivering in postop patients, and hyperthermia. CaO2 – Cv̄O2 may decrease with increased cardiac output, skeletal muscle relaxation due to sedatives, peripheral shunt, cyanide poisoning, and hypothermia. Oxygen extraction ratio (O2 ER). O2 ER is calculated by dividing the arterial to venous oxygen content difference by the arterial oxygen content:

O2 ER = (CaO2 – Cv̄O2) ÷ CaO2 Normal O2 ER is 0.25 to 0.30, which means that normally the tissues extract 25% to 30% of the available oxygen from the arterial blood. Measures of Ventilation Tidal Volume, Respiratory Rate, Minute Ventilation ∎ Tidal volume (VT). Normal adult VT is about 500 mL or about 7 mL/kg IBW with a range of 400 to 700 mL. ∎ Respiratory rate (f). Normal adult respiratory rate is about 12 to 18 or 20 breaths/min. ∎ Minute ventilation (V̇E). Normal adult minute ventilation (aka minute volume) is approximately 6 L/min with a range of about 5 to 10 L/min. If tidal volumes are consistent from breath to breath, minute ventilation may be calculated as follows: V̇E = VT × f Physiologic Dead Space ∎ Dead space to tidal volume ratio (VD/VT) may be calculated: VD/VT = (PaCO2 – PĒCO2) ÷ PaCO2 Normal VD/VT is 0.3 with a range of 0.20 to 0.40 (20% to 40% dead space ventilation), although it is not unusual to have a VD/VT up to 0.50 in mechanically ventilated patients with normal lungs Physiologic dead space (VD). Normal adult physiologic VD is about 150 mL or 20% to 40% of the tidal volume. Physiologic VD may be calculated as follows: VD = VD/VT × VT Alveolar Ventilation ∎ Alveolar ventilation (V̇A). Normal adult V̇A is about 4 to 5 L/min where: V̇A = (VT – VD) × f

Mechanical Circulatory Assistance Mechanical circulatory assist devices include the intra-aortic balloon pump (IABP), left ventricular assist devices (LVAD), right ventricular assist devices (RVAD), and biventricular assist devices (BiVAD).45 Total artificial heart devices are also available.

The primary purpose of mechanical circulatory assist devices is to improve cardiac output and end-organ perfusion in patients with severe heart failure. Increasingly, mechanical circulatory assist devices are used as a bridge to heart transplant or to provide time for the failing heart to recover. The IABP is a widely used circulatory assist device for short-term support in the critical care environment.46 IABP counterpulsation works by inserting a catheter with a 30- to 50-mL helium-filled balloon at its tip. The catheter is threaded into the aorta and the balloon is inflated during cardiac diastole and deflated during systole. This inflation and deflation cycle decreases aortic pressures during systole, increases pressures during diastole, and improves cardiac output. Specific indications for IABP include left ventricular failure (often following acute myocardial infarction), inadequate cardiac output following cardiac surgery, intractable angina, and as a bridge to additional therapy.46 IABP devices are often set up by perfusionists, but are routinely monitored by critical care nursing or respiratory care personnel. Respiratory care clinicians must be alert to the many complications associated with mechanical circulatory assist devices. Patients experiencing complications may develop dyspnea, tachypnea, hypoxemia, increased lactate levels, and decreased hemoglobin and hematocrit due to bleeding. Arrhythmias, hypotension, ventricular failure or dysfunction, and cardiac tamponade may develop. Other complications include pneumothorax, device failure, hemoptysis, hemolysis, chest pain, syncope, gastrointestinal bleeds, kidney failure, hematuria, infection, and stroke.

Other Assessment Parameters Other parameters that should be routinely monitored in patients receiving mechanical ventilatory support include vital signs (pulse, respirations, and temperature), mental status and neurologic function, pain assessment, kidney function and urine output, chest tube function and chest tube drainage, and nutritional status.

Assessment of the Mental Status and Neurologic Function Critical care patients often have compromised neurologic function and impaired mental status.47 Patients may be confused, delirious, lethargic, obtunded, stuporous, semicomatose, or comatose. These changes may be due to hypoxia, hypercarbia, acid-base disturbances, compromised cardiac output, shock, hypotension, sleep deprivation, and/or administration of sedatives, tranquilizers, or narcotics. Other sources of neurologic compromise include head trauma, seizures, strokes, traumatic brain injury, and other neurologic disease.47 Mental status assessment includes sensorium, level of consciousness (LOC), and orientation to person, place, time, and situation (i.e., oriented × 4). Neurologic assessment includes examination of reflexes, pupillary response, sensory function, motor assessment (e.g., symmetry of movement, motor weakness), evidence of seizures, and cerebellar function (e.g., have patient touch each fingertip to thumb tip in succession). Cough reflex can be assessed during suctioning. The Glasgow Coma Scale (GCS) is commonly used to assess changes in patients’ level of consciousness.48 Scores range from a low of 3 points, which suggests brain death, to a maximum total of 15, which indicates full consciousness. Other scoring systems to assess patients’ sedation and agitation are the Ramsay Sedation Scale and the Richmond Agitation-Sedation Scale. Chapters 2 and 8 provide additional information regarding assessment of patients’ cognitive and neurologic status.48

Pain Monitoring Patients in the intensive care unit may have suffered traumatic injury, surgery, or other painful medical procedures. Endotracheal intubation, insertion of invasive lines (e.g., IVs, CVP), insertion of chest tubes, urinary catheterization, airway suctioning,

arterial and venous puncture, thoracentesis, tracheostomy, mechanical ventilation, and bronchoscopy are all potential sources of pain. Inadequate pain control in the ICU may result in anxiety, tachypnea, tachycardia, increased oxygen consumption, and ventilator asynchrony (e.g., “fighting the ventilator”).49 Pain assessment may include physical assessment for the presence of grimacing, writhing, tachycardia, hypertension, tachypnea, or sweating.49 Patients may be asked rate their pain on a scale of 0 to 10, where 0 indicates no pain and 10 indicates the worst possible pain. The Behavioral Pain Scale (BPS) and the CriticalCare Pain Observation Tool (CPOT) provide two additional instruments for monitoring and evaluating patients’ pain.

Intracranial Pressure Monitoring Intracranial pressure (ICP) monitoring is commonly employed in the neurointensive care unit in patients with closed head injury. In addition to acute severe traumatic brain injury, ICP monitoring may be useful in patients with increased intracranial pressures due to other causes and patients with a reduced Glasgow Coma Scale score associated with severe brain injury (GCS ≤ 8). Normal ICP in the supine patient is about 10 to 15 mmHg. Elevated ICP may reduce cerebral blood flow and extremely high ICP will severely compromise cerebral perfusion. Techniques to reduce intracranial pressure include head elevation, hyperventilation (PaCO2 26 to 30 mmHg), intravenous mannitol or hypertonic saline infusion, and correction of the underlying cause. Hyperventilation can rapidly reduce ICP, but is not effective for more than 24 hours. Hyperventilation may be used emergently to lower ICP due to cerebral edema, intracranial hemorrhage, or tumor. As noted, its effect is short-lived, and hyperventilation should not be used for an extended period of time. Hyperventilation is generally not recommended in patients with acute stroke or traumatic brain injury, as the resulting vasoconstriction may decrease cerebral perfusion and worsen brain injury.

Renal Function and Urine Output Monitoring Kidney function tests include measurement of blood urea nitrogen (BUN) and serum creatinine and estimation of glomerular filtration rate (GFR). Urine output monitoring

provides a measure of patients’ fluid balance and kidney function. Most patients receiving mechanical ventilatory support have indwelling urinary catheters attached to a calibrated urine collection drainage system for monitoring urine output. Monitoring urine output can assist in the evaluation of renal function and acute kidney injury and guide fluid resuscitation.50–52 Normal adult urine output is about 0.5 mL/kg/day or about 60 mL/hour. Chapter 8 provides additional information regarding urine output monitoring and assessment of kidney function and fluid balance.

Dialysis Renal replacement therapy (RRT) is sometimes necessary for ICU patients with acute kidney injury (AKI) or chronic kidney disease. Renal replacement therapy may be accomplished using peritoneal dialysis, hemodialysis, or certain other techniques (e.g., hemofiltration). Clinical indications for urgent RRT include fluid overload (refractory to diuresis), severe metabolic acidosis (pH < 7.1), severely elevated potassium levels (> 6.5 mEq/L), signs of uremia (decline of mental status), and alcohol or drug intoxication. Early identification of patients likely to require RRT prior to the development of these urgent indications may improve outcomes. Ongoing assessment of electrolytes, pH, and renal function indicators such as BUN can be helpful in determining when therapy should be initiated.53

Chest Tubes, Drainage, and Management Chest drainage tubes are inserted into the pleural space to treat pleural effusions, pneumothorax, and hemothorax. Chest tubes are also sometimes placed following thoracic surgery. Chest tube insertion allows for the removal of air and fluid from the pleural space and the restoration of negative pleural pressures, in cases of pneumothorax. Chest tubes should be monitored for proper function, and volume and nature of drainage fluid. Chapter 8 provides additional information regarding assessment and management of chest drainage systems.

Temperature Monitoring and Regulation in the ICU Vital sign monitoring in the ICU includes measurement of body temperature, usually at least every 4 hours; unstable patients may require continuous invasive temperature monitoring.54–56 Fever may be caused by viral, bacterial, fungal, or

parasitic infection. History and physical exam, complete blood count (CBC), blood cultures, blood chemistries, urinalysis, and chest radiograph may be helpful in identifying the source of fever. In the ICU, fever may be caused by infection, sepsis, or ventilator-associated pneumonia.54–56 Other common causes of fever in the ICU include catheter-related bloodstream infection and surgical site wound infection. Other infectious causes include sinusitis, abdominal abscess, empyema, urinary tract infections, and endocarditis. Fever may also be caused by noninfectious inflammatory disease, postoperative fever, medication allergy, gallbladder inflammation, deep vein thrombosis, or malignancy. Hyperthermia (as opposed to fever) may be caused by excessive heat production or inadequate heat dissipation. Hypothermia may be caused by exposure to environmental cold.

Therapeutic Hypothermia Neurologic injury sometimes occurs following cardiac arrest and resuscitation. Development of fever in these patients is associated with poorer neurologic outcomes and temperature management has been suggested. Therapeutic hypothermia (TH) employs a cooling device with a feedback mechanism to control the patient’s core body temperature. In patients with signs of cerebral edema, deep coma, or a malignant EEG pattern, body temperature may be lowered to 32° C to 36° C for 24 hours, followed by gradual rewarming (0.25° C/hour). It should be noted that TH may cause a mild coagulopathy, and patients should be observed for signs of bleeding. TH has also been associated with increased risk of infection if it is extended beyond 24 hours. Finally, cold diuresis may result in excessive urine output leading to hypovolemia or serum electrolyte abnormalities.57

Nutritional Support Patients in the ICU are often malnourished and may be in a catabolic stress state. Nutritional assessment in the ICU should include determination of nutritional risk using a standardized assessment tool such as the Nutritional Risk Screening 2002 (NRS 2002) or the Nutrition Risk in Critically Ill Score (NUTRIC). In the ICU, ventilated patients are occasionally assessed using a metabolic cart for measurement of oxygen consumption (V̇O2), carbon dioxide production (V̇CO2), and resting energy expenditure (REE) to determine energy requirements. For example,

resting energy expenditure can be significantly increased in burn patients, sepsis, trauma, and following major surgery. REE measurement can help avoid over- or underfeeding. Nutritional support should ensure the appropriate delivery of calories, protein, electrolytes, vitamins, minerals, trace elements, and fluids to meet the patient’s needs.58 Enteral nutrition may be provided through a feeding to tube through the mouth or nose into the stomach or small bowel. Percutaneous endoscopic gastrostomy (PEG) tubes may be used to provide nutritional support in patients with stroke, head and neck cancer, brain injury, or other neurologic disorders. The PEG feeding tube is inserted through the abdominal wall and into the stomach using endoscopy. Providing enteral feeding early in the course of critical illness may be beneficial. Enteral nutrition should be avoided in patients who are hemodynamically unstable and those with gastrointestinal disease. Complications of enteral nutrition include constipation, diarrhea, abdominal distention, vomiting, and regurgitation. Parenteral nutrition may be necessary in cases where enteral nutrition is contraindicated. Parenteral nutrition is provided intravenously. Complications of parenteral nutrition include catheter occlusion, catheter-related infections, and hyperglycemia. Refeeding syndrome may occur in patients in which nutritional support is provided to malnourished patients following a period of severe nutritional deprivation. Refeeding syndrome may result in neurologic complications and cardiac failure. Chapter 2 (Respiratory Failure) provides additional information regarding nutritional assessment.

Managing and Monitoring the Patient Airway Assessing and monitoring the patient’s airway in the ICU is an interdisciplinary responsibility. Many patients require an artificial airway to allow for positive-pressure ventilation and maintain airway patency. Airway management, such as endotracheal intubation, may be required in the presence of upper airway obstruction, sedative/narcotic overdose, reduced or absent ventilatory drive, respiratory failure, cardiac arrest, and reduced levels of consciousness.4 Nasopharyngeal or oropharyngeal airways may be helpful in certain patients with soft-tissue obstruction; however, pharyngeal airways do little to protect the lower airway. Endotracheal intubation provides a secure and patent airway, protects the lower airway, and is required to provide invasive mechanical ventilatory support. Emergency cricothyroidotomy may be required in rare circumstances (e.g., complete airway obstruction) when oral or nasotracheal intubation is unsuccessful or contraindicated. A tracheostomy tube may be placed in patients that will require an artificial airway for an extended period of time (most often > 14 days; however, earlier procedures are often considered in select subgroups) and to improve patient comfort, reduce the need for sedation, facilitate suctioning, decrease work of breathing, and (perhaps) facilitate weaning from the ventilator. Endotracheal tubes (ETT) are placed to ensure ventilation and prevent aspiration.60 Specific indications where emergency intubation may be required include cardiac arrest, persistent apnea, and upper airway obstruction. Upper airway obstruction (including laryngeal obstruction) may be caused by angioedema, infection (e.g., epiglottitis, abscess), and laryngeal edema. Massive upper airway bleeding, massive hemoptysis, or traumatic upper airway obstruction may also require emergency intubation. Coma or reduced/absent airway protective reflexes and inability to protect the airway from aspiration provide clear indications for endotracheal intubation.64 Endotracheal tubes are usually inserted using a laryngoscope to visualize the epiglottis, glottis, and vocal cords when placing the tube. A number of airway assessment tools have been suggested to evaluate the patient’s airway prior to intubation. These include oropharyngeal examination of the tongue, hard palate, soft palate, uvula, and posterior pharynx; and visualization of airway structures during direct laryngoscopy (e.g., modified Mallampati Difficulty Classification). The inability

to visualize specific anatomic structures upon oropharyngeal examination or direct laryngoscopy can be predictive of a difficult intubation.64 Endotracheal intubation is required prior to initiation of invasive mechanical ventilation. Occasionally, accidental premature extubation in patients receiving mechanical ventilatory support occurs requiring prompt and successful reintubation. To perform endotracheal intubation using direct laryngoscopy, the appropriate equipment, supplies, and medications are gathered, and the airway is assessed. The patient is prepared, positioned, and preoxygenated with 100% oxygen using a bagvalve mask system with a PEEP valve. The patient’s mouth is opened, and the laryngoscope is introduced and advanced until the epiglottis and glottis can be visualized. The tube is guided to the glottis and inserted through the vocal cords into the trachea. Once passed through the cords to an appropriate depth, the ETT is secured, with tape or a commercial tube-holding device. Generally, an initial ETT placement marking of 21 cm at the teeth (adult females) or 23 cm (adult males) is acceptable. Immediately following intubation, spontaneous or mechanically supported (i.e., ventilator or manual resuscitator bag) breath sounds should be assessed and proper tube placement verified by capnometry.67 Equal and bilateral breath sounds should be confirmed by auscultating the patient’s chest. Clinical Focus 9-3 reviews key points regarding endotracheal intubation.

CLINICAL FOCUS 9-3 Endotracheal Intubation Endotracheal intubation may be required to protect the airway, particularly in patients who are unconscious or obtunded. Endotracheal intubation may also be indicated to relieve upper airway obstruction, facilitate suctioning, and provide mechanical ventilatory support. Endotracheal intubation should be performed by the most qualified and experienced personnel available. Respiratory therapists are often called upon to perform nonelective intubations such as following a cardiac or respiratory arrest. As with any procedure, an organized, stepwise approach should be used. Emergent intubations performed during cardiac resuscitation are often hurried, and the patient’s airway is sometimes obstructed with vomitus or other material. In these situations, suctioning of the airway prior to intubation is almost always required. If the patient does vomit, always turn the head to the side and clear the airway immediately to avoid aspiration. With elective intubations the situation is

more controlled, vomiting is less likely, and preprocedure medications may be used to sedate (e.g., etomidate [Amidate], ketamine [Ketalar], or midazolam [Versed]) and briefly paralyze (e.g., succinylcholine [Anectine]) the patient. Prior to performing an endotracheal intubation, the patient should be assessed for characteristics associated with a difficult airway. Exceptions to this rule are cases where intubation cannot be delayed or avoided (e.g., “crash” airway seen during cardiac arrest). The LEMON approach for airway assessment includes Looking for unusual anatomy; Evaluating the ease of access to the airway, volume of space below the mandible and location of the larynx relative to the base of the tongue; calculating the Mallampati score to predict difficult intubation; noting the presence of Obstruction or obesity; and observing for Neck mobility. Equipment needed to perform endotracheal intubation in adults using direct laryngoscopy includes a manual resuscitator bag with oxygen source and appropriate adapters, suctioning equipment to include suction catheters and Yankauer suction tip, monitoring equipment (blood pressure, pulse oximeter, cardiac monitor, capnography), oropharyngeal airway and nasopharyngeal airway, intravenous access, and appropriate medications for intubation (induction agents, neuromuscular-blocking agents, and emergency medications). Equipment needed to perform laryngoscopy and intubation includes the laryngoscope handle and assorted blades, a selection of endotracheal tubes, sterile lubricant, 10-mL syringe to inflate the cuff, endotracheal tube holder, tape, and carbon dioxide monitoring system to ensure tracheal placement. Video laryngoscopes are now in common use at many institutions, and they may be especially useful when a difficult intubation is anticipated. Oral intubation can sometimes be facilitated by use of a stylet or endotracheal tube introducer (e.g., gum bougie). If intubation fails, a laryngeal mask airway (LMA) or similar rescue airway may be needed. The laryngoscope blade of choice is an individual decision based on personal experience. There are several types of curved and straight blades, including the Macintosh (curved), Miller (straight), and Wisconsin blades (straight). Always check the lightbulb to ensure it works and that the bulb is not loose. Inspect the endotracheal tube and inflate the cuff to ensure that it is functional. Be sure the 15-mm adapter is properly connected. The manual resuscitator must be functional; check to make sure it works. All of the equipment should be arranged within arm’s reach including additional endotracheal tubes. Patient positioning is critical. Place the patient in the sniffing position without hyperextension. A rolledup towel or small pillow under the patient’s head may help. Suction the mouth and oral cavity and preoxygenate the patient. Standing behind the bed, the approach with the laryngoscope blade is made using the left hand to hold the laryngoscope while the right thumb is at the front

teeth with the forefinger underneath the chin. This prevents the blade from hitting the teeth at entry and also prevents using the teeth as a fulcrum during the procedure. The wrist and arm should form a stationary axis and be used as a single, unhinged unit. Flexion of the arm and wrist will increase the risk of trauma and poor visualization. Use of the biceps and shoulder will reduce the risk of trauma and enhance visualization of the cords. The laryngoscope blade is then introduced orally deflecting the tongue and soft tissue to the left side of the mouth with the flange of the blade. The blade is advanced until the epiglottis and glottis are visualized. Following visualization of the glottis, the endotracheal tube should be introduced carefully beginning on the right side of the mouth and then advanced with care. The tube should be passed through the glottis, larynx, and into the trachea. Never force the tube into place. The tip of the tube should reside in the middle one-third of the trachea, 3 to 5 cm above the carina (or at least 2 cm above the carina). Proper placement for the average adult is about 20 to 21 cm for women and 22 to 23 cm for men at the front incisors. Following tube placement, inflate the cuff and auscultate the right and left sides of the anterior chest to ensure adequate ventilation during manual inflation using the manual resuscitator. Confirm proper tube placement via capnography or other CO2-sensing system. Once you have confirmed good bilateral breath sounds and CO2 is detected, secure the tube with an endotracheal tube holder or tape. If tape is used, a bite block or oropharyngeal airway should be placed so that the patient cannot bite down on the endotracheal tube. Be aware that oropharyngeal airways are designed to be used with unresponsive patients and may solicit gagging in the semi-alert or conscious patient. Note the tube’s position and depth in centimeters (cm) at the patient’s front incisors and record this information in the medical record and on the patient’s bedside flow chart. Proper tube placement should be confirmed via a chest radiograph. Following successful intubation, reassess the patient (heart rate, blood pressure, SpO2, cardiac monitor) and initiate appropriate respiratory care. This may include mechanical ventilatory support in patients with inadequate ventilation. Spontaneously breathing patients may be placed on a T-piece and air entrainment nebulizer with an appropriate oxygen concentration.

RC Insights Assessment of the airway for intubation may include application of the 3–3–2 rule. A difficult airway may be present if the one or more of the following are present: patient’s mouth cannot be opened to permit placement of three fingers between the upper and lower teeth, three fingers do not fit under the chin between the tip of the jaw and the beginning of the neck, or there is not space for two fingers between the thyroid notch and the floor of the mandible.

Various technology is available for measuring end-tidal carbon dioxide (PETCO2) following intubation to assure proper tube placement. Assessment for the presence of exhaled CO2 is the most accurate method to confirm successful tracheal intubation, except in cases of cardiac arrest. Capnography devices range from sophisticated PETCO2 monitors to simple colormetric measurement devices. As a point of reference, normal PETCO2 values should represent alveolar and arterial PCO2 and normally range from about 35 to 45 mmHg (or within 0 to 5 mmHg of the patient’s PaCO2 levels). Colormetric devices change colors based on exhaled CO2 levels. For example, purple may indicate PETCO2 < 3 mmHg while yellow may indicate PETCO2 > 15 mmHg. Many factors can influence PETCO2, and these should be taken into account when assessing measured values. Measurement of exhaled CO2 for confirmation of proper ETT placement should include at least six consecutive expiratory gas samples with consistent expiratory CO2 levels. Following verification of proper position, the ETT should be secured with tape or a commercially available ETT holder. Portable chest x-rays are extremely useful in the ICU for monitoring and assessing the position of invasive lines and tubes, and identifying specific problems and issues.59,60 Following endotracheal intubation, it is recommended that a chest x-ray be obtained to verify proper tube position. Bedside ultrasound may also prove to be valuable in assessing proper endotracheal tube position by confirming ventilation of both lungs and ruling out bronchial intubation.60 In an adult patient, the distal tip of the ETT should be at least 2 to 3 cm above the carina (range: 2 to 6 cm above the carina). The carina should be approximately between the fifth and seventh thoracic vertebrae. If the carina is not visible on the chest x-ray, an alternative is to verify the tip of the tube is approximately at the level of the aortic knob. To prevent inadvertent extubation or mainstem intubation, the tip of the ET should be positioned midway between the carina and bottom border of the larynx. Modern endotracheal tubes are marked with centimeter distance markers that can be used to record the tube’s insertion depth. As noted, the recommended adult ETT insertion depth is about 21 cm in females and about 23 cm in males.60 This distance is measured from the incisors at the midline. When an ETT is inserted too far, it typically enters the right mainstem bronchus. Right mainstem intubation

may cause hyperinflation of the ventilated (right) lung and deflation and atelectasis of the left lung.60 Once proper ETT position is confirmed it is imperative that the position be noted and documented in the medical record.60 A major complication of endotracheal intubation is inadvertent placement of the tube into the esophagus (i.e., esophageal intubation). This should be immediately suspected if breath sounds are absent when providing ventilatory support via manual resuscitator bag and expired CO2 is absent. With inadvertent esophageal intubation, there will usually be a rapid and serious decline in the patient’s condition; if the situation is not quickly corrected cardiac arrest may occur. In addition to breath sounds and PETCO2 measurement to assess for ETT placement, auscultation over the abdomen may be performed during application of positive pressure via manual resuscitator bag.60 Esophageal intubation may be detected by the presence of sounds of gas movement while auscultating over the stomach while squeezing the resuscitator bag. As noted above, following cardiac arrest, PETCO2 may be absent, making verification of proper ETT placement more difficult. Esophageal detector devices are available and may be of value for verification of tube placement in the presence of cardiac arrest. These devices use a squeeze bulb or syringe to apply vacuum to the ETT connection. With successful tracheal intubation, the bulb or syringe refills easily, while a slow or difficult refill indicates possible esophageal intubation.64 If it is difficult to provide positive-pressure breaths once the ETT is in position, decreased airway patency may be the cause. This may be caused by kinks, blockages, or obstruction of the ETT. For example, patients may bite down on the tube and cause obstruction, or the tube may become partially or fully occluded with secretions. Bite blocks or an oropharyngeal airway may be inserted to prevent patients from biting down on the tube. Newer ETT holders often incorporate a bite block. A flexible suction catheter may be inserted to verify ETT patency and remove secretions. In order to avoid accidental extubation or inadvertent bronchial intubation, it is important that the ETT be properly secured.64 In the past, ETTs were often secured using medical adhesive tape; however, there are many commercially available devices that can be used to secure the tube. The ICU environment can pose challenges to ensure ETT stability. As the patient turns or is repositioned, or as the

ventilator circuit is repositioned, the ETT may be dislodged, resulting in accidental extubation. The ETT may also be inadvertently pushed farther down the airway, resulting in bronchial intubation.64 Intubated patients with free hands will often reach for the endotracheal tube and, if successful in grasping it, extubate themselves. Occasionally, personnel will move the ventilator, the bed, or the patient not realizing that the patient and the endotracheal tube are connected to the ventilator via the ventilator circuit. It is important to keep the ventilator circuit positioned in such a way to avoid pulling on the artificial airway, particularly when moving the patient, bed, or ventilator.64

Endotracheal Tube Characteristics Modern endotracheal tubes are made of polyvinyl chloride (PVC) and have been implantation tested to ensure that they do not react with tissue.64 This PVC material makes the ETT strong enough to be inserted without a stylet, although a rigid stylet inserted into the tube may be used to hold the tube’s shape and ensure passage of the ETT. Once inserted, the tube’s material will become softer as it is exposed to the warm, moist environment of the airway.64 Endotracheal tubes have a radiopaque line to allow them to be visualized on radiography.64 ETT size should be based on patient size, and the largest diameter tube that can be easily inserted should be used in order to facilitate suctioning and reduce airway resistance. Typical adult tube sizes used range from 7.0 to 7.5 mm inner diameter (ID) (females) and 8.0 to 8.5 mm ID (males). Smaller diameter endotracheal tubes (< 7 mm in adults) can significantly increase airway resistance and imposed work of breathing. Figure 9-32 illustrates a typical 8-mm ID oral/nasal ETT.

FIGURE 9-32 Intubation Equipment (A) Laryngoscopes. (B) Adult endotracheal tube. (C1) and (C2) Tube cuff pressure monitoring systems. (A) © Jones & Bartlett Learning. Courtesy of MIEMSS; (B) © YJPTO/Shutterstock; (C) Courtesy of Posey Company.

Description Some ETTs are designed to reduce the likelihood of ventilator-associated pneumonia (VAP). VAP occurs in up to 15% of patients receiving mechanical ventilation and is a serious cause of increased morbidity and mortality and generally develops 48 to 72 hours after endotracheal intubation.61 ETTs with subglottic secretion removal ports help to reduce secretion accumulation above the cuff. ETTs lined with an antimicrobial silver coating may have beneficial effects by blocking the formation of a bacterial biofilm on the surface of the tube.62 Other strategies to avoid the development of VAP include use of noninvasive ventilation or a high-flow nasal cannula (to avoid endotracheal intubation), minimal sedation, early mobility, elevation of the head of the bed, and proper ventilator circuit maintenance. Additional modifications of ETT design have been introduced to solve specific problems. The anode tube is reinforced with steel wire within the wall of the tube itself and can prevent the tube from kinking.64 Double-lumen tubes have been developed for selective bronchial intubation and can be used during certain surgical procedures and for independent lung ventilation (Figure 9-33).64

FIGURE 9-33 Double-Lumen Endotracheal Tube. (A) © 2018 Medtronic. All rights reserved. Used with the permission of Medtronic.

In the event of an ETT cuff leak or faulty pilot balloon, the ETT may need to be exchanged. When this occurs, clinicians are faced with the challenge of safely exchanging the tube without causing harm to the patient. This can be done by direct laryngoscopy, visualization by use of a video laryngoscope, or a tube exchanger. Tube exchangers are designed to aid in the placement of an ETT without the use of a laryngoscope. Whenever a decision is made to exchange an ETT, experienced clinicians in airway management should be present.

Cuff Pressure and Volume Monitoring of endotracheal tube intracuff pressure is performed routinely in intubated patients in order to prevent complications associated with high pressures exerted against the tracheal wall mucosa.63 Most cuffs used today are high-volume, lowpressure cuffs to avoid cuff pressures impeding tracheal wall blood flow and causing tracheal mucosa necrosis or other complications associated with high cuff pressures.64 Intracuff pressures are maintained between 20 to 30 cm H2O, with 30 cm H2O being the maximum pressure recommended.64 This pressure is generally enough to seal the airway and decrease the risk of aspiration of secretions. Maintaining pressures greater than 30 cm H2O may increase the risk of tracheal tissue ischemia.64 If the pressure against the tracheal wall exceeds the capillary perfusion pressure (25 to 35 mmHg) tracheal tissue damage may result. High pressures against the tracheal wall can cause tracheal stenosis, tracheal malacia, and tracheoesophageal fistula.63,64 When small ETTs (≤ 7.0 mm ID) are placed in larger adults, a higher-than-recommended cuff pressure may be required to seal the airway. The lowest cuff pressure needed to provide a seal and prevent aspiration of secretions should be used. The volume of air needed to inflate the cuff and maintain an effective airway seal varies, depending on ETT, patient size, and airway anatomy.63 ETT cuff pressures are measured by devices that allow for simultaneous pressure adjustment. Other techniques sometimes used to manage ETT cuffs include minimal

occluding volume (MOV) and minimal leak technique (MLT). For MOV, only enough volume is inserted into the ETT cuff to achieve a complete seal of the airway at the ventilator’s peak inspiratory pressure (PIP). MOV is achieved by inflating the cuff while listening for a leak at PIP during positive-pressure ventilation; just enough air is added to seal the leak.64 With MLT, the cuff is inflated to a volume that allows a small leak to occur at end inspiration during a positive-pressure breath. To determine volumes using MLT and MOV, it is necessary to auscultate over the neck; concerns remain about the possibility of aspiration.64 That said, intracuff pressure monitoring to ensure the cuff pressure of 25 cm H2O may be effective in preventing aspiration.

Managing the Artificial Airway While the gold standard for securing and protecting the airway is the ETT, other methods and appliances include oropharyngeal airways, nasopharyngeal airways, and laryngeal mask airways (Figure 9-34).

FIGURE 9-34 (A) Oropharyngeal Airways. (B) Nasopharyngeal Airways. (C) Laryngeal Mask Airways. (A) © Praisaeng/iStock / Getty Images Plus; (B) © Michael Pervak/ Shutterstock; (C) Courtesy of LMA North America, Inc.

Oropharyngeal airways (OPA) are useful to treat or prevent soft-tissue obstruction and ensure airway patency in patients with reduced or absent gag reflex. They are made of plastic and are rigid in their design, making them optimal for use in maintaining a patent airway and preventing patients from biting down on endotracheal tubes. The OPA has three parts to its design: the flange, body, and air channel.64 The flange prevents the OPA from being inserted too deeply into the patient’s airway. This is a major concern in edentulous patients. The body of the OPA lies distal to the flange. The air channel allows for air movement.64 Oropharyngeal airways are mainly used in unconscious or sedated patients with no gag reflex. Semiconscious or awake patients may gag on the device, which may cause aspiration of gastric contents.64 This device is often used during manual bagvalve mask ventilation to keep the airway patent and allow for adequate ventilation. It is important to insert a properly sized OPA. To assure a proper size, hold the device against the patient’s cheek, with the curvature pointed downward and the flange at the corner of the patient’s mouth (Figure 9-35). The tip of the OPA should not extend further than the patient’s angle of the jaw. If the device is too long or extends past the jaw angle, the tip could occlude the patient’s airway and also stimulate a gag reflex. If the device is too small, it can push the tongue posteriorly into the oropharynx, creating an airway obstruction. Prior to inserting this device, ensure that it is the proper size to avoid further airway compromise.64

FIGURE 9-35 Oropharyngeal Airway (OPA) Insertion. (A) © Jones & Bartlett Learning. Courtesy of MIEMSS.

The nasopharyngeal airway (NPA) may be considered when an oropharyngeal airway is contraindicated or impractical (Figure 9-36). The NPA is inserted in either nare and advanced until the distal tip sits the behind the tongue, above the epiglottis. These devices are not as rigid as an OPA; however, they too have a flange that prevents the device from being inserted too far into the nose. Like the OPA, proper measurement is key to patient comfort and effectiveness. NPA length is measured from the nare to the tragus of the same ear (i.e., right nare to tragus of right ear or left nare to left tragus). Patients who may benefit from an NPA include those who are conscious, have an intact gag reflex, or have the inability to open their mouth.64

FIGURE 9-36 Nasopharyngeal Airway (NPA) Insertion. © AB Forces News Collection / Alamy Stock Photo.

Description The laryngeal mask airway (LMA) is a supraglottic ventilatory device that does not pass through to the vocal cords (Figure 9-37). Designed primarily for the operating room for surgical procedures in short duration, it has become more popular in the emergency setting as an important accessory for the difficult to manage airway.67 Manual ventilation (e.g., bag-valve resuscitator bag) can be accomplished with an LMA, and use of the LMA may reduce the likelihood of inadvertent gastric insufflation. LMAs can be inserted with relative ease and with relatively little training. While LMAs are useful in emergencies and for some elective procedures, they should not be considered for longer-term use.64

FIGURE 9-37 Methods for Securing the Airway. (A) Endotracheal intubation with a curved blade. (B) Endotracheal intubation with a straight blade. (C) Endotracheal intubation using Magill forceps. (D) through (I) Insertion technique for laryngeal mask airway. Courtesy of LMA North America, Inc.

Description Description The ETT remains the preferred method for securing the airway for most critically ill patients requiring mechanical ventilatory support. Endotracheal intubation is not a benign procedure; risks and complications must be considered. All equipment should be carefully checked for proper function prior to the intubation procedure. Equipment failure once the procedure has begun can be harmful to the patient. Prior to the intubation, the patient should be assessed. If possible, determine if there is a prior history of difficult intubation. Once the assessment is complete and the equipment prepared and checked, the intubator should position him or herself at the head of the bed with enough room to perform the procedure without physical interference. The person performing the procedure should also ensure all needed equipment (suction, ETCO2 device, laryngoscope, etc.) is within easy reach. The bed should be raised to an appropriate height for the person performing the procedure. The patient is then positioned (supine) with the head in the sniffing position (neck slightly extended and tilted). Sedation and/or neuromuscular-blocking agents may be necessary to facilitate intubation; however, apneic patients will generally not require sedation/paralysis. When considering sedation and neuromuscular blockade for intubation, the clinician should be on the alert for additional hazards, including unwanted changes in cardiac rhythm and blood pressure. Further, paralyzing a patient can complicate the procedure, especially if the intubation is difficult. Box 9-6 describes the steps for endotracheal intubation.

BOX 9-6 Endotracheal Intubation The steps needed to perform oral endotracheal intubation follow. STEP

SKILL

KEY POINTS

1

Gather correct equipment and supplies.

a. Equipment should include: laryngoscope and blades, stylet, Magill forceps, bite block, 10-cc

syringe, tape, hemostat, sterile 4 × 4s, E/T tubes, sterile lubricant, CO2-sensing device. Have suction on and ready. Have several ETT sizes available in duplicate. Video laryngoscopes are now in common use in many facilities. 2

Inspect and check functionality of all equipment.

a. Ensure laryngoscope batteries are charged and the bulbs of the blades are functional by attaching and locking blade at a 90-degree angle to handle. b. Check bulbs to ensure they are tight. c. Ensure selected ETT is functional by inflating its cuff fully, connect all adapters, 15 mm and valve (if applicable), and visually inspect tube to ensure patency.

3

Prepare for intubation.

a. Arrange equipment at the bedside table within easy reach. If a stylet is to be used, it should be placed within E/T tube, but not to extend out the distal end. Bend the stylet over at proximal end to prevent forward movement. b. Have suction on with a Yankauer suction tip or catheter connected. c. Aspirate cuff to fully deflate it, have syringe ready to reinflate cuff.

4

Preoxygenate and ventilate the apneic patient as necessary.

a. All patients should be preoxygenated prior to tube insertion. Patients breathing spontaneously should receive oxygen via partial or nonbreather mask. Patients who are already having respirations augmented should be on supplemental oxygen prior to ETT insertion.

5

Position the patient (supine position).

a. It is essential to establish as straight a line as possible between mouth and glottis to facilitate intubation of the larynx via oral intubation. Flexion of the cervical spine and extension at the atlantooccipital joint facilitates this. The patient’s head should be at a level above the shoulders by placing it on a firm pad or pillow at about a 4-inch elevation (sniffing position). Place your right hand at the back of the head extending the head and neck at the junction of the spine and skull. THIS IS NOT HYPEREXTENSION. Maintain oxygenation. Manually ventilate if patient is apneic.

6

Initial insertion of the blade (straight blade).

a. The laryngoscope is held in the LEFT hand. The right hand is used to open the jaw widely for introduction of the blade and to protect the lips from being wedged between teeth and blade. • The use of adhesive tape or a plastic shield over the upper incisors can help prevent damage. DO NOT TOUCH THE TEETH with the b. laryngoscope blade. c. The blade is introduced at the right side of the mouth, the blade tip moving forward parallel to the right side of the tongue while sweeping the blade

toward the left moving the tongue with it. The blade is advanced until the epiglottis is visualized. 7

Visualization (straight blade).

a. At this point, your wrist and arm should become fixed and no longer act as an axis but as a single unit. This prevents trauma by avoiding using the upper teeth as a fulcrum. The tip of the straight blade is advanced to a position beneath the tip of the epiglottis to expose the glottis. b. Pressing lightly downward over the patient’s thyroid cartilage may help to visualize the glottis. • Too deep of an insertion of the blade will result in elevation of the entire larynx and esophagus visualization. c. Lift the left hand upward and forward to expose the glottis.

8

Use curved blade.

a. The blade’s tip rests in the vallecula indirectly lifting the epiglottis. In some cases, only the arytenoids will be seen if the larynx is anterior. The use of stylet with Magill forceps will help direct the tube anteriorly.

9

Tube placement.

a. The tube is held in the right hand with its concavity directed laterally passing to the right of the tongue to that point where the cuff just disappears beyond the vocal cords. • Sometimes the tube must be rotated during introduction, but it is always returned to its forward position (natural curve of tube pointed anteriorly) once within the larynx. b. Remove the blade. Do not touch the teeth. c. MAXIMUM TOTAL TIME = 40 SECONDS. If not successful, resume oxygenation/ventilation until the patient is stable, then repeat Steps 6 to 9.

10

Assess tube location (time allowed for cuff inflation and auscultation = 5 seconds).

a. b. c. d. e. f.

g.

h.

The cuff is inflated with 6 to 8 cm3 of air. The chest is observed for bilateral movement. Ventilate with oxygen. Anterior auscultation bilaterally with a stethoscope should follow. Tube position should be further confirmed using a CO2 detection device. Absence of breath sounds indicates possible esophageal intubation while unilateral breath sounds (typically right side) indicate a mainstem intubation. If the tube is in the esophagus, listening over the stomach while manually ventilating may reveal entry of air into the stomach as the bag is compressed. Extubate immediately, oxygenate and ventilate and then reattempt insertion. If mainstem intubation has occurred, manually ventilate with high FIO2 then deflate cuff and withdraw tube while auscultating until bilateral breath sounds are heard.

i. Chronic coughing following intubation may be due to the tip of E/T touching the carina. j. If compliance as determined by manual ventilation seems poor and/or does not relate to disease (i.e., pulmonary edema, ARDS, restrictive lung disease, pneumothorax), suspect problems with tube placement. 11

Complete tube placement.

a. Maintain oxygenation and ventilation manually. b. Mark ETT at incisors and secure with tape (note distance marker) or ETT holder. Notation of tube depth will facilitate future assessment of the tube’s position in reference to the carina. c. The ETT should always be secured to upper lip (not jaw) line to prevent movement of the tube with the opening and closing of the mouth. d. Use of a bite block (not airway) will insure patency. Patients who require an artificial airway may seize or bite down. Use of a bite block will prevent occlusion of the ETT. e. Order chest x-ray to confirm tube position. Never assume the presence of bilateral breath sounds guarantees proper tube placement. The chest film will confirm placement and aids in determining whether adjustment in tube position is needed for insertion or withdrawal of the E/T tube. The tip should be at approximately T-4 or about 4 to 5 cm above the carina.

12

Gather equipment to secure the tube.

a. 1-inch-wide cloth tape, bit block, tincture of benzoin. b. ETT holder, Velcro straps.

13

Secure the tube.

a. Movement of the ETT must be prevented once placement is complete. Using a single piece of 1inch wide cloth, tape around the head, below the ears, which will secure the ETT. b. The tape should be back to back as it passes in back of the head so that it does not stick to the patient’s hair. c. Apply tincture of benzoin to the face to improve bonding to the skin. d. At the lip line, each end is split. e. The corners of the mouth can be protected by creasing the tape at that point. f. A bite block is inserted. g. The tape itself has its upper half wrapped around the E/T tube several times. h. The very end of the tape is folded to facilitate removal. i. A commercially available ETT holder may be used in place of tape.

ETT, endotracheal tube.

Tracheostomy Tubes Tracheostomy tubes are artificial airways that can be surgically placed at the bedside (usually in an ICU) or in the operating room (OR). Like endotracheal tubes, tracheostomy tubes must be made of material that is quality tested and does not react adversely with human tissue. Sizes range from 2.5 to 11.5 internal diameter (ID). For most tracheostomy tubes, ID and outer diameter (OD) are provided as a guide for the user. Tracheostomy tube shapes vary, but typically mimic the anatomy of the airway. An open surgical tracheostomy is a procedure that is typically performed in the operating room (OR), while a percutaneous tracheostomy may be performed at the bedside, typically in the ICU. In the ICU, for patients who are mechanically ventilated, the procedure can be done with a local anesthetic, using appropriate sedation and analgesic control. In the OR, the procedure is usually performed using general anesthesia. Whether at the bedside or in the OR, the field of operation is isolated and cleansed. The surgical tracheostomy is generally performed in the region of the second to fourth tracheal cartilages while a percutaneous tracheostomy is done between the first and second or second and third tracheal cartilages. If there is an existing ETT in place, it is retracted and removed as the tracheostomy tube is inserted. Not until about 2 weeks after insertion is the stoma considered mature. Because of this, special care should be taken to reduce the likelihood of accidental decannulation. If this were to occur, it may be difficult to reinsert the tracheostomy tube. In the event that reinsertion is difficult or takes additional time, oral intubation may be necessary.64 There are a number of different types of tracheostomy tubes (Figures 9-38, 9-39 and 9-40), a few of which are described below:64

FIGURE 9-38 Standard Cuffed Tracheostomy Tube. Courtesy of Dean Hess.

FIGURE 9-39 Tracheostomy Tubes. (A) Trach tube with foam cuff. (B) Fenestrated tracheostomy tube. (A) Courtesy of Smiths Medical; (B) Courtesy of Pulmodyne.

Description

FIGURE 9-40 Metal Tracheostomy Tube. Courtesy of the Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins Medicine.

Metal tracheostomy tubes (Jackson Trach Tube): Named after laryngology pioneer, Chevalier Jackson, these silver tracheostomy tubes were once held as the standard for relieving airway obstruction. While popular in the past for its advantages, which included silver’s ability to not react with human tissues, the Jackson tracheostomy tubes are now uncommon. Uncuffed tracheostomy tubes: Uncuffed tracheostomy tubes, like other artificial airway adjuncts mentioned (with the exception of the silver Jackson trach tube), are made of PVC, Teflon, or silicone materials. They consist of an outer and inner cannula, the latter of which can be removed for cleaning and/or disposal. They are labeled as uncuffed on the flange and lack a pilot balloon and cuff. These tubes are used in patients that may require relief of airway obstruction, individuals who cannot protect or clear the natural airway, but do not require positive-pressure ventilation.64 Cuffed tracheostomy tubes: These tubes are the most common type used in the ICU and have outer and inner cannulas, as well as a pilot balloon and cuff

(Figure 9-39). Cuff inflation allows for positive-pressure ventilation. Like ETTs, these tubes are visible on a chest radiograph and should be evaluated for proper placement. Fenestrated tracheostomy tubes include a fenestration or “window” in the outer cannula (Figure 9-40). When the inner cannula is inserted this window is blocked allowing for mechanical ventilatory support with the cuff inflated. When the inner cannula is removed this fenestration is “open” allowing the patient to breathe through his or her upper airway. With the cuff deflated and inner cannula removed a speaking valve can be used that will divert gas flow to the upper airway, allowing the patient to talk. Fenestrated tubes are available that include a regular inner cannula, speech inner cannula, and low-profile speaking valve. Such tubes may also incorporate a subglottic suction channel with a port that can be connected to intermittent or continuous suctioning for removal of secretions above the tracheostomy tube cuff.

Patient Care Critical respiratory care provided in the ICU often includes therapy to improve oxygenation and ventilation, provide secretion management and airway care, treat bronchospasm and mucosal edema, and/or deliver lung expansion therapy to treat or prevent atelectasis. Mechanical ventilation seeks to maintain oxygenation, ventilation, and acid-base balance. Critical respiratory care is also concerned with maintaining adequate circulation, blood pressure, and cardiac output. Mechanical ventilation may incorporate specific techniques to improve oxygenation. These include the application of PEEP, RMs, and prone positioning. Respiratory care personnel may also be responsible for managing extracorporeal membrane oxygenation (ECMO) in cases where more conventional techniques are ineffective. Respiratory care personnel are also sometimes responsible for management and monitoring of mechanical circulatory assistance devices (e.g., aortic balloon pumps). In addition to mechanical ventilatory support, patients in the intensive care unit often receive other forms of respiratory care. These include conventional oxygen therapy, bronchial hygiene and secretion management, suctioning and airway care, aerosolized medications for treatment of bronchospasm and mucosal edema (e.g., bronchodilators, anti-inflammatory agents, anti-asthma agents), and lung expansion therapy. Additional aerosolized agents are sometimes employed that may include narcotics, antimicrobials, or vasodilators. Occasionally, airway installations of specific agents may be performed such as lidocaine, epinephrine, cold saline, or topical thrombin. Topical epinephrine, cold saline, or topical thrombin may be helpful in treating hemoptysis, while lidocaine is a topical anesthetic. Helium–oxygen specialty gas mixtures are sometimes given to reduce airway resistance and decrease the work of breathing. Inhaled vasodilators such as nitric oxide and prostacyclin may be given to reduce pulmonary arterial pressures. Routine nursing care may include frequent turning of critically ill patients (e.g., every 2 hours), mouth inspection and care, maintenance of patient hygiene (e.g., skincare, bed baths), routine dressing changes, and medication administration and monitoring. Physical therapy techniques for range of motion, chest physical therapy, and/or patient mobility are also often performed.

Bronchial Hygiene and Airway Care While some sputum production is normal, increased sputum production is often a sign of pulmonary disease. Increased sputum production may occur due to pulmonary mucosal inflammation and may be seen in patients with infection, inhalational injury, pneumonia, asthma, acute or chronic bronchitis, bronchiectasis, cystic fibrosis, and COPD. Endotracheal intubation may also impair secretion clearance. In the acute care setting, sputum produced should be monitored for volume, color, and consistency. The ease with which the patient is able to cough and expel excess secretions should also be noted. In nonintubated, cooperative patients, sputum volume can be estimated by placing a clean sample canister/container at the bedside for 24 hours. The patient is then instructed to deposit secretions in the container and the results noted. In normal health, sputum is colorless. In the presence of inflammation or infection, sputum may become creamy, white, red, green, brown, rust-colored, or yellowgreen. Color, consistency, and viscosity of the sputum should be observed and recorded. Normally, sputum is thin and mucoidal. In the presence of inflammation, infection, or dehydration, sputum consistency may change to thick, viscous, and tenacious (sticky). Thick, viscous sputum may lead to retained secretions, mucus plugging, and atelectasis. A number of pharmacologic and nonpharmacologic airway-clearance therapies have been employed in an attempt to mobilize and remove secretions in the acute care setting. Airway clearance therapies sometimes used to mobilize secretions include active cycle breathing technique (ACBT), chest physiotherapy (CPT), forced exhalation technique (FET), positive expiratory pressure (PEP), interpulmonary percussive ventilation (IPV), high-frequency chest wall compression (HFCWC), and mechanical insufflation–exsufflation. Indications for nonpharmacologic airwayclearance therapies include difficulty with secretion clearance (noted by inability to cough secretions out and clear breath sounds), evidence of retained secretions (course breath sounds), and atelectasis associated with mucus plugging.68 Unfortunately, there is no strong evidence for the effectiveness of nonpharmacologic airway-clearance therapies in patients who do not have cystic fibrosis to improve oxygenation, reduce time on the ventilator, reduce time in the

ICU, or treat atelectasis and lung consolidation.69 IPV may decrease ICU stay for nonintubated patients with COPD, and there is some evidence that FET and PEP may be effective in these patients.69 There is also some evidence that airwayclearance therapies may be considered in COPD patients with symptoms of secretion retention.69 Airway-clearance therapies are not recommended for patients with an effective cough. These patients should receive instruction on appropriate cough techniques.69 ACBT may be effective in secretion clearance for patients with bronchiectasis.69 In hospitalized patients without cystic fibrosis, CPT is not recommended for the routine treatment of uncomplicated pneumonia and the routine use of incentive spirometry has also not been shown to be effective in prevention of postoperative complications.69 A number of aerosolized medications have been used over the years to promote mucus clearance. These include bronchodilators (e.g., albuterol [Proventil], salbutamol [Ventolin], ipratropium [Atrovent]) and mucoactive drugs (Nacetylcysteine, dornase alfa). Aerosolized sterile, distilled water, normal saline, and hypertonic saline have also been sometimes used in an attempt to mobilize secretions. In hospitalized patients without cystic fibrosis, clinical practice guidelines suggest aerosolized bronchodilators, mucokinetics, or mucolytics (e.g., Nacetylcysteine, dornase alpha [Pulmozyme]) should not be routinely used as an aid to secretion clearance.70 To summarize, in patients who do not have cystic fibrosis, available evidence does not support the routine use of nonpharmacologic airway-clearance therapies for postoperative patients, mechanically ventilated patients, or patients with COPD.69 These therapies may be considered in individual patients based on patient preference, difficulty clearing airway secretions, and in cases where retained secretions are affecting gas exchange or lung mechanics. Manual and mechanicalassisted cough maneuvers may be beneficial in cases where the cough is weak (e.g., neuromuscular disease, muscle weakness, spinal cord injury, or impaired cough). Insufficient evidence is available to support or reject the use of IPV or HFCWC for secretion clearance for these patients.69 Evidence for the effectiveness of bronchodilators or mucosal active medications to improve airway clearance and prevent complications such as atelectasis is lacking. That said, absence of evidence is not the same as evidence of absence (in terms of benefit), and clinical decision-

making should be made based on individual patient needs and preferences, response to therapy, cost, and potential for harm. Airway care includes providing appropriate humidification, airway suctioning, monitoring and correcting endotracheal tube position, monitoring and adjusting endotracheal/tracheostomy tube cuff pressures, and performing tracheostomy tube care. Endotracheal intubation and tracheostomy bypass the humidification function of the upper airway, which may lead to bronchospasm, atelectasis, retained secretions, and airway obstruction. These patients should receive humidification of their inspired gases. Humidification can be provided through a heated humidifier (i.e., active humidification) or a heat and moisture exchanger (i.e., passive humidification). All patients receiving invasive mechanical ventilation should receive some form of humidification, and active humidification in patients receiving noninvasive mechanical ventilation may improve patient comfort and adherence.71 Active humidification during invasive mechanical ventilation should provide 33 to 44 mg H2O/L of gas with a relative humidity 100% saturation at a temperature of 34° to 42°C at the patient “Y” connection.71 For invasive ventilation, the heat and moisture exchanger (HME) should provide at least 30 mg H2O/L at the patient “Y”. HMEs are not recommended for use with noninvasive ventilation or invasive low-tidal volume ventilation.

Patient–Ventilator System Monitoring Assessment of the patient–ventilator system should begin with the patient. The patient should be observed for overall condition, level of consciousness, airway patency, circuit connection, and patency of the circuit. The patient’s color and condition of the extremities (e.g., skin temperature, capillary refill, edema) should be noted. Physical assessment should include inspection, auscultation, palpation, and percussion of the chest. The clinician should be on the alert for signs of respiratory distress, accessory muscle use, retractions, absence of bilateral symmetrical chest wall movement, abnormal respiratory rate or rhythm, asymmetrical chest to diaphragm motion, and chest wall stability. Breath sounds should be bilateral, and any adventitious breath sounds should be noted to include crackles, wheezing, or absent or diminished breath sounds. Percussion notes should be evaluated for resonance, hyperresonance, or dullness. The position of the trachea should be evaluated as a tracheal shift may be caused by tension pneumothorax or major atelectasis. The respiratory care clinician should also observe the cardiac monitor and pulse oximeter, as well as ventilator airway pressures and exhaled volumes to assure that the patient is being adequately ventilated. Prior to performing the ventilator check, the respiratory care clinician should drain the ventilator circuit tubing and service the humidifier (if needed) and attend to the patient’s airway. Endotracheal or tracheostomy tube position and stability should be assessed and the tube cuff pressure and volume to properly inflate should be noted. If the patient needs suctioning or the ventilator circuit needs adjustment, this should occur prior to the actual patient–ventilator system check. Assessment of the patient–ventilator system should occur at regularly scheduled intervals (e.g., every 1 to 2 hours) and before obtaining blood gas samples for analysis so that values obtained can be correlated with specific physiologic monitoring data. Assessment of the patient–ventilator system should also occur concurrent with or just prior to obtaining other physiologic or hemodynamic measures. Assessment of the patient–ventilator system should occur after any change in ventilator settings, and as soon as possible following deterioration in the patient’s condition or should questions about the effectiveness of ventilator’s performance arise. The patient–ventilator system check typically involves observation and recording of:

Date and time of the system check Ventilator mode Ventilatory volumes and rates (VT, V̇E, f) Airway pressures (PIP, Pplateau, PEEP/CPAP, autoPEEP, IPAP/EPAP, mean P̄AW) Trigger effort or sensitivity setting FIO2 (set, analyzed) Inspiratory time and/or peak flow setting Inspiratory flow wave form Inspiratory, expiratory and respiratory cycle time (TI, TE, Ttot,) TI/Ttot, and I:E ratio Airway temperature Alarm settings Pulmonary mechanics (compliance, airway resistance) Oximetry and arterial blood gas values (Spo2, Pao2, Sao2, Cao2, Paco2, pH, HCO3–, B.E./B.D, Hb) Mixed venous or central venous blood gases if available (Pv̄O2, Cv̄O2, CaO2 – Cv̄O2) Capnography, and related values, if available (PETCO2, PĒCO2, VD/VT) Hemodynamic variables (pulse, BP, CVP, PAP, PCWP, cardiac output, cardiac index, SVR, PVR) Spontaneous breathing variables (MIP, MEP, VC, spontaneous rate and volumes [VT, V̇E, f], RSBI [f/VT]. Observation of the ventilator graphics package to confirm mode, assess adequacy of gas flow rate during volume ventilation, assess trigger effort and work of breathing, adjust rise time and termination criteria in pressure ventilation modes, assess for patient–ventilator asynchrony, detect auto PEEP, and assess for lung overdistention Additional physiologic data sometimes collected during patient–ventilator system monitoring includes additional measures of oxygenation (e.g., PaO2/FIO2, PaO2/Pao2, Q̇s/Q̇T), additional measures of ventilation (VD/VT, V̇A), measures of ventilatory load (e.g., effective static compliance, dynamic compliance, work of breathing); and measures of ventilatory capacity (e.g., occlusion pressure [PO.1], vital capacity, MIP, MVV, pressure-time index). Normal values for respiratory and cardiac/physiologic monitoring data are found in Table 9-4 and Table 9-5. TABLE 9-4 Respiratory Physiologic Monitoring Dataa

Oxygenation

Normal (Clinically Acceptable Values)

Arterial oxygen pressure (Pao2)

80 to 100 mmHg (60 to 100 mmHg)

Arterial oxygen saturation (Sao2)

96% to 98% (> 90%)

Oxygen saturation by pulse oximeter (Spo2)

96% to 98% (> 90%)

Transcutaneous oxygen partial pressure (Ptco2)

80 to 100 mmHg (60 to 100 mmHg)

Alveolar to arterial oxygen tension gradient on 100% O2 (P[A-a]o2)

100 to 150 mmHg (< 350 mmHg)

Arterial to alveolar oxygen tension ratio (Pao2/PAO2)

0.80 (> 0.6)

P/F ratio (Pao2/FIO2)

380 to 500 (> 300)

Percentage shunt (Q̇S/Q̇T)

3% to 5% (< 15% to 20%)

Mixed venous oxygen content (Cv̄o2)

15 mL/dL (> 10.0 mL/dL)

Mixed venous oxygen partial pressure (Pv̄o2)

35 to 40 mmHg (> 30 mmHg)

Mixed venous oxygen saturation (Sv̄o2)

70% to 75% (> 65%)

Arterial-venous oxygen content difference (CaO2 Cv̄O2)

3.5 to 5.0 mL/dl (< 7 mL/dL)

Arterial oxygen content (Cao2 = 1.34 × Hb × Sao2 + 0.003 Pao2)

20 vol% (16 to 20 vol%)

Oxygen delivery (ḊO2 = Cao2 × Q̇T)

1000 mL/min

Oxygen consumption (V̇O2= [FIO2 – FEO2]V̇E)

250 mL/min (3.5 to 4.0 mL/kg/min)

Oxygen extraction ratio [O2ER = [Cao2 – Cv̄o2] ÷ Cao2]

25% (25% to 30%)

Ventilation Respiratory rate

12 to 18 or 20 breaths/min (< 30 bpm)

Tidal volume

400 to 700 mL (> 300 mL)

Minute ventilation (V̇E)

5 L/min (5 to 10 L/min)

Arterial carbon dioxide (Paco2)

40 mmHg (35 to 45 mmHg)

Transcutaneous carbon dioxide partial pressure (Ptcco2)

40 mmHg (35 to 45 mmHg)

End-tidal carbon dioxide partial pressure (PETco2)

40 mmHg (35 to 45 mmHg or 4.6% to 5.6%)

Dead space/tidal volume ratio (VD/VT)

0.20 to 0.40 (< 0.6)

Minute ventilation vs. carbon dioxide partial pressure (V̇E vs. Paco2)

V̇E < 10 L/min with normal Paco2

Ventilatory Load Dynamic compliance (total impedance) (Cdyn = VT ÷ [PIP – PEEP])

< 100 mL/cm H2O (35 to 50 mL/cm H2O)

Effective static compliance (CST = VT ÷ [Pplateau – PEEP])

100 mL/cm H2O (60 to 100 mL/cm H2O)

Airway resistance (cm H2O/L/sec)

1 to 2 cm H2O/L/sec (< 10 cm H2O/L/sec)

Work of breathing (static total) (WOB = kg × m/L or J/L)

0.5 to 1.0 J/L (< 0.15 kg × m/L; < 1.5 J/L)

Ventilatory Capacity Occlusion pressure (P0.1)

1 to 2 cm H2O (< 6 cm H2O)

Mean inspiratory flow (VT/TI)

500 mL/sec

Vital capacity (VC)

70 mL/kg (< 10 to 15 mL/kg)

Maximal inspiratory pressure (MIP; PImax)

–70 to –130 cm H2O (< –20 to –30 cm H2O)

Maximum expiratory pressure (MEP)

88 to 238 cm H2O (> 40 cm H2O)

Maximum voluntary ventilation (MVV)

80 to 180 L/min (> 20 L/min or 2 × V̇E)

Ratio of minute ventilation to MVV (V̇E/MVV)

(< 1 : 2)

Pressure–time index ([Pdi/Pmax]*Tl/Ttot)

(< 0.15)

a Adult values listed are approximate and vary with age, size and gender.

TABLE 9-5 Hemodynamic Monitoring Data Data

Normal Values (range)

Heart rate (HR)

80 beats/min (60 to 100 bpm)

Arterial blood pressure (ABP)

120/80 mmHg (90 to 140/60 to 90 mmHg)

Mean arterial blood pressure (MAP)

90 mmHg (80 to 100 mmHg)

Electrocardiogram (ECG)

Normal heart rate and rhythm

Central venous pressure (CVP)

4 to 8 mmHg

Pulmonary artery pressure (PAP)

25/10 mmHg (20 to 35/5 to 15 mmHg)

Mean pulmonary artery pressure (PAP)

15 mmHg (10 to 20 mmHg)

Pulmonary capillary wedge pressure (PCWP)

6 to 12 mmHg ( 90%. Tidal volume should be monitored to ensure that it remains at 5 to 8 mL/kg predicted body weight (PBW). Patients may remain on NIV for period of time, up to 90 minutes, to ensure recovery from the procedure.

Community-Acquired Pneumonia Community-acquired pneumonia (CAP) that requires hospitalization is associated with higher morbidity and mortality. The use of NIV in severe CAP is controversial and is associated with failure rates that may be as high as 76%.36,37 Although this has not been well studied, it appears that the use of NIV in CAP should be limited to mild respiratory failure and that the clinician should have a low threshold to convert to invasive support. Lower failure rates have been reported when NIV is used in patients with a lower severity of illness and when there is good response to initial supportive medical therapy.38

Sleep Apnea and Obesity Hypoventilation Syndrome Obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS) are two

commonly recognized sleep-disordered conditions.39 Loss of muscle tone during sleep creates an obstruction when the tongue falls on the soft palate and obstructs the passage of air. Apnea is defined as cessation of airflow (breathing) for 10 seconds or more and hypopnea by a decrease in airflow by 30% or more and associated with a > 4% decrease in oxygen saturation. These episodes cause a decrease in blood oxygen levels that may lead to disordered sleep architecture. Often, patients are unaware of the source of their problem but show signs of poor sleep such as excessive daytime sleepiness.40 Obese patients hypoventilate during sleep because of a heavy chest wall from the extra adipose tissue. Patients with undiagnosed OSA or OHS have a higher risk of mortality associated with analgesic therapy exacerbating their condition and leading to acute respiratory failure.41 Attempts should be made to screen patients for these conditions before planned surgeries whenever feasible.42

Trauma In the industrialized world, the incidence of blunt chest trauma has been progressively on the rise. Injuries associated with blunt chest trauma include pulmonary contusions, rib fractures, flail chest, increased lung water, and release of cytoactive modulators.43–45 Derangements from these injuries include an increase in ventilation/perfusion (V̇/Q̇) mismatching, pulmonary hemorrhage, and a decrease in pulmonary compliance. Many of these patients receive mechanical ventilation due to the severity of their injuries. NIV may be considered for trauma patients with blunt chest trauma and associated pulmonary derangements not severe enough to require intubation. The application of CPAP may aid in reversing intrapulmonary shunting caused by damaged lung parenchyma or atelectasis.45 Unlike a medical ARDS patients, trauma patients may be less tolerant of lower oxygen levels. For patients with flail chest or significant ribs fractures, NIV augments tidal volume and minute ventilation.43,44 Special considerations should be given to patient selection in the setting of trauma. NIV should be avoided in patients with severe facial trauma and those unable to protect their airway. Low Glasgow Coma Scale scores of < 8 have been associated with NIV failure. NIV should be avoided in patients with severe encephalopathy.43 Other contraindications include high risk for aspiration, upper airway obstruction, and

organ failure. Close monitoring is required for trauma patients due to concerns over hidden injuries such as an esophageal fistula.44,45

Long-Term Applications Patients who suffer from chronic respiratory failure may benefit from NIV. Examples of such patients include those with chronic restrictive disorders and those with COPD. Examples of patients with restrictive disease who may benefit from NIV include those with spinal cord injury, neuropathies, myopathies, and dystrophies, ALS, chest wall deformity, kyphoscoliosis, and sequelae of polio. Some patients with COPD and chronic hypercapnia may also benefit from NIV. Long-term application of NIV should be established with clear goals in terms of symptom relief and for the overall management of the chronic disease process. It is important for clinicians in the critical care environment to consider chronic disease. This may help to guide the care plan to account for chronic, underlying processes. Additionally, if long-term NIV use is to include several hours per day or continuous use, the placement of a tracheostomy should be considered.

Neuromuscular Disease Neuromuscular diseases, such as ALS, myasthenia gravis, or Duchenne muscular dystrophy, can lead to muscle weakness and respiratory failure. Often, patients with diseases like ALS will face an insidious decline in physical function and eventually death. As the patient’s functional capacity declines, some patients may be placed on NIV in the outpatient setting. However, for patients with neuromuscular disease presenting to the intensive care unit (ICU) or the emergency department (ED), the use of NIV has been shown to reduce the need for intubation and shorten hospital stay.46 Guillain-Barré syndrome is an exception; when these patients initially present with acute respiratory failure, the clinical course will often continue to rapidly decline. Recognizing respiratory failure in patients with neuromuscular disease is important because of the often-progressive nature of the disease. Some patients can sustain their ventilatory status even when severe muscle weakness is present and these patients require careful monitoring. Application of NIV in patients with neuromuscular disease is generally facilitated

with an oronasal mask, as they often breathe through their mouths. The use of a sufficient inspiratory pressure to augment tidal volume is highly recommended. CPAP alone is often inadequate; although it does improve FRC, it does not adequately offload the WOB. Using a backup rate is also recommended.46 RC Insight: Proper patient selection is key to the success of noninvasive ventilation.

Box 10-1 provides a summary of the indications and contraindications for NIV.

BOX 10-1 Indications and Contraindications for Noninvasive Ventilation (NIV) Possible Indications for CPAP and/or NIV ∎ Chronic obstructive pulmonary disease (COPD) • Acute exacerbation/respiratory failure • Domiciliary NIV in patients with hypercarbia may benefit select patients. ∎ Acute asthma • Acute hypoventilation is present, but intubation and mechanical ventilation are not immediately indicated. • Invasive ventilatory support should not be delayed, if needed. ∎ Cardiogenic pulmonary edema ∎ Immunocompromised patients in respiratory failure ∎ Postextubation ventilatory support • Patients at high risk of extubation failure may benefit. • NIV is a poor rescue modality for patients who fail several hours after extubation. ∎ Preintubation oxygenation to avoid acute desaturation ∎ Acute respiratory distress syndrome (ARDS) • Mild hypoxemic respiratory failure may respond to NIV. • Do not delay providing invasive mechanical ventilatory support if there is no timely improvement. • May not be appropriate with moderate to severe ARDS. ∎ Palliative care • Progressive neuromuscular disease (e.g., ALS).

Use during comfort measures is controversial. ∎ Bronchoscopy • NIV may improve oxygenation and ventilation during the procedure. ∎ Community-acquired pneumonia (CAP) requiring hospitalization • Use of NIV for CAP is controversial and may have a high failure rate. • Limit the use of NIV to patients with mild respiratory failure. • Do not delay initiation of invasive ventilatory support when indicated. ∎ Sleep apnea ∎ Obesity hypoventilation syndrome ∎ Trauma • NIV should be limited to those who do not require intubation. • NIV should be avoided in patients with facial trauma. • NIV is contraindicated in patients who cannot protect their airway (e.g., Glasgow Coma Score < 8). ∎ Neuromuscular disease • NIV may reduce the need for intubation in patients presenting to the ICU or emergency department. • NIV is probably not appropriate in patients with Guillain-Barré due to the often rapidly progressive nature of the disease. Contraindications to NIV ∎ Inability to protect airway or clear secretions ∎ Poor neurologic status (GCS < 8) ∎ Significant facial trauma/burns ∎ Cardiac or respiratory arrest ∎ Unstable hemodynamic status ∎ Untreated pneumothorax ∎ Active myocardial infarction or acute coronary syndrome (with pulmonary edema) ∎ Inappropriate candidate: severe agitation, vomiting, need for emergent intubation ∎ Recent esophageal surgery

•

Equipment Initiation of noninvasive ventilation requires selection of an appropriate patient interface and ventilator.

Interface Patient interfaces for use in the application of NIV with positive pressure include the nasal mask, oronasal mask, total facemask, and helmet (see Figure 10-1). Appropriate interface selection is pivotal in terms of efficacy and tolerance/compliance of NIV. It is generally accepted that some form of full-face mask, or an interface that covers both the nasopharynx and oropharynx should be used in the setting of acute respiratory distress/failure. There are multiple types and variations of interfaces.47–49

FIGURE 10-1 Types of NIV Patient Interfaces. (A) Face mask. (B) Nasal mask. (C) Nasal interface. (D) Helmet. (A) © ResMed 2010. Used with permission; (B) and (C) Courtesy of Philips Respironics; (D) Courtesy of StarMed SpA.

Description Factors that should be considered when selecting the appropriate interface include

face shape and size, the type of support needed, and likely patient compliance with the interface chosen. There should be balance between patient tolerance and effective delivery of NIV. As stated previously, patients in acute respiratory distress or failure will need a “closed” system provided by a total face mask that covers both the mouth and nose. This provides optimal gas exchange. Patients with nocturnal needs only may benefit from nasal mask or modern nasal interfaces designed for comfort and chronic use. Table 10-1 compares the advantages and disadvantages of four types of NIV patient interfaces. Figure 10-1 provides examples of typical NIV patient interfaces. TABLE 10-1 CPAP/NIV Interfaces Interface

Advantages

Disadvantages

Nasal mask

Less risk for aspiration Easier secretion clearance Less claustrophobia Easier speech May be able to eat Easy to fit and secure Less dead space

Mouth leak Higher resistance through nasal passages Less effective with nasal obstruction Nasal irritation and rhinorrhea Upper airway dryness with mouth leak

Oronasal mask

Better oral leak control More effective in mouth breathers

Increased dead space Increased aspiration risk Increased difficulty speaking and eating Asphyxiation with ventilator malfunction

Total face mask

May be more comfortable for some patients Easier to fit Less facial skin breakdown

Potentially greater dead space Potential for drying of the eyes Cannot deliver aerosolized medications

Helmet

May be more comfortable for some patients Easier to fit (one size fits all) Less facial skin breakdown

Rebreathing Poorer patient–ventilator synchrony Less respiratory muscle unloading Asphyxiation with ventilator malfunction Cannot deliver aerosolized medications

Application Applying the interface is one of the most important and challenging aspects of NIV. It is during the initial phase of the application of NIV that the patient may become intolerant or refuse to move forward with the process. This can directly influence success or failure of NIV. Care should be taken to position the patient appropriately

and make him or her as comfortable as possible while keeping the head of bed at an angle of about 30 degrees. Often, it is helpful to initiate NIV while on low-pressure settings to help the patient ease into the change of having flow and positive pressure introduced into his or her upper airway. It may be helpful to allow patients to place the mask on themselves and hold it until they become used to it. RC Insight Placing a patient on noninvasive ventilation can be challenging. If needed, allow the patient to hold the mask on his or her face until he or she becomes acclimated to the mask and positive pressure.

Types of Ventilators There are options when choosing the type of ventilator to be used in the delivery of NIV. The clinician will need to take many factors into consideration, including equipment availability, cost, and limitations of the equipment itself, such as the ability to compensate for leaks in the system. The clinician can choose either a critical care ventilator or a machine specifically designed for noninvasive ventilation. Intermediate ventilators that may be used for NIV or provision of invasive mechanical ventilatory support are also available.

Noninvasive Ventilators Noninvasive ventilators are those that are designed specifically for NIV and have features that are different from critical care ventilators. A single-limb circuit is often used that incorporates a leak port allowing for washout of carbon dioxide. This port may be incorporated into the circuit proximal to the patient or in the mask. Additionally, these machines have the ability to compensate for leaks that occur at the interface. When using low levels of support and a single-limbed circuit, clinicians should be aware that flow levels could be inefficient to clear CO2 effectively from the circuit. Figure 10-2 provides examples of ventilators designed specifically for NIV, as well as several intermediate ventilators that may be used for NIV.

FIGURE 10-2 Ventilators That May Be Used for NIV. (A) Intermediate ventilators that can be used for NIV. (B) Bilevel ventilators that can be used for NIV. (A-1) Courtesy of Philips Respironics; (A-2) Reproduced with permission from CareFusion; (A-3) © ResMed 2014. Used with permission; (B-1) © Drägerwerk AG & Co. KGaA, Lubeck,. All rights reserved. No portion hereof may be reproduced, saved, or stored in a data processing system, electronically or mechanically copied, or otherwise recorded by any other means without our express prior written permission; (B-2) Reproduced with the permission of Koninklijke Philips N.V. All rights reserved; (B-3) © ResMed 2014. Used with permission; (B-4) Reproduced with the permission of Koninklijke Philips N.V. All rights reserved.

Critical Care Ventilators There are advantages and disadvantages to using a critical care ventilator to deliver NIV.50 Advantages include their general availability in the intensive care unit and fewer CO2 rebreathing issues (critical care ventilator circuits incorporate inspiratory and expiratory limbs and exhalation valves). Software that allows for leak compensation is available on many modern ICU ventilators. As with any application of mechanical ventilatory support, the clinician should be very familiar with the equipment used. Disadvantages of using critical care ventilators to provide NIV include cost and access. For example, using a critical care ventilator to provide NIV to patients may limit the number of such ventilators available for other patients who require more sophisticated modes of ventilation and ventilator monitoring. In addition, many institutions have policies limiting the use of critical care ventilators to the ICU, while NIV ventilators may be acceptable on general care wards. RC Insight It is important that clinicians responsible for the delivery of noninvasive ventilation understand the nuances of each device available to them for use.

Initiation As with the initiation of any form of mechanical ventilatory support, the clinician should begin with an assessment of the patient’s ventilatory needs and the goals addressed by the institution of NIV. Following this assessment and choice of an appropriate NIV interface and ventilator, initial support settings must be selected.

Settings Although interrelated, oxygenation and ventilation may be approached separately, just as would be done with invasive ventilation. The clinician’s primary concerns should be to ensure adequate oxygenation and ventilation while avoiding iatrogenic injury, and settings should be determined with these goals in mind. Patients with primary hypoxemic respiratory failure (type 1) may be treated with CPAP alone; this requires adequate spontaneous ventilation with an acceptable spontaneous ventilation workload. CPAP is typically initiated with pressures of 5 to 10 cm H2O but may be titrated higher if clinically warranted. FIO2 may be started at 1.0 and quickly titrated down as low as possible, while maintaining satisfactory oxygenation. Balance should be found between CPAP levels and FIO2 levels that complement each other to achieve the therapeutic goal. In other words, if the FIO2 requirements remain high after initiation, the CPAP level should be titrated in order to allow for a lower FIO2 to be used. Figure 10-3 provides an example of a CPAP system for use in the ICU.

FIGURE 10-3 CPAP System for Patients with Adequate Spontaneous Breathing. (A) CPAP system with blender, reservoir bag, humidifier, pressure manometer and threshold PEEP valve. (B) PEEP valves. (C) Face mask with PEEP valve. (B) Courtesy of Ambu, Inc.; (C) © Vital Signs, Inc. Used with permission of GE Healthcare. All Rights Reserved.

Description When there is ventilatory failure or significant WOB, NIV may be needed. NIV incorporates an inspiratory pressure level that is added to the baseline pressure. When using ventilators specifically designed for NIV, the inspiratory positive

airway pressure (IPAP) and expiratory positive airway pressure (EPAP) are set. Baseline pressures should be set similar to CPAP and titrated to meet the patient’s oxygenation goals. Baseline pressures should be initially set at 5 to 10 cm H2O and titrated to achieve an acceptable oxygenation status, while minimizing patient discomfort. The expiratory airway pressure (EPAP) is adjusted for oxygenation while the inspiratory pressure (IP or IPAP) is adjusted to support ventilation and reduce the WOB. Initial inspiratory pressures should be set to achieve a delta pressure (ΔP) of about 5 to 15 cm H2O, where ΔP = IPAP – EPAP. Titration should be done to achieve optimal gas exchange and alleviation of WOB. Evaluating for improvement should include physical assessment, vital signs (i.e. respiratory rate and heart rate), pulse oximetry, and arterial blood gas analysis. Determining initial ventilator settings is accomplished differently, depending on whether using an NIV ventilator or more sophisticated critical care ventilator. For example, when using a critical care ventilator the clinician may decide to use either pressure-support ventilation (PSV) or pressure assist/control ventilation. When using pressure-support ventilation, the PEEP and PSV levels should be set to achieve the desired ΔP. If the baseline pressure is 5 cm H2O and the desired ΔP is 15 cm H2O, then the PEEP should be set to 5 cm H2O and the PSV level should be set at 15 cm H2O. This would result in a peak inspiratory pressure (PIP) of 20 cm H2O for ventilators that automatically adjust PIP based on the set PEEP (i.e. ΔP = PIP – PEEP = 20 cm H2O – 5 cm H2O = 15 cm H2O. Achieving these same settings with pressure-controlled ventilation will depend on the type of ventilator in use and ΔP will be achieved differently depending on the ventilator. Some ventilators require the clinician to set the ΔP directly by setting a specific inspiratory pressure, whereas others will require the clinician to set the ΔP indirectly by setting a pressure limit. Adjunctive settings are important as well, depending on the type of ventilator being used. In some modes, rise time settings and expiratory cycle sensitivity may be adjusted to improve patient–ventilator synchrony or compensate for large air leaks. Backup controlled rates should be used cautiously in patients with unstable ventilatory patterns and variable spontaneous effort. Such patients may be more appropriately and safely managed with invasive mechanical ventilatory support. Alarms should be set in the same manner as with invasive ventilation. These

should include alerts that indicate high minute volume, low minute volume, large leaks, apnea, patient disconnect, and high and low respiratory rate. RC Insight Noninvasive ventilation requires a lot of “front-end” time and effort from the clinician. Expect frequent adjustments to settings and mask interface when initiating NIV.

Ongoing Management Ongoing management should focus on supporting appropriate gas exchange, decreasing the work required to breathe, and preventing iatrogenic injury to the lungs. A careful balance is required, and a level of patience is required of the clinician. The clinician may need to spend a considerable amount of time at the patient’s bedside to ensure that the goals of support are met. Box 10-2 describes specific management strategies for CPAP and NIV.

BOX 10-2 Management Strategies for CPAP and NIV As previously discussed, there are two pressures in NIV (e.g., IPAP and EPAP) and one delivered pressure in CPAP. The following guidelines outline management strategies for CPAP and NIV.

CPAP for obstructive sleep apnea CPAP should be adjusted to mitigate obstructive sleep apnea by splinting or holding the airway open. Alleviation of obstructive apnea should be observed and monitored to assure appropriate CPAP levels. If possible, a formal sleep study should be performed. If unable to perform a formal sleep study, then clinical observation should be made to make sure that there is no obstruction during the patient’s inspiratory effort. Ongoing monitoring should be performed in the ICU via continuous ECG, oximetry, and respiratory rate. Titration of CPAP levels should be made based on observation of the above monitoring parameters. CPAP for hypoxemic respiratory failure CPAP alone may be effective in improving oxygenation in patients with hypoxemic respiratory failure who are able to maintain adequate spontaneous ventilation without a high level of spontaneous ventilatory work. When using CPAP to support such patients, great care should be taken to monitor for worsening hypoxemia and any increase in respiratory distress or WOB. In the

event the patient begins to tire or oxygenation is insufficient, invasive mechanical ventilatory support should be instituted. CPAP and FIO2 should be adjusted to maintain an adequate arterial oxygen saturation (e.g., SaO2 ≥ 0.90) on an acceptable FIO2 (e.g., FIO2 ≤ 0.40 to 0.50). Balance between FIO2 and CPAP levels should be the focus. Achieving the lowest FIO2 by increasing CPAP levels should be the goal. Monitoring the patient’s respiratory rate, heart rate, SpO2, and other appropriate vital signs should be performed. If the patient does not seem to be responding well, there should be a low threshold for converting to invasive ventilatory support.

NIV for hypoxemic and or hypercapnic respiratory failure EPAP should be adjusted to maintain a patent airway and to support oxygenation. FIO2 should be titrated in concert with EPAP levels. IPAP levels should be adjusted for appropriate tidal volume, carbon dioxide tension (PaCO2), acid-base status, and WOB. Monitoring should include vital signs, physical assessment, observation of physiologic monitors, and blood gas analysis when needed.

It is not clear how much influence tidal volume, pressure strain, and change in pressures have on iatrogenic secondary pulmonary injury during NIV. Careful consideration of these factors should be made while adjusting settings in any mode that delivers positive pressure to the lungs. Tidal volumes should probably be maintained at ~6 mL/kg PBW and peak airway pressure maintained < 30 cm H2O to reduce the possibility of ventilator-induced lung injury (VILI). In addition, esophageal sphincter opening pressures are reported to be about 20 to 25 cm H2O.51 NIV pressurizes the upper airway and care should be taken to avoid exceeding this threshold and causing gastric insufflation. Also, be aware that patients can remove the mask on their own. Consider closer monitoring for patients who are restrained or unable to remove the mask on their own. Patient–ventilator asynchrony may sometimes occur, and the clinician should carefully monitor for its presence. Appropriate ventilator changes should be made promptly in the presence of asynchrony to eliminate it. Inappropriate cycling due to inspiratory times that are either too long or too short, or when there is a leak that cannot be compensated for by the machine, should be monitored for and aggressively managed. Other types of asynchrony may occur and can be addressed much in the same way that they are addressed during invasive mechanical ventilation. Trigger

asynchrony can be caused by inappropriate trigger thresholds that are too sensitive or not sensitive enough. Autotriggering can occur if the ventilator is too sensitive. If the ventilator is not sensitive enough, patients may be unable to spontaneously trigger the ventilator. Trigger asynchrony can be corrected by either manipulating the sensitivity threshold and/or increasing the baseline pressure when air trapping is present. Appropriate humidity should be provided to inspiratory gas to avoid ciliary damage or impairment of mucociliary function.52,53 Appropriate, heated humidity may improve patient compliance and tolerance as well. Heat-moisture exchangers are not recommended for use with NIV. RC Insight The use of protocols, algorithms, or guidelines can assure timely and consistent adjustments to noninvasive ventilator settings.

Monitoring Monitoring the patient receiving NIV is similar to monitoring any patient receiving mechanical ventilatory support and includes assessment of the patient’s oxygenation status, ventilatory status, and hemodynamic variables. Noninvasive monitoring may include pulse oximetry and capnography. Cardiac and hemodynamic monitoring may include heart rate, blood pressure, electrocardiogram (ECG), central venous pressure (CVP), hemodynamic waveforms, and other hemodynamic variables (e.g., cardiac output, pulmonary artery pressures). Additional assessment data should be obtained as needed, including the results of arterial blood gas analysis, other laboratory studies, and imaging studies. Observation of ventilator settings; airway pressures, flows, volumes, and related ventilator graphics; patient trigger effort; oxygen concentration; airway temperature; and alarm settings should occur on a regular basis and whenever a change or problem seems to be occurring. Mental status and neurologic function, renal function and urine output, pain assessment, nutritional assessment, and recognition of common problems should be included. Chapters 8 and 9 provide additional detail regarding monitoring of the ICU patient receiving mechanical ventilatory support.

Recognizing Failure of NIV Careful monitoring of the patient’s status with respect to the primary indication for NIV (i.e. reason NIV was initiated) should occur to determine if the patient is improving and continues to require ventilatory support. Monitoring for deterioration in the patient’s condition requiring alterations in ventilatory support is also essential. At a minimum, the following should be monitored on an ongoing basis: Vital signs (respiratory rate, heart rate, and blood pressure) Oxygenation via pulse oximetry Neurologic status Level of dyspnea and WOB Arterial blood gas analysis as needed A low threshold should be maintained to convert to invasive ventilatory support when there is no improvement in the indications that supported the initiation of NIV.

Where NIV Should Be Started and Managed There is controversy as to locations within the hospital that patients needing NIV may be managed. The major consideration on where patients are best managed should be the availability of appropriate monitoring and support. Also, it is generally accepted that NIV support should not be delayed based on location within the hospital, and that it may be started anywhere when needed urgently. Once stabilized, the patient then can be transferred appropriately.

Discontinuing NIV It is not clear what the most appropriate method of discontinuing NIV may be. It is probably best to discontinue NIV/CPAP when the initial indication for its use has resolved. In some cases, there will be a need for long-term NIV. Short periods of NIV/CPAP suspension may be acceptable to allow for eating, or trips to the restroom. These short trials may also have some utility in helping the clinical team determine if the patient is ready for a more formal trial of NIV discontinuation.

Complications and Hazards As with any form of mechanical ventilatory support, complications include inadequate or inappropriate levels of ventilatory support resulting in hypoventilation or hyperventilation, inadequate support of oxygenation resulting in acute hypoxemia, and machine or system malfunction. Inappropriate application of NIV may increase the WOB and worsen ventilatory fatigue. Inappropriate ventilator settings may result in patient–ventilator asynchrony. Patients may not tolerate the patient interface or the ventilator and remove the mask or other interface device resulting in acute hypoxemia and/or hypoventilation. Because an artificial airway is not in place, patients are at greater risk for vomiting and aspiration. Facial pressure ulcers may occur due to the interface if it is not well fitted or straps are fitted too tightly. Specific contraindications to NIV include cardiac or respiratory arrest, untreated pneumothorax, inability to cooperate, inability to protect the airway or clear secretions, high aspiration risk, and severely impaired consciousness. NIV may not be appropriate for certain patients following facial surgery, craniofacial trauma or burns, or those with upper airway swelling, edema, or other airway problems. Gastric insufflation may also occur, particularly with patients in which higher pressures are employed. As noted, NIV should not employed in patients requiring airway protection due to high risk of aspiration. NIV should also not be employed in patients who are hemodynamically unstable, those with unstable ventilatory patterns, or patients who are uncooperative or neurologically compromised. NIV is also contraindicated in patients who have recently undergone esophageal surgery (e.g., esophageal anastomosis).

Facial Pressure Ulcers The application of NIV places the patient at risk for the development of pressure ulcer formation at the site where the mask comes into contact with the skin. Skin breakdown can contribute to NIV intolerance which in turn could necessitate intubation. The type of mask and duration of NIV usage are independent risk factors for development of pressure ulcers. Full face masks have been shown to have alower incidence of pressure ulcer formation than oronasal masks as they distribute

the pressure across a wider area of the patients face. The reported incidence of skin breakdown with NIV varies but suggest that pressure ulcer formation may occur in 13% to 20% of patients54–59 Patients receiving NIV should undergo routine assessment of the area where the skin comes into contact with the mask with attention being focused on the face, forehead, and the bridge of the nose. Pressure ulcers can begin to form as soon as 1 to 2 hours after initiation of therapy.59 The clinician should assess for redness or discoloration and if the skin blanches when touched.58 Strategies that may help mitigate skin breakdown include rotating mask types on a scheduled basis to alter pressure points, use of skin barrier devices such as Tegasorb or Tegaderm, or the use of a helmet interface.58,59 Table 10-2 summarizes risk factors and problems associated with NIV. Clinical Focus 10-3 reviews strategies to reduce the risk of developing facial pressure ulcers during NIV. TABLE 10-2 Risk Factors and Problems Associated with NIV General risks • Sensory impairment • Acute Illness • Chronic Illness • Hypoxia or low blood pressure • Extremely young or extremely old age • Diminished level of consciousness • Psychological status • Vascular disease • Malnutrition/dehydration • Chronic skin condition • History of a previous pressure damage • Medicines (such as chronic steroid use) Extrinsic factors • Straps fitted too tightly • Ill-fitting masks • Pressure, shear, or friction from the mask/straps • Allergy to the materials Other factors • Skin damage • Edema • Shape and size of the nose/face • Time period mask is worn • Inability to self-manage the mask Data from: Brill AK. How to avoid interface problems in acute noninvasive ventilation. Breathe 2014;10:230– 242.

CLINICAL FOCUS 10-3 Facial Pressure Ulcer A 67-year-old female with end-stage COPD was admitted to the hospital for a COPD exacerbation. The patient arrived intubated and on mechanical ventilation. On hospital Day #2, the patient was placed on a spontaneous breathing trial (SBT) followed by extubation to NIV. Now on hospital Day #6, the patient remains on NIV with an IPAP of 20 cm H2O and EPAP of 10 cm H2O (ΔP of 10 cm H2O). The patient has not tolerated attempts to remove her from NIV or wean her settings. She can only tolerate very short periods off the NIV, and she is not strong enough to remove the mask. She has nursing support at her bedside at all times. Question 1. What are the risk factors for this patient developing a facial pressure ulcer? This patient has multiple risk factors for developing a facial pressure ulcer. First and foremost, she has been on NIV for 4 days and can only tolerate short times with the mask off. She also has a chronic lung condition, end-stage COPD. Chronic steroid use in COPD patients can make the skin fragile and easy to tear. Note that if the patient feels facial pain from high mask pressures, she is unable to adjust the mask herself. Question 2. What should be done to monitor for possible pressure sores? Although caregivers may not be able to completely prevent facial pressure sores, every effort needs to be taken for prevention, identification, and treatment. Routine removal of the mask for inspection should occur. The caregiver should inspect the patient’s face, bridge of the nose, and anywhere the mask’s straps contact the skin. New redness and blanching of the skin when touched are signs that a pressure sore is developing. Question 3. What are some strategies to reduce the risk of patients on NIV from developing pressure sores? First, identifying risk factors will be helpful. Routine assessment such as every 2 or 4 hours of the face, bridge of the nose, and straps will be helpful in early identification. The use of a skin-protecting material such as Tegaderm, as well as keeping the mask and skin dry, can also help. Lastly, rotating masks with different pressure points will prevent any one area from being exposed to high pressure for a sustained period of time.

Special Considerations Alternatives to NIV using positive-pressure ventilation include the high-flow nasal cannula (HFNC) and use of other modes of NIV support (e.g., negative-pressure ventilation). Several noninvasive techniques to augment ventilation have been used in the past. These include the iron lung, chest cuirass, and body suit, which are all forms of negative-pressure ventilation. The rocking bed and pneumobelt provide two other examples of techniques used in the past to augment ventilation in patients with chronic disease. Some of these techniques may be considered in certain patients based on patient preference and need, although positive-pressure NIV has largely supplanted these older methods.

High-Flow Nasal Cannula HFNC has gained popularity in recent years as a method to provide high gas flows (up to 60 L/min in adults) via a nasal cannula using warmed and humidified gas.60 Although HFNC is not a true form of NIV, there are advantages to its use, and it may have some positive effect on ventilation and the removal of CO2. Many studies regarding the efficacy of warmed, humidified, high-flow nasal cannulas have been published in the last decade. HFNC using warmed and humidified gas may facilitate mucociliary clearance, reduce the likelihood of retained secretions, and avoid the development of atelectasis or V̇/Q̇ abnormalities secondary to mucous plugging. HFNC provides accurate oxygen flow and low-level positive airway pressure not unlike CPAP. The HFNC does not greatly impede mobility, oral intake, or speaking (as compared to NIV). HFNC has shown a lower 90-day mortality when compared to standard oxygen therapy and NIV.61 HFNC should be considered when there is hypoxemic respiratory failure with absent or only mild hypercapnea.62–69

Specialty Modes of NIV Support Average volume-assured pressure support (AVAPS) and neurally adjusted ventilatory assist (NAVA) are two modes of NIV that are currently available from some manufacturers.70–72 AVAPS allows clinicians to set parameters such as tidal volume, FIO2, frequency, and expiratory pressure.72,73 The inspiratory pressure varies within a set range to assure the target tidal volume is met. This mode has been shown to be effective in the setting of obesity hypoventilation syndrome and chronic, stable COPD.72–75 AVAPS may also be useful in the setting of acute hypercapnic respiratory failure due to COPD.73–75 NAVA may be administered using invasive or noninvasive ventilation. NAVA differs from other modes in that it is controlled by electrical diaphragmatic activity (Edi) that is detected by a special catheter placed in the esophagus. Each breath is triggered by and delivered proportional to the Edi. Interestingly, NAVA is not affected by gas leaks, allowing patients to trigger the NIV breath in the presence of leaks. NAVA can reduce patient–ventilator asynchrony and improve the overall interaction between the device and patient. When used for NIV, it is not yet clear if NAVA has any advantages over other modes in terms of avoiding intubation and reducing mortality.76

Key Points Noninvasive ventilation (NIV) is used to support patients in respiratory distress in the absence of artificial airways. Proper patient selection is key when considering the use of NIV. There is strong literature support for the use of NIV in acute exacerbations of COPD and acute cardiogenic pulmonary edema (CPE). An interface that covers both the mouth and nose is generally recommended in the setting of acute respiratory failure. Placing an interface on a patient can be challenging. Clinicians should allow the patient to acclimate to the device before securing the head straps. There are various types of ventilators used to deliver NIV. It is imperative that clinicians understand the equipment they have in their facility. The best way to set NIV settings is unknown; however, it is generally recommended that pressures be initially set relatively low and subsequently increased to meet therapeutic objectives. Gastric insufflation can occur when NIV pressures are high, around 25 cm H2O. NIV requires ongoing management and monitoring. Settings are adjusted based on the patient response and improvement/worsening of the underlying condition. The best method to discontinue NIV support is not yet known. It is reasonable to discontinue support when the underlying condition is resolved. Ongoing assessment of facial skin should be done when NIV is being utilized to avoid the development facial pressure ulcers.

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CHAPTER

11 High-Frequency Oscillatory Ventilation for Acute Respiratory Distress Syndrome in Adults Stephen Derdak*

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Oxygenation Lung Recruitment Maneuvers During HFOV Ventilation Adjuncts to HFOV Prone Positioning Aerosol Medication Delivery Inhaled Nitric Oxide Tracheostomy Transition to Extracorporeal Membrane Oxygenation Fluctuation of mPaw and ∆P Transition from HFOV to Lung-Protective Conventional Ventilation Transport of Patients on HFOV Bronchoscopy During HFOV Troubleshooting During HFOV Pneumothorax Endotracheal Tube Misplacement or Obstruction Infection Control

OBJECTIVES

1. 2. 3. 4. 5. 6. 7.

Identify current indications for high-frequency oscillatory ventilation (HFOV). Understand basic mechanisms of oxygenation and ventilation during HFOV. Describe the role of endotracheal tube cuff leaks during HFOV. Describe the role of adjunctive therapies with HFOV (e.g., prone positioning). Identify common troubleshooting issues that may arise during HFOV (e.g., pneumothorax). Describe principles of weaning from HFOV to conventional ventilation. Describe principles of transition from HFOV to extracorporeal membrane oxygenation (ECMO).

KEY TERMS acute respiratory distress syndrome (ARDS) extracorporeal membrane oxygenation (ECMO) frequency hertz (Hz) high-frequency oscillatory ventilation (HFOV) lung-protective conventional ventilation (LPCV) mean airway pressure (mPaw) pressure amplitude of oscillation (∆P)

Introduction High-frequency oscillatory ventilation (HFOV) is primarily used as a rescue oxygenation mode for adults with acute respiratory distress syndrome (ARDS) complicated by severe oxygenation failure despite optimized lung-protective conventional ventilation (LPCV).1–4 The use of HFOV for less-severe forms of ARDS (e.g., patients already meeting gas exchange goals within acceptable LPCV parameters) is of unproven benefit, may increase mortality, and is not recommended for routine use.5–9 HFOV has not been demonstrated to reduce the incidence of barotrauma (e.g., pneumothorax) and is not recommended for bronchopleural fistula treatment alone in the absence of persistent hypoxemia on LPCV. Similarly, HFOV is not recommended for isolated hypercapneic respiratory failure associated with obstructive lung diseases, although it has been used successfully in patients with combined obstructive lung disease and severe ARDS.10,11 HFOV is usually considered after optimal LPCV with high positive end-expiratory pressure (PEEP), neuromuscular blockade, prone positioning, and correction of fluid overload have failed to achieve oxygenation goals. In clinical practice, a trial of HFOV may be utilized prior to initiating extracorporeal membrane oxygenation (ECMO) or when ECMO is considered relatively contraindicated (e.g., uncontrollable bleeding, intracranial hemorrhage).2 In its most basic form, HFOV may be viewed as delivering continuous positive airway pressure (CPAP) with superimposed small tidal volumes (50 to 250 mL) at cycling frequencies between 180 (3 Hz) and 900 (15 Hz) cycles per minute/sec (Figure 11-1). Note that 1 hertz (Hz) is 1 cycle per second or 60 cycles per minute. HFOV is sometimes referred to as “CPAP with wiggle.” The only HFOV ventilators approved in the United States for clinical use are the SensorMedics 3100A and 3100B (CareFusion, Yorba Linda, CA).

FIGURE 11-1 The SensorMedics 3100B HFOV. Courtesy Stephen Derdak.

This section will focus on clinical application of the SensorMedics 3100B HFOV in adult and/or large patients (> 35 kg) (Table 11-1). Respiratory therapists should refer to detailed information in the 3100B Operators Manual and receive specific 3100B clinical training before caring for patients.12 The SensorMedics 3100A HFOV is primarily used for neonates, infants, and children weighing < 35 kg.

TABLE 11-1 SensorMedics 3100B Features Bias flow

0 to 60 L/min

mPaw

3 to 55 cm H2O

mPaw alarms

0 to 59 cm H2O

mPaw dump valve

60 cm H2O

∆P

≥ 90 cm H2O (maximum power)

Frequency

3 to 15 Hz

Inspiratory time

30% to 50%

Expiratory filter

Change every 24 hours

Oxygenation Oxygenation on the HFOV 3100B is primarily adjusted by the mean airway pressure (mPaw) control. Setting mPaw for HFOV is similar to setting continuous positive airway pressure (CPAP) mode during conventional ventilation with the important exception that there is no demand inspiratory flow augmentation if the patient has spontaneous inspiratory efforts. If a patient is breathing spontaneously, the mPaw display will fluctuate in proportion to inspiratory efforts. In order to minimize ventilator asynchrony, chest wall elastance, skeletal muscle oxygen utilization, and fluctuation of mPaw, patients with severe oxygenation failure are usually pharmacologically paralyzed with a neuromuscular-blocking drug during the transition between conventional ventilation (CV) and starting HFOV. Neuromuscular blockers are often utilized on LPCV prior to starting HFOV and have been reported to improve both oxygenation and mortality if used early for severe ARDS.13 Initial setting of HFOV mPaw should approximate what Pplateau was during LPCV prior to starting HFOV (Table 11-2). Typically, this equates to setting mPaw at 30 to 34 cm H2O for the initial phase of HFOV (assuming a patient has normal chest wall compliance, normal intra-abdominal pressure, and a Pplateau in this range during optimized LPCV). Alternatively, initial mPaw setting during HFOV can be set approximately 5 cm H2O above the mPaw value during LPCV or to the value of Phigh or mPaw during airway pressure-release ventilation (APRV). TABLE 11-2 HFOV Initial Settings FIO2

100%

Bias flow

40 L/min

mPaw

30 to 34 cm H2O

mPaw high and low alarms

+/– 10 cm H2O around set mPaw

∆P

90 cm H2O

Frequency (Hz)

7

Inspiratory time

33%

Endotracheal tube (ETT) cuff leak

5 cm H2O

Higher mPaw may be necessary for patients with low chest wall compliance and/or intra-abdominal hypertension and low lung inflation on portable chest radiograph (Figure 11-2). Measurement of urinary bladder pressure (as a surrogate for intra-abdominal pressure) or esophageal pressure (as a surrogate for regional pleural pressure) to estimate transpulmonary distending pressure (Ptl) should be considered if higher mPaw appears to be required.14,15 Experimental animal models have demonstrated that approximately half of intra-abdominal pressure may be transmitted to inspiratory plateau pressure during volume-cycled conventional ventilation and a similar increment in pressure may limit transpulmonary distending pressure during HFOV.16

FIGURE 11-2 Chest Radiographs Showing Varying Levels of Lung Inflation. (A) Normal inflation (sixth anterior rib at right hemidiaphragm, mPaw 34 cm H2O). (B) Low lung inflation (fourth anterior right rib at right hemidiaphragm, mPaw 40 cm H2O, bladder pressure 28 cm H2O; mPaw should be increased). (C) Lung hyperinflation (seventh/eighth anterior right rib at right hemidiaphragm, mPaw 38 cm H2O; mPaw should be reduced). (A) through (C) Courtesy Stephen Derdak.

Lung recruitment maneuvers may be considered if significant desaturation occurs during the transition from the conventional ventilator circuit to the HFOV circuit. Lung recruitment maneuvers (e.g., sustained inflations with the piston paused) using HFOV are discussed below. Once a starting mPaw is chosen and HFOV is initiated, it may take 4 to 6 hours for oxygenation to equilibrate. Similarly, subsequent increases in mPaw may take at least an hour to achieve a new oxygen equilibrium.17,18 mPaw should be adjusted slowly in 2 to 3 H2O increments allowing adequate time (e.g., ≥ 1 hours) for observing oxygenation effects, similar to adjusting PEEP during LPCV.

Once oxygenation goals are achieved (e.g., arbitrarily, an SpO2 ≥ 88% with FIO2 ≤ 60%), mPaw may be slowly decreased in 2 to 3 cm H2O decrements every 4 to 6 hours with careful observation for oxygen desaturation and low inflation on chest radiographs. Using an FIO2 : mPaw table similar to the FIO2:PEEP table approach used by the ARDS Network conventional ventilation strategy may provide a general roadmap for respiratory therapists and clinicians caring for a patient on HFOV (see Appendix 11-A: HFOV Algorithm).19 However, it is important to realize that a low SpO2 or low PaO2 does not always mean that mPaw should be increased on HFOV. A low SpO2 may be due to fluid overload, pneumothorax, lung collapse, lung overinflation, inspissated secretions, or airway occlusion—all of which require different specific treatment approaches. Normally as HFOV frequency decreases, tidal volume and ventilation increase (assuming no change in mPaw and percent inspiratory time). It should be noted, however, that a rising PaCO2 does not always mean that frequency should be decreased. A rising PaCO2 can be due to mucus occlusion of the endotracheal tube (ETT) or airway, atelectasis, or loss of a desired ETT cuff leak. Recent negative clinical trials of HFOV for moderate severity ARDS that followed strict algorithms triggered by SpO2, PaO2, or PaCO2 values alone may not have incorporated these important caveats.2–5 Caution should be utilized when sustained high mPaw (e.g., > 34 cm H2O) appears necessary to achieve oxygenation goals. Estimating the degree of lung inflation on chest radiograph and measuring transpulmonary distending pressure (e.g., mPaw – Ppl or mPaw – [abdominal pressure × 0.5]) may be important to minimize ventilator-induced lung injury (VILI) during HFOV. Lung inflation may be estimated by counting the lowest anterior rib to cross the right hemidiaphragm.20 The fourth rib crossing the right hemidiaphragm indicates underinflation, the sixth rib suggests normal inflation, and those beyond the seventh/eighth ribs indicate hyperinflation. Hyperinflation on chest radiograph suggests the need to reduce mPaw (Figure 112). In contrast, low inflation on chest radiograph in conjunction with elevated abdominal pressures or low chest wall compliance (e.g., thoracic burn eschar) suggests the need to increase mPaw above 34 cm H2O if SpO2 or PaO2 remains low.

Obtaining a portable chest radiograph 60 to 90 minutes after initiating HFOV is recommended to assess the degree of lung inflation. Respiratory therapists should confer with physicians about the estimated degree of lung inflation on chest radiograph to assist with decision making about mPaw settings. Determining whether clinical outcomes improve with use of advanced lung imaging technologies, such as electroimpedance tomography, lung ultrasound, or bedside computed tomography (CT) scanners, to estimate lung inflation compared with conventional chest radiograph when setting mPaw will require future clinical trials.21

Lung Recruitment Maneuvers during HFOV Patients with severe oxygen desaturation following lung derecruitment events (e.g., circuit changes, bronchoscopy, suction) or who have low lung inflation on chest radiograph associated with reduced chest wall compliance or high abdominal pressures may benefit from a lung recruitment maneuver (RM). Whether routine RMs should be done prior to increases in mPaw steps for a low PaO2 or SpO2 remains controversial. The use of relatively high, continuous mPaw (30 to 35 cm H2O) during HFOV may be viewed as a lung-recruiting pressure itself, and the author does not recommend performing routine RMs unless a derecruiting event associated with oxygen desaturation has occurred. As stated above, adequate time (e.g., ≥ 1 hour) should be allowed following an increase in mPaw to observe oxygenation effects. Lung RMs are contra-indicated in patients with hemodynamic instability, active air leaks from the lung (e.g., bubbling chest tubes, mediastinal emphysema), or elevated intracranial pressure. An RM should be discontinued if desaturation or hemodynamic instability develops during the maneuver. Use of an RM checklist is recommended to ensure the correct sequence of steps are performed (see Appendix 11-A). Performing an RM with the HFOV piston turned off is recommended to avoid delivering potentially injurious tidal volumes during sustained inflation of the lung with higher mPaw. RC Insight Lung recruitment maneuvers (e.g., sustained inflation) may be considered following lung derecruiting procedures (e.g., bronchscopy, suction) if associated with significant oxygen desaturation. Recruitment maneuvers should be performed with the piston turned off.

Ventilation PaCO2 clearance during HFOV is primarily determined by delivered tidal volume (VT) and establishment of an endotracheal tube cuff leak. Delivered VT is not directly measured or displayed on the 3100B but is adjusted by the combination of pressure amplitude of oscillation (ΔP) (e.g., ∆P = peak oscillatory pressure – trough oscillatory pressure) and frequency (e.g., cycles/sec or Hz). Experimental models of HFOV and limited clinical data reported VT delivery ranging between 40 to 250 mL, depending on frequency, ∆P, ETT diameter, and % inspiratory fraction settings.12,22,23 ∆P is set by the power control (e.g., higher power settings result in higher ∆P). The lowest VT delivery to achieve a targeted PaCO2 and pH is obtained by using a high ∆P and high frequency (in contrast to a low ∆P and lower-frequency strategy). Highest VT delivery occurs when a low frequency is used in combination with a high ∆P. VT delivery may approach 240 mL when using an 8 mm I.D. ETT, frequency of 3 Hz, and ∆P of 90 cm H2O (e.g., approximating 4 mL/kg ideal body weight [IBW] in a 60-kg patient). Use of high-power, low-frequency settings (e.g., higher VT) in conjunction with high mPaw and lung hyperinflation may potentially contribute to VILI and should be avoided.24 Use of an endotracheal tube cuff leak (see below) may be lung protective in this situation and allow for use of higher frequency (e.g., lower VT). VT delivery approximates 140 mL when ∆P is 90 cm H2O and frequency is 7 Hz. This is close to the anatomical dead space of a 140-lb (IBW) patient. In order to achieve sub-dead space VT delivery and minimize lung stretch, a goal should be to achieve frequency ≥ 7 Hz whenever possible. Use of higher frequency may result in hypercapnia during HFOV, and a pH target of 7.25 to 7.30 (e.g., similar to permissive hypercapnea targets used for LPCV) is recommended. HFOV should be avoided or used cautiously in patients who are poor candidates for permissive hypercapnia (e.g., elevated intracranial pressure, right ventricular (RV) failure with pulmonary hypertension, pregnancy, unstable coronary artery disease, sickle cell disease, etc.). Transcutaneous CO2 monitoring (PtcCO2) may be useful to follow PaCO2 trends during HFOV and should be considered in higher-risk patients expected to be intolerant of hypercapnia. In the past, setting power (rather than a specific ∆P) to achieve “chest wiggle

down to the mid-thigh” was commonly done and is still utilized in some centers and for neonatal applications. With increased understanding of tidal volume delivery during HFOV and the potential for causing VILI at low frequency (higher VT) and high mPaw settings, the author does not recommend titrating to “chest wiggle down to the mid-thigh” in adults. Prolonging the inspiratory time has a modest effect on delivered VT compared with frequency and ∆P and is usually set at 33% (corresponding to an inspiratory:expiratory ratio of 1:2). A longer inspiratory time (e.g., 50%) may result in air trapping and distal alveolar pressure that may be higher than the mPaw displayed on the 3100B, analogous to the development of occult PEEP during conventional ventilation.25 VT is also influenced by the size of the endotracheal tube, with smaller internal diameter ETTs delivering less VT than larger ETT.12 A rising PaCO2 in an otherwise stable patient may indicate a narrowing inside the ETT tube or airways from inspissated mucus. Placement of an ETT cuff leak during HFOV often improves PaCO2 clearance and allows use of higher frequency.26 It is important to document the presence of a leak with an end-tidal CO2 monitor at the nose and/or mouth. Oral or nasal airway adjuncts may be necessary to facilitate a leak if oropharyngeal edema or a large tongue prevents leakage of gas around the partially deflated ETT cuff. Typically, a 5 cm H2O ETT cuff leak is sufficient to improve PaCO2 clearance and is less likely to destabilize mPaw than complete deflation of the cuff. Induced ETT cuff leaks can vary with patient head positioning and must be checked frequently, particularly if the patient is repositioned (e.g., for portable chest radiographs, prone positioning, bathing, etc.). RC Insight Abrupt increase in PaCO2 during HFOV may signify loss of a desired endotracheal tube cuff leak.

If a transmissible airway infection is suspected and an ETT cuff leak is being utilized, the mouth and nose should be loosely covered with a surgical mask to minimize aerosol exposure to intensive care unit (ICU) personnel. Sequential steps for placing an ETT cuff leak during HFOV are outlined in 11-1 HFOV Algorithm for Severe ARDS Period A 5 cm H2O ETT cuff leak can be placed by briefly increasing

the bias flow until mPaw increases by 5 cm H2O, followed by slow cuff deflation until the mPaw is reduced back to the desired pre-leak mPaw setting. The presence of a cuff leak can be confirmed during HFOV ventilator checks by gently squeezing the ETT cuff and seeing a rise in mPaw. For patients who develop low PaCO2 during HFOV (e.g., respiratory alkalosis), removing the ETT cuff leak and gradually increasing frequency (increase 1 Hz every 30 to 60 minutes), guided by PaCO2, PETCO2, or PtcCO2, should be done until target pH and PaCO2 are achieved.

Adjuncts to HFOV Patients on HFOV are critically ill and may receive the same adjuncts that are used during LPCV (Table 11-3). Adjuncts to HFOV include prone positioning, aerosol medication delivery, inhaled nitric oxide, and tracheostomy. TABLE 11-3 Adjuncts to HFOV Chest radiograph estimate of lung inflation (right anterior rib count) Transcutaneous PCO2 monitoring End-tidal Petco2 monitoring (ETT, mouth, nares) Prone positioning Neuromuscular paralysis (cisatracurium) Diuresis Endotracheal tube cuff leak Lung recruitment maneuvers Inhaled nitric oxide Aerosolized medications (prostacyclin [Flolan], heparin, antibiotics, saline)

Prone Positioning Prone positioning has been demonstrated to improve mortality in severe ARDS and can be initiated during HFOV (if not already being done during LPCV prior to transition).27 Special care must be employed to avoid circuit kinking, endotracheal tube malposition or occlusion, and loss of the ETT cuff leak during prone positioning. Use of a specialized prone positioning bed (e.g., RotoProne, ArjoHuntleigh, Malmo, Sweden) facilitates prone positioning, although this is not an absolute requirement. The respiratory therapist should perform frequent (every 1 to 2 hours) checks to confirm ETT cuff leak presence, position of oral and/or nasal airways, endotracheal tube patency by passage of an inline suction catheter, and stability of mPaw and ∆P settings—especially in the initial hours following prone positioning. Prone positioning should be initiated in the morning (e.g., during day shift when the most ICU personnel are available) with resumption of supine position after 12 to 16 hours. Use of a prone positioning checklist is recommended. Details on the physiology and mechanics of prone positioning are found in Chapter 3. Clinical Focus 11-1 demonstrates the use of HFOV.

CLINICAL FOCUS 11-1 A 56-year-old male with severe ARDS (PaO2/FIO2 ratio 80 mmHg) is on HFOV (mPaw 34, ΔP 90, frequency 6 Hz, bias flow 40 L/min, FIO2 80%) with an endotracheal tube cuff leak in place to maintain pH 7.30 with PaCO2 60 mmHg. One hour following prone positioning, he is noted to have improvement in PaO2/FIO2 ratio to 140 mmHg; however, pH is now 7.20 and PaCO2 is 75 mmHg. Question 1. What has likely occurred, and what should be done next? Patients with severe ARDS on HFOV often improve oxygenation in the prone position, similar to patients on conventional ventilation. This patient required an endotracheal tube cuff leak to improve CO2 clearance and with repositioning of the head or tongue while turning from the supine to prone position likely lost some of the leak. The first step in assessment is to verify that a cuff leak is still present by gently squeezing the cuff and noting a rise in mPaw (at least 5 cm H2O). Additionally, PetCO2 can be confirmed at the nares and mouth and should be similar to values observed when supine. If a leak is not present or diminished when prone, an oral or nasal airway should be considered (or repositioned) to restore the leak.

Aerosol Medication Delivery Aerosol delivery of drugs during HFOV is most efficiently achieved by inserting a vibrating mesh nebulizer (VMN) between the ETT tube and circuit Y.28,29 Drug doses delivered using a VMN have been reported in the range of 14% to 22% of the instilled dose and are similar to the ranges reported for conventional ventilation. Delivery of aerosolized medication during HFOV is optimized by use of largerdiameter endotracheal tubes, higher frequency, lower ∆P, higher mean airway pressures, and higher bias flows. Use of flow-driven nebulizers will cause mPaw fluctuations and are not recommended during HFOV. Drugs that can be aerosolized during HFOV include bronchodilators, corticosteroids, prostacyclins, heparin, and antibiotics. The indications for specific aerosolized medications during mechanical ventilation are discussed in Chapter 9.

Inhaled Nitric Oxide Inhaled nitric oxide (iNO) is a pulmonary vasodilator approved by the U.S. Food and

Drug Administration (FDA) to improve oxygenation and reduce the need for extracorporeal membrane oxygenation in term and near-term (> 34 weeks gestation) neonates with hypoxic respiratory failure associated with clinical or echocardiographic evidence of pulmonary hypertension. It is not approved by the FDA for adult use, however iNO is commonly used off-label in the evaluation and treatment of adults with pulmonary artery hypertension (PAH) and/or right ventricular (RV) failure. In addition to use in adults with PAH, iNO may be considered as a rescue oxygenation therapy for patients with persistent, severe hypoxemia despite optimized mechanical ventilation in an attempt to improve V̇/Q̇ . Clinical trials of iNO for adult ARDS have demonstrated short-term (e.g. 48–72 hr) oxygenation improvement, but failed to demonstrate improved mortality. The routine use of iNO for oxygenation failure during HFOV is not recommended based on lack of evidence for improved outcomes and concerns that iNO may increase the risk of acute kidney injury.30 A trial of iNO may still be considered in patients in whom severe ARDS is associated with right ventricular failure and pulmonary hypertension (e.g., postcardiac surgery ARDS with RV failure, massive pulmonary embolism associated with shock, post-traumatic pneumonectomy RV failure, etc.) If used, iNO should be titrated to the lowest effective parts per million (ppm) dose that produces an objective improvement in measured hemodynamics or oxygenation. Daily iNO ppm dose de-escalation and retitration should be performed to ensure that objective improvement is maintained (e.g., improved PaO2/FIO2 ratio > 20%, improvement in pulmonary artery pressure, improved right ventricle function) and that the lowest effective dose is utilized for the shortest time.

Tracheostomy Bedside or operating room (OR) open tracheostomy can be performed during HFOV. Bronchoscopy-assisted percutaneous tracheostomy is not recommended during HFOV due to the need to occlude the ETT with a bronchoscope (e.g., causing acute hypercapnea) as well as the risk of potential loss of the airway with ETT withdrawal during the procedure. The respiratory therapist may be asked to briefly pause the piston during specific parts of an open tracheostomy procedure. Oxygen desaturation during and/or following tracheostomy placement is common due to

transient loss of mPaw with ETT tube removal. Additionally, PaCO2 may increase if blood and/or clots occlude the tracheostomy tube lumen or distal airway. Respiratory therapists should anticipate these events and be prepared to suction blood from the airway, perform a lung recruitment maneuver if severe desaturation occurs, and install a cuff leak with the new tracheostomy tube (especially if one was being used prior to the procedure). Monitoring continuous transcutaneous PCO2 is recommended for early detection of hypercapnea during and following tracheostomy.

Transition to Extracorporeal Membrane Oxygenation Patients who fail to achieve gas exchange goals while on lung-protective HFOV settings (e.g., mPaw ≤ 34 cm H2O if normal chest wall and abdominal compliance, or if measured, a transpulmonary distending pressure ≤ 25 cm H2O) may be transitioned directly to venovenous ECMO (VV-ECMO) while continuing HFOV at lower lung-protective settings. A persistent oxygenation index > 40 (or mPaw > 40) with failure to achieve gas exchange goals for > 4 to 6 hours has been suggested as a criterion for considering transition to VV-ECMO. Calculation of the respiratory ECMO survival prediction (RESP) score may be useful in estimating patient prognosis at the time of VV-EMCO initiation.31 Once cannulation and effective VV-ECMO gas exchange is underway, FIO2 can usually be reduced to ≤ 40%, HFOV mPaw reduced to 22 to 24 cm H2O, and frequency increased to ≥ 7 Hz for an initial phase of ultra-low tidal volume lung protection while maintaining some degree of lung inflation. If an ETT cuff leak had been utilized during HFOV, it can be removed after transition to VV-ECMO because of the efficiency of PaCO2 clearance with sweep gas flow. Maintaining frequency > 7 Hz facilitates minimal VT delivery (e.g., VT < 140 mL) while buying time for the lung to heal. If the ARDS lung injury improves, chest radiography or CT scan may demonstrate increasing lung inflation while maintaining a relatively low mPaw of 22 to 24 cm H2O. An increasing PetCO2 may also indicate the lung is improving (e.g., decreasing dead space) if associated with decreasing PaCO2 (or PtcCO2) and suggests that a trial of gradual sweep flow reduction can be undertaken to see if the patient can sustain adequate gas exchange on HFOV alone.

Alternatively, if the patient is on VV-ECMO as a “bridge” to lung transplant, it may be appropriate to transition from HFOV to a lung-protective LPCV strategy with the goal of weaning completely off the ventilator while continuing VV-ECMO and physical therapy until transplant can be performed. The goal of ECMO for individual patients (e.g., bridge to recovery versus bridge to lung transplant versus bridge to decision) and the priority of whether to “wean the ventilator first” versus “wean ECMO first” will impact both duration of ECMO and the specific ventilator strategies used. ECMO and ventilator goals should be clearly defined and coordinated by the critical care and respiratory teams. Emergency HFOV settings should be established and updated frequently in the event ECMO must be suddenly stopped. Early in the course of ECMO, this would typically require resuming HFOV settings similar to those used prior to transitioning to ECMO. Additionally, an RM may be necessary if lung inflation is reduced from the lower mPaw settings used during ECMO. Mechanical ventilation strategies during ECMO are discussed in more detail in Chapter 14.

Fluctuation of mPaw and ∆P Fluctuation or “drift” of mPaw and/or ∆P is common during HFOV. A cyclic decrease and increase in mPaw may indicate the patient is breathing spontaneously. This may be occurring from diaphragm contractions even though the patient does not appear to be breathing. Fluctuation of mPaw ≥ 5 cm H2O is common with shallow spontaneous breathing and may not be associated with oxygen desaturation. If associated with oxygenation desaturation or respiratory distress, fluctuating mPaw may indicate the need for increased sedation and/or neuromuscular paralysis. Bracketing the targeted mPaw with low and high mPaw alarms at +/– 10 cm H2O will alert the respiratory therapist and critical care team if excessive mPaw fluctuation is occurring. Patients in whom ARDS is improving (e.g., weaning mPaw phase) can often breathe spontaneously without desaturation and may tolerate reduction or discontinuation of neuromuscular-blocking drugs. Another important cause of mPaw fluctuation is variability in the degree of ETT cuff leak as head or tongue position changes. The presence of an ETT cuff leak can be confirmed by gently squeezing the ETT cuff pilot balloon and observing for a rise in mPaw; no rise in mPaw with this maneuver indicates absence of a leak. Absence of cuff leak can also be confirmed if no PetCO2 is detectable at the mouth or nares. Head and neck repositioning and/or placement of oral or nasal airways may be required to ensure a continuous ETT cuff leak. An increasing power setting to maintain the same set ∆P may occur if lung compliance increases, airway resistance decreases, bronchopleural fistula leakage increases, or with increasing ETT cuff leak. In contrast, a decreasing power setting to maintain the target ∆P may indicate an increase in airway resistance (e.g., inspissated mucus or blood occlusion of the ETT or airway), decreased lung compliance, or atelectasis. Monitoring (and recording) both ∆P and the power setting needed to achieve the desired ∆P is important so that trends can be observed and incorporated into clinical decision making.

Transition from HFOV to Lung-Protective Conventional Ventilation Patients can usually be transitioned back to LPCV when mPaw has been weaned to 22 to 24 cm H2O while maintaining satisfactory oxygenation on FIO2 40% to 50%. A rise in PaCO2 during mPaw weaning may be due to lung derecruitment, particularly if associated with decreasing lung inflation on chest radiograph. Alternatively, a rising PaCO2 during mPaw weaning may be due to retrograde entrainment of exhaled PetCO2 into the inspiratory limb of the circuit, particularly if a high ∆P is maintained during weaning of mPaw.32 This phenomenon can be minimized by decreasing ∆P, utilizing an ETT cuff leak, and increasing bias flow. Before changing between the HFOV and conventional ventilator circuit, the ETT tube cuff leak should be removed and the ETT briefly clamped in order to avoid abrupt lung derecruitment during the circuit change. Neuromuscular paralysis can usually be reduced or discontinued during the weaning phase before the patient is placed back on LPCV. As with conventional ventilation for ARDS, discussion between the respiratory therapist and physician regarding use of neuromuscular blockers is essential. Initial LPCV settings are typically set with a respiratory rate of 20 to 25 breaths/min, VT of 6 mL/kg/IBW in either assist/control-pressure control (A/C-PC) or assist/control-volume control (A/C-VC) modes, PEEP 14 to 16 cm H2O, and FIO2 10% higher than the value on HFOV. Subsequent conventional ventilator parameter changes and weaning can be performed using the lung-protective approach of the ARDSNet algorithm.33 Alternatively, patients can be transitioned to airway pressure-release ventilation (APRV) with Phigh set to match the mPaw while on HFOV. Subsequent APRV settings are adjusted to facilitate adequate minute ventilation with a VT < 6 to 8 mL/kg IBW and spontaneous breathing augmentation with automatic tube compensation (ATC) and/or pressure-support ventilation (PSV).

Transport of Patients on HFOV Because of electromagnetic emissions, the SensorMedics 3100B is not approved for aeromedical transport applications. For patients who require transport, transition to a portable conventional ventilator or pneumatic high-frequency percussive ventilator (e.g., Bronchotron transport ventilator, Percussionaire, Sagle, ID) is necessary. Care should be taken during the circuit change to prevent loss of mPaw and rapid lung derecruitment by first removing the ETT cuff leak and briefly clamping the endotracheal tube while the change is made. LPCV or high-frequency percussive ventilation (HFPV) parameters should be set to approximate the mPaw utilized during HFOV. A 30- to 60-minute period of observation with blood gas monitoring is advisable to ensure patient stability prior to initiating transport. For operating room (OR) use, a 3100B can be set up and running before the patient arrives. Inhalational anesthesia is not recommended during HFOV due to the loss of anesthetic gas from the exhalation valves of the circuit and/or airway if an ETT cuff leak is being used. Total intravenous anesthesia is recommended if the patient is to remain on HFOV during surgery. A qualified respiratory therapist should remain in the OR to assist the OR team with managing the 3100B and throughout the perioperative recovery period while the patient is out of the ICU. Brief pauses of the piston may be requested by the surgeon to reduce motion in the operative field (e.g., during tracheostomy).

Bronchoscopy During HFOV Bronchoscopy is frequently performed during HFOV to assess airway humidification, evaluate ETT and airway patency, and to obtain bronchoalveolar lavage specimens (e.g., for cultures, differential cell count, or evaluate the etiology of ARDS). Initial placement of an inline-suction adapter at the HFOV circuit Y that contains a bronchoscopy port facilitates performance of bronchoscopy during the course on HFOV and minimizes lung decruitment that occurs with circuit disruption needed to place a conventional PEEP-saver adapter (Figure 11-3).

FIGURE 11-3 (A) AirLife Verso Adapter, CareFusion. (B) The Halyard MultiAccess Catheter Port Adapter. (A) and (B) Courtesy Stephen Derdak

Equipment and medications necessary for bronchoscopy during mechanical ventilation are discussed in Chapter 12. Prior to performing bronchoscopy, FIO2 should be increased to 100%. An additional neuromuscular paralysis bolus dose should be considered for patients who cough or move with passage of a suction catheter to the carina. Patients who move or desaturate with catheter suctioning can be expected to desaturate during bronchoscopic suction. Bronchoscopy should be performed as quickly as feasible in critically ill patients on HFOV. Monitoring transcutaneous carbon dioxide tension (PtcCO2) as a surrogate for PaCO2 along with SpO2 may be useful in deciding when to terminate the procedure. “Quick look” bronchoscopy to inspect the ETT lumen, proximal airway, and bronchial mucosal appearance (e.g., humidity assessment) can usually be done without destabilizing the patient. In contrast, oxygen desaturation and hypercapnea should be anticipated if prolonged bronchoscopy and/or bronchoalveolar lavage (BAL) is performed. If this occurs, performance of a lung recruitment maneuver following bronchoscopy, or alternatively, use of a 2 to 3 cm H2O higher mPaw for several hours until oxygenation recovers, may be necessary.

Troubleshooting During HFOV Complications and hazards that may occur during HFOV include pneumothorax, endotracheal tube or airway obstruction, inadequate airway humidification, and sudden HFOV stoppage.

Pneumothorax It is important for respiratory therapists to understand that during HFOV, no ventilator alarms occur as a tension pneumothorax develops. As intrathoracic tension develops, oxygenation and ventilation will deteriorate, but mPaw will remain constant. An important clinical clue is the development of oxygen desaturation associated with new hypotension and tachycardia. Immediate bedside lung ultrasound or portable chest radiograph is essential to evaluate for pneumothorax (see Clinical Focus 11-2).

CLINICAL FOCUS 11-2 A 32-year-old female with severe viral pneumonia has been on HFOV for 48 hours with stable ventilator settings (mPaw 30, ΔP 90, frequency 7 Hz, bias flow 40 L/min, FIO2 50%) with pulse oximeter SpO2 varying between 92% to 94%. Over the last 2 hours, SpO2 has gradually decreased to 80% and a norepinephrine infusion has been started for new hypotension. No ventilator alarms are observed. Question 1. What should be ruled out as soon as possible? A decreasing SpO2 along with new hypotension developing while on HFOV is a tension pneumothorax until proven otherwise. Similar to conventional pressurelimited modes of ventilation, no pressure alarms on the HFOV will be triggered as a tension pneumothorax develops. Although septic shock, congestive heart failure, and pulmonary embolism can also result in a decreasing SpO2 associated with new hypotension, the first action to take is immediate lung ultrasound or portable chest x-ray to rule out a pneumothorax. If pneumothorax is confirmed, a chest tube should be placed. A decreasing SpO2 may prompt consideration of increasing the HFOV mPaw when following an algorithm for oxygenation; however, in the setting of a pneumothorax, this will worsen the situation. Clinical assessment of the patient by the respiratory therapist prior to increasing mPaw for a low SpO2 is important when following HFOV (or any) ventilator protocols.

Endotracheal Tube Misplacement or Obstruction Similar to pneumothorax, no ventilator alarms may occur in the presence of a right mainstem bronchus intubation or with partial occlusion of the ETT or distal airway with inspissated mucus or blood clots. Passage of the inline suction catheter every 2 to 4 hours is recommended to ensure ETT patency. Suction does not need to be done every time the catheter is passed if minimal return is obtained. If SpO2 drops with suction, the patient should be pre-oxygenated with FIO2 100%.19 RC Insight Tension pneumothorax, right mainstem intubation, or an occluded endotracheal tube may not cause any HFOV ventilator alarms to trigger.

A low threshold to perform bronchoscopic inspection for ETT and distal airway patency is important. Patients with overt pulmonary edema or blood flowing into the ETT and airway will require suction to clearing before HFOV can be successfully used. Humidification during HFOV is achieved with use of an expiratory filtered circuit with integrated heated wire and a conventional humidifier. Heat moisturizer exchangers (HME) should not be used during HFOV. Airway humidification may be reduced if a large ETT cuff leak is used. If bronchoscopy suggests airway drying, saline aliquots (4 to 8 mL) may be instilled through the suction catheter positioned at the carina every 2 to 4 hours. It is important to periodically visualize the airway with bronchoscopy to ensure patency, mucosal integrity, and adequacy of humidification. It may be necessary to remove the ETT cuff leak if airway humidity is insufficient. If the mPaw dump pressure is exceeded (> 59 cm H2O) or airway pressure is suddenly lost (e.g., a circuit valve pops off), the 3100B may abruptly stop. It is essential to keep a selfinflating bag-valve mask with an attached PEEP valve immediately available at the head of the bed at all times. If sudden stoppage occurs, the patient should be manually ventilated with FIO2 100% and PEEP (15 to 20 cm H2O) while the cause is quickly determined and corrected.

RC Insight Abrupt stoppage of the 3100B may occur if a circuit pressure valve leaks or pops off. A self-inflating manual ventilation bag with PEEP valve should always be immediately available at the head of the bed.

Infection Control Infectious droplets and medication aerosols may escape from the expiratory valve of the HFOV circuit. The 3100B expiratory filter should be utilized to minimize escape of infectious droplets from the expiratory valve (Figure 11-4). This filter should be changed every 24 hours or if overt contamination with secretions is visualized. An increase in mPaw may indicate that resistance across the expiratory filter has increased, indicating the need for a filter change. The use of an ETT cuff leak may also result in airborne infectious droplets emitting from the nares and/or mouth. A surgical mask can be placed over the patient’s mouth and nose to capture airborne infectious droplets that may escape into the room. These precautions are especially important for patients with suspected airborne infectious causes of ARDS (e.g., influenza, adenovirus, tuberculosis, etc.) and should be considered for all patients on HFOV to minimize occupational exposure to bedside personnel. The use of negative airflow rooms, personal protective equipment, and environmental infection control should comply with current standards for transmission-based precautions specified by the Centers for Disease Control and Prevention (available at www.CDC.gov).

FIGURE 11-4 The Halyard MultiAccess Catheter Port Adapter. Courtesy Stephen Derdak

Key Points HFOV is primarily used as a rescue oxygenation mode for patients with severe ARDS. HFOV may be considered for patients with severe oxygenation failure on LPCV prior to ECMO (and/or if ECMO is contraindicated). HFOV delivers small tidal volumes (e.g. 50 to 250 mL) at cycling frequencies between 3 and 15 Hz (180 and 900 cycles/min). mPaw is the main determinant of oxygenation during HFOV. Increasing ∆P and decreasing frequency increases tidal volume delivery and carbon dioxide clearance during HFOV. Endotracheal tube cuff leaks facilitate carbon dioxide clearance during HFOV. Adjuncts to HFOV include prone positioning, neuromuscular paralysis, lung recruitment maneuvers, aerosolized pulmonary vasodilators, and inhaled nitric oxide. HFOV should be avoided or used cautiously in patients who are poor candidates for permissive hypercapnia. Routine use of inhaled nitric oxide (iNO) is not recommended for oxygenation failure during HFOV. With proper monitoring and care, bedside or operating room open tracheostomy can be performed during HFOV; percutaneous tracheostomy is not recommended. Patients can usually be transitioned from HFOV to lung-protective conventional ventilation when the mPaw has been weaned to 22 to 24 cm H2O with FIO2 of 0.40 to 0.50. Bronchoscopy is frequently performed during HFOV to assess humidification, obtain bronchoalveolar lavage specimens, and evaluate airway and ETT patency. HFOV complications and hazards include pneumothorax, endotracheal tube or airway obstruction, inadequate humidification, and sudden HFOV ventilator stoppage. Infection control precautions for infectious aerosols are important when caring for patients on HFOV.

References 1. Derdak S, Mehta S, Stewart TE, et al. High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med. 2002;166:801–808. 2. Meade MO, Young D, Hanna S, et al. Severity of hypoxemia and effect of high-frequency oscillatory ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2017;196:727–733. 3. Nguyen AP, Schmidt UH, MacIntyre NR. Should high-frequency ventilation in the adult be abandoned? Respir Care. 2016;61:791–800. 4. Sklar MC, Fan E, Goligher EC. High-frequency oscillatory ventilation in adults with ARDS: past, present, and future. Chest. 2017;152:1306–1317. 5. Ferguson ND, Cook DJ, Guyatt GH, et al. High-frequency oscillation in early acute respiratory distress syndrome. N Engl J Med. 2013;368:795–805. 6. Malhotra A, Drazen JM. High-frequency oscillatory ventilation on shaky ground. N Engl J Med. 2013;368:863–865. 7. Marini J. Does high-pressure, high-frequency oscillation shake the foundations of lung protection? Intens Care Med. 2015;41:2210–2212. 8. Dreyfuss D, Ricard JD, Gaudry S. Did studies on HFOV fail to improve ARDS survival because they did not decrease VILI? On the potential validity of a physiological concept enounced several decades ago. Intens Care Med. 2015;41:2076–2086. 9. Goligher HC, Munshi L, Adhikari NKJ, et al. High-frequency oscillation for adult patients with acute respiratory distress syndrome: a systematic review and meta-analysis. Ann Am Thorac Soc. 2017;14:S289–S296. 10. Frerichs I, Achtzehn U, Pechmann A, et al. High-frequency oscillatory ventilation in patients with acute exacerbation of chronic obstructive pulmonary disease. J Crit Care. 2012;27:172–181. 11. Friesecke S, Stecher SS, Abel P. High-frequency oscillation ventilation for hypercapnic failure of conventional ventilation in pulmonary acute respiratory distress syndrome. Crit Care. 2015;19:201. 12. CareFusion. 3100B high frequency oscillatory ventilator operator’s manual. Yorba Linda, CA: CareFusion. Available at http://www.bd.com or http://www.carefusion.com. 13. Papazian L, Forel J-M, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107–1116. 14. Keller SP, Fessler HE. Monitoring of oesophageal pressure. Curr Opin Crit Care. 2014;20:340–346. 15. Sahetya SK, Brower RG. The promises and problems of transpulmonary pressure measurements in acute respiratory distress syndrome. Curr Opin Crit Care 2016;22:7–13. 16. Cortes-Puentes GA, Cortes-Puentes LA, Adams AB, et al. Experimental intra-abdominal hypertension influences airway pressure limits for lung protective mechanical ventilation. J Trauma Acute Care Surg. 2013;24:1468–1473. 17. Chiumello D, Coppola S, Froio S, et al. Time to reach a new steady state after changes of positive end expiratory pressure. Intens Care Med. 2013;39:1377–1385. 18. Brower RG. Time to reach a new equilibrium after changes in PEEP in acute respiratory distress syndrome patients. Intens Care Med. 2013;39:2053–2055. 19. Fessler HE, Derdak S, Ferguson ND, et al. A protocol for high-frequency oscillatory ventilation in adults: results from a roundtable discussion. Crit Care Med. 2007;35:1649–1654. 20. Ely EW, Bowton DL, Reed JC, et al. Portable chest radiographs identify mechanical ventilator-associated hyperinflation. Chest. 1994;106:545^551. 21. Pesenti A, Musch G, Lichtenstein D, et al. Imaging in acute respiratory distress syndrome. Intens Care Med. 2016;42:686–698. 22. Sedeek KA, Takeuchi M, Suchodolski K, et al. Determinants of tidal volume during high frequency oscillation. Crit Care Med. 2003;31:227–231. 23. Hager DN, Fuld M, Kaczka DW, et al. Four methods of measuring tidal volume during high frequency oscillatory ventilation. Crit Care Med. 2006;34:751–757. 24. Derdak S. Lung-protective higher frequency oscillatory ventilation. Crit Care Med. 2008;36:1358–1359. 25. Pillow JJ, Neil H, Wilkinson MH, Ramsden CA. Effect of I/E ratio on mean alveolar pressure during highfrequency oscillatory ventilation. J Appl Physiol. 1999;87:407–414. 26. Fessler HE, Hager DN, Brower RG. Feasibility of very high-frequency ventilation in adults with acute respiratory distress syndrome. Crit Care Med. 2008;36:1043–1048.

27. Guerin C, Reignier J, Richard J-C, et al. N Engl J Med. 2013;368:2159–2168. 28. Fang T-P, Lin H-L, Chiu S-H, et al. Aerosol delivery using jet nebulizer and vibrating mesh nebulizer during high frequency oscillatory ventilation: an in vitro comparison. J Aerosol Med Pulm Drug Deliv. 2016;29(5):447–453. 29. Parker D, Shen S, Zhiang J, et al. Inhaled treprostinil delivery using a vibrating mesh nebulizer in mechanically ventilated adult, pediatric, and infant lung models (abstract). Respir Care. 2014;59(10):OF6. 30. Afshari A, Brok J, MØller AM, Wetterslev J. Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) and acute lung injury in children and adults. Cochrane Database Syst Rev. 2010 Jul 7; (7):CD002787. 31. Schmidt M, Bailey M, Sheldrake J, et al. Predicting survival after extracorporeal membrane oxygenation for severe acute respiratory failure: the respiratory extracorporeal membrane oxygenation survival prediction (RESP) score. Am J Respir Crit Care Med. 2014;189:1374–1382. 32. Bostick AW, Naworol GA, Britton TJ, et al. Inspiratory limb carbon dioxide entrainment during highfrequency oscillatory ventilation: characterization in a mechanical test lung and swine model. Respir Care. 2012;57:1865–1872. 33. NIH-NHBLI ARDS Clinical Network. Mechanical ventilation protocol summary. Available at http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf. Accessed July 1, 2016.

11-1 – HFOV Algorithm for Severe ARDS



*Note: The views expressed in this chapter are those of the author and do not represent the offi cial policy or views of the Department of the Air Force or other departments of the U.S. government.

CHAPTER

12 Diagnostic and Supportive Procedures in the ICU Adriel Malave and Kevin Proud

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Bronchoscopy Diagnostic Bronchoscopy Thoracentesis Supportive Procedures Temperature Regulation in the ICU Dialysis in the ICU Overview and Definitions Nutrition in the ICU Extracorporeal Membrane Oxygenation Indications Methods Monitoring During ECMO Discontinuance Mechanical Circulatory Assistance Indications Methods Monitoring Discontinuance of Mechanical Circulatory Support

OBJECTIVES 1. 2.

Contrast diagnostic and therapeutic bronchoscopy in the ICU. Describe the steps in performing bronchoscopy with bronchoalveolar lavage (BAL).

3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.

Recognize the risks associated with bronchoscopy. Review the indications for performing a thoracentesis. Describe the steps in performing thoracentesis. Determine the potential complications of a thoracentesis. Review the indications and methods for managing environmental hyperthermia. Review the indications and methods for managing environmental hypothermia. Describe the indications and goals of targeted temperature therapy after cardiac arrest. Provide an overview of the role of dialysis in the ICU. Highlight the importance of providing adequate nutritional support in the ICU. Explain the benefits of early enteral nutrition. Contrast the risks and benefits associated with parenteral nutrition. Determine barriers to providing nutritional support. Provide an overview of indications, goals, and contraindications for extracorporeal membrane oxygenation (ECMO). Describe the two major types of ECMO and disease processes that lead to mode selection. Explain the steps in starting and managing ECMO. Review key parameters to be monitored during ECMO. Describe the criteria and processes for discontinuing ECMO. Review key parameters to be monitored during mechanical circulatory support (MCS). Describe the different modes of MCS and conditions associated with the use of each mode. Describe methods of MCS initiation. Review key parameters to be monitored during mechanical circulatory support. Describe the criteria for and processes of discontinuing mechanical circulatory support.

KEY TERMS acute respiratory distress syndrome (ARDS) bronchoscopy bronchoalveolar lavage (BAL) cardiopulmonary bypass continuous renal replacement therapy (CRRT) continuous venovenous hemodialysis (CVVHD) continuous venovenous hemofiltration (CVVH) dialysis echocardiography ejection fraction enteral nutrition Extracorporeal Life Support Organization (ELSO) extracorporeal membrane oxygenation (ECMO) exudative pleural effusion hyperthermia hypothermia hypoxemic respiratory failure intra-aortic balloon pump (IABP) left ventricular assist device (LVAD) mechanical circulatory support (MCS) parenteral nutrition percutaneous pleural effusion right ventricular failure slow, extended daily dialysis (SLEDD) sustained low-efficiency dialysis (SLED) thermodilution thoracentesis

total artificial heart (TAH) total parenteral nutrition (TPN) venoarterial (VA) venovenous (VV)

Introduction The purpose of this chapter is to overview several important diagnostic and supportive procedures and techniques used in the care of patients in the intensive care unit (ICU). Invasive diagnostic procedures sometimes performed in the ICU include bronchoscopy and thoracentesis. Bronchoscopy allows the physician to evaluate the airway and remove specimens or secretions for diagnostic purposes. Thoracentesis allows for removal of fluid from the pleural space for analysis in order to evaluate pleural effusions. Thoracentesis may also be useful in certain patients with pleural effusions to relieve symptoms (e.g., dyspnea) and in patients with large pleural effusions or those with hemothorax or tuberculosis that may otherwise cause pleural thickening. Supportive procedures performed in the ICU include techniques for temperature regulation, dialysis, and nutritional support. Techniques to regulate temperature may be applied in patients who have an abnormally elevated temperature (e.g., fever, heat stroke) or abnormally low temperature (e.g., environmental hypothermia). Dialysis may be necessary in certain patients with kidney failure. Nutritional support may be required in ICU patients who are malnourished with increased metabolic demands. Other cardiopulmonary supportive measures sometimes used in the ICU include extracorporeal membrane oxygenation (ECMO) and mechanical circulatory assistance. ECMO is sometimes used in adult patients with severe cardiac or respiratory failure in order to support oxygenation. Mechanical circulatory assistance may be useful in certain patients with heart failure and as a bridge to heart transplantation. Noninvasive diagnostic imaging procedures used in the ICU include critical care ultrasonography, which will be discussed in Chapter 13.

Bronchoscopy Diagnostic bronchoscopy typically involves inspection of the airway and removal of tissue specimens, cell washings, or respiratory tract secretions for analysis. Therapeutic bronchoscopy may be performed to manage secretions or remove abnormal endobronchial tissue, foreign bodies, or other foreign material. RC Insight Bronchoscopy performed in the ICU may be diagnostic or therapeutic or both.

Diagnostic Bronchoscopy There are a host of indications for the use of rigid or flexible bronchoscopy; however, flexible bronchoscopy is most commonly used in the ICU, while rigid bronchoscopy is generally performed in the operating room under general anesthesia. The flexible bronchoscope is comprised of a malleable sheath containing the necessary cables to allow flexion and extension of the tip of the scope, while harboring encapsulated fibers that transmit the endobronchial images onto a screen. The instrument also has a light source and a working channel to facilitate usage of the tools for diagnostic or therapeutics purposes. The tools include forceps, sterile brush, cytology brush, and fine needle aspiration. The working channel enables suctioning of bronchoalveolar samples or mucus secretions that are obstructing the airway.1 The flexible bronchoscope can also be used as tool to facilitate endotracheal intubation, especially in a patient with a difficult airway. The scope is typically inserted through the nose or the mouth past the epiglottis and through the vocal cords into the trachea. When entering through the oral cavity, a mouthpiece or a protecting device is used to protect the scope from the patient biting the instrument. Flexible bronchoscopy is specifically indicated for sampling of parenchymal masses or nodules suspicious for cancer, obtaining bronchoalveolar samples to diagnose infection, confirmation and localization of hemoptysis, evaluation of interstitial lung disease, and persistent chronic cough.2 Flexible bronchoscopy can also be used for diagnostic sampling of mediastinal lymphadenopathy, evaluating the endobronchial tissue for an obstructing lesion, and sampling of endobronchial and

parenchymal tissue to assess for diseases such as sarcoidosis or other granulomatous diseases.2,3 Bronchoscopy can also be used for removal of foreign bodies and clearing of airway obstruction secondary to mucus impaction that is compromising the patient’s oxygenation and/or ventilation. Removal of mucus impaction with the bronchoscope should be performed after noninvasive methods and medical therapy have failed. As with any invasive procedure, consent needs to be provided by the patient, or his or her surrogate. Possible contraindications include a recent history of myocardial infarction (within the last 6 weeks), unstable arrhythmias, unstable bronchial asthma, coagulopathy, hemodynamic instability, and severity of hypoxic/hypercarbic respiratory failure. Depending on the patient’s respiratory status, the procedure may necessitate intubation of the airway to proceed. In the intensive care unit (ICU), bronchoscopy is routinely performed through the endotracheal tube.1 Before the procedure is initiated, patients undergo a pre-bronchoscopy assessment. This includes assessment of the patient’s upper airway anatomy, use of dentures, social history (including recreational drugs and alcohol), home medications, allergies, smoking history, and medical history. Flexible bronchoscopy does not require general anesthesia, and most physicians use conscious sedation.4 Endotracheal intubation can be done just prior to bronchoscopy in order to protect the airway and ensure adequate oxygenation and ventilation during the procedure. Intubation is considered if patient cannot oxygenate adequately with a nasal cannula, facemask, or other noninvasive forms of oxygen therapy. Another indication for intubation to facilitate bronchoscopy is determination of a difficult airway after evaluation of the upper airway anatomy. Patients with complicated health status or medical problems that increase the risk of difficulties during the procedure should also be considered for endotracheal intubation. Assessment should include vital signs, adequacy of oxygenation and ventilation, and factors that may lead to the development of hypercapnia. These guide the administration of analgesics and sedatives and helps determine whether the patient will be able to tolerate the procedure. The patient’s respiratory status should be optimized prior to bronchoscopy to ensure the patient will be able to tolerate the procedure and minimize the likelihood of complications. Once the procedure is underway, the bronchoscope is advanced through the

oropharynx, and passed just posterior to the epiglottis, until the vocal cords are visualized. A lidocaine solution is then administered through the working channel of the scope to anesthetize the vocal cords. This improves patient comfort and decreases the cough reflex. The scope is next advanced through the vocal cords into the trachea. The trachea is anesthetized with lidocaine to optimize control of the cough reflex that occurs with the sensation of a foreign body (the scope) in the airway. The bronchoscopist will then proceed with a visual endobronchial exam of the airway anatomy. The bronchial tree, left and right, are examined to ensure that all lobes and subsegments are patent and without abnormalities. After the endobronchial exam is completed, samples are taken based on the indication for the procedure. For example, a sterile brush is used for microbiology, while a cytologic brush sample is used to assess for malignant cells. Transbronchial biopsies may be taken of lung tissue, and bronchoalveolar lavage (BAL) may be performed to evaluate for infection, inflammatory disease, malignancy, or other pathology. Independent of the sampling technique to be used, the scope is wedged into the area of concern. To obtain a BAL, approximately 20 to 40 mL of saline solution is introduced into the working channel of the scope, and then suctioned into a collection container that is attached to the outside of the scope.5,6 The BAL can be used to obtain a sample from the distal bronchial subsegments or small airways that cannot be visualized during the procedure.5,6 Transbronchial biopsies, cytology, and microbiology brush of the lung parenchyma are done in similar fashion, often using live imaging technology (most often fluoroscopy). The forceps and bronchial brushes are advanced through the working port of the bronchoscope into the distal airway of interest. Fluoroscopy guidance confirms advancement and location. The forceps and/or brush are then advanced into the distal tissue to collect tissue and secretion samples to send for microscopic and microbiologic assessment. Complications associated with bronchoscopy include infection, bleeding, and pneumothorax due to trauma from the scope and/or biopsy samples taken.1 Other complications include difficulty with oxygenation and ventilation leading to acute respiratory failure, hypertension, and tachycardia due to pain or underlying cardiac conditions. Death is a very rare potential complication of bronchoscopy.

Bronchoscopy in the Intensive Care Unit As described above, bronchoscopy can be performed on patients that are in the ICU. There are many clinical settings in which this may be indicated, whether for diagnostic or therapeutic purposes. For example, a patient receiving invasive mechanical ventilatory support may experience a sudden hypoxic event with an associated chest radiograph showing complete opacification of the lung on the affected side. This may suggest lung collapse distal to a mucus plug obstruction of the airway. Bronchoscopic evaluation may confirm the mucus plug and enable removal using suction to evacuate the plug and associated thick secretions, resulting in improved oxygenation and ventilation. Secretions can be sent to the microbiology lab to evaluate for infection. Biopsy of lung tissue or transbronchial biopsies are not usually performed in the ICU setting, as this is best accomplished using fluoroscopic guidance, which is not always readily available in the ICU. Bronchoscopy performed on patients receiving mechanical ventilation with endotracheal tubes (ETT) in place is technically different than bronchoscopy without an ETT in place. Most patients tolerate the procedure well, since they are already receiving sedation and the cough reflex is suppressed. Also, the administration of sedatives to achieve patient comfort is done more freely because there is less concern for airway compromise and ventilatory support is being provided. Administration of medications to treat potential hemodynamic issues is also readily available. The ETT allows the bronchoscope direct access to the trachea without having to navigate the scope through the natural upper airway. The practitioner stands at the side or at the head of the patient’s bed. The mechanical ventilator settings are adjusted by the respiratory therapist. Oxygen concentration and the peak pressure and associated alarm limits are maximized, given that once the scope is introduced into the ETT, there is partial occlusion of the ETT lumen. This will increase airflow resistance during the procedure and elevate the peak inspiratory pressures (assuming volume-control ventilation); if the pressure-limit settings are not increased during the procedure, minute ventilation may be significantly reduced. The fraction of inspired oxygen (FIO2) is increased to a maximum setting of 100% during the procedure (FIO2 = 1.0) to ensure oxygen delivery to the tissues and minimize hypoxemic events. A size 8 mm ID ETT or larger will decrease the impact of the

bronchoscope on airway resistance, reduce peak airway pressures, and minimize reduction in delivered minute ventilation. A minimum 7.5 mm ID ETT is required to accommodate the bronchoscope in most adults. Smaller ETTs will require smaller instruments, likely a pediatric scope. However, using a smaller scope in adults may impair visualization and limit the ability to effectively suction and remove secretions. Prior to bronchoscope insertion, a bronchoscopic adapter is connected to the patient’s ETT, allowing passage of the bronchoscope into the airway without interrupting the ventilator circuit. Following insertion, bronchoscopic evaluation is performed in a similar fashion as described above. The risk and frequency of complications associated with bronchoscopy are higher in critically ill ICU patients, especially if they have lung pathology or are receiving mechanical ventilation; types of complications are similar to those listed earlier. The key to ensuring that critically ill patients tolerate the procedure is being alert for the factors likely to lead to complications (i.e., relative contraindications). These include patients requiring a high FIO2 and/or high positive end-expiratory pressure or PEEP (e.g., refractory hypoxemia), active bronchospasm, and hemodynamic instability. Most patients in the ICU tolerate bronchoscopy well; thus it is an indispensable tool for diagnosis and treatment. Figure 12-1 illustrates flexible fiberoptic bronchoscopy at the bedside in the ICU.

FIGURE 12-1 Flexible Fiberoptic Bronchoscopy Performed at the Bedside. Courtesy of Kevin Proud

Thoracentesis Thoracentesis is a valuable diagnostic procedure in patients with pleural effusions of unknown origin. Pleural fluid analysis can help guide clinicians in determining the effusion’s cause and selecting therapeutic options. Effusions are classified as a transudate (a product of unbalanced hydrostatic forces) or an exudate (a product of increased capillary permeability or lymphatic obstruction).7 Common causes of transudative fluid pleural effusions include congestive heart failure and liver disease. Medical treatment of the underlying disease is recommended and thoracentesis to drain the fluid is generally not required unless it is complicating the patient’s respiratory status by compressing lung tissue and causing atelectasis.7 Common causes of exudative pleural effusions include cancer and infections. For example, infection may cause an exudative process resulting in pleural fluid containing

bacteria, dead white blood cells, and cellular debris (i.e., pus) called empyema. Traditionally, exudates have been characterized by an increase in pleural fluid protein to serum protein ratio (0.5), increased pleural lactate dehydrogenase (LDH) to serum LDH ratio (> 0.6), or pleural fluid LDH in the upper range of the laboratory’s normal serum LDH range. Empyemas may need to be procedurally drained, as medical therapy alone is usually ineffective. RC Insight Analysis of fluid samples obtained during thoracentesis can allow for discrimination between exudates and transudates and help identify the cause of pleural effusion.

The medical staff must consider whether the patient can tolerate the procedure with respect to necessary positioning, requirements for analgesia, and the patient’s ability to follow the commands necessary to successfully complete the procedure. Thoracentesis is often performed with the patient sitting on the edge of the bed, leaning forward, with his or her arms resting on a bedside table. This tends to better expose the intercostal spaces where the needle will be inserted. If the patient is unable to sit upright, the lateral recumbent or supine position may be used. In the past, the level of the effusion was estimated on the basis of diminished or absent breath sounds, other physical examination findings, and chest radiograph or computed tomography (CT) scan to guide where to perform the thoracentesis to obtain a fluid sample. Today, with the advent of bedside ultrasonography (US), thoracentesis is commonly guided by live, direct ultrasound imaging and this is now considered the standard of care. Bedside ultrasonography allows for identification of deep fluid pockets away from anatomic structures, such as the diaphragm and lung tissue, thus further minimizing the risk of complications.8 Once the best site has been located via ultrasound guidance, it is marked and the area is cleansed with a sterilizing solution such as chlorhexidine or povidone-iodine solution. The medical staff will be gowned in sterile clothing and the patient’s back draped using sterile technique. The operator will then anesthetize the skin with lidocaine, as well as numbing deeper soft-tissue structures, including the pleura. The next step is to advance the needle, going over the rib, simultaneously withdrawing on the syringe plunger (creating negative pressure) until fluid is seen in the syringe. Ensuring the

needle goes over the superior margin of the ribs helps avoid the intercostal nerves and vascular structures that are located in the inferior margin.9 Once pleural fluid is obtained within the syringe, the depth of penetration is noted prior to withdrawing the needle. This allows the clinician to determine the depth required to advance a larger drainage needle to obtain larger volumes of pleural fluid. This also minimizes the risk of creating a pneumothorax when the larger needle is introduced. An 18-gauge overthe-drainage needle catheter is then attached to a syringe, and advanced along the superior surface of the rib to the predetermined depth while continuously pulling back on the syringe plunger. Once pleural fluid is obtained, the needle is no longer advanced, and the catheter is guided over the needle, and then the needle is removed. A large syringe is connected to the catheter tubing, and fluid is aspirated. The clinician must be careful of the volume of fluid removed during thoracentesis, as patients can experience re-expansion pulmonary edema and acute respiratory decompensation. This complication is rare and can be avoided by limiting the volume of fluid removed to less than 1500 mL.9,10 Pneumothorax is a possible complication caused by thoracentesis. A significant pneumothorax may require placement of a chest tube with suction, particularly if it is causing respiratory distress.9,10 A post-procedure chest radiograph can confirm the size of the pneumothorax, and in conjunction with the patient’s symptoms, guide whether a chest tube will be needed. Bedside US has also become an integral tool for evaluating patients for the presence of pneumothorax following thoracentesis. Bedside US can rapidly (in real time) identify findings that are consistent with pneumothorax.7 The ultrasound probe is used to examine the side of the chest where the thoracentesis was performed. On ultrasound examination, the presence of “lung sliding” (shimmering of the visceral and parietal pleura) confirms lung expansion. Lack of lung sliding is consistent with the presence of a pneumothorax. Ultrasonography can be used to guide the placement of a chest tube, if needed, as well.7 Figure 12-2 illustrates thoracentesis performed at the bedside.

FIGURE 12-2 Thoracentesis Performed at the Bedside.

Common complications of thoracentesis include chest pain, coughing (due to the lung re-expanding as the fluid is being drained), and localized infection. Besides pneumothorax and re-expansion pulmonary edema, other serious complications include hemothorax due to procedure trauma to the vascular structures surrounding the pleural space and bleeding into the pleura. Intra-abdominal organ injury and air embolism are both very rare complications. Contraindications to thoracentesis include bleeding diathesis (unusual susceptible to bleeding), coagulopathy (clotting disorder), small pleural fluid volume, and poorly defined anatomical landmarks that would make the procedure more challenging to perform. The presence of loculations could make the thoracentesis more difficult and US can assist in finding the best location to obtain fluid when loculations are present.7 In summary, thoracentesis is a common procedure in pulmonary medicine and may be helpful in certain ICU patients with pleural effusion in clarifying the underlying disease and reducing dyspnea.

Supportive Procedures Supportive procedures sometimes performed in the intensive care unit include methods for temperature regulation, dialysis, and nutritional support. Cardiopulmonary support techniques include ECMO and mechanical circulatory assistance. Each of these supportive measures are discussed below.

Temperature Regulation in the ICU The need for therapeutic regulation of body temperature is not uncommon in the care of critically ill patients. Therapeutic maneuvers for temperature regulation can be necessary in either direction; i.e., there are situations in which the goal is to correct an abnormal body temperature back to normal, and there are situations when a normal body temperature is manipulated to obtain a nonphysiologic target to achieve certain goals. Examples of each situation and their corresponding strategies are provided below.

Making the Hot Patient Cool: Management of Environmental Hyperthermia Hyperthermia is broadly defined as an elevation in temperature wherein the body loses control of thermoregulation, and compensatory mechanisms become overwhelmed and fail. The loss of physiologic control separates hyperthermia from the common fever. Hyperthermia is often categorized as either environmentally induced (heat exhaustion and heat stroke) or nonenvironmentally induced, typically related to metabolic derangements, drugs, or medications (thyrotoxicosis, sympathomimetic syndromes, and malignant hyperthermia). RC Insight Heat stroke is characterized by signs of neurologic impairment, hemodynamic instability, or end-organ damage.

Environmental hyperthermia can be related to exposure to high ambient temperatures or extreme physical exertion. Heat exhaustion and heat stoke are two syndromes of environmental hyperthermia largely differentiated by severity and multiorgan system involvement. Both include symptoms of malaise, nausea, muscle

cramping, and hypovolemia; however, with heat stroke there are also signs of hemodynamic compromise, neurologic impairment, and end-organ damage. Treatment of environmental hyperthermia depends on its severity, but hinges on returning body temperature to normal. In the setting of heat exhaustion, removal of the patient from the hot environment, rehydration, and observation are often adequate. However, if the patient progresses to, or presents with, signs of heat stroke, more aggressive interventions are likely necessary. With heat stroke, supportive care, including airway and hemodynamic management, is often necessary. Additionally, some form of cooling technique will be the basis of definitive management. RC Insight Treatment of environmental hyperthermia depends on severity, but the goal is to restore normal body temperature.

No consensus exists on preferred method of cooling. Cooling methods are categorized as internal or external. External methods include evaporative techniques, cold water immersion, and ice packing. Internal methods include cold water gastric and rectal lavage, as well as peritoneal lavage.

Evaporation Techniques Evaporation technique involves exposure of the majority of the body surface area and spraying exposed skin with cool water (approximately 15°C). Forced air is then applied to the patient’s wet skin via an electric fan. The advantage of this technique is that it is easy to apply, and avoids shivering and skin vasoconstriction that occurs at skin temperatures below 30°C. No good head-to-head comparison between cooling methods exists, however, this evaporation technique has been shown to decrease core temperature as quickly as 0.31°C/min in healthy volunteers, and as slowly as 0.05°C/min in a small case series of heat stroke patients.11 Given this discrepancy, it has been suggested that healthy volunteers may not be good study surrogates.11,12 Some clinicians advocate the technique as described above, but include covering the patient with a wet sheet. Ice packs applied to the neck, axillae, and groin are easily added to the method, but the benefits of this are largely unknown. Interestingly, in one report involving military personnel, the downdraft of a

helicopter blade was used to effectively cool a patient.13

Immersion Techniques Immersion technique involves placing the patient in a bath of cold water, typically ice water. Use of this method remains somewhat controversial, but it is frequently touted that immersion is the most rapid cooling method, with rates of cool ranging from 0.15°C/min to 0.2°C/min. However, as noted above, the literature lacks good headto-head comparisons of cooling techniques. Also, no standardization exists with regard to temperature of the water, volume of water, and percentage of body surface submerged. Opponents to this immersion method believe that decreasing the skin temperature below 30°C will induce shivering and skin vasoconstriction, thereby limiting effectiveness. Advocates believe the large thermogradient between the skin and the ice water overcomes any skin vasoconstriction that could theoretically hinder cooling. Without good outcome data to date, this argument remains theoretical. The larger issue regarding this technique resolves around the pragmatic challenges. The availability of an immersion tub or tub-like patient bed in the hospital setting is limited. Patients suffering heat stroke by definition have some neurologic or hemodynamic compromise and this results in an additional safety concern regarding patient immersion in cold water. Mechanical ventilation or vasopressor support would generally preclude the use of immersion techniques.

Making the Cold Patient Warm: Management of Environmental Hypothermia While there are disease states or conditions that can result in hypothermia (hypothyroidism, sepsis, adrenal insufficiency), most hypothermia requiring temperature-regulation management techniques are related to environmental exposure (i.e., environmental hypothermia). Hypothermia is commonly defined as a core temperature of less than 35°C. In the United States there are approximately 1300 deaths annually from hypothermia, which is approximately twice that related to heat stroke.14,15 Hypothermia severity is defined by patient’s core temperature: mild is 35°C to 32°C, moderate is < 32°C to 28°C, and severe is < 28°C. Although these definitions are numerically specific, clinical symptoms associated with each

temperature range vary with different patients. As a result, the definitions should serve as an approximate guide to assist in medical decision making. Symptoms follow a spectrum that roughly reflects the degree of hypothermia, and nearly all organ systems are involved. Neurologic function, for example, ranges from impaired judgement and amnesia in mild hypothermia to coma mimicking death in severe hypothermia. Even pupillary reflexes decrease and become absent as core temperature decreases. Arrhythmias and hemodynamic instability also become more common as severity progresses from moderate to severe. Most patients are hypovolemic due to poor oral (PO) fluid intake, increased vascular permeability, and so-called “cold-induced diuresis.”16 Treatment involves supportive care and some form of rewarming, both of which are largely dictated by clinical signs and symptoms as well as severity. Advanced airway care and mechanical ventilation are required in most cases of moderate to severe hypothermia. Close monitoring for hemodynamic stability and arrhythmias is recommended in all hypothermic patients. Care should be taken to minimize rolling or jostling the patient, as this can precipitate ventricular arrhythmias. Rewarming is categorized as passive or active. Passive rewarming involves moving from the cold environment, removal of wet clothing, and wrapping the patient in blankets. This technique relies on the patient’s physiologic mechanisms to contribute to the rewarming process, and therefore is only indicated for mild hypothermia in relatively stable patients. Active rewarming includes noninvasive techniques such as warmed forced air, warmed intravenous fluids, and warmed humidified oxygen in the ventilator circuit if the patient is intubated. During these interventions, it is important to warm the trunk first as warming the extremities can result in vasodilation and hypotension. In more severe cases or in patients who are not improving, more invasive techniques are available. Invasive active-rewarming techniques include peritoneal lavage with isotonic saline warmed to 40ºC or thoracic lavage with warmed saline infused through a large thoracotomy tube. In rare instances, ECMO circuits can be used to warm the blood and circulating fluids. This technique is very invasive and not available at all centers and may be reserved for patients without a perfusing heart rhythm. Specific evidence supporting one method over another is lacking. Active noninvasive rewarming is probably suitable for most patients.

Making the Normal Patient Cold: Therapeutic Hypothermia Anoxic brain injury is probably the most dreaded complication of any patient who suffers cardiac arrest and is successfully resuscitated. Anoxic brain injury results in irreversible neuronal damage that often has a devastating impact on the patient’s functional status and can carry a high mortality rate. Until the past few decades, there has been no specific therapy to treat or prevent anoxic brain injury, and postresuscitation care focused on treating the event that triggered the cardiac arrest and supportive care. To date, there is very little effective therapy once brain damage has occurred. In the 1980s, experimental models in dogs showed that systemic hypothermia decreased anoxic neurologic damage. Since that time, therapeutically induced hypothermia has been used as a postresuscitative treatment. In 2002, two randomized trials suggested some benefit to decreasing core temperature temporarily following cardiac arrest.17,18 Postcardiac arrest temperature management (therapeutic hypothermia) was adopted into national guidelines as a part of postresuscitation care in 2010.19 Since then, a large, multicenter, randomized trial failed to show the benefit of targeting a 33°C core body temperature comparted to 36°C.20 The recommendation remains in place, however, but now states that all comatose postarrest patients should receive targeted temperature management with a target core body temperature between 32°C and 36°C for at least 24 hours.21 Due to variability in clinical trial results and institutional protocols, there is no widely accepted consensus on target temperature or duration of cooling. Most clinical trials have targeted core temperatures ranging from 32°C to 34°C and maintained this temperature for 12 to 24 hours. At least one trial suggested that simply avoiding hyperthermia and keeping core temperature at or below 36°C may be as effective as targeting lower temperatures.20 Our institution targets a core temperature goal of 33°C to be achieved over 4 hours. The patient is then to be maintained at the goal temperature for 24 hours, with the 24-hour time period starting when the target temperature has been reached. After 24 hours at the target temperature, the core temperature target is raised by 0.25°C to 0.5°C every hour until the patient’s temperature is 37°C. Rewarming generally takes 8 to 16 hours. It should be noted that it is our practice to raise the target temperature (keeping the target below 36°C) if the patient develops signs of

adverse effects of the hypothermia such as bleeding, prolonged QT, or hemodynamic instability not easily controlled with vasopressors. As with target temperatures, no standard exists for timing of initiation of therapy and contraindications to therapeutic hypothermia. One of the initial trials of therapeutic hypothermia excluded patients if the time between return of spontaneous circulation (ROSC) and initiation of hypothermia exceeded 6 hours. As a result, 6 hours is a common cut-off point for starting therapeutic hypothermia at many institutions. Our institution’s protocol extends this window up to 8 hours after achieving return of spontaneous circulation. Of note, at least one small trial compared early versus late initiation of therapeutic hypothermia and found early initiation to be associated with worse outcomes.22 Hemodynamic instability, underlying coagulopathy, hyperkalemia, and baseline QTc (i.e. heart rate corrected QT interval) of greater than 500 milliseconds are common relative contraindications, but again these are institution dependent and are based on concern for potential complications rather than strong evidence. Clinical Focus 12-1 provides an example of a patient that may require therapeutic hypothermia.

CLINICAL FOCUS 12-1 A 60-year-old male is admitted to the medical ICU after experiencing cardiac arrest at home. According to the emergency medical service (EMS) providers, the patient’s family initiated cardiopulmonary resuscitation (CPR), and on the EMS arrival, he was noted to be in ventricular fibrillation. After standard advanced cardiac life support (ACLS) therapy, ROSC is achieved after approximately 10 minutes of resuscitation. The patient is endotracheally intubated, on minimal ventilator settings, and hemodynamically stable. He is not responsive to verbal stimuli and unable to follow commands. Question 1. What therapies should be attempted to minimize neurologic injury in this patient? In cardiac arrest patients, therapeutic hypothermia has been shown to improve neurologic outcome in patients at high risk for anoxic brain injury. It is recommended that targeted temperature therapy be initiated in patients that are not alert enough to follow commands following cardiac arrest. Though no studies of therapeutic hypothermia have been done in all types of cardiac arrest, ventricular fibrillation cardiac arrest is the best studied.

Question 2. What are potential adverse effects of therapeutic hypothermia? Inducing hypothermia can worsen hemodynamic instability by causing hypotension, bradycardia, or cardiac arrhythmias. Prolonged QT interval is commonly seen. Hypothermia also results in several electrolyte abnormalities including hypokalemia. Hypothermia also induces coagulopathy, which predisposes the patient to bleeding. Question 3. What temperature should be targeted for therapeutic hypothermia? The optimal temperature target and duration remains unknown. Common targets range between 32°C and 36°C, typically for 24 hours. One large trial showed no benefit of targeting 32°C compared to 36°C. It is clear that avoiding hyperthermia is important, as fevers worsen neurologic injury.

Dialysis in the ICU Renal replacement therapy (e.g., dialysis) may be required in ICU patients with acute, severe kidney injury. Indications include uremia, fluid overload unresponsive to conventional treatment, severe electrolyte disturbances (e.g., severe hyperkalemia), severe metabolic acidosis, and certain types of drug overdose (e.g., theophylline [Theolair], lithium [Eskalith, Lithobod], or salicylate poisoning). Patients with chronic kidney disease may also require renal dialysis in the ICU. Several methods for renal replacement therapy are available, including continuous renal replacement therapy (CRRT), intermittent hemodialysis (iHD), and peritoneal dialysis.

Overview and Definitions Acute kidney injury (AKI) is defined by an acute (hours to days) decline in urine output or rise in serum creatinine concentration. AKI is common among patients that require ICU care. Causes may be prerenal, intrinsic or postrenal. Prerenal causes of AKI include hemorrhage, fluid loss, sepsis, or other causes of reduced perfusion of the kidney. Intrinsic AKI may be caused by a variety of vascular, glomerular, tubular, or interstitial diseases. Postrenal AKI is associated with obstruction of urinary flow (e.g., bladder or urethral obstruction). While not all acute kidney injury requires dialysis, the need for renal replacement therapy (RRT) is common. The exact timing

for starting nonemergent dialysis is debatable and varies in clinical practice. As noted, the major indications for urgent or emergent dialysis include severe acidosis, electrolyte abnormalities, volume overload, uremia, and certain toxic ingestions. RC Insight Indications for dialysis in patients with AKI include life-threatening acidosis, volume overload, electrolyte abnormalities, certain toxic ingestions, and uremia.

The details for performing dialysis are beyond the scope of this chapter; however, there are several modes of dialysis available for the critically ill patient. It is important to note that with any method selected, RRT simply “does the job” of the kidney; it does not improve recovery of the injured kidney itself. Similarly, there is no role for prophylactic RRT to prevent kidney damage. In patients who undergo chronic dialysis and are hemodynamically stable, traditional intermittent hemodialysis can be performed in the ICU using the patient’s normal fistula. However, critical illness often results in hemodynamic instability, which decreases the patient’s tolerance for large fluid shifts during intermittent dialysis (which sometimes can be several liters per hour of fluid removal). In selected cases where the patient’s blood pressure is low but adequate at baseline, the added instability induced by dialysis can be managed with the addition of vasopressors. In cases where the patient requires vasopressors at baseline, or when there are signs of inadequate perfusion, other methods of “slower” dialysis involving lower flow rates can be used. Figure 12-3 illustrates conventional hemodialysis equipment.

FIGURE 12-3 Conventional Hemodialysis Equipment. Fresenius SE & Co. KGaA

Continuous renal replacement therapy (CRRT) is a complex intervention sometimes performed on ICU patients with severe, acute kidney injury. Lower-flow “continuous” filtration systems fall under the umbrella term of CRRT. CRRT can be done as either continuous venovenous hemodialysis (CVVHD) or continuous venovenous hemofiltration (CVVH). The major difference is that with the latter, fluid is being removed, but not truly dialyzed. These methods (CVVHD and CVVH) are performed using different machines and equipment than the standard iHD (intermittent hemodialysis) machines, and CRRT may often be managed by the bedside ICU nurse rather than a dedicated dialysis nurse. The goal is to perform CRRT continuously (24 hours per day) for as long as needed, although temporary interruptions are common. Another available option is slow, extended daily dialysis (SLEDD), also known as extended daily dialysis (EDD) or sustained low-efficiency dialysis (SLED), in which dialysis is performed over 6 to 12 hours on a daily or near-daily basis. One

advantage to these methods is that they can be performed with standard dialysis equipment, obviating the need to purchase specific CRRT devices. There is no definitive evidence to show one mode is superior to another. As a result, practice is primarily dictated by institutional resources and physician preference. Even in patients receiving chronic dialysis accessed through a fistula, if CRRT is to be performed, some form of dialysis catheter needs to be placed. Dialysis catheters can be temporary catheters that are essentially larger versions of standard central venous catheters, generally with two 12-gauge lumens. These can be placed at the bedside by the intensivist or nephrologist. Another option is having a tunneled dialysis catheter placed. Tunneled catheters have lower rates of infection and are generally for longer term uses than nontunneled temporary catheters. Tunneled catheters require special training and hence are usually placed by interventional radiology, surgery, or interventional nephrology in some institutions. Treatment of AKI varies depending on the cause and the patient’s condition. For example, treatment of prerenal AKI includes improving renal perfusion by correcting volume depletion or treating other causes of reduced circulating blood volume (e.g., heart failure or septic shock). In the ICU, patients with AKI may require RRT, which may include acute hemodialysis or CRRT.

Nutrition in the ICU Critically ill patients are often malnourished and may be in a catabolic stress state. Energy requirements can be determined in the intensive care unit using a metabolic cart for measurement of oxygen consumption, carbon dioxide production, and resting energy expenditure (REE) to determine caloric requirements and avoid underfeeding. More commonly, however, a calorie goal is set based on the patient’s body weight using a standard nutrition formulation. Nutritional support should provide patients with the appropriate protein, electrolyte, vitamin, mineral, and caloric intake.

Introduction Nutritional support in the ICU is likely one of the most underappreciated aspects of critical care today. Despite extensive data demonstrating the benefits of good and timely nutritional support and low chance of harm, it is frequently a lower than deserved priority. This is demonstrated by the fact that 78% of patients on

mechanical ventilation received less than the recommended amount of nutritional support in the ICU in one clinical audit.23 Barriers to providing nutritional support are numerous, but include omission due to underappreciation of benefits, overestimated possible harms, and practical constraints such as lack of access or time for required procedures.

Routes Nutrition can be administered either enterally (via the gastrointestinal tract), or parenterally (intravenously). Obviously, differences exist between solutions that are absorbed by the gut mucosa compared to those that can be directly infused into a vein. Each method is associated with different risks and benefits. As such, the method of the feeding may vary depending on the patient’s specific clinical situation.

Enteral Nutrition Enteral nutrition (EN) generally refers to feeding provided via nasogastric tube, orogastric tube, or (in long-term situations) percutaneous endoscopic gastrostomy (PEG) tube. While there currently are no clinical practice guidelines suggesting the best tube location, there are clinical conditions in which certain routes may be preferable. For example, in mechanically ventilated patients, oral gastric tubes may be preferable because the oral route largely eliminates the chance of developing a sinus infection, which may occur with nasogastric tubes. However, in awake nonintubated patients, oral gastric tubes are not well tolerated, and nasogastric tubes are much more commonly used. RC Insight Adequate enteral nutrition in the ICU is associated with improved outcomes.

In addition to selecting the site for tube insertion, there are several options for type of feeding tube. Feeding can be provided through either standard gastric tubes such as the Salem Sump or specialized smaller, flexible tubes that carry tradenames such as Dobhoff or Corpak tubes. While no preference exists when placed solely for providing nutrition, generally the smallest tube possible is desirable. Placement of nasogastric tubes is generally a simple bedside procedure, and in

most cases, does not require sedation or local anesthetic. While generally a safe procedure, nasal gastric tubes should not be inserted in patients with significant facial or anterior head trauma. Also, in the setting of severe coagulopathy or thrombocytopenia, one should always consider the risks and benefits of placement, as severe bleeding can occur. To place a nasogastric tube the depth of placement is first estimated by measuring the distance from the nose to the posterior ear then down to the xiphoid process. After lubrication, the tube is inserted through the nares in a mostly posterior rather than cranial direction. Flexion of the patient’s neck, putting the chin to the chest often helps align the posterior nasal sinus with the esophageal inlet, and facilitates passage. Having the patient attempt to swallow during tube passage is frequently helpful. Significant coughing may suggest that the tube has inadvertently gone into the trachea; however, coughing is not sensitive or specific for accidental tracheal tube placement. Pushing air through a large syringe into the tube while auscultating over the stomach is frequently done to suggest proper tube placement. Abdominal radiography (KUB [kidneys, ureters, bladder] x-ray) is more specific and required by many institutions. It should be noted that the presence of an endotracheal tube does not protect against misplaced feeding tubes and can actually increase the chance of accidental tracheal cannulation with a feeding tube. Other tools exist for placement of the small flexible feeding tubes, which use a type of electromagnetic navigational technology (i.e., electromagnetic tracing) to direct and verify tube placement. The purpose of this technology is to obviate the need for radiographic confirmation of proper tube placement; there is not yet sufficient comparative evidence of the technology’s relative effectiveness and radiographs remain the gold standard. Lastly, there is debate about whether gastric or postpyloric placement for temporary feeding tubes is beneficial. Specifically, does placement of the feeding tube in the duodenum (i.e., beyond the gastric pylorus) decrease the risk of aspiration and pneumonia? This has been studied extensively and remains controversial. Three meta-analyses have been done to address this question. Two studies found no difference in the incidence of pneumonia, while one showed a slight decrease in the incidence of pneumonia with postpyloric tubes.24–26 Hence, national guidelines state that either gastric or postpyloric feeding tube placement is

acceptable unless the patient is at high risk of aspiration or has impaired gastric motility, in which case, postpyloric tube placement is recommended.27 Our practice is to use gastric feeding except in select cases; postpyloric placement can require several attempts resulting in numerous x-rays and delays in feeding.

Benefits of Enteral Nutrition Enteral nutrition is beneficial in critically ill patients for a number of reasons. In addition to preventing starvation ketosis and tempering catabolism during illness, enteral nutrition appears to have some protective value in preventing infection. It is well known that lack of enteral nutrition induces villus atrophy of the gut mucosa and loosening of cellular tight junctions. Enteral nutrition has also been shown to help maintain areas of gut-associated lymphoid tissue (GALT). Thus, it is believed that enteral nutrition decreases the rate of bacterial translocation across the gut mucosa. Additionally, enteral nutrition stimulates bowel motility, and thereby helps prevent ileus. There are also studies that indicate that enteral nutrition is associated with better outcomes including lower infection rates, decreased length of stay, and (in some studies) survival.28–29

Parenteral Nutrition Parenteral nutrition (PN) is given ether as total parenteral nutrition (TPN) or, less frequently, peripheral parenteral nutrition (PPN). The major difference between the two is osmotic load. TPN has a higher osmotic load, rendering it potentially more caustic to small veins. Therefore, TPN must only be given via a central venous catheter. PPN contains less calories with a lower osmolality and can be given through a peripheral intravenous (IV). As a result, PPN better serves as a supplemental rather than primary source of nutrition RC Insight Early parenteral nutrition has been associated with increased infections, cholestasis, and increased need for mechanical ventilation.

It should be noted that parenteral nutrition should only be considered when enteral nutrition is not possible and will not be possible in the foreseeable future. Parenteral nutrition has been associated with complications including increased rates of

infection, liver dysfunction, and candidemia. In a large clinical trial, patients unable to tolerate EN where randomized to receive PN either within 48 hours or at 8 days. This trial showed no benefit to early PN, and higher rates of infection, cholestasis, and duration of mechanical ventilation in the early PN group.30 Guidelines recommend against starting PN within the first 7 days of patients being unable to receive EN, particularly if there is no evidence of malnutrition.

Barriers to Enteral Nutrition Barriers to providing adequate EN largely come from one of three sources. First, an underappreciation of the benefits of enteral nutrition cause tube feeding to be delayed. Second, the practical issue of obtaining enteral access and procedures that require the patient to be NPO (nothing by mouth) may delay initiation of enteral nutritional support. For example, patients presenting with gastrointestinal hemorrhage are frequently kept NPO in preparation for esophagogastroduodenoscopy (EGD or gastrointestinal [GI] endoscopy). Similarly, patients with esophageal varices who undergo variceal banding (for treatment) are generally discouraged from having gastric tubes placed for fear of dislodging the bands. The last barrier is probably the most common and most frustrating, but also has the most potential for improvement: the overestimation risk associated with enteral nutrition. Several misconceptions by nurses and physicians lead to unnecessary withholding of tube feeding. For example, there is a common (but incorrect) belief that patients with high gastric residuals should have tube feeds stopped because of increased risk of aspiration. Gastric residual is the amount of fluid remaining in the stomach during enteral feeding and can be measured by withdrawing fluid from the feeding tube using a large syringe. Gastric residuals are sometimes measured in the ICU at specific intervals (e.g., every 4 to 8 hours). Two studies have shown that stopping feeding because of higher gastric residuals does not affect rates of aspiration; one trial has shown that not monitoring gastric residuals is safe and does not result in increased aspiration.31–33 RC Insight Monitoring gastric residuals has not been shown to decrease the rate of aspiration pneumonia in mechanically ventilated patients.

Another common misconception is that enteral feeds cannot be given to patients receiving vasopressors. The 2009 American Society for Parenteral and Enteral Nutrition (ASPEN) guidelines acknowledge that the complication of bowel ischemia is a rare complication of EN (< 1% of cases) but advise against enteral nutrition in the setting of a mean arterial pressure < 60 mmHg or with increasing doses of vasopressors.27 These guidelines do state that EN can be given cautiously in patients receiving stable doses of vasopressors. The belief is that vasopressorinduced vasoconstriction reduces gastrointestinal blood flow and that enteral feeds will increase gastrointestinal oxygen demand and therefore lead to ischemia. This recommendation, however, is largely theoretical with little to no clinical evidence (essentially case reports) to support it; several studies have provided evidence to the contrary. There is now evidence that enteral nutrition may, instead increase gastrointestinal blood flow in these situations. A large retrospective study comparing outcomes of patients receiving early vs late enteral feeds showed that early enteral nutrition was associated with improved mortality, including patients on vasoactive agents. In fact, the benefit was more pronounced in the sickest patients (those requiring more than one vasopressor).28 We start tube feeding routinely in patients with low to moderate vasopressor requirements and hold them if clinical signs of intolerance (rising lactate, or ileus) develop.

Special Considerations Two other settings in which practices regarding nutritional support are slowly changing include patients with pancreatitis and patients with gastrointestinal surgery. Historically, acute pancreatitis was treated with bowel rest by making the patient NPO. However, this approach has been challenged in the recent decades, and is now thought to be incorrect. In 2013, the American College of Gastroenterology guideline supported early enteral nutrition in patients with acute pancreatitis.34 Additionally, the guidelines supported the notion that gastric feeds are as safe and efficacious as postpyloric feeds. Similarly, patients have traditionally been treated with bowel rest following gastrointestinal surgery, given the concern for postoperative ileus and possible bowel ischemia. Again, these concerns are based on very limited data; more recent

evidence suggests early enteral nutrition is safe in these patients and may decrease infection rates as well as hospital length of stay.29,35,36

Extracorporeal Membrane Oxygenation Extracorporeal membrane oxygenation (ECMO) or extracorporeal life support (ECLS) is a form of cardiopulmonary bypass that is a mainstay of therapy in neonatal and pediatric patients with life-threatening respiratory and/or cardiac failure. Historically, the use of ECMO in adults has been limited; however, after the 2009 H1N1 influenza pandemic and subsequent technological advances, there has been increased utilization of ECMO in adult patients with severe respiratory failure. ECMO can also be used in adults with cardiac failure. Survival rates between 60% to 70% have been reported in adult patients requiring ECMO for refractory respiratory failure. One study utilizing a specialized ECMO center demonstrated a mortality benefit when compared to tertiary care centers.37 Whether ECMO will continue to be used as a rescue therapy for refractory acute respiratory distress syndrome (ARDS) remains a topic of continuing debate.

Indications ECMO buys time for making a diagnosis or to allow recovery from a life-threatening underlying disease. It is a support modality, not a treatment; it is only beneficial in patients whose primary disease is reversible or as a bridge to heart or lung transplant. This brings with it the challenge of patient selection and determination of candidacy. There are some reports of emerging utilization as an adjunct to cardiopulmonary resuscitation.38 This rescue treatment is primarily reserved for circumstances in which patients are refractory to escalating conventional therapies. The Extracorporeal Life Support Organization (ELSO) guidelines suggest that ECMO be considered in adult patients with severe hypoxemic respiratory failure and when predicted mortality exceeds 50%.39 Severe hypoxemic respiratory failure mortality can be roughly estimated based on PaO2/FIO2 and Murray score where:39 PaO2/FIO2 < 150 mmHg on an FIO2 of 0.9 and a Murray score of 2 to 3 is associated with a predicted mortality of 50%. PaO2/FIO2 < 100 mmHg on an FIO2 of 0.9 and a Murray score of 3 to 4 is associated with a predicted mortality of 80% if not improving after 6 hours of conventional treatment. Other indications for ECMO in adults include respiratory acidosis refractory to

conventional therapies with high plateau pressures (Pplateau) > 30 cm H2O, cardiorespiratory collapse after a pulmonary embolus or other inciting etiology, and severe air leak. ECMO contraindications include mechanical ventilation at high settings (FIO2 > 0.9, Pplateau > 30) for 7 days, immunosuppression (absolute neutrophil count < 400/mm3), patients who have an irreversible cause of critical illness, advanced multiorgan failure, increased risk of bleeding, or severe neurological injury that limits the quality of life.39

Methods Cannula access for ECMO may be by femoral and jugular veins with two cannulas or a double-lumen cannula via the internal jugular (IJ) vein. Placement of the cannula can be done at the bedside percutaneously or surgically in the operating room. Introduction of a double-lumen venovenous (VV) ECMO cannula that drains blood from both the superior and inferior vena cava and directs the return of blood directly across the tricuspid valve allows for single site percutaneous cannulation.37,39 It avoids femoral vein cannulation, and thus increases patient mobility and lowers the complication rates. Venoarterial (VA) access via IJ or femoral vein and femoral artery is preferred in patients with a low cardiac output. VV ECMO is primarily used in respiratory failure with adequate cardiac function, while VA ECMO is used with significantly depressed cardiac function requiring circulatory support. The additional components of a traditional ECMO circuit include the pump, oxygenator, circuit components, and various monitoring devices. Depending on the clinical setting, the parameters of these components can be adjusted to support oxygenation, ventilation, and hemodynamics. ECMO patients require heavy sedation during the initial phase; this is gradually decreased once the patient is stable and showing improvement. Figure 12-4 illustrates an ECMO system.

FIGURE 12-4 Extracorporeal Membrane Oxygenation (ECMO) System. (A) and (B) can be reduced in size a bit to make room for (C).

Description

Monitoring During ECMO Oxygenation parameters such as oxygen saturation, oxygen concentration, and flow requirements are evaluated daily. These parameters determine the management of ECMO circuit. In patients requiring vasoconstrictors and circulatory support from ECMO, hemodynamics are monitored. With status asthmaticus and other conditions in which the initial arterial carbon dioxide tension (PaCO2) is high, PCO2 is gradually reduced to avoid acid-base imbalance or cerebral complications. A suggested rate of decreasing arterial PCO2 is 20 mmHg/hour.37,38 Anticoagulation is critical to avoid the formation of clots in the ECMO circuit while balancing the patient’s risk of bleeding. An assigned perfusionist routinely manages the anticoagulation therapy. Heparin is commonly used to keep the whole-blood activated clotting time at a designated level (usually 1.5 times normal). Thrombocytopenia is a common problem, and regular platelet transfusions may be necessary to keep the platelet count over an arbitrary limit and decrease the risk of spontaneous bleeding.

Discontinuance Removal from the ECMO circuit can be attempted after the patient has improved sufficiently with reasonable ventilator settings (e.g., FIO2 < 0.4, peak inspiratory pressure [PIP] < 25 cm H2O, and respiratory rate < 30/min).1 With VV ECMO, weaning is achieved by simply turning off the oxygen. With VA ECMO, the flow rate is reduced to 1 L/min. Echocardiography is useful for assessing cardiac function or the presence of pulmonary hypertension. If circulation and gas exchange are stable with reasonable ventilator settings and low-dose inotropes, the circuit is clamped for a few minutes. Once the patient demonstrates being able to remain stable (e.g., SaO2 > 95 and PaCO2 < 50 for 60 minutes) on conventional treatments, ECMO is discontinued. If the patient has irreversible lung damage or severe brain damage with no chance of recovery, cessation of ECMO may be recommended. If the patient

does not improve within several weeks or 1 month after the onset of ARDS, continuing ECMO may be considered futile. The period for which ECMO can be continued is unknown, and there have been some reports of a successful outcome after more than 1 month of treatment.40,41 There is debate regarding ECMO as a rescue mode for refractory severe respiratory failure. Advances in ECMO technology may provide this option if an experienced center is readily available. That said, these are often difficult cases where conventional treatment is failing and there is a high risk of mortality. Clinical Focus 12-2 introduces a patient who initially requires bronchoscopy in the ICU and then is considered for ECMO.

CLINICAL FOCUS 12-2 A 40-year-old woman is admitted to the intensive care unit for hypoxia in the setting of severe pneumonia. She has been previously healthy and was diagnosed with influenza 4 days ago. Today she required intubation and mechanical ventilation. Current ventilator settings are assist/control with tidal volume of 400 (6 cc/kg ideal body weight [IBW]), respiratory rate of 18 bpm, FIO2 of 60%, and PEEP of 10. Her chest x-ray reveals bilateral infiltrates without pleural effusions. Question 1. What diagnostic modality could be considered to further clarify the diagnosis? Bronchoscopy with bronchoalveolar lavage (BAL) would be a reasonable diagnostic test in this patient. Other conditions such as secondary bacterial infection or diffuse alveolar hemorrhage (sometimes induced by infection) could be diagnosed. Question 2. What are contraindications to performing bronchoscopy on a patient on mechanical ventilation? Potential contraindications to bronchoscopy on mechanically ventilated patients include high ventilator requirements, hemodynamic instability, active arrhythmia, and inadequate size of endotracheal (ET) tube to accommodate the bronchoscope. Most of these are relative contraindications, which means there is no exact definition for “high ventilator settings” that would preclude bronchoscopy. This definition likely varies by institution and medical practitioner. Similarly, the definition of hemodynamic instability often varies by practitioner. For example, if

a patient has adequate blood pressure on stable doses of a vasopressor, many providers would be comfortable proceeding with bronchoscopy. There is much higher risk of worsening active arrhythmia (atrial fibrillation with rapid ventricular response [RVR], severe bradycardia, frequent runs of ventricular tachycardia) during bronchoscopy and should probably be controlled prior to bronchoscopy. It should be noted that coagulopathy is generally not considered a contraindication to BAL, as the risk of inducing significant bleeding is very low. Question 3. What steps should be taken to set up for bronchoscopy? Once the decision is made to proceed with bronchoscopy, several steps are taken before starting the procedure. First, consent must be obtained. Next, the ventilator must be prepped, typically by setting the ventilator to 100% FIO2, increasing the high-pressure alarm, increasing the high respiratory rate alarm, and lowering the minimal minute ventilation alarm. All of these parameters will be difficult for the ventilator to accurately measure during the procedure and the ventilators response to inaccurate readings could limit support to the patient. A bite block should be placed around the ET tube to prevent the patient from biting and damaging the scope. A connector with a port for the bronchoscopy should be connected to the ventilator circuit at the ET tube. Supplies including sterile traps, tubing for suction, saline, and 30 to 60 mL syringes should be readily available for BAL. Lidocaine or other topical anesthetic should be available for intrabronchoscopic administration. Appropriate sedation should be available for the patient, and vital sign monitoring should be increased to every 3 minutes or more frequently. Lastly, when all required members of the team are present, a time-out should be performed just prior to initiation of the procedure. A bronchoscopy with bronchoalveolar lavage was performed and cultures from the BAL revealed staphylococcal pneumonia. Despite adequate antimicrobial therapy, the patient’s condition continued to worsen over the next 24 hours. Her oxygen requirements and plateau pressures have continued to rise. She has been started on paralytic therapy, and prone ventilation has been initiated. With pronation and paralytics, she now requires an FIO2 of 90% and PEEP of 16, and her PaO2 is 54. Despite this, she remains in single-organ failure. Question 4. How would you describe the patient’s condition currently? Are there any other modalities you would consider to support her respiratory status? At this point, the patient has developed clinical ARDS, and based on her P:F ratio she would be categorized as severe ARDS. She is on near-maximal therapy from the ventilator and has received adjunctive therapies for severe ARDS (prone ventilation and paralytics). Even on maximal therapy, her PaO2 is just below goal, which suggests a poor prognosis. At this point, it would be

reasonable to consider extracorporeal membrane oxygenation (ECMO) to improve oxygenation (and ventilation if needed). This patient was previously healthy, has no comorbidities (single-organ failure), and has been on the ventilator for less than 7 days, all of which make her a good candidate for ECMO. Question 5. What are typical indications for ECMO? The Extracorporeal Life Support Organization (ELSO) guidelines recommend that ECMO be considered in adult patients with severe hypoxemic respiratory failure and when predicted mortality is greater than 50%. Having a P:F ratio < 150 on an FIO2 of 90% with a Murray score of 2 or higher would meet such criteria.

Mechanical Circulatory Assistance The medical community has used implantable mechanical circulatory support (MCS) devices at increasing rates for patients with end-stage heart disease.42 The primary purpose of mechanical circulatory assist devices is to improve cardiac output and end-organ perfusion in patients with severe heart failure. Increasingly, mechanical circulatory assist devices are used as a bridge to heart transplant or to provide time for the failing heart to recover. With the innovation in technology and more reliable left ventricular assist devices (LVADs), there has been a rise in implantation of devices as the definitive therapy for end-stage cardiomyopathy without the intention of cardiac transplantation or other forms of definitive treatments.43 The intra-aortic balloon pump (IABP) is the most commonly used mechanical circulatory support device and is commonly seen in cardiac ICUs. It can be rapidly and easily inserted and is the least expensive of the mechanical circulatory devices. One of its advantages is that it can managed by the physician, nursing staff, and respiratory therapist, with intermittent assistance by a skilled perfusionist. IABP is a temporary measure with the goal of supporting improved myocardial perfusion. Patients requiring IABP are generally expected to have additional definitive therapy provided or recovery of cardiac function is anticipated. The total artificial heart (TAH) is another type of mechanical device used in patients with advanced right ventricular failure or other anatomic abnormalities and who are poor candidates for isolated left ventricular mechanical support. The majority of TAH implantations are performed in patients with critical cardiogenic shock or other cardiac disease that leads to rapid decline.42,44

Indications MCS can be used for cardiac disorders in patients who have failed more conventional medical treatment. MCS may be indicated in the following settings:39 High-risk percutaneous coronary intervention Advanced heart failure (ejection fraction < 35%) or decompensated heart failure Complications of acute myocardial infarction (cardiogenic shock, mitral regurgitation, or ventricular septal rupture)

Bridge to heart transplant Cardiac valvular disease Severe underlying left ventricular dysfunction in patients who may not tolerate sustained ventricular arrhythmias Medically refractory (particularly ventricular) arrhythmias associated with ischemia Acute cardiac allograft failure or post-transplant right ventricular failure. MCS should not be used in the following settings: Aortic regurgitation or prosthetic aortic valve Aortic aneurysm or dissection Severe aortic or peripheral artery disease Left ventricular or left atrial thrombi Bleeding diathesis Uncontrolled sepsis

Methods Mechanical circulatory assist devices include the IABP, LVAD, right ventricular assist devices (RVAD), and biventricular assist devices (BiVAD). Total artificial heart (TAH) devices are also available. As noted, the IABP is a widely used circulatory assist device for short-term support in the critical care environment. IABP counterpulsation works by inserting a catheter with a 30- to 50-mL helium-filled balloon at its tip. The catheter is threaded into the aorta, generally with fluoroscopy guidance. Due to the risk of limb ischemia at the site of insertion, peripheral pulses are documented prior to placing the IABP. Once the correct location and function are documented by fluoroscopy, the balloon is inflated during cardiac diastole and deflated during systole. This inflation and deflation cycle decreases aortic pressures during systole, increases pressures during diastole, and improves cardiac output. Specific indications for IABP include left ventricular failure (often following acute myocardial infarction), inadequate cardiac output following cardiac surgery, intractable angina, and as a bridge to additional therapy. Devices are often set up by perfusionists, but routinely monitored by critical care nursing or respiratory care personnel. Figure 12-5 illustrates an intraaortic balloon pump.

FIGURE 12-5 Intra-Aortic Balloon Pump.

LVADs are continuous-flow pumps with retrograde inflow across the aortic valve into the left ventricle. A pump draws blood out of the left ventricle and ejects it into the ascending aorta. Some of LVADs require surgical placement while smaller devices can be placed percutaneously. LVADs are placed via a graft to the ascending aorta or subclavian artery or for percutaneous placement via the femoral artery.42,43,45,46 Figure 12-6 illustrates a LVAD.

FIGURE 12-6 Left Ventricular Assist Device (LVAD).

TAH is currently approved as a bridge to heart transplantation. The native right

and left ventricles are excised and replaced with two 70-mL polyurethane pneumatic chambers. Each chamber has two mechanical disc valves replicating the function of the excised cardiac structures. Pneumatic drive lines tunneled through the abdominal wall connect each chamber to an external driver. The artificial heart provides high cardiac output (6 to 8 L/min) with lower vasoconstrictor requirements. Physicians have control of the patient’s hemodynamics, including heart rate, flow, time spent in systole, and ejection and filling times. The patient must be on systemic anticoagulation during initial placement and afterwards. Figure 12-7 illustrates a TAH.

FIGURE 12-7 Total Artificial Heart (TAH).

Monitoring Respiratory care clinicians must be alert to the many complications associated with mechanical circulatory assist devices. Patients experiencing complications may develop dyspnea, tachypnea, hypoxemia, increased lactate levels, and decreased

hemoglobin and hematocrit due to bleeding. Arrhythmias, hypotension, ventricular failure or dysfunction, and cardiac tamponade may develop. Other complications include pneumothorax, device failure, hemoptysis, hemolysis, chest pain, syncope, gastrointestinal bleeds, kidney failure, hematuria, infection, and stroke. Hemodynamic management can be particularly challenging. Echocardiography is used to assess LV function, whereas different methods are available for cardiac output (CO) estimation. Echocardiography provides useful data to determine the response to mechanical circulatory support. Ejection fraction, cardiac chamber structure appearance, and other data are monitored and assist in the clinical decision making. Cardiac output estimation can also be done through the thermodilution technique. This technique employs a bolus of fluid with reduced temperature (cooler than blood) that is injected into the right atrium via a pulmonary artery catheter. The change in temperature detected in the blood of the pulmonary artery at the catheter tip is used to calculate cardiac output. This is still the standard method for cardiac output measurement in the cardiac catheterization lab. Transpulmonary thermodilution allows cardiac output to be assessed less invasively, using a central venous catheter (to allow injection of the indicator) and an arterial catheter, rather than needing to introduce a catheter into the pulmonary artery.47 Newer technologies have evolved where patients’ pulse waveform can be analyzed and estimates of cardiac output, stroke volume, and systemic vascular resistance provided. With the advent of bedside ultrasound and these new technologies, invasive assessment of hemodynamics is becoming less common in intensive care units.

Discontinuance of Mechanical Circulatory Support MCS devices are generally used for short-term patient stabilization until recovery of jeopardized myocardium is achieved or as a bridge to definitive treatment. Patients who receive MCS (either percutaneous or surgically placed) should always be evaluated for ventricular recovery, particularly in the setting of cardiogenic shock, myocardial infarction, or myocarditis. Weaning is performed using hemodynamics and echocardiographic left ventricular function as a guide while MCS is being reduced. Ventricular recovery can be detected first by the presence of native ventricular ejection on the arterial or pulmonary artery wave forms. Subsequent

confirmation of recovery is best performed by echocardiography. Percutaneous devices can be removed at the bedside and surgically placed MCS are preferably removed in the operating room.42

Key Points The risks and benefits of performing bronchoscopy in the intensive care unit must be considered for each individual patient. Thoracentesis is the primary diagnostic tool to determine the cause of pleural effusion. Hyperthermia is an elevation in temperature in which the body loses control of thermoregulation. Treatment of heat exhaustion starts with removal of the patient from the hot environment and rehydration. The presence of neurologic impairment, hemodynamic compromise, and endorgan damage separates heat stroke from heat exhaustion. Common cooling techniques include evaporation methods and immersion methods. Evaporation cooling for temperature regulation involves spraying exposed skin with cool water followed by applying forced air. Hypothermia severity is defined by core temperature: mild (35°C to 32°C), moderate (< 32°C to 28°C), and severe (< 28°C). Passive rewarming involves moving the patient from the cold environment, removing cold or wet clothing, and using blankets to rewarm. Noninvasive active rewarming includes applications of forced air and using warmed humidified oxygen through the ventilator. Invasive active rewarming includes peritoneal and/or thoracic lavage with warmed saline and warmed intravenous fluids. Therapeutic hypothermia (targeted temperature therapy) is often used following cardiac arrest to minimize anoxic brain injury. Potential adverse effects of the hypothermia include bleeding and coagulopathy, prolonged QT interval, bradycardia, and hypotension. Indications for urgent or emergent dialysis include life-threatening acidosis, volume overload, electrolyte abnormalities, certain toxic ingestions, and uremia, which cannot be safely reversed without dialysis. There is no convincing evidence that the need for vasopressors should prevent enteral nutrition. Parenteral nutrition is generally reserved for patients who have not been able to receive enteral nutrition for 7 days or more. Early parenteral nutrition has been associated with increased infections, cholestasis, and increased need for mechanical ventilation. Monitoring gastric residuals has not been shown to decrease the rate of aspiration pneumonia in mechanically ventilated patients. Extracorporeal and mechanical circulatory life support have become treatment options for acute respiratory, cardiac, and circulatory failure. Lung recovery is the main goal of ECMO in the setting of respiratory failure.

Mechanical circulatory support (MCS) uses technology to support patients with acute cardiac injury. Indications and contraindications for MCS support depend on the disease, type of organ failure, and other patient characteristics.

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CHAPTER

13 Point-of-care Ultrasound in Critical Care Kevin Proud, Sheila Habib, Patricio De Hoyos, and Nilam Soni

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction The History and Evolution of Point-of-care Ultrasound Types of Transducers Holding and Moving the Transducer Cardiac Ultrasound General Concepts Parasternal Long Axis View Parasternal Short Axis View Apical Four Chamber View Subcostal View Assessment of Volume Responsiveness Lung Ultrasound General Concepts Detection of Pneumothorax Evaluation of Pleural Effusion Characteristics of Pleural Effusion Pleural Drainage Procedures Determining the Etiology of Respiratory Failure Abdominal Ultrasound General Concepts Anatomic Landmarks Assessment for Ascites and Paracentesis

Vascular Ultrasound Vascular Access Detection of Deep Vein Thrombosis Ultrasound-Guided Lumbar Puncture

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Describe the evolution and role of point-of-care imaging ultrasound in critical care. Explain different types of transducers and how to hold them. Describe accepted terms for moving the transducer to obtain images. Review the four basic cardiac ultrasound views. Contrast strengths and weakness of each type of ultrasound view. Describe transducer position in image acquisition. Review anatomic landmarks in lung and pleural ultrasound. Describe ultrasound technique to evaluate for pneumothorax. Describe sonographic characteristics of pleural effusions. Review sonographic anatomical landmarks of the abdomen. Highlight benefits of using ultrasound for paracentesis. Review techniques and benefits of using ultrasound for vascular access placement. Review venous geography and techniques in detection of deep vein thrombosis (DVT). Describe the use of ultrasound to assist in lumbar puncture.

KEY TERMS ascites central venous catheter (CVC) deep vein thrombosis (DVT) frequency hyperechoic hypoechoic isoechoic parietal pleural pericardial effusion pleural effusion point-of-care ultrasonography transducer visceral pleural wavelength

Introduction Bedside point-of-care ultrasonography has had a significant impact in recent years in the care of patients in the emergency department (ED) and intensive care unit (ICU). This chapter will briefly describe the history and evolution of point-of-care ultrasonography, present techniques for obtaining ultrasound imaging at the bedside, and overview the basics of cardiac, lung, abdominal, and vascular ultrasound. Critical care ultrasonography (aka point-of-care ultrasonography) can be used to evaluate patients with traumatic shock, respiratory failure, pneumothorax, and pleural effusion. Vascular ultrasonography is useful in evaluation of deep vein thrombosis (DVT) and aortic rupture or dissection, and for placement of venous and arterial catheters. Abdominal critical care ultrasonography can be useful in evaluating abdominal pain, abdominal trauma, or other abdominal disorders. Critical care echocardiography may be used in the evaluation of shock and cardiogenic pulmonary edema. With critical care ultrasonography, the clinician is directly responsible for image acquisition and interpretation. This contrasts with conventional diagnostic medical sonography as performed by a skilled technician and evaluated by a radiologist or cardiologist trained in the interpretation of the resultant images. A word about terminology: Echogenicity refers to the ability of anatomic structures, tissues, or abnormalities to bounce sound waves back to the ultrasound equipment. Hyperechoic structures or substances appear lighter on imaging, while hypoechoic structures or substances appear darker. Anechoic structures do not return sound waves and appear black. For example, bones are hyperechoic, fat is hypoechoic, and arteries and veins are anechoic.

The History and Evolution of Point-of-care Ultrasound The use of sounds waves to generate images has a long history in medicine, with the experimental phase dating back to the 1940s. Certain fields of medicine such as cardiology, obstetrics, and radiology have used ultrasound similar to its modern form since the 1970s and 1980s. Improvements in technology have lowered the cost and decreased the size of ultrasound machines, which in turn has increased the availability of ultrasound imaging and broadened its clinical applications. For over a decade, “point-of-care” or “bedside” ultrasound has been used to guide

medical decision making without traditional formal interpretation by a radiologist or cardiologist. One of the best-known examples of this is the focused assessment with sonography in trauma (FAST) exam, which was incorporated into the Advanced Trauma Life Support course nearly two decades ago.1 Bedside ultrasound is now deeply integrated into the management of critically ill patients in many forms. Its use has been endorsed by numerous medical professional societies and has been recommended to be included in graduate medical education. Physicians, respiratory therapists, nurses, and others working in the ICU should be familiar with the use of bedside ultrasonography. In critical care, ultrasound is used to aid in diagnosis and to improve the safety and success of therapeutic interventions. In many institutions, ultrasound use for central line placement has become routine, likely due to the relative simplicity of ultrasound devices and less required training. Today, ultrasound is commonly used to guide bedside thoracentesis, paracentesis, and lumbar punctures, and in many institutions, has largely become the standard of care. From a diagnostic standpoint, the application of critical care ultrasound can be very focused, such as to specifically rule out certain diagnoses (i.e., pericardial effusion with tamponade), or very broad as an adjunct to the physical examination. For example, Drs. Lichtenstein and Mezière developed a systematic algorithm known as the BLUE protocol to identify the cause of respiratory failure based solely on a constellation of sonographic findings of different organs.2

Types of Transducers Ultrasound transducers convert electrical energy into sound energy by means of the piezoelectric transducer. Each transducer is composed of 60 to 600 piezoelectric elements, or crystals, with the ability to generate vibrations when electric current is applied. While the physics of ultrasound is beyond the scope of this chapter, a basic understanding of transducer characteristics and the resultant images is necessary for optimal image acquisition. In general, transducers that use higher-frequency sound waves produce higher-resolution images; however, the higher frequencies result in decreased penetration, which limits image depth. RC Insight

Higher-frequency soundwaves result in higher-resolution images but have limited depth of field.

The four main types of transducers used in point-of-care ultrasound are the linear, curvilinear, phased-array, and intracavitary transducers. Each transducer type differs by crystal arrangement, frequency, imaging depth, and beam pattern thus producing a unique image. Linear transducers contain elements that activate in parallel to form a narrow rectangular image. They operate at a high frequency (5 to 10 MHz) and shorter wavelength, thus providing optimal visualization of superficial (< 5 cm deep) structures such as blood vessels, eyes, skin or soft tissue, and joints. Because of the high image resolution for these superficial structures, this transducer is optimal for use in common ultrasound-guided procedures such as central venous catheter placement and arthrocentesis (i.e., joint aspiration). Curvilinear transducers contain a linear arrangement of elements in a convex, or curvilinear, arrangement. They produce a broader beam pattern, and thus a wider field of view, in the shape of a trapezoid. They operate at lower frequencies (2 to 5 MHz) and longer wavelengths than the linear transducer, thus producing images of deeper structures (5 to 30 cm depth), though with less resolution than the linear transducer. These transducers are optimal for visualization of intraabdominal structures. Phased-array transducers contain fewer elements than the linear transducers discussed above and activate in “phases” in different directions. This produces multiple waves at a lower frequency (1 to 5 MHz) in diverging directions that interfere with each other to produce a small, triangular image. Since the elements are activated in phases, the addition of various transducer movements (discussed in the next section) can be utilized to steer the sound waves and produce a wider field of view. This allows for the imaging of moving structures including the heart and lungs. Intracavitary transducers combine the high frequency (5 to 8 MHz) of the linear transducer with the beam pattern of the phased array to produce a focal, highresolution image. This is best utilized for vaginal, rectal, and oral structures.

Holding and Moving the Transducer The transducer should be held loosely between the thumb and index finger, like a

pencil. The other digits can be curled against the transducer or anchored against the patient’s body to stabilize the scanning hand in place. Each transducer has an orientation marker on the side that should be aligned with the corresponding orientation dot on the screen image. From this neutral position, there are four transducer movements that can be applied: sliding, tilting, rocking, and rotating. Sliding (also called scanning) is when the transducer is held at a fixed angle and is moved entirely without breaking contact from the patient’s skin. This allows for identification of structures of interest. Tilting (also called sweeping or fanning) is when the transducer is held at a fixed point against the patient and is angled up or down along the long axis of the transducer. This provides a series of cross-sectional images that coalesce to form a wider view of the target structures. This is particularly useful for imaging of solid organs, such as the heart, or fluid collections, such as pleural effusions. Rocking is when the transducer is again held at a fixed point and then angled along its short axis, to and from the orientation marker as though pushing a corner of a linear probe deeper into the skin. This motion can be helpful in centering the image. Rotating is when the transducer is held at a fixed point against the skin and is turned about its central axis. This allows for optimal alignment of the ultrasound beams with the underlying structures. The combination of these movements may be necessary for optimal image acquisition. RC Insight Sliding, rotating, rocking, and tilting are all terms to describe movements of the transducer to obtain images. Each term has a specific definition that enables sonographers to communicate effectively about how to improve image acquisition.

Cardiac Ultrasound Cardiac ultrasound, commonly known as critical care echocardiography, can be useful in evaluating patients with shock or cardiogenic pulmonary edema, and may be useful during cardiopulmonary resuscitation to identify certain conditions (e.g., cardiac tamponade, severe hypovolemia, thrombus). Point-of-care echocardiography should not be confused with traditional diagnostic echocardiography performed by a skilled technician and evaluated by a trained cardiologist. Diagnostic echocardiography allows for more sophisticated evaluation of the heart, to include assessment of heart size, heart wall motion, heart valves, the pericardium, and the presence of intracardiac shunts.

General Concepts The critical care ultrasound assessment of cardiac structures and function is less detailed and generally less sophisticated than formal echocardiography, but it still provides extremely useful information. In general, large, clinically significant defects can easily picked up by an experienced bedside sonographer. For example, the average critical care sonographer does not need to calculate ejection fraction, but can qualify it as hyperdynamic, normal, reduced, or severely reduced. Clinically, this is useful enough, as anything greater than severely reduced ejection fraction is not likely to cause hypotension; thus, cardiogenic shock can be reasonably ruled out. Similarly, detection of a clinically significant pericardial effusion is not a subtle finding. Even in cases where early tamponade cannot be ruled out, the bedside ultrasound can help guide decisions about urgency of further testing, such as a formal echocardiogram or a stat cardiology consult. RC Insight Point-of-care ultrasonography provides an excellent qualitative assessment for systolic function, with descriptors such as hyperdynamic, normal, mildly depressed, or severely depressed.

Critical care cardiac ultrasound generally involves four views: parasternal long axis, parasternal short axis, apical four chamber, and subcostal. Each view transects the heart in a different plane, provides slightly different information, and has different strengths and weaknesses. Not every view is obtainable in every patient. While each

view provides different information, all findings should be taken together to make a clinical assessment. Inconsistencies should be taken in context with findings in other views, as well as the strengths and weakness of each view.

Parasternal Long-axis View The parasternal long-axis view is typically a good starting point for bedside cardiac ultrasound. It provides the most consistent location relative to fixed anatomic landmarks and generally does not require repositioning of the supine patient. Telemetry leads will often need to be removed temporarily to achieve an adequate assessment. The parasternal long-axis image is obtained by placing the probe just lateral to the left sternal border with the probe orientation marker pointed towards the patient’s right shoulder. The exact rib space that provides the best window varies from person to person, but typically is at the level of the third or fourth intercostal space. Optimal windows in an intercostal space above or below this range are not uncommon. The probe should be slid up or down one intercostal space until an adequate window is obtained. Structures seen in this view include the left atrium (LA), mitral valve, left ventricle (LV), aortic valve (Ao), and the left ventricular outflow tract (Figure 13-1). A limited view of the right ventricular (RV) outflow tract may also be seen.

FIGURE 13-1 Parasternal Long Axis View. The parasternal long-axis view visualizes the left atrium (LA), left ventricle (LV), aorta (Ao), and right ventricle (RV). It provides an assessment of LV size and function, LA size, the aortic and mitral valves, and pericardial effusion. Courtesy of Kevin Proud.

The parasternal long-access view gives a good assessment of left ventricular contraction, left atrial size, and mitral valve appearance. It is also a good view to assess for pericardial effusion. Though partially visualized, significant information about the aortic valve is rarely obtained in this view. The parasternal long-axis view provides a limited view of the right side of the heart; thus, it is not an optimal view to

assess right ventricular function or cardiac tamponade. RC Insight A qualitative assessment of systolic function and evaluation for pericardial effusion can quickly rule in or rule out cardiac causes of hypotension in most cases.

Parasternal Short-axis View The parasternal short-axis view is obtained by starting in the parasternal long-axis view, then rotating the probe clockwise until the probe orientation marker is pointed towards the patient’s left shoulder, or approximately 90 degrees from the parasternal long orientation. A circular appearance of the left ventricle is a good indicator that the probe is in the proper axis to yield a cross-sectional view. Structures visualized in the parasternal short-access view include the left ventricle, the mitral valve, the pericardium, the papillary muscles, and the right ventricle (Figure 13-2). Visualization of the papillary muscles indicates that the ultrasound beam is traversing the heart at approximately the mid-portion of the left ventricle.

FIGURE 13-2 Parasternal Short Axis View. The parasternal short axis view visualizes the left ventricle (LV), right ventricle (RV), and the interventricular septum (IVS). This view provides an assessment of global LV function and wall motion, shape and function of the IVS, and RV size. Courtesy of Kevin Proud.

This view provides valuable information about left ventricular function and is often the best view for assessing focal wall motion abnormalities. It also provides one of the best views of the mitral valve structure, which is achieved by sliding the probe to the level of papillary muscles, and then tilting the probe so that the beam is aimed cephalad. The irregular nature of the crescent-shaped right ventricle makes assessment of right ventricular size and function unobtainable in this view.

Apical Four-chamber View The apical four-chamber view provides a great deal of clinically useful information but is often one of the most challenging views to obtain. The view is obtained by

sliding the probe from the parasternal short-axis view to a more lateral and slightly inferior location, typically to the area of the cardiac point of maximal impulse (PMI). The transducer is again rotated clockwise until the orientation marker is pointed to the patient’s left side (referred to as the 3 o’clock position). Often the probe must be tilted more sharply than in other views in order to get the ultrasound beam in plane with the heart. Additionally, the transducer often has to be rocked to the left or right to achieve the proper axis. In this view, the transducer is often placed on the curved part of the chest wall and is prone to inadvertent sliding resulting in the loss of the window. The apical four-chamber view is often limited by aerated lung tissue obscuring the view. Image acquisition can be improved by having the patient rotate partially onto his or her left side. Structures included in this view are the right and left ventricles, right and left atria, the mitral and tricuspid valves, and the pericardium (Figure 13-3). With tilting of the transducer, this can sometimes be easily modified into a five chamber view, which includes the aortic valve.

FIGURE 13-3 Apical Four Chamber View. The apical four-chamber view provides visualization of all four chambers of the heart: right atrium (RA), right ventricle (RV), left atrium (LA), and left ventricle (LV). This view allows for assessment of RV and LV size and function relative to each other, tricuspid and mitral valve function, and pericardial effusion. Courtesy of Kevin Proud.

The apical four-chamber view is the single best view to assess right ventricular size and function. It provides a side-by-side comparison of the right and left ventricular size, the ratio of which is used to assess for right ventricular strain. This view also gives a good assessment of left ventricular function, though it must be

interpreted in the context of the other views obtained since only two ventricular walls are visualized. It is a good view to evaluate for pericardial effusion, structure of the mitral and tricuspid valves, and left ventricular wall motion. If color flow Doppler is used, the apical four-chamber view can give a good assessment of mitral valve or tricuspid valve regurgitation.

Subcostal View The subcostal view can be especially useful in intubated patients because the liver can be used as an acoustic window to project the sound waves that would otherwise be blocked by aerated lungs. This view is obtained by placing the probe directly inferior to the xyphoid process with the probe orientation marker pointed to the patients left side or the 3 o’clock position. The probe generally needs to be tilted so the ultrasound beam projects up toward the patient’s head, and often a fair amount of pressure needs to be applied to position the probe under the ribs. Structures visualized in this view include the right and left ventricles and the right and left atria (Figure 13-4). This view can give a qualitative estimate of right ventricular size; however, because of differences in axis, it is not as good as the apical four-chamber view for assessment for right ventricular strain.

FIGURE 13-4 Subcostal Four Chamber View. The subcostal four-chamber view provides visualization of all four chamber of the heart: right atrium (RA), right ventricle (RV), left atrium (LA), and left ventricle (LV). This view provides a comparison between right and left chambers of the heart, assessment of pericardial effusion, and visualization of RV free wall (especially useful in the setting of cardiac tamponade). Courtesy of Kevin Proud.

The subcostal view does provide a good view of the right ventricle and atrium and approaches the heart from an inferior angle. As a result, this is a good view to assess for pericardial effusion and for diastolic collapse seen in cardiac tamponade. The below the chest transducer position for this view provides two other advantages over the other views. First, this view can be obtained continuously during cardiopulmonary resuscitation (CPR) without interrupting chest compressions.

Second, because of this view’s inferior window to the right atrium, the junction of the right atrium and inferior vena cava (IVC) can be seen. The IVC can then be traced inferiorly into the abdomen and is often used to assess for volume responsiveness, as described in the next section.

Assessment of Volume Responsiveness One major area of uncertainty in critical care today is the degree to which volume resuscitation is beneficial. This is especially true for patients with severe sepsis and septic shock. It is evident that early fluid resuscitation is key to improving outcomes,3 but there is also evidence to suggest that too much fluid administration can be detrimental and worsen outcomes.4 Determining whether a patient will benefit from intravenous fluids, i.e., be “fluid responsive,” is a key area of investigation today, but remains largely difficult to determine. Most often, fluid responsiveness is defined as an increase in cardiac output or stroke volume by at least 15% following intravenous (IV) fluid administration. Ultrasound assessment of the inferior vena cava (IVC) has been shown to be potentially useful in this regard. The degree to which the IVC diameter (Figure 13-5) varies throughout the respiratory cycle in patients on mechanical ventilation has been shown to correlate with fluid responsiveness with good sensitivity and specificity.5,6 Exact cutoffs depend on the calculation used, but in general, the greater the difference between the maximum and minimum diameter of the IVC, the more likely the patient will be responsive to fluid resuscitation. These measurements can be difficult to obtain in some patients, and determining the exact amount of variability can also be challenging. For example, assessing for a 12% change in a 2-cm diameter structure would mean looking for a 2.4-mm difference! This can be aided by the use of M-mode and careful measurement of a frozen image. Often a more qualitative assessment is done, describing the IVC as collapsed, distended, or in between. This qualitative method is less refined, but often a good decision-making tool.

FIGURE 13-5 Longitudinal View. (A) A longitudinal view of the inferior vena cava (IVC) as it enters the right atrium (RA) can be obtained from the subcostal four chamber view. (B) M-mode can be utilized to analyze the IVC’s maximal diameter just distal to the hepatic vein–IVC junction. This assessment of the IVC’s diameter and collapsibility may be useful in guiding fluid management. (A) and (B) Courtesy of Kevin Proud.

Lung Ultrasound Although lung ultrasonography has a number of limitations, it can be very useful in confirming the presence or absence of pneumothorax, identifying alveolar or interstitial abnormalities, and in the evaluation and treatment of pleural effusion.

General Concepts The role of ultrasound of the lung was once believed to be extremely limited due to the poor acoustic properties of air. More recently, ultrasound has proven to be a useful tool for assessing the lung despite this issue. In fact, with practice, some sonographic findings can be highly sensitive and specific for certain specific pathologies. When applied in a broad but algorithmic manner, the etiology of respiratory failure can be determined by sonography with accuracy in many cases.2 Though it is true in most ultrasound examinations, in lung ultrasound, it is particularly important to identify key anatomic structures to orient the image and position. Because the chest wall is a large surface area that overlies several organs, it can contain a broad range of pathologies, some of which may have similar sonographic appearances. Additionally, the presence of the air in the lung can cause significant artifact and obscure the view. Orienting the images based on clearly identifiable structures is essential to prevent misinterpretations of images. Because normal lung is filled with air, which scatters ultrasound waves, normal lung appears as nonspecific noise and blocks visualization of discrete structures beyond the pleura. However, some sonographic artifacts are useful in distinguishing normal lung from abnormal lung. In contrast to the parenchyma, the pleura is well visualized with ultrasound and appears as a thin white line no more than 5 mm deep to the rib shadows. A reverberation artifact occurs as the result of sound waves repetitively bouncing off the pleural line. This reverberation creates parallel horizontal lines and consistent intervals known as A-lines. While not perfectly predictive, the presence of A-lines in the setting of normal pleural sliding (i.e., no pneumothorax) is indicative of normal, aerated lung. A second useful finding is the presence of vertical “spotlight-like,” cone-shaped lines originating from the pleural line and extending to the full depth of the ultrasound

field. These are referred to as B-lines or “comet tails.” This finding, particularly when three or more are present in the ultrasound field, suggests increased fluid density of the lung, most typically seen with pulmonary edema. As discussed below, B-lines seen in isolation are suggestive of cardiogenic pulmonary edema; however, if in conjunction with other findings, they could suggest pneumonia. The last common sonographic appearance of the lung is a dense consolidation of the lung, which often occurs in the setting of pneumonia. This results in an increased echogenicity similar to that of the liver and is often termed “hepatization” of the lung. Within this dense consolidation, it is common to see hyperechoic dots, which represent pockets of air or air bronchograms within the diseased or atelectatic lung. Similarly, this density often creates a ragged border between the aerated lung and the pleura. While these findings lack specificity for pneumonia, they may help refine the clinical picture.

Detection of Pneumothorax One very specific use of ultrasound of the lung is to evaluate for the presence of pneumothorax. Using a linear probe, the pleural line can be easily visualized. It is represented as a hyperechoic thin line that should be no more than 5 mm deep to the bottom of the rib shadows. The visualization of the pleural line itself is not useful for ruling out pneumothorax. However, as the visceral pleural and the parietal pleural slide past each other during normal respiratory motion, a shimmering appearance of the pleural line is created. The detection of this shimmering (also referred to as “lung sliding”) virtually rules out a pneumothorax in that area. To properly assess for pneumothorax, it is important to look for lung sliding in nondependent areas of the chest wall. Analogous to the air bubble in a level, gravity will push the air into the highest point in the chest cavity (assuming no loculation). A reasonably thorough assessment can be done quickly by scanning several upper intercostal spaces at the midclavicular line, the anterior axillary fold, and the midaxillary line. While typically it is not difficult to discern whether or not lung sliding is present, the use of M-mode during respiration with the transducer focused on the pleura can often provide additional clarity. The motion of the pleural line from lung sliding will create a variation on M-mode above and below the pleural line. This is commonly

referred to as “the sandy beach” or “the seashore sign” because the still chest wall generates smooth horizontal lines while the moving pleura generates a more heterogeneous appearance, similar to smooth water reaching a sandy shore (referred to as the “bar code sign”). Additionally, on a two-dimensional (2-D) view, identifying a transition point from normal lung sliding to no motion is known as a “lung point” sign and correlates highly with the presence of a pneumothorax. RC Insight The absence of lung sliding on a close evaluation of the pleura is highly suggestive of a pneumothorax.

Evaluation of Pleural Effusion Ultrasound is an excellent tool for assessing pleural effusions. For this task, the phased-array probe is the most commonly used. Ultrasound easily outperforms chest x-ray in sensitivity and specificity, and it likely outperforms computed tomography (CT) scan for clinically relevant effusions. The use of ultrasound during thoracentesis has been shown to increase the accuracy of site selection and decrease the rate of complications such as pneumothorax.7,8 As previously stated, finding anatomic landmarks is essential during assessment of pleural effusions, particularly if there is a plan for an invasive procedure such as thoracentesis or tube thoracotomy. Dense pneumonias can sonographically mimic the liver; conversely, volume loss due to atelectasis can lead to elevation of the hemidiaphragm well above the mid-chest. The diaphragm is generally the most reliably identifiable structure in the lower chest. It is a hyperechoic band that typically forms an arc-like shape. Its identification can be further confirmed by seeing movement when the patient is asked to inhale and exhale deeply. The presence of lung coming in and out of view during respiration, forming the “curtain sign,” can also help confirm the location of the diaphragm. Lastly, the liver or spleen should be easily identifiable just below the diaphragm, depending on the side of the patient being assessed. Identification of the kidney in relation to these structures is also recommended. There are anecdotal reports of the upper pole of the kidney being misidentified as the diaphragm prior to

thoracentesis. RC Insight Identifying anatomic landmarks such as the diaphragm, liver or spleen, kidney, and atelectatic lung is key to safely performing a thoracentesis.

A pleural effusion should appear as an anechoic (solid black) space just above the diaphragm in most cases; however, variations in the appearance exist depending on the nature of the pleural effusion. Atelectatic lung is commonly seen floating within the hypoechoic region.

Characteristics of Pleural Effusion A great deal of qualitative information can be gained about a pleural effusion with the use of ultrasound. Though calculations exist to determine the specific volume of fluid based on ultrasound measures, there is little clinical utility for this quantitative measurement. More often, pleural effusion size is described qualitatively as small, moderate, or large. Clinically, the most important size determinant is whether or not the effusion is large enough to be sampled safely via thoracentesis, as discussed in the next section. Generally speaking, almost all transudative effusions appear as simple, homogenous, anechoic fluid collections. However, simple, homogenous, anechoic effusions can be either transudates or exudates. If the effusion is anechoic but contains septations (divided by a septum); has free-floating, heterogeneous, echogenic material; or has increased echogenicity (similar to that of the liver), the fluid is almost certainly an exudate (Figure 13-6).9 Similarly, the appearance of debris swirling around in the fluid, often referred to as “plankton sign,” is very suggestive of an exudative effusion. The presence of two fluid densities or two fluids of different echogenicity that layer with gravity is very suggestive of a hemothorax. This is often referred to as the “hematocrit sign,” though it can also be seen in the case of an empyema.

FIGURE 13-6 Complex Multiloculated Pleural Effusion with Numerous Septations. Courtesy of Kevin Proud.

Pleural Drainage Procedures Bedside ultrasound has proven to be very useful for pleural drainage procedures. The use of ultrasound can help confirm the presence of effusions suspected based on chest x-ray, help determine if the effusion is large enough to safely sample, increase the rate of success, and decrease the rate of complications. Most sources recommend a minimum of 1.5 cm of fluid between the chest wall and underlying structures in order to safely perform a thoracentesis. While this number serves as a good guide, other factors should be taken into consideration, including motion of underlying structures with respiration, the quality of the angle or window achieved on ultrasound, and general patient factors. Real-time ultrasound can be performed with direct visualization of the needle; however, point-of-care

marking of a safe site is more commonly performed. Real-time ultrasound is more technically challenging than point-of-care marking, and currently there is no proven benefit for one method versus another. As a result, point-of-care marking with bedside ultrasound is more commonly performed and is acceptable, provided the patient does not change position following the marking. The use of ultrasound has reduced the rate of complications significantly. The rate of pneumothorax has decreased from as high as 18% without ultrasound to approximately 1% to 5% with ultrasound based on some case series.7,8,10–12 RC Insight A pocket of fluid that creates a depth of greater than 1.5 cm between the chest wall and underlying lung is felt to be large enough to be safely accessed by thoracentesis.

Determining the Etiology of Respiratory Failure The role of bedside ultrasound in critical care has been pushed beyond assessment for specific abnormalities in some cases. As discussed earlier, ultrasound of the thorax can be focused to assess for pleural effusion or pneumothorax, but when all findings are taken together, a constellation of findings can lead to the diagnosis in the majority of cases. In a study by Lichtenstein and Mezière,2 the authors used a protocolized ultrasound assessment of the lungs in 260 patients admitted to the ICU for dyspnea to determine the etiology while being blinded to any other information about the patient. After excluding rare or unusual cases, the authors reported making the correct diagnosis in 90% of cases.2 In this study, the authors used predetermined constellations of findings to categorize patients as having one of the following five diagnoses: cardiogenic pulmonary edema, obstructive lung disease (chronic obstructive pulmonary disease [COPD] or asthma), pulmonary embolism, pneumothorax, or pneumonia (Table 13-1). While there were cases in each diagnosis that had findings not anticipated by the predetermined constellations, their use of ultrasound alone to make the diagnosis performed very well. Most clinicians likely do not follow such a rigid protocol, but clearly lung ultrasound is a useful diagnostic tool. TABLE 13-1

Lung Profiles & Suspected Diagnoses based on Blue Protocol Profile

Description

Suspected Diagnosis

A

bilateral A-lines, lung sliding present

If DVT present: pulmonary embolism If PLAPS present: pneumonia If no additional findings: asthma or COPD

A’ (A prime)

bilateral A-lines, abolished lung sliding

If lung point present: pneumothorax If no lung point: Additional studies needed

B

bilateral B-lines, lung sliding present

B’ (B prime)

bilateral B-lines abolished lung sliding

AB

B-lines on one slide with predominant Alines on the other

C

Pulmonary edema

Pneumonia

anterior alveolar consolidation, air bronchograms

PLAPS: posterolateral alveolar and/or pleural syndrome (a combination of small pleural effusion and consolidated lung typically located in a dependent area on a supine patient) Data from Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol2.

Abdominal Ultrasound Abdominal ultrasonography in the emergency department or intensive care unit can be extremely useful in evaluating patients following abdominal trauma, those with abdominal pain, and for detection of gallbladder disease, bladder distention, or urinary tract obstruction. Abdominal ultrasonography may also allow for detection of free air or fluid in the abdomen and recognition of rupture of the abdominal aorta (e.g., aortic aneurysm).

General Concepts The role of abdominal ultrasound in critical illness is broad and can be useful in a wide range of clinical scenarios. For example, it can be used in the setting of trauma as part of the FAST exam to assess for intra-abdominal hemorrhage or used in a stable patient with cirrhosis to assess for the presence of ascites. Abdominal ultrasound can also be focused to assess specific organs such as the liver, gall bladder, kidneys, or spleen. Abdominal ultrasound can also be used in more dynamic settings such as to assess for fluid responsiveness by measuring IVC collapsibility as described above, or to assess for obstructive uropathy by evaluating the fullness of the bladder. The best transducers for abdominal ultrasound are the phased array or the curvilinear transducers because they allow for adequate depth to assess deep structures. Typically, the exam mode should be set to “abdomen” to ensure the proper frame rate for optimal image acquisition. The patient is generally in the supine position. By convention, the transducer orientation marker is pointed towards the patient’s head.

Anatomic Landmarks The diaphragm serves as a good starting anatomic landmark because it is consistent and easily identifiable. As described in the thoracic ultrasound section, it appears as a dense, hyperechoic, arc-shaped line that moves with respiration. Immediately below the diaphragm on the right is the liver, which appears as a large, isoechoic structure. On the left, just below the diaphragm, is the spleen. Sonographically, the spleen and the liver are very similar in appearance, but fortunately, the laterality of

these structures is almost universal. The gall bladder is also in the right upper quadrant tucked underneath the liver, typically between the right and left lobes. As the transducer is slid caudal to the liver, and typically between the mid and anterior axillary line, the right kidney is seen as a curved-elliptical “kidney or bean-shaped” structure. The center portion (the calyx) usually appears hyperechoic, while the somewhat triangular-shaped renal pyramids appear isoechoic. The left kidney is located just below the spleen and is typically more superior and posterior compared to the position of the right kidney. In the setting of hydronephrosis, the calyx becomes enlarged, and the pyramids become progressively smaller with increasing severity of hydronephrosis.

Assessment for Ascites and Paracentesis A common use for abdominal ultrasound in critical care is the identification of ascites and paracentesis. As mentioned above, the phase array or curvilinear transducers can be used. If present, ascites will appear as anechoic pockets, typically in dependent areas such as the right or left lower quadrant. In cases of large-volume ascites, free-floating bowel is commonly seen. The long thin loops of undulating bowel floating in the ascitic fluid is often referred to as the “palm tree” sign. It should be noted that numerous patients that appear to have tense ascites on physical exam, can have virtually no ascites on ultrasound. In these cases, bowel wall edema or bowel gas results in a scattered sonographic image similar to aerated lung. RC Insight Ultrasound is excellent at differentiating ascites from bowel wall edema as a cause of distended abdomen.

Using ultrasound when performing a paracentesis is beneficial because it confirms the presence of ascites, identifies the largest pockets of fluid, and makes the user aware of underlying structures to avoid. Much like with thoracentesis, a minimum safe distance of 1.5 cm between the abdominal wall and any underlying structures is recommended. Paracentesis can be performed in real time or with point-of-care marking. If point-of-care marking is used, it is important to avoid significant repositioning of the patient between the marking and the needle insertion, as the free-flowing nature of the fluid could result in a change of pocket size or location.

Lastly, it has also become our practice to use color flow Doppler to look for aberrant abdominal wall vessels that could cause bleeding if paracentesis were performed in that location. RC Insight Prior to paracentesis, the use of color flow can help identify blood vessels that would otherwise be in the path of the needle.

Vascular Ultrasound Vascular ultrasonography can be useful in identification of deep vein thrombosis (DVT), a common cause of pulmonary embolus. Vascular ultrasonography can also guide the placement of central or peripheral venous catheters, as well as arterial lines. Vascular ultrasonography may also be useful in identification of a ruptured abdominal aortic aneurysm or dissection.

Vascular Access Point-of-care ultrasound of the vascular system was first introduced into the intensive care unit in the 1980s; however, at that time it was largely felt to be too expensive and cumbersome to use. Advances in technology, especially in the development of smaller, portable ultrasound units, have allowed for more routine and integrated use of ultrasound imaging in the ICU. Real-time ultrasound guidance for the placement of central venous catheters (CVC) has become widespread and is now the standard of care. The linear transducer is the transducer of choice for vascular assessment. For CVC placement, ultrasound is used to identify the internal jugular or femoral veins. The subclavian vein can also be assessed by ultrasound; however, acoustic shadows from the clavicle can make visualization challenging. Despite this, there is some evidence that ultrasound can increase the success rate of subclavian line placement.13,14 The detailed technique of CVC placement is beyond the scope of this chapter; however, it is worth highlighting a few points. First, bilateral ultrasound assessment before line placement is strongly recommended, if possible. Patients have a high degree of anatomic variation, and often one side will present technical challenges while the other is anatomically ideal. Second, it is often helpful to view the vessel in both short-axis and long-axis views, both before and during the procedure. The longaxis view is more challenging in real time, but it can give valuable information about trajectory of the vessel before the procedure and is the best view for confirming proper placement of the guidewire during the Seldinger technique. RC Insight Due to significant asymmetry within the vascular system, bilateral sonographic assessment of central vessels should be done before any attempt at cannulation.

Detection of Deep Vein Thrombosis Bedside ultrasound can also be used to assess for the presence of deep vein thrombosis (DVT). Images of the veins of interest are best obtained using the linear transducer. In the lower extremities, the common femoral artery and vein can be identified just inferior to the inguinal ligament and tracked distally. As the operator scans further down, the first branch point is the takeoff of the greater saphenous vein, followed by the lateral perforator, and finally the division between the superficial and deep femoral veins. Detection of DVT relies primarily on the lack of compressibility of the vein (wall to wall), but suspicion may be increased by intraluminal abnormalities. During scanning, assessment of compressibility is performed at 1 to 2 cm intervals until just past the bifurcation of the deep and superficial femoral veins. The exam should then continue to assess the popliteal vein, posterior to the knee. Special attention should be given to vessel bifurcations, as they have the highest frequency of DVT. It is important to note that acute thrombi will appear less echogenic than well-formed subacute or chronic thrombi due to the initial gelatinous consistency of acute thrombi. Color flow Doppler can also be a useful adjunct to vessel compression to assess for DVT. Sensitivity and specificity are undoubtedly affected by operator experience, but with training most clinicians can achieve reasonable efficacy. Though practices vary, our practice is to confirm any abnormal bedside findings with formal studies, for both documentation purposes and confirmation; however, clinical decisions can be made based on bedside findings. RC Insight If a vein does not collapse under a small amount of applied pressure, the presence of a clot is likely.

Ultrasound-Guided Lumbar Puncture Ultrasound has been shown to useful in performing lumbar puncture by decreasing the number of failed attempts as well as improving diagnostic yield by decreasing traumatic taps.15 As with other ultrasound-assisted procedures, lumbar punctures can be performed with real-time image guidance or point-of-care ultrasound marking. Real-time ultrasound guidance with ultrasound can only be done in the paramedian approach, which will not be discussed in detail here. The point-of-care marking is less technically difficult, but still very beneficial compared to performing the procedure based on palpation of landmarks alone. RC Insight Sonographic identification of the spinous processes and interspinous space in the transverse and longitudinal views can be used to create a crosshair over the interlaminar foramen. Sonographic identification of the spinous processes in the transverse and longitudinal views can be used to create a crosshair over the interspinous space.

The point-of-care marking can be performed with the patient in the sitting or lateral decubitus position. The image acquisition is best obtained with the linear array probe. The first goal is to identify the midline, an imagery line connecting the spinous processes. This is achieved by positioning the probe in the transverse position, with orientation marker pointed toward the patient’s side (or pointed toward the ceiling for patients in the lateral decubitus position) at the patient’s gluteal cleft. As the probe is slid cephalad, the sacrum should come into view. The probe is then slid to the patient’s right or left as needed to keep the sacrum in the midline. As the probe is slid gradually more cephalad, individual spinous processes should be identified as thin white (hyperechoic) flat or slightly arc-shaped images. A dark area of shadowing should be visible below the spinous process. The probe is again slid to the patient’s right or left as needed to keep the spinous process in the midline. This midline should be marked as the probe is slid more cephalad. Each spinous process can be counted individually until the L3–L4 space is identified. Once the midline is identified, the probe is rotated 90 degrees. In the longitudinal view with the probe orientation marker pointed towards the patient’s head, the spinous processes are seen as more elongated, bright white arches. In the longitudinal view, two spinous processes are identifiable in one ultrasound field with the interspinous space between the two

structures. By sliding the transducer cephalad or caudal the interspinous space can be marked perpendicular to the previously marked midline, creating “crosshairs” over the ideal needle entry site. Once marked, the procedure is performed as usual. Case Study 1 A 50-year-old male patient is intubated and on vasopressors with a decrease in blood pressure to 70/40 mmHg and a heart rate of 130 beats per minute. He is on 100% Fio2 with a PEEP of 20 cm of H2O. The medical doctor wants to increase the vasopressors but an ultrasound image of the inferior vena cava (IVC) shows IVC collapse. Which of the following would you do in this situation? 1. Increase the vasopressors to maintain a mean arterial pressure (MAP) of 65 mm Hg or greater. 2. Observe the patient over 30 minutes and if the MAP remains low, then increase vasopressors. 3. Reduce the PEEP from 20 cm to 15 cm since PEEP reduces blood flow back to the right side of the heart. 4. Bolus fluid and repeat ultrasound of the IVC and reassess blood pressure. Correct answer: 4. Collapse of the IVC is an indication of inadequate intravascular volume. Additionally, vasopressors are not effective in patients who are volume depleted. Measuring the size of the IVC and determining the percentage of collapse during the respiratory cycle is a useful method for assessing the volume status of a patient.

Case Study 2 A 60-year-old female presented to the emergency room with acute shortness of breath, substernal chest tightness, and hypoxemia. The electrocardiogram (EKG) had nonspecific T-wave changes and demonstrated sinus tachycardia. The physical exam revealed mild wheezing, and her exam was otherwise normal except for mild bilateral lower extremity edema. How would a point-of-care ultrasound exam help you with this patient? 1. 2. 3. 4.

You could assess the left ventricular (LV) function and look for wall abnormalities, You could compare the size of the right ventricle (RV) to the left ventricle, You could evaluate the lower extremity for evidence of DVT, All of the above are correct.

Correct answer: All of the above are correct. This patient demonstrated normal LV function but the RV was larger than the LV, suggesting right ventricular overload. There was paradoxical motion of the ventricular septum, suggesting that there was RV failure consistent with either a pulmonary embolism or cardiac tamponade (seen with a pericardial effusion that was not noted in this case). The medical team performed Doppler exam of the lower extremity and found a large DVT in the common femoral vein; the presumptive diagnosis of pulmonary emboli was made and anticoagulation started in the emergency room. It is not uncommon for patients with pulmonary emboli to wheeze in the first few hours after the clot enters the pulmonary vasculature. The respiratory therapist initatiated oxygen and albuterol (Proventil), which resulted in improvement in the patient’s heart rate and dyspnea.

Key Points Ultrasound use has been increasing in many areas of medicine over the last 30 years, and point-of-care ultrasound often supplements the physical examination in some fields. Echogenicity refers to the ability of anatomic structures, tissues, or abnormalities to bounce sound waves back to the ultrasound equipment. Hyperechoic structures or substances appear lighter on imaging, while hypoechoic appear darker. Anechoic structures do not return sound waves and appear black. Bones are hyperechoic, fat is hypoechoic, and arteries and veins are anechoic. The focused assessment with sonography in trauma (FAST) exam was incorporated into the Advanced Trauma Life Support course nearly two decades ago. The BLUE protocol is used to identify the cause of respiratory failure based on a constellation of sonographic findings of different organs. Higher-frequency soundwaves result in higher-resolution images but have limited depth of field. The four main types of transducers are the linear, curvilinear, phased-array, and intracavitary; each differs by crystal arrangement, frequency, imaging depth, and beam pattern, thus producing a unique image. The four transducer movements are sliding, tilting, rocking, and rotating. Point-of-care cardiac ultrasound typically involves four views: the parasternal long, parasternal short, apical four chamber, and the subcostal. Point-of-care cardiac ultrasound is excellent for the evaluation of pericardial effusion and gives a qualitative assessment of left ventricular function. The subcostal view is often the mostly obtainable four-chamber view in ventilated patients because the liver can be used as an acoustic window through which sound waves are well transmitted. The degree to which volume resuscitation may be beneficial is important for patients with severe sepsis and septic shock; determining if a patient will be “fluid responsive” is a key area of investigation today. Ultrasound assessment to determine the degree to which inferior vena cava diameter varies throughout the respiratory cycle in ventilated patients has been shown to correlate with fluid responsiveness. Ultrasound assessment for detection of pneumothorax is an important tool in the ICU; the absence of “lung sliding” or shimmering on close evaluation or the pleural line is highly suggestive of pneumothorax. Ultrasound is an excellent tool for assessing pleural effusions. The presence of septations, heterogeneity in echogenicity, or debris floating in pleural fluid is very suggestive of an exudative effusion. Point-of-care ultrasound has been shown to increase the safety of thoracentesis

and decrease the number of unsuccessful attempts. A minimum distance of 1.5 cm between the fluid and the chest wall and underlying structures is recommended to safely perform a thoracentesis. Point-of-care ultrasound can be used to distinguish between ascites and abdominal distention from other causes. Point-of-care ultrasound can guide the placement of central or peripheral venous catheters and arterial lines. Bedside ultrasound can be used to assess for the presence of deep vein thrombosis (DVT), a common cause of pulmonary embolus. Point-of-care ultrasound has been shown to increase the success rate of lumbar punctures.

References 1. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Program For Doctors. 7th ed. Chicago, IL: American College of Surgeons; 2004. 2. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134:117–125. 3. Rhodes A, Evan LE, Alhazzani W, et al. Surviving Sepsis Campaign. International Guidelines for Management of Sepsis and Septic Shock: 2016. Intens Care Med. 2017;43(3):304–377. 4. Boyd JH, Forbes J, Nakada TA, et al. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. 2011;39:259–265. 5. Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intens Care Med. 2004;30:1740–1746. 6. Feissel M, Michard F, Faller JP, Teboul JL. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intens Care Med. 2004;30:1834–1883. 7. Diacon AH, Brutsche MH, Soler M. Accuracy of pleural puncture sites: a prospective comparison of clinical examination with ultrasound. Chest. 2003;123:436–441. 8. Barnes TW, Morgenthaler TI, Olson EJ, et al. Sonographically guided thoracentesis and rate of pneumothorax. J Clin Ultrasound. 2005;33:442–446. 9. Yang PC, Luh KT, Chang DB, et al. Value of sonography in determining the nature of pleural effusion: analysis of 320 cases. Am J Roentgenol. 1992;159(1):29–33. 10. Mercaldi CJ, Lanes SF. Ultrasound guidance decreases complications and improves the cost of care among patients undergoing thoracentesis and paracentesis. Chest. 2013;143(2):532–538. 11. Patel PA, Ernst FR, Gunnarsson CL. Ultrasonography guidance reduces complications and costs associated with thoracentesis procedures. J Clin Ultrasound. 2012;40(3):135–141. 12. Raptopoulos V, Davis LM, Lee G, et al. Factors affecting the development of pneumothorax associated with thoracentesis. Am J Roentgenol. 1991;156(5):917–920. 13. Fragou M, Grawanis A, Dimitriou V, et al. Real-time ultrasound-guided subclavian vein cannulation versus the landmark method in critical care patients: a prospective randomized study. Crit Care Med. 2011;39(7):1607–1612. 14. Gualtieri E, Deppe SA, Sipperlt M, Thompson D. Subclavian venous catheterization: greater success rate for less experienced operators using ultrasound guidance. Crit Care Med. 1995;23(4):692–697. 15. Shaikh F, Brzezinski J, Alexander S, et al. Ultrasound imaging for lumbar punctures and epidural catheterizations: systemic review and meta-analysis. BMJ. 2013 March 26:346:f1720.

CHAPTER

14 Mechanical Ventilation During Extracorporeal Membrane Oxygenation Stephen Derdak

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Goals of ECMO Decision to Transition to ECMO Approach to ECMO Transitioning Off ECMO Emergent Transition from ECMO to Mechanical Ventilation Special Respiratory Care Issues During ECMO

OBJECTIVES 1. 2. 3. 4. 5. 6.

Explain the indications and contraindications for adult extracorporeal membrane oxygenation (ECMO) in respiratory failure. Describe the basic principles of venovenous ECMO support for oxygenation and ventilation. Evaluate strategies to improve oxygenation during ECMO. Apply the principles of lung-protective mechanical ventilation during ECMO. Determine oxygenation and ventilation targets during ECMO. Contrast the strategies of extubation first versus decannulation first.

KEY TERMS

acute respiratory distress syndrome (ARDS) arterial oxygen content (CaO2) cardiac output (CO) electrical activity of the diaphragm (EAdi) extracorporeal lung support (ECLS) extracorporeal membrane oxygenation (ECMO) lung-protective conventional ventilation (LPCV) neurally adjusted ventilatory assist (NAVA) oxygen consumption (V̇O2) oxygen delivery (ḊO2) venovenous ECMO (VV-ECMO) ventilator drive pressure (ΔP)

Introduction Respiratory therapists are an integral part of multidisciplinary extracorporeal lung support (ECLS) teams and should understand the basis for mechanical ventilation strategies used during ECLS, commonly referred to as extracorporeal membrane oxygenation (ECMO), in which both oxygenation and carbon dioxide clearance are provided by peripheral blood vessel cannulation and a pump-driven extracorporeal circuit. The most common type of ECLS for severe oxygenation and/or ventilation failure in adults is venovenous ECMO (VV-ECMO), in which venous blood is drained from a cannula inserted into a femoral or jugular vein (with the aid of a centrifugal pump), oxygenated through a hollow-fiber membrane, and returned to the circulation through the right internal jugular or opposite femoral vein.1–6 Systemic oxygenation of blood is determined by adjustment of the ECMO pump flow rate (minus recirculation of returned oxygenated blood that may be pulled back into a venous drainage cannula) relative to the patient’s cardiac output (CO). Efficient carbon dioxide elimination is achieved by adjustment of sweep flow gas through the hollow permeable fibers of the membrane oxygenator. In contrast to VVECMO, venoarterial ECMO (VA-ECMO) and venovenous-arterial hybrid support (VVA-ECMO) are primarily utilized for patients with circulatory failure (e.g., cardiogenic shock, postcardiac surgery, cardiopulmonary resuscitation, massive pulmonary embolism) or who have combined respiratory and circulatory failure. Because blood clotting is activated when exposed to the ECMO circuit and oxygenator membrane, systemic anticoagulation is utilized to prevent circuit and patient thrombosis. ECMO circuits can be managed without anticoagulation if active bleeding is present or surgery is required; however, the risk of patient and circuit clotting increases. There are numerous cannulation options for venous and arterial ECMO, including single-site, dual-lumen venous catheters for venous drainage and reinfusion of oxygenated blood via the right internal jugular vein (e.g., Avalon Elite catheter).7 The focus of this chapter is on adult mechanical ventilator strategies and respiratory therapy interventions utilized during VV-ECMO for primary respiratory failure. Ventilator approaches necessarily vary depending on the goals of ECMO for a specific patient, underlying pathophysiology, and phase of disease.8 ECMO is discussed in more detail in Chapter 12.

Goals of ECMO ECMO is a potential consideration for any patient with severe oxygenation and/or ventilation failure that is refractory to optimal lung-protective conventional ventilation (LPCV), alternative ventilator techniques (e.g., high-frequency oscillatory ventilation, high-frequency percussive ventilation), and/or ventilator adjuncts (e.g., prone positioning, neuromuscular paralysis, diuresis, inhaled pulmonary vasodilators). Patient selection criteria for ECMO, relative contraindications, and long-term outcomes compared to mechanical ventilation alone are being investigated in ongoing clinical trials.9 The ability for ECMO to support gas exchange in a critically ill patient who is awake, extubated, and ambulating is remarkable, but as with mechanical ventilation, ECMO is a supportive mode only and not inherently therapeutic. It should be viewed as a technique to buy time until the underlying disease process (e.g., pneumonia, inhalation injury, pulmonary contusion) resolves or a patient can receive a lung transplant. In contrast to implantable cardiac mechanical assist devices, which are increasing utilized as a long-term alternative to cardiac transplant, ECMO is not currently a destination therapy for indefinite use in end-stage lung failure.

Decision to Transition to ECMO The decision to transition to ECMO is often complex, multidisciplinary, and depends on whether the patient is thought to have a survivable extrapulmonary illness in addition to the presence of severe oxygenation and/or ventilation failure. For example, a patient with severe acute respiratory distress syndrome (ARDS) who also has a catastrophic brain injury or terminal metastatic cancer is not a good candidate for ECMO. In contrast, a previously healthy adult with severe viral pneumonia (e.g., influenza) and oxygenation failure on LPCV would be a good candidate in whom to consider ECMO.10 Similarly, a patient with chronic end-stage lung disease (e.g., cystic fibrosis) who decompensates while on a lung transplant waiting list could be a good candidate for ECMO as a bridge to transplant.11,12 For such a patient, achieving adequate gas exchange through single-site ECMO (e.g., with a dual-lumen ECMO catheter in the right internal jugular vein) could allow for early extubation from mechanical ventilation and facilitate physical therapy with

ambulation while awaiting lung transplant (e.g., awake ECMO pretransplant conditioning).13 ECMO may be viewed as a bridge to recovery (e.g., anticipated recovery from severe pneumonia in a previously healthy adult), bridge to lung transplant (end-stage lung disease patients who are transplant candidates), or as a bridge to decision (e.g., a time-limited trial in a patient with an uncertain prognosis or transplant eligibility).14 The duration of ECMO in a specific patient will depend on resolution of the underlying disease, the goals of ECMO (“extubation to awake ECMO” versus “decannulation from ECMO and continued mechanical ventilation”), and the mechanical ventilation strategy utilized while on ECMO (e.g., “ultra-low tidal volume strategy” versus a “lung-protective strategy”).

Approach to ECMO Emergency mechanical ventilator settings should be anticipated and updated frequently in the event that ECMO is interrupted (e.g., during a circuit change) or unplanned flow reductions occur (e.g., malpositioned cannula, clots on cannula tip).15 It is important for respiratory therapists to understand that VV-ECMO may only provide partial gas exchange (e.g., the ECMO flow rate provides gas exchange proportional to the patient’s cardiac output); therefore additional gas exchange may be required from the native lung through ongoing mechanical ventilator support, especially in patients with high cardiac output (Table 14-1). TABLE 14-1 Methods to Improve Tissue Oxygenation Delivery During VV-ECMO ▪ Increase ECMO blood flow (e.g., increase pump flow rate, add venous drainage cannulas; additional membrane oxygenator). ▪ Reposition cannulas to reduce recirculation. ▪ Increase hemoglobin (Hb) (e.g., transfuse packed red blood cells [PRBCs] to Hb 15 g/dL target). ▪ Decrease hyperdynamic cardiac output (e.g., decrease heart rate with esmolol [Brevibloc], a cardioselective beta1 blocker with rapid onset and short duration of effect). ▪ Therapeutic hypothermia to reduce V̇ O2 (e.g., reduce temperature to 34ºC using ECMO circuit). ▪ Increase mechanical ventilation positive end-expiratory pressure (PEEP), mPaw (HFOV), or FIO2. ▪ Prone or vertical positioning. Abbreviations: HFOV, high-frequency oscillatory ventilation; mPaw, mean airway pressure during HFOV.

Targets for Oxygenation, PaCO2, and Hemoglobin

There is limited outcome evidence comparing different systemic oxygenation or hemoglobin targets during VV-ECMO, and practice varies among centers. Some ECMO clinicians allow for a low systemic PaO2 of 40 to 50 mmHg (SaO2 70% to 80%) as long as estimated oxygen delivery (Ḋ O2) (e.g., ḊO2 = cardiac output × arterial oxygen content [Cao2]) can be maintained at some multiple (e.g., ḊO2: V̇O2 > 3) above oxygen consumption (V̇O2) without evidence of tissue ischemia, whereas others advocate maintaining a systemic SaO2 ≥ 88%, similar to oxygenation goals targeted during LPCV.1,4 In the absence of clinical outcome data, the author recommends targeting oxygenation goals similar to those used during mechanical ventilation alone when possible. A systemic PaCO2 goal of 40 mmHg is usually readily achieved by adjusting ECMO sweep flow gas across the membrane oxygenator. PaCO2 goals should also be viewed in the context of pH. Patients with chronic hypercapnea prior to ECMO may have compensatory elevated serum bicarbonate levels, which can result in severe respiratory alkalosis if PaCO2 is abruptly lowered to a normal range with the ECMO sweep flow gas. For these patients, setting a pH goal, rather than an absolute PaCO2, may be more appropriate (e.g., pH 7.30 to 7.45). Some ECMO centers advocate using similar hemoglobin (Hb) transfusion targets (e.g., transfuse if Hb < 7 g/dL) as those used for other critically ill patients, whereas others advocate transfusing to higher Hb (e.g., 15 g/dL) to optimize oxygen content and oxygen delivery, especially if patients have evidence of tissue hypoxia while on ECMO.1,4 Patients with high cardiac output (e.g., ECMO flow: CO ratios < 0.6) may have low systemic PaO2 during VV-ECMO, and improve oxygenation with the use of beta blockers to reduce heart rate (and cardiac output) if ECMO flow rates and Hb have already been optimized.16,17 These patients may also require a more aggressive (but still within lung-protective thresholds), conventional ventilator or high-frequency oscillatory ventilation approach rather than an ultra-low tidal volume lung rest strategy (e.g., resulting in an atelectatic, consolidated lung). RC Insight Poor oxygenation while on VV-ECMO may result from high cardiac output states that exceed the flow rate of the ECMO pump.

As a general principle, systemic hypoxemia and/or hypercapnea should be corrected by optimizing ECMO pump flow and sweep gas flow parameters and/or hemoglobin rather than employing potentially injurious ventilator settings or high ventilator FIO2. There is a lack of high-quality evidence comparing patient outcomes or ECMO duration using different ventilator strategies (e.g., “ultra-low tidal volume lung rest“ versus “lung protection“ versus high-frequency oscillatory ventilation), and approaches vary among institutions.18,19

FIO2 and PEEP Data from a retrospective study supports the use of higher PEEP during LPCV prior to ECMO and during initial ECMO phases, but exactly how to choose the appropriate level of PEEP is uncertain.20 A reduction in ventilator drive pressure (∆P) (∆P = Pplateau – PEEP) with PEEP increments during volume-limited lung-protective ventilation in non-ECMO patients suggests that lung recruitment is occurring and is a favorable prognostic indicator.21 Similarly, a reduction in ventilator drive pressure during ECMO may indicate lung opening and herald the onset of lung recovery. As a general principle, patients on potentially injurious ventilator settings prior to ECMO (e.g., VT > 6 mL/kg/ideal body weight [IBW] or Pplateau > 30 cm H2O with normal chest wall and abdominal compliance or HFOV mPaw > 40 cm H2O) should have tidal volume and inspiratory airway pressures reduction as soon as ECMO circuit gas exchange is established. PEEP should probably be maintained in a range of 10 to 15 cm H2O to minimize cyclic end-expiratory derecruitment and atelectrauma. Higher PEEP settings may be required in patients with elevated abdominal pressures and/or low chest wall compliance. RC Insight PEEP should be utilized to minimize development of complete lung atelectasis while on VV-ECMO.

Ventilator FIO2 should be reduced to ≤ 40% if possible. Respiratory rate may be reduced to 10 to 15 breaths/min (if it was higher pre-ECMO). If HFOV is continued during ECMO, frequency should be increased to ≥ 7 Hz (e.g., approximating VT ≤ 2 mL/kg/IBW) and mPaw reduced to ≤ 30 cm H2O. Whether a conventional VT target of 4 to 6 mL/kg/IBW (e.g., conventional lung protection ranges) or VT of 0.5 to 3

mL/kg/IBW (e.g., ultra-low tidal volumes) should be utilized is uncertain in the absence of outcome data comparing these approaches.

Mode Whether a volume-limited mode versus a pressure-limited mode results in outcome differences (assuming both achieve the same targeted VT and airway pressures in an awake, comfortable, and spontaneously breathing patient) is uncertain. Optimal mechanical ventilation during ECMO is an area of active research and may lead to higher level evidence-based recommendations in the future.22

Monitoring Monitoring ventilator drive pressure (e.g., during volume-limited modes) and tidal volume changes (e.g., during pressure-limited modes) is suggested. Monitoring transpulmonary pressure (e.g., with an esophageal balloon catheter) and abdominal pressure (e.g., urinary bladder pressure) for non-ECMO ARDS patients has been demonstrated to allow safer use of higher PEEP while improving lung compliance and oxygenation and is an area of active investigation during ECMO.23,24 It is important to appreciate that true drive pressure (and transpulmonary distending pressure) may be greater than ventilator drive pressure if a patient has active inspiratory efforts associated with negative pleural pressures. An individualized approach to mechanical ventilation using lung-protective principles is recommended based on ECMO goals for a specific patient (Table 14-2). TABLE 14-2 Mechanical Ventilation Strategies During VV-ECMO

Description Description Abbreviations: CXR, chest radiograph; HFOV, high-frequency oscillatory ventilation; Hz, Hertz; IBW, ideal body weight; L/min, liters per minute; LRM, lung recruitment maneuver; NAVA, neurally adjusted ventilatory assist; NMB, neuromuscular-blocker drugs; ∆P, ventilator drive pressure; PC, pressure-control assisted ventilation; Petco2, end-tidal partial pressure of carbon dioxide; Ppeak, inspiratory peak airway pressure; Pplateau, inspiratory plateau pressure; PSV, pressure-support ventilation; Ptl, transpulmonary pressure; VC, volumecontrol assisted ventilation; V̇E, minute ventilation.

RC Insight A reduction in ventilator drive pressure (ΔP = Pplateau – PEEP) during VV-ECMO has been associated with reduced in-hospital mortality.

CLINICAL FOCUS 14-1

A 42-year-old morbidly obese female (150 kg actual body weight) with severe ARDS from viral pneumonia is on VV-ECMO and pressure control/assisted ventilation with PC 15 cm H2O above PEEP 10 cm H2O (Pplateau 25 cm H2O), inspiratory time 1 sec, VT 70 mL, set RR 12, FIO2 30%, and PetCO2 4 mmHg (recall that very low PetCO2 may occur with very low tidal volumes). She is not triggering the ventilator. Physical exam is notable for a morbidly obese abdomen. Urinary bladder pressure is elevated at 30 cm H2O. Chest x-ray demonstrates low lung volumes with dense bilateral lung opacification and no air bronchograms. Question 1. What is the ventilator drive pressure? What is the transpulmonary distending pressure? Answer: This patient has a measured inspiratory ventilator drive pressure (ΔP) of 15 cm H2O (ΔP = Pplateau – PEEP). In contrast, the inspiratory transpulmonary distending pressure (Ptl-ins = Pplateau – Ppleural) is likely significantly lower because of elevated pleural pressure due to abdominal hypertension associated with morbid obesity. With an elevated abdominal pressure of 30 cm H2O, and assuming half of abdominal pressure is transmitted to the pleural space, the true inspiratory transpulmonary distending pressure may be only 10 cm H2O (Ptl-ins = Pplateau – Ppleural) or (25 cm H2O – 15 cm H2O = 10 cm H2O).25 Expiratory transpulmonary pressure (Ptl-exp = PEEP – Ppleural) is actually negative (Ptl-exp = 10 cm H2O – 15 cm H2O = –5 cm H2O), which further contributes to the lung atelectasis observed. In this patient, high pleural pressure (transmitted from elevated abdominal pressure) reduces inspiratory and expiratory Ptl resulting in low lung volumes, atelectasis, and reduced PetCO2. Ventilator drive pressure overestimates true drive pressure (e.g., transpulmonary distending pressure) if pleural pressure is abnormally elevated. Estimation of pleural pressure utilizing an esophageal balloon manometer would confirm elevated pleural pressures (which may also be increased from reduced chest wall compliance). Question 2. What could be done to improve her low lung volumes? Answer: In order to have an inspiratory transpulmonary pressure (Ptl-ins) of 15 cm H2O, this patient would need ventilator PC peak pressure increased to 30 cm H2O (Ptl-ins = Pplateau – Ppl) or (Ptl-ins = 30 cm H2O – 15 cm H2O = 15 cm H2O). To improve expiratory lung collapse, PEEP could be increased to 20 cm H2O (Ptl-exp = PEEP – Ppleural) or (Ptl-exp = 20 – 15 = 5 cm H2O). Patients with elevated abdominal pressures (and/or low chest wall compliance) often have low lung inflation and are undertreated with PEEP if abdominal pressure and/or esophageal pressure

is not measured and considered in estimating true drive pressures.26 In this patient on VV-ECMO, PEEP was increased to 20 cm H2O, resulting in an increase of VT to 200 mL, a decrease in ventilator drive pressure (ΔP) to 10 cm H2O; ΔP = 30 cm H2O – 20 cm H2O = 10 cm H2O), improved aeration on chest xray, and increased PetCO2. A recent large meta-analysis found that a reduction in ventilator drive pressure early in the course of VV-ECMO was the only ventilator parameter showing an independent association with ARDS mortality.27

Transitioning Off ECMO For patients bridging to recovery on ECMO, improvement in the underlying lung disease may be observed as an improving tidal volume (e.g., if using a pressurelimited mode) or decreasing Pplateau and/or Ppeak (e.g., a decrease in ventilator drive pressure, ∆P) if using volume-limited modes). An increase in lung inflation and improved aeration of previously consolidated lung zones may be also be apparent on portable chest radiographs or chest CT scans. Bronchopleural fistulas (e.g., bubbling in chest tube drainage systems) and subcutaneous air may resolve. A trial of gradual ECMO sweep gas flow reduction may show a progressive increase in PetCO2 as gas exchange from the native lungs improves. Similarly, an increase in pressure-support pressure level in a spontaneously triggering patient (with a corresponding increase in tidal volume) may demonstrate an increase in PetCO2. Increased CO2 should be allowed to develop gradually as sweep flow is reduced to avoid abrupt air hunger, tachypnea, tachycardia, agitation, elevated intracranial pressure, and increased pulmonary vascular resistance leading to hemodynamic decompensation. RC Insight An increasing PetCO2 trend with sweep flow gas reduction while on stable ventilator settings may herald lung recovery during VV-ECMO.

During sweep flow reduction trials, ventilator settings need close monitoring and may need frequent adjustment (e.g., increase the PC or PSV pressure) to facilitate an adequate VT, minute ventilation (V̇E), PEEP, and ventilator FIO2% as the patient’s lungs assume more of the gas exchange and work of breathing. Careful monitoring of V̇E and PetCO2 is essential during the transition phase toward coming off ECMO. Transcutaneous PtcCO2 monitoring may also be useful during this phase for rapid assessment of the patient’s systemic PaCO2 trends.28 Similarly, PEEP and ventilator FIO2 may need to be increased if oxygen desaturation occurs. Patients transitioning off VV-ECMO to mechanical ventilation may not maintain a normal PaCO2 (although it was maintained in a normal range during ECMO) similar to the permissive hypercapnia that is sometimes tolerated in patients treated with

mechanical ventilation alone. Abrupt, large decreases in sweep flow gas (e.g., from 7 L/min to 1 L/min) in a patient with an atelectatic, consolidated lung while on ECMO may cause acute tachypnea with ventilator asynchrony and should be avoided. Once a patient has maintained adequate gas exchange with sweep flow at nominal levels (0 to 1 L/min), ECMO may be discontinued while continuing lung-protective conventional ventilation settings. Progression to spontaneous breathing trials and liberation from mechanical ventilation may then proceed as for non-ECMO patients. Patients with end-stage lung disease who are lung transplant candidates may be transitioned completely off mechanical ventilation (e.g., “wean the ventilator first” strategy) to VV-ECMO alone (“awake ECMO”) and either extubated or maintained with a humidified tracheostomy collar if tracheotomy has already been performed.12 Physical therapy, ambulation, and aggressive nutritional support proceeds while extubated to ECMO awaiting lung transplant. Patients undergoing early extubation to ECMO alone may have limited respiratory reserve with rapid shallow breathing, poor cough, and secretion clearance, and will continue to require aggressive pulmonary toilet. Intermittent noninvasive ventilation (e.g., bilevel positive airway pressure [BiPAP], intrapulmonary percussive ventilation) by mask interfaces (nasal or full face), mouthpiece, or connected to tracheostomy tubes may reduce work of breathing, and improve comfort, lung inflation, and cough efficiency. Suggested criteria for early extubation to ECMO alone include a primary indication of chronic obstructive lung disease (COPD) and/or decompensated chronic lung disease bridging to transplant, an awake, cooperative patient (Richmond AgitationSedation Score [RASS] –1 to +1), hemodynamic stability, absence of major bleeding, and ability to augment tidal volume and cough with coaching.29 Patients who demonstrate reduced respiratory rate, reduced esophageal pressure swings (an index of work of breathing), or reduced electrical activity of the diaphragm (EAdi) peak signal (e.g., monitored with a neurally adjusted ventilatory assist [NAVA] catheter) in response to increases in sweep flow gas may have a higher likelihood of successful extubation to ECMO alone. Preliminary observational studies indicate that monitoring EAdi and NAVA-mode ventilation may have particular utility for ECMO patients during the recovery phase from severe ARDS and in assessing respiratory drive response during sweep flow reduction trials.30,31

RC Insight A trial of an increase in sweep flow gas that results in a decrease in the patient's respiratory rate and work of breathing may identify patients in whom extubation to VV-ECMO alone is likely to be successful.

In contrast to chronic obstructive lung disease and “bridge to transplant” patients, severe ARDS patients have a high failure rate when extubated to early, awake ECMO alone and often require noninvasive ventilation or reintubation.29 Reasons for failure of ARDS patients extubated to ECMO include persistent dyspnea, tachypnea, agitation, and high work of breathing despite using high sweep flows. Poor cough and secretion clearance is commonly observed after extubation. Preliminary observational studies report that less than 30% of severe ARDS patients on ECMO can be successfully extubated to ECMO alone.29 ARDS patients on ECMO should be carefully evaluated with the above criteria prior to considering extubation. Prone positioning and vertical positioning (e.g., using a specialized tilt bed) may be utilized during VV-ECMO and continued following transition off ECMO.32–35 Tidal volume increases (in pressure-limited modes), Ppeak and Pplateau decreases (in volume-limited modes), and PetCO2 increases may occur with vertical positioning during physical therapy. Observation of these changes may suggest a decrease in lung atelectasis (and potential lung recruitment) in the upright position.

Emergent Transition from ECMO to Mechanical Ventilation Patients sometimes require urgent transition off ECMO to mechanical ventilation alone (e.g., membrane lung, circuit, or cannula malfunction). For patients with severe ARDS on ultra-low tidal volume lung rest settings (e.g., ≤ 3 mL/kg/IBW) and a consolidated, atelectatic lung on chest radiograph (e.g., ≤ four anterior ribs at the right hemidiaphragm), immediate use of lung-protective ventilator settings with either a pressure-limited or volume-limited mode set to achieve a tidal volume 6 mL/kg/IBW, rate 30 to 35, FIO2 100%, PEEP 16 to 18 cm H2O, with further titration of tidal volume and PEEP to maintain Pplateau < 30 cm H2O is recommended. If the patient is hemodynamically stable without active bronchopleural fistulas (e.g., no bubbling chest tubes), a lung recruitment maneuver (RM) can be considered. Lung recruitment can be attempted using a sustained inflation (e.g., continuous positive airway pressure [CPAP] 40 cm H2O for 40 to 50 sec) followed by conventional lung-protective ventilator settings or with HFOV, depending on the severity of hypoxemia. Ventilator adjuncts (e.g., neuromuscular blocker, prone positioning, diuresis, continuous renal replacement therapies) should be employed similarly to their use in non-ECMO–treated ARDS patients. Patients with persistent hypoxemia (e.g., PaO2 < 60 on FIO2 1.0 > 4 to 6 hours) on optimal LPCV may be considered for a trial of highfrequency oscillatory ventilation if ECMO cannot be resumed. The use of HFOV as a rescue oxygenation strategy is discussed in Chapter 12.

Special Respiratory Care Issues During ECMO During mechanical ventilation while on ECMO, usual respiratory therapy techniques such as airway humidification, aerosol medication delivery, and secretion clearance modalities are continued. Airway humidification should be maintained with a heated humidifier (e.g., not a heat-moisture exchanger), particularly if therapeutic hypothermia is being employed to reduce V̇O2. Aerosolized medication delivery with a vibrating mesh nebulizer may be utilized depending on specific patient indications (e.g., heparin and N-acetylcysteine for severe inhalation injury, bronchodilators and corticosteroids for obstructive lung disease, antibiotics for cystic fibrosis, epoprostenol [Flolan] for pulmonary hypertension with right ventricular failure, etc.).36–39 Patients may experience persistent cough during the healing phase of severe airway injury (e.g., associated with burn-inhalation injury, toxic epidermal necrolysis, toxic gases, etc.). Nebulized lidocaine (4 mL of 4%) or directly instilled lidocaine (4 mL of 1% to 2%) through a suction catheter positioned at the carina may reduce refractory cough.40 Caution should be exercised to avoid lidocaine toxicity from systemic absorption (e.g., limit total lidocaine dose to < 4 mg/kg). Airway bleeding may occur during aggressive suctioning and may be aggravated by systemic anticoagulation. If bleeding is significant, bronchoscopy may be indicated to inspect the airway and/or obtain samples for cultures. The clinical diagnosis of pneumonia is particularly difficult when using a lung rest strategy with ultra-low tidal volumes and temperature that is being controlled with the ECMO circuit. A chest radiograph or chest computed tomography (CT) scan demonstrating bilateral collapsed and consolidated lungs can mask an underlying pneumonia or diffuse alveolar hemorrhage. If pneumonia is suspected, tracheal aspirates may be obtained for quantitative aerobic cultures (if no instilled saline was required), cytology, and special studies (e.g., fungal, acid fast, and respiratory viral cultures). Additional blood testing for biomarkers of fungal (e.g., galactomannan, 1-3-beta-Dglucan) and bacterial (e.g., procalcitonin) organisms may support a clinical diagnosis of infectious pneumonia before confirmatory cultures return. Bronchoscopy with bronchoalveolar lavage may be indicated to obtain additional specimens for cultures and/or to evaluate for alveolar hemorrhage on ECMO. Bronchoscopy preparation and technique during ECMO is similar to bronchoscopy performed on other critically ill and/or intubated patients, with the exception that

patients are usually anticoagulated (e.g., transbronchial biopsies are not performed).

Key Points VV-ECMO may be considered for select patients with severe oxygenation or ventilation failure on optimal lung-protective mechanical ventilation. Oxygenation on VV-ECMO is primarily set by the ECMO pump flow rate. Ventilation on VV-ECMO is primarily set by the sweep gas flow rate. Patients on VV-ECMO may still require mechanical ventilation support for oxygenation and work of breathing. Mechanical ventilation parameters during ECMO should emphasize lungprotective principles and a reduction in ventilator drive pressure (ΔP). Patients extubated to awake VV-ECMO may still require aggressive pulmonary toilet and/or noninvasive ventilatory or high-flow nasal cannula oxygen support.

References 1. Brodie D, Bachetta M. Extracorporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011;365:1905–1914. 2. Del Sorbo L, Cypel M, Fan E. Extracorporeal life support for adults with severe acute respiratory failure. Lancet Respir Med. 2014;2:154–164. 3. Ventetuolo CE, Muratore CS. Extracorporeal life support in critically ill adults. Am J Respir Crit Care Med. 2014;190:497–508. 4. Bartlett RH. Physiology of gas exchange during ECMO for respiratory failure. J Intens Care Med. 2017;32(4):243–248. 5. MacLaren G, Combes A, Bartlett RH. Contemporary extracorporeal membrane oxygenation for adult respiratory failure: life support in the new era. Intens Care Med. 2012;38:210–220. 6. Schmidt M, Hodgson C, Combes A. Extracorporeal gas exchange for acute respiratory failure in adult patients: a systematic review. Crit Care. 2015;19:99. doi: 10.1186/s13054-015-0806-z. 7. Reeb J, Olland A, Renaud S, et al. Vascular access for extracorporeal life support: tips and tricks. J Thorac Dis. 2016;8:S353–S363. 8. Schmidt M, Pellegrino V, Combes A, et al. Mechanical ventilation during extracorporeal membrane oxygenation. Crit Care. 2014;18:203–213. 9. Assistance Publique – Hospitaux de Paris. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome (EOLIA). Available at: www.ClinicalTrials.gov. Identifier: NCT01470703. Accessed January 18, 2018. 10. Pham T, Combes A, Roze H, et al. Extracorporeal membrane oxygenation for pandemic influenza A (H1N1)–induced acute respiratory distress syndrome—a cohort study and propensity-matched analysis. Am J Respir Crit Care Med. 2013;187:276–285. 11. Nosotti M, Rosso L, Tosi D, et al. Extracorporeal membrane oxygenation with spontaneous breathing as bridge to lung transplantation. Interact Cardiovasc Thorac Surg. 2013;16:55–59. 12. Lafarge M, Mordant P, Thabut G, et al. Experience of extracorporeal membrane oxygenation as bridge to lung transplantation in France. J Heart Lung Transplant. 2013;32:905–913. 13. Langer T, Santini A, Bottino N, et al. “Awake” extracorporeal membrane oxygenation (ECMO): pathophysiology, technical considerations, and clinical pioneering. Crit Care. 2016;20:150. 14. Abrams DC, Prager K, Blinderman CD, et al. Ethical dilemmas encountered with the use of extracorporeal membrane oxygenation in adults. Chest. 2014;145:876–882. 15. Ruisanchez C, Sarralde JA, Gonzalez-Fernandez C, Dominguez MJ. Sudden dysfunction of veno-venous extracorporeal membrane oxygenation caused by intermittent cannula obstruction: the key role of echocardiography. Intens Care Med. 2017;43:1055–1056. 16. Pappalardo F, Zangrillo A, Pieri M, et al. Esmolol administration in patients with VV-ECMO: why not? J Cardiothorac Vasc Anesth. 2013;27(4):e40. 17. Kimmoun A, Vanhuyse F, Levy B. Improving blood oxygenation during venovenous ECMO for ARDS. Intens Care Med. 2013;39:1161–1162. 18. Marhong JD, Telesnicki T, Munshi L, et al. Mechanical ventilation during extracorporeal membrane oxygenation: an international survey. Ann Am Thorac Soc. 2014;11:956–961. 19. Marhong JD, Munshi L, Detsky M, et al. Mechanical ventilation during extracorporeal life support (ECLS): a systematic review. Intens Care Med. 2015;41:994–1003. 20. Schmidt M, Stewart C, Bailey M, et al. Mechanical ventilation management during extracorporeal membrane oxygenation for acute respiratory distress syndrome: a retrospective international multicenter study. Crit Care Med. 2015;43:654–664. 21. Amato MBP, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372:747–755. 22. University of Toronto. Optimal Lung Ventilation in ECMO for ARDS: The SOLVE ARDS Study (SOLVE ARDS). Available at: https://www.ClinicalTrials.gov. Identifier: NCT01990456. Accessed January 18, 2018. 23. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359:2095–2104. 24. Beijing Chao Yang Hospital. Applied Research of New Lung Ventilation Strategies Guided by Transpulmonary Pressure in Extracorporeal Membrane Oxygenation for Acute Respiratory Distress Syndrome. Available at: https://www.ClinicalTrials.gov. Identifier: NCT02439151. Accessed January 18,

2018. 25. Cortes-Puentes GA, Cortes-Puentes LA, Adams AB, et al. Experimental intra-abdominal hypertension influences airway pressure limits for lung protective mechanical ventilation. J Trauma Acute Care Surg. 2013;24:1468–1473. 26. Henderson WR, Chen L, Amato MBP, Brochard LJ. Am J Respir Crit Care Med. 2017;196:822–833. 27. Neto AS, Schmidt M, Azevedo LCP, et al. Associations between ventilator settings during extracorporeal membrane oxygenation for refractory hypoxemia and outcome in patients with acute respiratory distress syndrome: a pooled individual patient data analysis. Intens Care Med. 2016;42:1672–1684. 28. Rodriguez P, Lellouche F, Aboa J, et al. Transcutaneous arterial carbon dioxide pressure monitoring in critically ill adult patients. Intens Care Med. 2006;32:309–312. 29. Crotti S, Bottino N, Ruggeri GM, et al. Spontaneous breathing during extracorporeal membrane oxygenation in acute respiratory failure. Anesthesiology 2017;126:678–687. 30. Karagiannidis C, Lubnow M, Philipp A, et al. Autoregulation of ventilation with neurally adjusted ventilatory assist on extracorporeal lung support. Intens Care Med. 2010;36:2038–2044. 31. Mauri T, Graselli G, Suriano G, et al. Control of respiratory drive and effort in extracorporeal membrane oxygenation patients recovering from severe acute respiratory distress syndrome. Anesthesiology 2016;125:159–167. 32. Richard JC, Maggiore SM, Mancebo J, et al. Effects of vertical positioning on gas exchange and lung volumes in acute respiratory distress syndrome. Intens Care Med. 2006;32:1623–1626. 33. Guérin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013;368:2159–2168. 34. Kimmoun A, Roche S, Bridey C, et al. Prolonged prone positioning under VV-ECMO is safe and improves oxygenation and respiratory compliance. Ann Intens Care. 2015;5:35. 35. Culbreth RE, Goodfellow LT. Complications of prone positioning during extracorporeal membrane oxygenation for respiratory failure: a systematic review. Respir Care. 2016;61:249–254. 36. Miller AC, Elamin EM, Suffredini AF. Inhaled anticoagulation regimens for the treatment of smoke inhalation-associated acute lung injury: a systematic review. Crit Care Med. 2014;42:413–419. 37. Kashefi NS, Nathan JI, Dissanaike S. Does a nebulized heparin/N-acetylcysteine protocol improve outcomes in adult smoke inhalation? Plast Reconstr Surg Glob Open 2014;2:e165. 38. Sheridan RL. Fire-related inhalation injury. N Engl J Med. 2016;375:464–469. 39. Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11:811–822. 40. Slaton RM, Thomas RH, Mbathi JW. Evidence for therapeutic uses of nebulized lidocaine in the treatment of intractable cough and asthma. Ann Pharmacother. 2013;47:578–585.

CHAPTER

15 Neonatal and Pediatric Critical Care Craig Wheeler and Craig D. Smallwood

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Fetal Lung Development Fetal Circulation Transition to Extrauterine Life Recognizing Respiratory Distress Is the Process of Primary Cardiac or Respiratory Origin? Other Causes of Respiratory Distress Assess the Gestational Age of the Patient Common Neonatal Respiratory Conditions Respiratory Distress Syndrome Transient Tachypnea of Newborn Persistent Pulmonary Hypertension of the Newborn Meconium Aspiration Syndrome Chronic Lung Disease Other Conditions Seen in Premature Infants Common Pediatric Respiratory Conditions Pediatric ARDS Asthma Neurologic Conditions Neuromuscular Diseases Bronchiolitis Cystic Fibrosis Monitored Parameters Expected Values for Important Respiratory Parameters Endotracheal Tube Selection and Management Securing the Endotracheal Tube Noninvasive Support

Conventional Mechanical Ventilation Inhaled Gas Mixtures Helium–Oxygen Mixtures Nitric Oxide Subambient Oxygen and Inhaled Carbon Dioxide Anesthetic Gas Mixtures Extracorporeal Membrane Oxygenation Indications Cardiac Applications Complications Patient Transport Adverse Events Mechanical Ventilation during Transport Safety Implications

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Outline the stages of fetal lung development. Describe fetal pulmonary circulation. Review the physiology of transitioning to pulmonary respiration. Describing signs and symptoms of respiratory distress. Review physiology and treatment of common neonatal respiratory conditions. Review physiology and treatment of common pediatric respiratory conditions. Highlight key aspects of endotracheal tube selection and management in a neonate. Review various types of noninvasive and invasive respiratory support. Describe key aspects of high-frequency ventilation. Describe several common inhalational gas mixtures and their uses. Highlight indications, limitations, and complications of inhaled nitric oxide. Describe the indications and complications of extracorporeal membrane oxygenation (ECMO). Compare and contrast venovenous (VV)- and venoarterial (VA)-ECMO. Describe the need for and risk associated with transporting a patient needing respiratory support.

KEY TERMS adverse events alveoli asthma bronchiolitis cystic fibrosis (CF) ductus arteriosus endotracheal tube extracorporeal membrane oxygenation (ECMO) foramen ovale head bobbing high-flow nasal cannula meconium nasal flaring nasal intermittent positive-pressure ventilation (NIPPV) neonate paradoxical chest movement respiratory distress syndrome retinopathy retractions surfactant

tachypnea venoarterial (VA)-ECMO venovenous (VV)-ECMO

Introduction Many respiratory care practices are shared between neonatal, pediatric, and adult clinicians, but there are important differences as well. This section is not meant to reiterate those skills that are important across all patient ages, such as auscultation, physical examination of the thorax, or understanding fundamental concepts such as basic pulmonary physiology or general mechanical ventilation (this foundation is laid out elsewhere). Rather, the unique features of the neonatal and pediatric population will be highlighted. This will begin with an overview of fetal lung development, understanding the wide range of expected vital signs and respiratory parameters in this population, discussion of neonatal and pediatric diseases and management, as well as a discussion of devices and therapies commonly utilized in this population.

Fetal Lung Development Lung development begins with the formation of the large conducting airways at approximately 4 weeks after conception and continues through birth until the child reaches 8 years old.1 In Table 15-1, the major developmental stages of intrauterine lung development are outlined.2 Following formation of the alveoli at ~37 weeks to birth, the chest wall and lungs continue to develop. Infants born before 37 weeks are premature or preterm. Infants born at 37 or 38 weeks are sometimes considered early term, whereas infants born after 42 weeks are considered post-term. TABLE 15-1 Major Phases of Intrauterine Lung Development Developmental Stage

Time (weeks after conception)

Notes

Embryonic

3 to 8

Large airways develop (trachea and bronchi).

Pseudoglandular

7 to 16

Smaller conducting airways are formed.

Canalicular

16 to 26

Vascular bed is formed and respiratory acini (immature sacs that will eventually become alveoli) begin to form; also known as type II pneumocytes (alveolar cells).

Saccular

24 to 36

Respiratory acini continue to develop and increase in complexity; surfactant begins to be secreted into the alveoli.

Alveolar

36 to birth

Alveoli are formed.

As the fetal lung matures, surfactant begins to be secreted by type II alveolar cells beginning at about 20 weeks of gestation. Mature surfactant does not appear until about week 35. The Dubowitz and new Ballard scoring systems provide methods to help determine the gestational age of the newborn at the time of birth. The full-term infant is born with approximately 50 million alveoli and a surface area of 3 m2. The lungs continue to grow, until approximately 300 million alveoli are formed by age 8. Once fully grown, the lung surface area is 50 to 75 m2— approximately equal to the area of a tennis court.

Fetal Circulation Fetal circulation is distinct from circulation after birth, since the fetus does not exchange gas with its lungs (Figure 15-1). The fetus relies upon the mother to provide nourishment and oxygen. The placenta, an organ formed within the mother’s uterus, is connected to the fetus by the umbilical cord. Blood that carries nutrients and oxygen is delivered to the fetus from the placenta via the umbilical vein. The ductus venosus is a fetal shunt that directs a proportion of the left umbilical blood flow to the inferior vena cava. Doing so permits oxygenated blood to bypass the fetal liver and flow to the heart. The proportion of shunting through the ductus venosus decreases as the fetus matures.3 The oxygenated blood delivered by the ductus venosus mixes with oxygen-depleted blood from the systemic circulation in the fetal right atrium. Within the right atrium, the majority of blood flow from the inferior vena cava crosses to the left atrium via the foramen ovale, a hole in the atrial septal wall. The blood remaining in the right atrium is pumped to the right ventricle, through the pulmonary arteries, and into the vasculature of the developing lung. An extremely important concept for the respiratory care clinician to appreciate is that the pulmonary vascular resistance (PVR) of the fetus is very high. The two main factors that account for the increased PVR are: (1) low oxygen concentration in pulmonary blood results in hypoxic pulmonary vasoconstriction and (2) direct compression of the vessels occurs as a function of low lung volumes. Only about one-fifth of the blood from the right atrium reaches the fetal lung vessels.4

FIGURE 15-1 Fetal Circulation.

Description Blood from the pulmonary veins flows to the left atrium (mixing with fresh oxygenated blood that came across the foramen ovale), is directed to the left ventricle and then pumped through the ascending aorta to supply oxygen and nutrients to the head, coronary vessels, and right arm. Importantly, the fact that the

right arm receives oxygenated blood is the reason clinicians will place an oxygen saturation monitor on the right hand to monitor “preductal” saturations. The ductus arteriosus is a fetal blood vessel that connects the pulmonary artery to the proximal descending aorta. The high PVR causes most of the blood from the right atrium to bypass the pulmonary vasculature and flow directly into the systemic circulation. A preductal oxygen saturation, therefore, reflects the richest oxygenated blood before mixing with deoxygenated blood, which occurs at the ductus arteriosus. Blood that enters the systemic circulation after the ductus arteriosus has a lower concentration of oxygen; preductal oxygen saturation will be higher than postductal oxygen saturation (this is most pronounced in utero and in a pathologic process that precludes the transition from fetal to newborn circulation).

Transition to Extrauterine Life Upon birth, a drastic change in circulation occurs in the baby (Figure 15-1). Blood flow from the placenta is discontinued when the umbilical cord is clamped, and no further nutrients or oxygen are received from the mother’s circulatory system. Once the baby takes its first breath, the PVR is significantly reduced and a marked increase in pulmonary blood flow occurs. An increase in the baby’s systemic blood pressure, along with reduced PVR, means that the amount of blood passing through the ductus arteriosus is greatly reduced. This leads to an increase in left atrial pressure and a decrease in right atrial pressure. These changes in atrial pressure cause the foramen ovale to close. A successful transition to newborn circulation means that the ductus arteriosus and foramen ovale are essentially closed. Although changes in blood flow through the ductus arteriosus begin to occur rapidly, complete closure does not typically occur until 3 to 4 days after birth.5 Over a period of a few weeks, a process by which the ductus is anatomically closed occurs. There are many types of cyanotic and acyanotic congenital heart disease. Cyanotic congenital heart disease includes coarctation of the aorta, Ebstein’s anomaly, hypoplastic left heart syndrome, pulmonary atresia, tetralogy of Fallot, transposition of the great vessels, tricuspid atresia, and truncus arteriosis. Acyanotic congenital heart disease includes atrial septal defect, aortic stenosis, patent ductus arteriosis, and ventricular septal defect.

Recognizing Respiratory Distress Since respiratory illness is the top reason for children to be admitted to the hospital, it is paramount for neonatal and pediatric clinicians to recognize the signs and symptoms of respiratory distress quickly and accurately. Although in many cases, the underlying disease process is pulmonary in origin, respiratory distress can be associated with sepsis, heart failure (or undiagnosed congenital heart disease in the neonate), and compensation for metabolic acidosis (that can occur from ingestion of toxins, severe dehydration, or some other disorders). Tachypnea is the most common sign of distress and is defined as an increased respiratory rate (RR) above normal. Because RR varies with age, it is important to note the differences in expected RR. The normal range for infant respiratory rate is 30 to 40 breaths/min. RR for children ranges from 18 to 30 breaths/min, depending on age. Increasing respiratory rate is an infant’s first attempt to compensate for an increased production of CO2 or as a function of impaired gas exchange. This occurs because infants have a more elastic chest cavity relative to adults, weaker intercostal muscles, and therefore limited capacity to increase tidal volume (VT). Tachypnea patient’s can be isolated or associated with increased work of breathing. In the case that it is associated with increased work of breathing (nasal flaring and retractions), the proportion of energy required to sustain this effort can be significant and should be monitored closely for signs of respiratory failure. Nasal flaring occurs as a function of the patient’s effort to reduce airway resistance. The upper airway is particularly small in infants and has a high resistance. Flaring the nostrils serves to increase the diameter of the airway and reduce resistance to airflow. Retractions occur when a muscle pulls inward and is visibly detected. There are several areas that should be assessed for retractions in children: Suprasternal: Noted at the jugular notch in the area close to the trachea. Sometimes referred to as tracheal retractions or tracheal tugging. Intercostal: At the area of the intercostal muscles between the ribs. Substernal or subcostal: Beneath the ribs at the level of the abdomen, caused by a contraction of the abdominal muscles that reveals the bottom portion of the rib cage. Typically associated with an obstructive disease process as the patient works to exhale against a constricted airway. Sternal: Over the sternum; in young infants with compliant chest walls,

increased inspiratory breathing efforts can cause partial collapse of the soft/cartilaginous sternum inward. Grunting is a low-pitched expiratory noise that originates at the level of the pharynx where the glottis is located. In cases where the patient is attempting to maintain an adequate end-expiratory volume, he or she partially closes the glottis and exhales against it. The maneuver serves to increase the expiratory pressure that can prevent end-expiratory lung collapse and maintain alveolar volume. Paradoxical chest movement occurs as the chest appears to fall during inspiration and rise during exhalation. It is sometimes noted in infants and children with a severe lower airway obstruction such as bronchiolitis or asthma. It occurs as a result of the abdominal muscles contracting to forcefully exhale gas. Paradoxical chest movement is sometimes described as “see-saw” breathing, as it is a rocking motion of the chest. Head bobbing occurs in infants and is a late-stage physical manifestation of increased work of breathing and respiratory failure. It occurs as the infant becomes lethargic but is still utilizing accessory muscles to augment respiratory efforts. Respiratory failure is defined as the inability of a patient to maintain adequate oxygenation and ventilation. Upon recognition of respiratory distress, it is necessary to assess other factors in the newborn infant. In the following section, key features of the neonatal exam are noted, but the section is not meant to provide a complete introduction of assessment skills outlined elsewhere.

Is the Process of Primary Cardiac or Respiratory Origin? Although congenital heart diseases are very rare, the primary diagnosis of previously unrecognized congenital cardiac problems can occur in the neonatal or pediatric intensive care (NICU or PICU) unit. In this case, chest radiographs and echocardiography can be utilized to assess the cardiac structures and function of the newborn.

Other Causes of Respiratory Distress Other causes of respiratory distress can be metabolic, renal, or neurologic in origin.

As such, additional testing can be completed in the intensive care unit (ICU) to rule out these factors. For metabolic processes, an indirect calorimetry test may be indicated. Indirect calorimetry is a noninvasive technique incorporating a device affixed to the breathing system either by direct connection or hood. Metabolism (breaking down a substrate in order to produce energy) consumes oxygen and produces CO2. Measurements of the rate of oxygen consumption (V̇O2) and carbon dioxide elimination (V̇CO2) can be combined using the modified Weir equation to determine energy expenditure (number of calories burned; typically expressed in kcal/day).6 Although a typical indirect calorimeter is a standalone device that can be applied to various subjects, more and more mechanical ventilators offer gas exchange monitoring. If offered, V̇CO2 is typically computed while some devices measure both V̇O2 and V̇CO2. Many factors affect gas exchange: temperature, agitation, pain/discomfort, nutrition prescription, seizure activity, etc. Although these factors should be considered carefully, typical ranges for V̇CO2 and V̇O2 are depicted in Table 15-2. TABLE 15-2 Estimated Gas Exchange Values for Infants and Children Age

V̇CO2 (mL/kg/min)

V̇O2 (mL/kg/min)

< 0.5 year

7.6 (6.0 to 9.2)

8.0 (6.5 to 9.5)

0.5 to < 8 years

5.8 (5.2 to 6.4)

6.5 (5.6 to 7.4)

≥ 8 years

3.5 (3.0 to 4.0)

3.8 (3.3 to 4.3)

Values are expressed as mean (95% CI). V̇CO2 is carbon dioxide production and V̇O2 is oxygen consumption. Reproduced from Smallwood CD, Walsh BK, Bechard LJ, Mehta NM. Carbon dioxide elimination and oxygen consumption in mechanically ventilated children. Respir Care. 2015;60(5):718–723.

To rule out renal conditions, additional blood testing is typically indicated; likewise, for ruling out neurologic conditions, additional testing such as electroencephalography (EEG) may be needed.

Assess the Gestational Age of the Patient The following sections provide a general guideline to help the reader gain insights into the relationship between gestational age and select conditions. It should be

noted that careful examination of the patient and consideration of all conditions is warranted. That said, if the patient is preterm (< 37 weeks), he or she is more likely to have respiratory distress syndrome (see disease states and conditions). If the patient is term (37 to 42 weeks), the cause of respiratory distress is more likely to be transient tachypnea of the newborn, and if the patient is post-term (> 42 weeks), one should consider meconium aspiration.

Common Neonatal Respiratory Conditions Common neonatal respiratory conditions include neonatal respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN), persistent pulmonary hypertension of the newborn (PPHN), and meconium aspiration syndrome (MAS) as described below. Chronic lung disease (e.g., bronchopulmonary dysplasia) may also occur.

Respiratory Distress Syndrome Respiratory distress syndrome (RDS), also known as hyaline membrane disease or surfactant deficiency syndrome, is characterized by an inadequate surfactant production and immature pulmonary vascular and cellular development. Pulmonary surfactant serves to reduce the surface tension of alveoli, reducing the amount of work required to inflate the lungs and prevent atelectasis. Typically, during the canalicular phase of lung development, type II alveolar cells begin to mature and start producing surfactant. As the neonate approaches term, the amount of surfactant that is produced increases. Infants born ≤ 28 weeks gestation have an underdeveloped pulmonary structure and are therefore at high risk for developing surfactant deficiency and respiratory distress syndrome. In general, RDS includes reduced functional residual capacity (FRC), decreased pulmonary compliance, hypoxia, and hypercapnia as a consequence of ventilation/perfusion mismatch. Significant hypoxia can be associated with pulmonary hypertension, as well as intraand extrapulmonary shunting. Shunted blood leads to heightened hypoxia, which increases pulmonary vascular resistance, causing increased shunting—a vicious cycle that can further limit surfactant production and proliferation. RDS occurs in approximately 1 in 100 live births and is inversely related to gestational age.8 Signs and symptoms of RDS occur rapidly, often appearing in the delivery room. Infants will present with profound tachypnea, grunting, nasal flaring, and retractions. The four main components to diagnosing RDS include: 1. Blood gas analysis: Hypoxia (reduced PaO2) and hypercapnea (increased PaCO2). In some cases, the PaCO2 may be normal or slightly low since the baby has increased respiratory rate to compensate for a low oxygen level. Eventually, PaCO2 will increase as the baby will be unable to sustain such a

high work of breathing. 2. Chest x-ray: A hallmark characteristic of RDS on chest x-ray is a “ground glass” appearance, with diffuse reticulogranular (fine, granular) densities (Figure 15-2).

FIGURE 15-2 Respiratory Distress Syndrome. Chest x-ray findings in an infant with respiratory distress syndrome. Note the appearance of bilateral ground glass and air bronchograms. Also, the tip of the endotracheal tube is low and should be withdrawn about 0.5 cm. Reproduced from Gallacher DJ, Hart K, Kotecha S. Common respiratory conditions of the newborn. Breathe (Sheff). 2016;12(1):30–42.

3. Lecithin-sphingomyelin (L:S) ratio: A test of the fetal amniotic fluid to assess the level of fetal lung maturity. Both lecithin and sphingomyelin are components of surfactant and can be found in the amniotic fluid. Since sphingomyelin concentration remains relatively constant during pregnancy and lecithin increases as the fetal lung matures, measuring both quantities provides a reasonable assessment of lung maturation. An L:S ratio < 2.0 is associated with RDS and is the standard in RDS testing. These tests may be unreliable in cases of Rh isoimmunization and gestational diabetes. 4. Phosphatidylglycerol (PG): A common phospholipid in surfactant that increases as the baby matures in utero. If PG is measured in the amniotic fluid, the patient will be at lower risk for RDS. Often, L:S ratio and PG results are used in combination to determine the likelihood of RDS development.

Treatment The general strategy for treating a patient with RDS includes surfactant replacement if indicated, respiratory support including oxygen therapy, high-flow nasal cannula, continuous positive airway pressure (CPAP), noninvasive ventilation, and invasive ventilation with a mechanical ventilator, depending on severity of illness.

Surfactant Replacement One of the pillars of treating neonates with established RDS is surfactant replacement therapy. In this case, surfactant replacement has been shown to reduce mortality, incidence of pulmonary air leak (pneumothoraces or pulmonary interstitial emphysema), and risk of chronic lung disease.10,11 Transient intubation in order to deliver exogenous surfactant to the lower airways in a neonate has also been shown to reduce the need for invasive mechanical ventilation.12 In brief, INtubation, SUrfactant Replacement, and Extubation to CPAP (INSURE) is a procedure often utilized in premature babies. In general, there are two strategies to surfactant administration: prophylactic and rescue. In prophylactic use, patients who are deemed eligible receive a dose of surfactant regardless of clinical presentation. Rescue surfactant is only given once a baby demonstrates a clinical deterioration that includes tachypnea, increased work of breathing, and evidence of insufficient gas exchange.

Indications Surfactant deficiency due to prematurity occurs in neonates of gestational age < 30 weeks and/or birth weight < 1250 g. Surfactant deficiency may also occur in neonates up to 2000 g, but evidence showing a benefit in this group is not as strong.13 Other indications may include pulmonary hemorrhage, meconium aspiration, and other circumstances that decrease surfactant production.

Procedure In addition to the steps outlined below, use personal protective equipment (PPE) and aseptic techniques as appropriate to reduce the risk of contamination and nosocomial infection. 1. Verify indications and appropriate placement of endotracheal tube. 2. Obtain exogenous surfactant and verify dosage (depending whether the surfactant is animal derived or synthetic). a. Most doses are approximately 100 mg/kg (must verify). 3. Warm surfactant to room temperature (in room air for ~ 20 minutes or warmed in hands for ~ 8 minutes). DO NOT SHAKE. 4. Aspirate appropriate dosage using a large-bore needle and syringe. Avoid foaming the surfactant.

5. Select appropriate catheter depending on endotracheal tube (ETT) inner diameter and available equipment. Catheters that can be used include: a. In-line surfactant delivery system b. Small-bore feeding tube (6 French) c. Umbilical catheter (6 French) 6. Determine safe catheter insertion depth (to tip of ETT). 7. Consider suctioning patient before the procedure if indicated. 8. Turn subject on left side ➝ insert catheter ➝ administer half of the total dose to the tip of the ETT ➝ remove catheter ➝ administer several breaths if manually ventilating or allow ventilator to deliver breaths for ~30 seconds. 9. Turn subject on right side and administer ➝ insert catheter ➝ administer half of the total dose to the tip of the ETT ➝ remove catheter ➝ administer several breaths if manually ventilating or allow ventilator to deliver breaths for ~30 seconds. 10. Monitor patient. Note that compliance may temporarily decrease, and the patient may experience a moderate desaturation as the surfactant is distributed. After a short time, compliance and oxygenation should improve. Also, avoid suctioning the patient for 1 to 2 hours following administration to ensure that surfactant is adequately delivered.

CLINICAL FOCUS 15-1 A neonate of 28 weeks gestation arrives in the NICU and shows signs of respiratory distress. You are asked to assist in surfactant replacement. You remember the mnemonic “INSURE.” How would you proceed? Question: What is the first thing that must be done? Answer: 1. Insert an appropriately sized endotracheal tube (ETT)and determine the correct insertion depth. Consider suctioning the airway before insertion of surfactant. 2. Draw up the appropriate dose of surfactant slowly (usually 100 mg/kg) with a large-bore needle to avoid foaming. 3. Instill half the dose with the patient on the left side, followed by several breaths over 30 seconds. Then, turn to position the patient with the right side down and instill the second half and again give several breaths over 30 seconds. 4. Determine if the patient requires mechanical ventilation. If not, extubate to high-flow oxygen, continuous positive airway pressure (CPAP), or bilevel

positive airway pressure (BiPAP). 5. Avoid suctioning the patient for 1 to 2 hours after instillation.

Transient Tachypnea of the Newborn Transient tachypnea of the newborn (TTN) is one of the most commonly diagnosed conditions in the NICU. A baby with TTN may have mild respiratory distress and a wet chest x-ray appearance (Figure 15-3). Although the specific etiology is not completely understood, “early-term birth,” that is, birth at 37 or 38 weeks gestation, may be at risk for developing TTN. It is also thought that risk of TTN is increased in infants born via cesarean section due to a delay in the reabsorption of lung fluid.14

FIGURE 15-3 Transient Tachypnea of the Newborn. Chest x-ray findings in an infant with transient tachypnea of the newborn. The lung fields appear wet, especially around the heart and caudal aspects of the lung. Reproduced from Gallacher DJ, Hart K, Kotecha S. Common respiratory conditions of the newborn. Breathe (Sheff). 2016;12(1):30–42.

Treatment TTN infants tend to have a resolution of symptoms with only supportive care. Support may include supplemental oxygen via standard cannula, high-flow nasal cannula, and sometimes noninvasive ventilation (nasal CPAP, typically at levels 5 to 7 cm H2O). Resolution of symptoms is often seen within days.

Persistent Pulmonary Hypertension of the Newborn Persistent pulmonary hypertension of the newborn (PPHN) occurs as the result of a failure of the pulmonary vasculature to adapt to ex utero environment after birth. In

utero, PVR is high in order to minimize blood flow through the lungs, since they do not participate in gas exchange and the baby relies on the mother for oxygenation. Blood is shunted to the systemic circulation through the patent ductus arteriosis (PDA) and foramen ovale. After the baby is born, oxygen (a potent vasodilator) and respiratory efforts of the baby cause a reduction in PVR. Failure of this transition to occur, plus continued shunting through the PDA and foramen ovale, manifest as pulmonary hypoperfusion, severe hypoxia, and hypercapnia. Early detection of shunting can be done using a series of oxygenation saturation probes. Preductal oxygen saturation is obtained by observing the SpO2 on the right arm. Postductal oxygen saturations are obtained by observing the SpO2 on the left arm or lower extremity. The difference between these measurements, where the preductal SpO2 is higher than the postductal SpO2, indicates right-to-left shunting (passage of blood from the right side of the heart to the left). In the context of PPHN, this occurs as a result of pulmonary hypertension. Definitive diagnosis is typically done by ultrasound since the clinical presentation can be very similar to other conditions.

Treatment Treatment of the newborn with PPHN includes high SpO2 targets (≥ 95%) and can require relatively high FIO2 concentrations. Other therapeutic interventions include inhaled nitric oxide (iNO). Nitric oxide (NO) is an important cellular signaling molecule and potent vasodilator. Its use is approved for newborns with persistent pulmonary hypertension. The medication is introduced into the mechanical ventilator circuit in gaseous form in concentrations from 1 to 80 parts per million (ppm). There are important considerations when caring for the newborn with PPHN receiving iNO. First, NO has an extremely short half-life; therefore discontinuation of the drug can result in severe and rapid decompensation. It is important to limit circuit disconnects and have a backup iNO delivery device should a fault occur. Second, high concentrations of delivered iNO can result in the formation of methemoglobin and lead to methemoglobinemia, a condition that reduces the ability of hemoglobin to transport oxygen and lead to hypoxemia.

Meconium Aspiration Syndrome

Meconium aspiration syndrome (MAS) is the inhalation of a meconium, a viscus, dark green substance formed from the digestion and defecation of materials (epithelial cells, mucus, amniotic fluid, etc.) by the baby in the uterus. An example of a chest x-ray of a baby with MAS is depicted in Figure 15-4. Typically, the material is retained in the infant’s bowels until after birth. However, meconium can sometimes be expelled before birth. Clinicians should look for meconium-stained amniotic fluid around the time of birth, which can be a risk factor for MAS. Upon birth, the infant may inadvertently inhale meconium, impeding air flow, resulting in respiratory distress, hypoxia, hypoventilation, and in severe cases, PPHN.

FIGURE 15-4 Meconium Aspiration Syndrome. Chest x-ray findings in a term infant with MAS. Note the patchy opacities throughout the lung fields. In addition, the lungs appear hyperexpanded. Reproduced from Gallacher DJ, Hart K, Kotecha S. Common respiratory conditions of the newborn. Breathe (Sheff). 2016;12(1):30–42.

Treatment Treatment of an infant with MAS includes diligent suctioning to remove the meconium from the airways and supportive therapy to ensure adequate gas exchange. In severe cases, this will include intubation and mechanical ventilation. As noted above, MAS can lead to PPHN. In that case, treatment in accordance with PPHN is indicated.

Chronic Lung Disease Chronic lung disease (CLD), also often referred to as bronchopulmonary dysplasia, is an unfortunate but common long-term condition associated with prematurity. CLD is defined as a supplemental oxygen requirement ≥ 28 days after birth and beyond

36 weeks corrected gestational age. A chest x-ray of a 24-week preterm infant is shown in Figure 15-5. Injury to the pulmonary system that occurs as a result of supportive therapy prevents the normal development of vascular and alveolar tissue. It is thought that inflammation as the result of mechanical ventilation, fluid overload, and postnatal sepsis contributes to the development of CLD.15 Degree of prematurity is the biggest risk factor for CLD, with the most premature infants being at highest risk.16

FIGURE 15-5 Chest X-ray Findings in an Infant with Chronic Lung Disease. Note the shadowing throughout both lung fields and the area of cystic changes. Reproduced from Gallacher DJ, Hart K, Kotecha S. Common respiratory conditions of the newborn. Breathe (Sheff). 2016;12(1):30–42.

Treatment Gentle ventilation and oxygen therapy aimed to provide adequate oxygen saturation but limiting hyperoxic damage is extremely important. Home oxygen may be required, and in severe cases, tracheostomy and long-term mechanical ventilation.

Other Conditions Seen in Premature Infants Other respiratory care–related conditions sometimes seen in premature infants include retinopathy of prematurity, apnea of prematurity, and congenital anomalies as described below.

Retinopathy of Prematurity In premature infants, retinopathy of prematurity is a condition of the eye in which inappropriate growth of retinal blood vessels, due to excessive oxygen therapy,

results in scarring and retinal detachment. There is a full spectrum of retinopathy of prematurity severity, from mild loss of eye function that can resolve spontaneously to the most severe that could result in blindness. The key with retinopathy of prematurity is prevention. In most centers, infants born < 30 weeks gestation or birth weight 10 mL/kg ideal body weight (IBW) were not associated with increased mortality or ventilator-free days.33,34 While the causal pathway between VT and mortality cannot be irrefutably ascertained from these types of studies, VT levels are set based upon the physiologic range with consideration of the underlying lung pathology and respiratory system compliance. As such, PALICC recommendations suggest targeting VT at 5 to 8 mL/kg for children with adequate respiratory system compliance and 3 to 6 mL/kg IBW in children with reduced pulmonary mechanics.24 Further, inspiratory plateau pressure or peak inspiratory pressure should ideally be limited to ≤ 28 cm H2O unless evidence of reduced chest wall compliance (i.e., extrapulmonary ARDS) is observed, in which case, slightly higher pressures (e.g., 29 to 32 cm H2O) may be used. Gas exchange goals should be considered in balance with the risks of using high levels of ventilator support to attain normal physiologic targets, as this could potentially exacerbate lung injury further. Permissive hypercapnia is a commonly accepted strategy in which PaCO2 levels are allowed to increase (e.g., 45 to 65 mmHg) and lower pH thresholds (7.15 to 7.30) are accepted. Some exceptions to this strategy include patients with concomitant pulmonary hypertension, specific types of congenital heart disease, or traumatic brain injury; in these scenarios, normal pH and PaCO2 targets are typically maintained. Importantly, increased

systemic oxygenation has not been correlated with improved outcomes in ARDS; as such, maintaining SpO2 between 88% to 92% in patients with moderate to severe ARDS and using elevated PEEP (e.g., 10 to 15 cm H2O) or higher is recommended. A subset of children with severe PARDS may exceed the proposed limits of lungprotective ventilation or exhibit further clinical deterioration unresponsive to therapy. In these patients, adjuncts such as prone positioning, high-frequency oscillatory ventilation, and extracorporeal membrane oxygenation (discussed later in the chapter) have been employed.

Asthma Asthma affects more than 300 million people and is one of the most common causes of pediatric hospital admissions. Acute asthma exacerbations are mostly preventable unless the disease is poorly controlled. Approximately 60% of children with asthma have at least one exacerbation each year, with younger children accounting for the majority of cases, and disease burden lessening with age.35 Of children presenting with severe asthma exacerbations, 8% to 16% require admission to intensive care, although most do not require mechanical ventilation.36 The pathophysiology of asthma includes three primary mechanisms: bronchospasm, inflammation, and increased mucus production. Environmental, infectious, or noxious “triggers” result in injury to the airway epithelium, which is subsequently followed by the inundation of proinflammatory cells and cytokines. Asthma is categorized by structural changes in the airway, such as remodeling, mucous gland hyperplasia, basement membrane thickening, fibrosis, and bronchial smooth muscle hypertrophy. Most children have mild to moderate asthma and present with symptoms including inspiratory and expiratory wheezing, crackles, tachycardia, pulsus paradoxus, and accessory muscle use. The majority respond to first-tier therapies including: inhaled beta2 agonists, anticholinergics, and systemic corticosteroids. Occasionally, children may continue to exhibit severe airflow limitation, fatigue, and impending respiratory failure despite receiving continuous albuterol (Ventolin, Proventil) and steroids. These children often receive adjuvant therapies in a stepwise fashion, such as intravenous magnesium sulfate (a bronchodilator), helium–oxygen (heliox; described later), and noninvasive ventilation, culminating in invasive mechanical ventilation for

the most severe cases. There are no specific guidelines or recommendations for when to initiate mechanical ventilation in unresponsive asthma (also known as status asthmaticus). The decision to intubate and mechanically ventilate is made in context with perceived patient exhaustion, altered mental status, signs of hypercarbic or hypoxic respiratory failure, and worsening metabolic acidosis. Once intubated, the goals of mechanical ventilation include providing adequate gas exchange and the avoidance of ventilator-induced lung injury. Permissive hypercapnia and a pH > 7.2 are acceptable, unless specific contraindications to hypercarbia (e.g., pulmonary hypertension) exist.35 Asthmatics are challenging to manage on the ventilator, as the physiologic manifestation of airway inflammation results in increased airway resistance and high ventilatory pressures. Ventilation is frequently complicated by a vicious cycle of expiratory flow limitation, gas trapping, hyperinflation, and the inability to fully exhale. Gas trapping can be discerned during mechanical ventilation by performing an autoPEEP maneuver (expiratory hold) in patients who are not spontaneously breathing or by observing the volume of end-expiratory flow (V̇EE) in those with preserved spontaneous efforts. Of note, if PEEPtotal (from autoPEEP maneuver) exceeds set PEEP, or if V̇EE is greater than 0 L/min, then dynamic hyperinflation or gas trapping is present. Ventilation strategies in patients with asthma aim to minimize gas trapping and warrant careful consideration of the precarious balance between inspiratory and expiratory time constants, and the appropriate selection of breathing frequency, inspiratory time (TI), and VT. The set mechanical rate is often lowered (e.g., 8 to 12 breaths/min) with efforts to maximize the exhalation phase. Airway resistance must also be taken into consideration when setting TI; as a minimum, often longer inspiratory phase (e.g., 1 to 1.5 seconds) may be needed to achieve adequate inflation. It is important to monitor waveforms, flow-volume loops, capnogaphy, autoPEEP, V̇EE, and vital signs in response to mechanical ventilation changes. For example, increasing the set breathing frequency to raise minute volume and lower PCO2 may not improve gas exchange (with severe air trapping) and could further exacerbate poor pulmonary mechanics. It is important to maintain the regimen of continuous albuterol and intravenous adjuncts such as steroids, magnesium sulfate, terbutaline (Brethine), and ketamine

(Ketalar) during mechanical ventilation. In rare cases, asthma exacerbations will remain refractory to escalation in treatment; at this stage third-tier therapies such as inhaled volatile anesthetics and extracorporeal membrane oxygenation should be considered (discussed later in chapter).36

Neurologic Conditions Brain injury or the acute disturbance of neurologic function resulting from a traumatic, hemorrhagic, infectious, or hypoxic insult are thought to be an underreported cause of death in children.37 Commonly encountered neuropathological processes include traumatic brain injury, refractory status epilepticus, central nervous system infection, or any condition complicated by increased intracranial pressure (ICP). Treatment strategies for children with brain injury consist of management of ICP, cerebral blood flow (CBF), and the avoidance of secondary brain injury through the prevention of precipitous fluctuations in PaCO2. It is important to understand that PaCO2 is a strong modulator of both CBF and vascular tone. Hypercapnia is accompanied by increase in CBF ~ 6% per 1 mmHg change in PaCO2, which can subsequently result in intracranial hypertension. In contrast, hypocapnia decreases CBF by ~ 3% per mmHg in PaCO2, thereby reducing cerebral blood volume and potentially increasing risk for cerebral ischemia. In children with traumatic brain injury, normal PaCO2 levels (35 to 40 mmHg) are targeted, as PaCO2 < 30 mmHg have been associated with cerebral ischemia and increased mortality.38 Arterial oxygen content, SpO2, and cerebral near-infrared spectroscopy are commonly employed surrogates for estimating whether the brain receives enough oxygen, since direct measurement is not possible. Adult guidelines suggest maintaining PaO2 > 60 mmHg since lower thresholds have been associated with exponential increases in CBF.39 Further, the application of PEEP during mechanical ventilation affects ICP, CBF, and cerebral perfusion pressure (CPP), denoted as the difference between mean arterial pressure and ICP. Although PEEP is a necessary component for mechanical ventilation, it is associated with decreased venous return, increased intrathoracic pressure, and possibly reduced cardiac output. Children suffering from traumatic brain injury may have impaired autoregulation or the ability

to maintain a constant blood flow in response to fluctuations in perfusion pressure.38 For example, when autoregulation is intact, decreased cardiac output is compensated for by cerebral vasodilation to maintain CPP. Alternately, when autoregulation is impaired, compensatory mechanisms are unresponsive and decreased CPP leads to ischemia.

CLINICAL FOCUS 15-2 A young child is admitted to the ICU with severe asthma after being intubated in the emergency department. The oxygen saturation is 97% on 0.30 FIO2. You are asked to assist in the patient’s management. Question 1: What medications would help the patient resolve this episode of status asthmaticus? Answer: Continuous inhaled beta-agonist therapy (albuterol) is the cornerstone of resolving bronchospasm and often combined with inhaled anticholinergic therapy (ipatropium [Atrovent]). This must be combined with systemic corticosteroids, since the airway is inflamed and corticosteroids are potent anti-inflammatory drugs. Question 2: What would be your ventilator strategy? Answer: In general, a large tidal volume (8-10ml/kg) and lower respiratory rate strategy is required. Permissive hypercapnia with a pH > 7.2 is acceptable. Assess for autoPEEP by applying an expiratory hold if the patient is not breathing spontaneously and try to adjust parameters to minimize hyperinflation. Question 3: If the patient fails to respond to inhaled bronchodilators and systemic corticosteroids, what other modes of therapy can be utilized? Answer: Magnesium sulfate, terbutaline, and heliox have been utilized in refractory cases. Volatile anesthetics are rarely used today, but the IV anesthetics ketamine and propofol (Diprivan) both have bronchodilating properties. In rare circumstances, ECMO can prove to be lifesaving in patients that have progressive hypercapnia and acidosis that is refractory to therapy.

Neuromuscular Diseases Neuromuscular diseases (NMD) represent a heterogeneous group of conditions, both genetic and acquired, that are associated with varied degrees of restrictive lung disease and pulmonary dysfunction. These disorders can be categorized as genetic (e.g., Duchenne muscular dystrophy and spinal muscular atrophy) or acquired (e.g., Guillain-Barré syndrome and myasthenia gravis), and differ in terms of onset, severity, and impact on quality of life. Examples of neuromuscular conditions often seen in children are depicted in Table 15-4. TABLE 15-4 Neuromuscular Disorders in Children

Description IVIG, intravenous immunoglobulin; NIV, noninvasive ventilation; NMJ, neuromuscular junction.

Respiratory failure in children with NMD can be separated into two overlapping etiologies: recurrent lung damage culminating in chronic respiratory failure and

respiratory muscle weakness. Aspiration of secretions during swallowing or periods of reflux is commonly associated with NMD, resulting in infections, chemical insult to the airways, pneumonia, bronchiectasis, and pulmonary fibrosis. These factors contribute to low lung compliance and increased work of breathing. Additionally, the compliance of the chest wall has important implications on work of breathing. Infants have highly compliant chest walls, which slowly transition to a low compliance state with increasing age. The negative pleural pressure required to move air into the lungs may cause collapse during inspiration, and paradoxical motion of the rib cage and abdomen. Further, children with NMD have decreased upper airway tone and can have significant airway obstruction. The increased work required of the respiratory muscles to overcome high airway resistance under these conditions predisposes patients with NMD to respiratory muscle fatigue and inefficient ventilation.40 Respiratory muscle fatigue is characterized by the inability to sustain contractile force in the face of a constant load. When patients with NMD become hypercarbic, they are generally unable to increase ventilation sufficiently to restore normocapnia even if the ventilatory drive remains intact.41 Further, these patients have insufficient respiratory muscle strength to generate an effective cough, leading to reduced airway clearance.

Treatment In the absence of curative treatments, the impetus on management is largely supportive, and focuses on attenuating the progressive decline in musculoskeletal and cardiopulmonary function.42 The provision of respiratory support through noninvasive or nocturnal mechanical ventilation are common treatments for respiratory muscle fatigue in children with neuromuscular disease. Manual insufflation–exsufflation therapies, which generate positive pressure followed by negative pressure, are used to facilitate secretion clearance and have become a mainstay of supportive care. Moreover, corticosteroid administration has been shown to improve respiratory muscle strength, mitigate decline in lung function, and delay the need for mechanical ventilation.41

Bronchiolitis

Bronchiolitis is the most common cause of hospitalization for children < 2 years old, and accounts for roughly 125,000 to 150,000 admissions annually.43 Bronchiolitis is a lower respiratory tract infection characterized by acute inflammation, edema, and increased mucus production. The necrosis and shedding of epithelial cells that line the small airways cause narrowing and increased resistance to flow. Respiratory syncytial virus (RSV) is the most common etiology of bronchiolitis, followed by human rhinovirus and influenza. Typically, bronchiolitis is preceded by a viral upper respiratory infection accompanied by tachypnea and increased work of breathing—notably grunting, nasal flaring, retractions, and wheezing. The course of illness is variable and is impacted by risk factors including congenital heart disease, prematurity, immunodeficiency, and chronic lung disease. For many patients, treatment is supportive, with clinical practice guidelines recommending suctioning and the maintenance of hydration to counter insensible losses secondary to increased work of breathing. The routine use of bronchodilators, hypertonic saline, systemic corticosteroids, chest physiotherapy, and suctioning is not recommended, as conclusive evidence is lacking in these areas.44 Clinical practice guidelines do not provide recommendations for the subset of children requiring admission to the ICU. In the absence of guidelines describing the escalation of care, considerable variability exists in management strategies. A multicenter prospective review of children with bronchiolitis found that 16% required ICU admission, which included CPAP and/or intubation within 24 hours of admission. Additionally, the choice of modality included CPAP, high-flow nasal cannula (HFNC), or intubation exhibited significant institutional-level variation.43 Further, studies describing the characteristics of children most likely to benefit from each of these modalities are needed. In lieu of evidence-based recommendations, a staged approach is often employed, for example, the application of CPAP or NIV if no improvement is noted with HFNC.

Cystic Fibrosis Cystic fibrosis (CF) is a genetic exocrine gland disorder that causes excessive lung secretions, repeated pulmonary infections, pancreatic enzyme insufficiency, and other symptoms. Specifically, CF is a monogenic autosomal recessive condition primarily occurring in the Caucasian population, affecting roughly 70,000 people

worldwide.45 CF is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR anion channel is responsible for regulation of chloride, bicarbonate, and sodium transport across cell membranes. Perturbations in anion channel transport impacts mucociliary clearance in the lungs, and affects the pancreas, gastrointestinal tract, and liver. Prior to the widespread expansion of newborn screening programs, infants and children presented with respiratory symptoms, meconium ileus, and failure to thrive.46 Early detection of CF using biochemical markers and genetic assays has been attributed to timely diagnosis and treatment and reduced disease severity. The sweat test with a chloride value ≥ 60 mmol/L continues to be the gold standard for diagnosis. Historically, life expectancy was limited to early childhood; however, with improvements in diagnosis and management, median survival has progressively increased to 40 years.47 The airway epithelium is an integral component of the mechanical and chemical barriers responsible for the lungs’ immune defenses. In the healthy airway, airway surface liquid has endogenous antimicrobial properties that destroy bacteria. Additionally, mucus production and cilia motility allow for mucociliary transport of pathogens and particles out of the lung.48 CFTR channels are thought to play a major role in the regulation of airway surface liquid via the osmotic transport gradient of chloride and sodium. Derangement of this function results in a reduced depth of the low-viscosity layer, which is hypothesized to attenuate the effectiveness of pathogen and secretion clearance. Children with CF endure repeated respiratory infections with bacteria and viruses, including Pseudomonas aeruginosa, Staphylococcus aureus, and Haemophilus influenzae.49 Over time, these organisms are able to establish a chronic presence in the airways as innate immunity is compromised. Pulmonary consequences of CF are characterized by persistent infections, repetitive cycles of inflammation, lung injury, airway remodeling, obstruction, and bronchiectasis. Typically, CF patients experience periodic exacerbations characterized by increased cough, sputum production, and reduced overall pulmonary function. These exacerbations begin in infancy with progressively worsening symptoms, decreasing lung function, and ultimately irreversible lung injury, with respiratory failure being the cause of death in over 90% of patients. Longer life expectancies have largely been attributed to the

application of effective airway clearance, development of effective mucolytics, vigilant treatment of infection, and optimizing nutritional status.45

Treatment Airway clearance therapies (ACT) are commonly recommended for CF patients. These include both physiologic and pharmacologic interventions. Antibiotics are also used as prophylaxis for preventing lung infections.

Physiologic Airway Clearance Therapies A wide range of devices have been used to facilitate airway clearance, including positive-pressure physiotherapy, high-frequency chest wall oscillation, intrapulmonary percussive ventilation, and manual insufflation–exsufflation. Conceptually, the physiologic principles for utilizing ACTs to increase sputum production are rational; however, no studies have demonstrated superiority of one device over another.50 Therefore, device selection depends often on the patient’s age, preferences, disease progression, and cost.

Pharmacologic Airway Clearance Therapies Dornase alfa (Pulmozyme), a mucolytic, and hyperosmolar medications including hypertonic saline and mannitol have been used to improve secretion clearance in patients with CF. A Cochrane review concluded dornase alfa improves lung function and decreases pulmonary exacerbations in patients with CF.51 However, evidence supporting the superiority of dornase alfa over hypertonic saline or mannitol is mixed and inconclusive.

Antibiotics Proactive measures to reduce infection, inflammation, and further lung injury are primary objectives in CF management. Antibiotic therapies are used for prophylaxis, suppression, and eradication of the major pathogens responsible for CF infections. Tobramycin (Tobrex) was the first aerosolized antibiotic approved for the treatment of CF and continues to be a mainstay in the suppression and prevention of Pseudomonas aeruginosa. A host of other antibiotics, delivered orally, intravenously, or aerosolized, are selected based upon the complexity of infection, species, and resistance to antibiotics.52

Monitored Parameters The neonatal and pediatric population exhibits tremendous heterogeneity in terms of age, weight, height, cognitive development, and pathophysiology. The vital signs— heart rate, respiratory rate, and blood pressure—vary greatly dependent upon age. In an intensive care unit, a 1-year-old patient could be breathing 35 breaths/min and would not be cause for alarm. But if a 15-year-old patient, in the very next bed space, had the same 35 breaths/min respiratory rate, this would indicate a significant derangement and may indicate the need for escalated respiratory support. The expected respiratory rate and heart rate are depicted in Figure 15-6.

FIGURE 15-6 Heart Rate and Respiratory Rate Percentile Curves in Hospitalized Children. Solid lines represent all subjects, and dotted lines represent subjects without respiratory disease.

Description

Expected Values for Important Respiratory Parameters One of the most difficult aspects of caring for the neonatal and pediatric patient is the vast differences in expected values depending on age or weight. Ventilator parameters are typically normalized to ideal body weight. As patients grow, the heart rate, respiratory rate, inspiratory flow, expected minute ventilation (V̇E), alveolar minute ventilation (V̇A), and dynamic pulmonary compliance (Cdyn) all change. In Table 15-5, expected values for these variables are depicted for patients with healthy lungs. In general, Cdyn is ~1.0 mL/cm H2O/kg for healthy (nonintubated) subjects and ~0.6 mL/cm H2O/kg for mechanically ventilated subjects. TABLE 15-5 Reference Values for Healthy Neonatal and Pediatric Subjects*

Description *It should be noted that in critical illness and during invasive mechanical ventilation in particular, individual values may be much worse than shown here.

Endotracheal Tube Selection and Management Historically, cuffless endotracheal tubes (ETTs) were utilized in the neonatal population and in some small pediatric subjects. This was a function of manufacturing limitations associated with developing an ETT cuff appropriate for small children and a desire to place the largest diameter tube without the bulk of the cuff. However, current ETTs and practice have evolved to include the use of many 3.5-mm inner diameter (ID) ETTs with inflatable cuffs and even some 3.0-mm ID tubes. An appropriately selected ETT ID can help to ensure an adequate seal around the tube that enhances accuracy of monitored tidal volume and end-tidal CO2 while minimizing the irritation or damage to the trachea. For children ≤ 35 weeks old, the suggested ID of the ETT is depicted in Table 15-6. For children > 35 weeks of age, Equation 15-1 can be utilized to determine the appropriate-size ETT ID. In both cases, it is important to note individual anatomic differences may require the clinician to select an ETT that deviates from the suggested size. Furthermore, the estimated insertion depth (in cm to the lip) for an ETT can be calculated by multiplying the ID (of the appropriately selected ETT) by 3. As an example, let us calculate the appropriate ETT ID and insertion depth for a 2-year-old child: ETT ID = (2 + 16)/4 = 18/4 = 4.5 mm, insertion depth = 4.5 × 3 = 13.5 cm at the lip. TABLE 15-6 Endotracheal Tube Inner Diameter for Neonates ≤ 35 Weeks of Age Age (weeks)

ETT Inner Diameter (mm)

Cuff

< 30

2.5

No

30 to 35

3.0

Possibly

> 35

≥ 3.5

Yes

Equation 15-1: Suggested Endotracheal Tube Inner Diameter for Children ≥ 6 Months of Age

Other considerations for ETT management include managing cuff inflation. Theoretically, the ideal volume of an ETT cuff is that which prevents leak but also minimizes pressure and physical displacement of the trachea. Although there is no consensus for cuff management, neonatal and pediatric centers will typically target a cuff pressure 20 to 30 cm H2O (if it can be physically monitored with a standalone device) or utilize a minimal occlusion volume (MOV) technique. MOV requires the clinician to auscultate the lateral neck, after which a syringe attached to the pilot balloon of the ETT slowly withdraws volume during positive-pressure ventilation. The cuff is slowly deflated until a gurgling or leaking sound is heard. This sound corresponds to an air leak around the ETT, and the pressure on the tracheal wall should be less than the maximum inflating pressure set on the mechanical ventilator. The clinician will then add just enough volume to ensure that no leak is heard. This procedure is utilized to confirm cuff pressures are not excessive and is typically done daily. It is important to note that the practice of deflating the ETT cuff comes with the risk of upper airway content seeping into the lower airway. Individual institutions typically offer quality-assurance programs for management of ETT and cuffs that should be followed closely.

Securing the Endotracheal Tube Often, an ETT can be adequately affixed to the patient using cloth tape. Various tape strategies exist and largely depend on size of the infant and institutional preferences. One of the limitations of the cloth tape method is the tendency of the tape to become saturated with secretions and become loose on the patient’s face. Respiratory therapists should assess the security of the tape frequently and re-tape if necessary to prevent movement or accidental extubation of the ETT. Other commercially available devices are available that include a rigid apparatus to place the ETT in the center of the infant’s mouth and cheek mounts that are sticky enough to resist some secretions.

Noninvasive Support Noninvasive respiratory support consists of devices that deliver mechanical ventilation without the presence of an established airway. Delivery of noninvasive support is accomplished using various interfaces, most commonly nasal prongs, nasal masks, or full-face masks. High-flow nasal cannula (HFNC) is a rapidly expanding modality for infants and children with respiratory distress. While not classified as noninvasive ventilation in the classic sense, this modality has been employed as an intermediate therapy for many infants and children whom otherwise would have received continuous positive airway pressure (CPAP).53 HFNC is thought to improve oxygen delivery by providing oxygen flow exceeding the patient’s peak inspiratory flow requirements, thereby mitigating the dilutional effect of entraining room air. Other proposed mechanisms through which HFNC decreases work of breathing include the generation of PEEP and associated alveolar recruitment and flushing extrathoracic dead space, thus minimizing CO2 rebreathing. At this time, there is no consensus on initial flow settings relative to patient size or weaning.54 CPAP provides a constant positive pressure upon which the patients breathe spontaneously. This effectively increases functional residual capacity (FRC) by counteracting some of the elastic forces imposed by the chest wall and small airways. Increasing FRC can help ameliorate and prevent atelectasis, thus reducing intrapulmonary shunt and improving gas exchange. It is important to note that CPAP does not directly influence ventilation, as VT delivery is not augmented. Ventilation is indirectly influenced by mechanism of alveolar recruitment and improving the balance of ventilation and perfusion. Therefore, CPAP is utilized in infants and children to improve gas exchange in the setting of mild to moderate respiratory failure.55 Nasal intermittent positive-pressure ventilation (NIPPV) has been increasingly used in neonates as a method of augmenting the beneficial effects of nasal CPAP (nCPAP), particularly in premature infants with respiratory distress syndrome. NIPPV provides two levels of positive pressure at a set frequency and inspiratory time. Clinical evidence has demonstrated that NIPPV provides additional benefits over nCPAP in premature infants, primarily reduced need for intubation and mechanical

ventilation.56 Other potential advantages over nCPAP include reduction in work of breathing, stimulation of the respiratory drive, and fewer apnea episodes.57 Bilevel positive airway pressure (BiPAP) is a commonly used modality that provides two-levels of pressure: inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). This mode can be triggered in synchronization with spontaneous efforts and has a preset backup rate should the patients’ spontaneous drive fall below the mandatory set frequency. The terminology associated with BiPAP settings and availability of pressure or volume delivery modes is variable between different manufacturers. While CPAP is used in hypoxemic respiratory failure, BiPAP is preferentially employed as a precursor to intubation in the setting of hypoxemic and hypercarbic respiratory failure.

Conventional Mechanical Ventilation The era of standalone neonatal ventilators has mostly passed. Today, many ventilators offer the required flow- and pressure-sensing capabilities needed for neonates in the same device that can deliver ventilation to pediatric and adult subjects. Variability in size, lung maturity, and the heterogeneous range of acute and chronic diagnoses make the development of a single ventilator strategy difficult. Therefore, the mode of ventilation and combination of settings vary considerably based upon the underlying condition and institutional preference. In efforts to further define a standard of care in children, the Pediatric Mechanical Ventilation Consensus Conference aimed to confer recommendations in regards to ventilation modalities, monitoring, gas exchange targets, and liberation from mechanical ventilation.58 Pressure-control and volume-targeted modes of ventilation have been predominately used in both neonatal and pediatric settings. Importantly, there are no conclusive data that suggest one mode of ventilation affords a long-term benefit over another; therefore, consistency is integral to providing safe and effective mechanical ventilation. Put another way, institutional preference and experience are more likely to generate positive outcomes, rather than the mode of ventilation used. Impetus is placed on the maintenance of spontaneous respiratory effort to maintain optimal ventilation to perfusion (V̇/Q̇) matching. Further, preserving the patient’s ability to assist ventilation generally requires lower inspiratory pressures. Often the most critically ill children with severe restrictive disease, obstructive disease, or combinations thereof require increased support. In these scenarios, controlled ventilation (volume or pressure) and continuous sedation and/or paralytics may be required. Tidal volume is generally set dependent upon two factors: (1) the patient’s condition (obstructive, normal, or restrictive) and (2) the severity of illness. PEEP is set to maintain adequate functional residual capacity and titrated based primarily upon oxygenation and work of breathing. Peak inspiratory pressure (PIP) is set directly to achieve a monitored VT in pressure-control modes or monitored in relation to set VT in volume-targeted or volume-controlled modes. In neonates and children with healthy lungs, the PIP required to achieve VT between 6 to 8 mL/kg is often in the range of 15 to 25 cm H2O. A general guide for initializing ventilator support is

shown in Table 15-7. TABLE 15-7 General Settings During Conventional Mechanical Ventilation

Description * This is a general guide, and specific targets and considerations may be important depending upon disease, prematurity, severity of illness, and other factors.

High-frequency ventilation (HFV) is a form of mechanical ventilation that employs rapid respiratory rates (240 to 900 breaths/min), to deliver VT that are generally smaller than anatomic dead space.59 Important concepts to consider about HFV are the mechanical factors that influence pressure, flow, and ventilation. For example, the resistance imposed by the endotracheal tube is a critical determinant of distal pressure transmission and ventilation efficiency. Pressure at the airway opening is attenuated significantly as it passes through the endotracheal tube, a process that continues in the conducting airways. Further, there is a direct relationship between smaller endotracheal tube size and pressure transmission to alveolar compartment. With smaller endotracheal tubes, resistance is higher, resulting in lower transmission of pressure to the alveolar compartment. The same phenomenon is true in reverse: With larger ETT lumens, there is less resistance, and therefore distal VT and pressure transmission are higher. In addition to these concepts, the fundamental mechanisms of gas exchange during HFV are different than in conventional mechanical ventilation, and numerous

mechanisms are thought to play a contributory role.60 Carbon dioxide elimination (V̇CO2) during HFV is impacted to a larger degree by changes in VT than frequency (f), and is expressed by the equation: V̇CO2 = f × VT2 The most commonly applied types of HFV in the United States include highfrequency oscillatory ventilation (HFOV) and high-frequency jet ventilation (HFJV). A typical high-frequency jet ventilator is shown in Figure 15-7, and a typical highfrequency oscillator is shown in Figure 15-8. Both of these devices have been used for over three decades and are considered standard alternatives for respiratory failure refractory to conventional mechanical ventilation. It is important to note that elective use of either HFV mode has not demonstrated superiority in outcomes over conventional mechanical ventilation. As such, the use of HFV is generally reserved for rescue use when conventional ventilation can no longer be applied in a protective manner.

FIGURE 15-7 High-Frequency Jet Ventilator. The Bunnell Life Pulse high-frequency jet ventilator is a typical example of a machine used in the neonatal intensive care unit. Courtesy of Craig Wheeler MS, RRT-NPS.

FIGURE 15-8 High-Frequency Oscillatory Ventilator. A typical high-frequency oscillatory ventilator used in the neonatal and pediatric intensive care unit. Courtesy of Craig Wheeler MS, RRT-NPS.

HFOV uses a continuous distending pressure or mean airway pressure (mPaw) that is generated by a fixed fresh gas flow (bias flow) as it passes through a restrictive valve before leaving the ventilator circuit. Manipulation of mPaw is the primary method of improving alveolar recruitment and oxygenation. HFOV employs an “open lung” strategy in which mPaw is increased to attain adequate oxygenation and lung expansion of eight to nine ribs on chest radiograph. A piston-driven membrane creates pressure oscillations (referred to as ΔP or amplitude) that are superimposed on the set mPaw. Adjustment of ΔP is the primary control of VT, and therefore adjusted up or down to achieve the targeted PaCO2 level. Frequency is a secondary control of PaCO2 and is adjustable between 3 to 15 hertz (Hz) or 240 to 900 breaths/min. Frequency selection is based upon the size of the patient and underlying physiology. For example, neonates are generally placed on 12 to 15 Hz, and larger children are often managed anywhere between 6 to 10 Hz. Importantly, HFOV employs a fixed inspiratory–expiratory (I:E) ratio (1:1 or 1:2), which influences the delivery of pressure and volume to the lung. The piston moves forward during the inspiratory phase and withdraws during the active exhalation phase. Since the I:E ratio is fixed, VT has a direct relationship with changes in set frequency. Explained another way, as frequency increases, the cycle time and VT are reduced. At lower frequencies (e.g., 3 to 4 Hz), VT delivery increases dramatically, thus potential lung-protective benefits of HFOV may be negated. Moreover, it is common strategy to utilize higher frequencies that are appropriate for patient size in order to afford lower VT, thereby maintaining the lung-protective properties of HFOV.61 HFJV delivers small VT in the form of rapid pulses through a specially designed endotracheal tube adapter. HFJV is characterized by the axial jet stream of gas that reaches the alveolar spaces quickly during a very short inspiratory time. The primary control of augmenting PaCO2 clearance is adjusting the HFJV PIP up or down to achieve the targeted threshold. Similar to HFOV, setting frequency on HFJV is based on the patient’s size and underlying disease process. For example, in disease states

in which longer exhalation time may be advantageous (e.g., meconium aspiration syndrome [MAS], air-leak syndromes, and bronchopulmonary dysplasia [BPD]), HFJV frequency is set between 4 and 6 Hz (or 240 to 360 breaths/min). In smaller infants with low compliance (RDS), a frequency of 7 Hz (420 breaths/min) is common. In contrast to HFOV, adjustment of frequency on HFJV does not impact VT, which is a principal mechanical difference between HFOV and HFJV. Additionally, exhalation during HFJV is passive and relies on the natural recoil of the lungs. Clinically, this distinction translates into the proper application of settings, particularly the adjustment of frequency and inspiratory time. For exhalation to occur passively there must be a long enough period of time for exhaled gas to exit or air trapping will occur. Conventional mechanical ventilation is always used in tandem with HFJV to generate PEEP and provide bias flow, and also effectively functions as the exhalation valve. Importantly, PEEP is the primary mechanism of adjusting mPaw, alveolar recruitment, and oxygenation. While it is generally preferred to use only PEEP, conventional mandatory breaths (sigh breaths) can be applied to remedy atelectasis and improve oxygenation. Sigh breaths are generally used following PEEP increases, thus using the larger conventional mechanical ventilation breaths to recruit and maintain expiratory lung volume. Additionally, sigh breaths may help restore lung volumes following suctioning or inadvertent disconnection from the ventilator. Sigh breaths should generally be avoided in the setting of air-leak syndromes or when there is concern for expiratory flow limitation. HFJV is commonly used in premature neonates and small children and is not designed for use in larger children (> 10 kg). There are insufficient data to recommend using HFJV in larger children, and it should be avoided in infants with obstructive airway disease because of the risk of dynamic hyperinflation.58

Inhaled Gas Mixtures The use of oxygen has been a cornerstone of respiratory therapy since its inception and has played a role in the transformation of respiratory care into the profession it has become. While the majority of patients do not typically require medical gases beyond oxygen, subsets of neonatal and pediatric patients have etiologies and pathophysiologic conditions for which treatment may be optimized by using adjunctive medical gases.

Helium–Oxygen Mixtures Helium (He) is a colorless, odorless, tasteless noble gas that has a lower density than ambient air and 100% oxygen. Helium is inert, meaning that it is neither chemically reactive nor toxic even after prolonged exposure, since it does not elicit any biologic effects.62 When helium is proportionally combined with oxygen, generally in concentrations greater than 50% (e.g., 60:40 or 80:20 He:O2), it is referred to as heliox. The key property of heliox is its low density in comparison with air and oxygen concentrations. The reduction in density allows for the conversion of turbulent gas flow to laminar flow, thereby reducing resistance to gas flow.62 It is important to recognize that decreased gas density is directly proportional to helium concentration; thus, lower concentrations (e.g., < 50%) may have limited effects. The Reynolds number (Re) quantifies the ratio of inertial to viscous forces and describes whether fluid flow is laminar or turbulent. In anatomical terms, each successive generation of the tracheobronchial tree provides a different challenge to airflow resultant from diminishing airway caliber and branching angles.63 Collectively, these factors contribute to turbulence and airway resistance, and are further compounded by conditions such as status asthmaticus, bronchiolitis, croup, stridor, or other forms of airway obstruction. Regardless of the etiology of obstruction (small or large airway), the low-density properties of heliox theoretically facilitate diffusion into the distal airways faster than air–oxygen mixtures, thereby reducing the work of breathing. This is explained by Graham’s law, which states that the flow rate of any gas is inversely proportional to the square root of its density. Moreover, additional mechanisms of action for heliox include a greater diffusion coefficient when compared with air, and the potential to augment the delivery of aerosolized

medications due to improved ventilation (although in theory, He:O2 is a poor vehicle for aerosols).64,65 Furthermore, by lowering airway resistance, heliox in conjunction with conventional mechanical ventilation may afford lower PIP requirements for intubated patients with asthma.66 No major adverse events have been reported in any of the randomized control trials, which suggest heliox is safe to utilize as a therapeutic adjunct.67 Evidence in support of heliox as an adjuvant is conflicting, and limited to small single center trials mostly in the context of asthma. A meta-analysis including adults and children with asthma suggests heliox improved pulmonary function only in the more severe cases.67 Other studies have found no differences in clinical asthma score, duration of continuous albuterol nebulization, or outcomes data including length of stay, admission, or intubation rate.36

Nitric Oxide Nitric oxide (NO) is a colorless, odorless gas, consisting of one nitrogen and one oxygen atom. NO is a free radical and highly reactive gas that is unstable in air and undergoes oxidation to form nitrogen dioxide (NO2), a toxic environmental pollutant.68 NO is synthesized as a byproduct following the conversion of L-arginine to L-citruline by nitric oxide synthase. NO rapidly diffuses across cell membranes where it comes in contact with smooth muscle, and activates guanylate cyclase, resulting in increased cyclic guanosine 3',5’ monophosphate (cGMP).69 Increased cGMP levels are accompanied by decreased intracellular calcium and the concomitant relaxation of vascular smooth muscle. Exogenous, or inhaled nitric oxide (iNO) enters the alveoli, and diffuses across the alveolar–capillary membrane to the pulmonary smooth muscle cells, which results in vasodilation. iNO has a high affinity for hemoglobin, where it is bound and deactivated. iNO has a very short half-life (3 to 5 seconds) and is considered a selective pulmonary vasodilator; thus, the vasodilatory effects are limited to ventilated lung regions, thereby minimizing effects on systemic circulation.70–72 The physiologic effects of iNO with pulmonary hypertension are multifactorial, and response often depends on the underlying cause of pulmonary hypertension. In neonates with pulmonary hypertension, iNO can reverse hypoxic vasoconstriction by improving the balance of ventilation and perfusion (V̇/Q̇) matching. By decreasing

pulmonary vascular resistance (PVR), pulmonary blood flow is increased to ventilated lung areas. A reduction in PVR, and improved V̇/Q̇ matching, decreases the amount of intrapulmonary shunt and intracardiac shunting through the ductus arteriosus and/or the foramen ovale.73,74 Physiologic responses to iNO typically occur within minutes after initiation of therapy, and manifest as improvements in arterial gas exchange and hemodynamic stability.

Indications Although the only approved use of iNO is PPHN in the neonatal population, it has also been used in children with PARDS, congenital heart disease, and certain offlabel uses.

Persistent Pulmonary Hypertension of the Newborn Persistent pulmonary hypertension of the newborn (PPHN) is characterized by the failure of the pulmonary circulation to transition normally following birth, which results in pulmonary hypertension. Intracardiac right-to-left shunting of blood across the foramen ovale and ductus arteriosus results in hypoxemia. Disorders that delay the normal relaxation of the pulmonary bed may be primary (e.g., idiopathic) or secondary conditions such as congenital diaphragmatic hernia, meconium aspiration syndrome (MAS), and respiratory distress syndrome (RDS).75 Methods of optimizing lung expansion including increased mean airway pressure, high-frequency ventilation, and surfactant should be employed prior to initiating iNO. iNO has only been approved by the U.S. Food and Drug Administration (FDA) for therapy in term and near-term neonates (> 34 wk) with hypoxic respiratory failure associated with PPHN and/or echocardiographic diagnosis of pulmonary hypertension.76,77 Multiple studies have demonstrated that iNO improves oxygenation, and reduces the need for extracorporeal membrane oxygenation (ECMO); however, none have shown a decrease in mortality.76–78 It should be noted that approximately 40% of neonates with PPHN do not respond, or sustain a limited response to iNO. If oxygenation and hemodynamic parameters do not improve despite these interventions, extracorporeal membrane oxygenation should be considered.79

Off-Label Use

Multiple randomized and quasi-randomized control trials have evaluated the efficacy and safety of iNO therapy in term or near-term newborns with hypoxic respiratory failure. Current evidence suggests it is safe and reasonable to give these infants a trial of iNO, with the exclusion of congenital diaphragmatic hernia.80 The available evidence does not support the routine or rescue use of iNO in premature infants < 34 weeks gestational age, and some reports suggest deleterious neurologic consequences.81 Despite potential adverse outcomes and recommendations against using iNO therapy in infants < 34 weeks gestational age, off-label use has increased and accounts for nearly half of all iNO use in the United States.82–84

ARDS Numerous trials have investigated strategies for improving oxygenation and outcomes in pediatric ARDS (aka PARDS). Despite the extensive adoption of lungprotective ventilation strategies, the mortality in PARDS ranges from 22% to 35%.24,33,85 The basis of delivering iNO to patients with ARDS is to reduce intrapulmonary shunting and pulmonary hypertension by diverting pulmonary blood flow to better-ventilated areas of the lung. In adult ARDS, iNO has been shown to improve oxygenation for 1 to 3 days; however, these results were not sustained and did not have a beneficial impact on outcomes (e.g., duration of ventilation or mortality).86 Similarly, pediatric trials demonstrated only transient improvement in oxygenation; however, these studies did not evaluate if iNO had impacted outcomes in PARDS.87,88 Bronicki et al. found that iNO decreased the duration of mechanical ventilation in pediatric patients with ARDS, which resulted in a greater rate of survival without ECMO.89 In contrast, a large meta-analysis found no beneficial effects of iNO on mortality in adult or pediatric ARDS, regardless of the degree of hypoxemia. The routine use of iNO for acute hypoxic respiratory failure in ARDS is not recommended.90,91 Considering that most patients with ARDS demonstrate a short-lived response to iNO, this therapy should be reserved for bridging moribund patients to alternative ventilator strategies or ECMO.21

Congenital Heart Disease Therapeutic benefits of using iNO have been reported during the perioperative management of infants and children with pulmonary hypertension and hypoxia

associated with congenital heart disease. Preoperatively, iNO is often used in the cardiac catheterization lab for assessment of pulmonary vascular resistance (PVR) and delineation of the operative plan and corrective surgery.92–94 In adults, pulmonary hypertension has been defined as a mean pulmonary artery pressure (PAP) of ≥ 25 mmHg, a pulmonary artery wedge pressure of ≤ 15 mmHg, and an indexed pulmonary vascular resistance of > 3 Woods units.95,96 In children with congenital heart disease, perioperative pulmonary hypertension is related to anatomic substrates that are not seen in adults, rendering these criteria less applicable. Clinically, pulmonary hypertension is often described as the ratio of systolic PAP, relative to systolic systemic artery blood pressure (e.g., greater than half of the systemic blood pressure).97 When the mean PAP acutely exceeds the mean systolic arterial pressure, this is referred to as a pulmonary hypertensive crisis. Congenital heart disease is responsible for about 50% of pulmonary hypertension cases in children, and the postoperative incidence of severe pulmonary hypertension has been reported at 2% to 5%.98–100 The use of cardiopulmonary bypass during surgical repair has been associated with pulmonary vascular damage, and the impairment of endothelial function resulting in the transient loss of NO production, manifesting in pulmonary hypertension.101 The rationale for using iNO in infants and children with congenital heart disease is to decrease PAP and PVR, with the goal of improving right ventricular function and subsequently cardiac output.102,103 Postoperative risk of pulmonary hypertension can be assessed based on the type of cardiac lesion, and then categorized into four causative mechanisms: increased PVR, increased pulmonary blood flow, combined increased pulmonary blood flow and PVR, and increased pulmonary venous pressure.104 Pulmonary hypertension is associated with high mortality and poor clinical outcomes; however, given the relatively small patient population, it remains difficult to conduct large randomized control trials. As a result, most of the evidence for using iNO in cardiac surgery stems from small, observational, single-center randomized trials, and very few multicenter trials. Several studies have identified hemodynamic improvement with iNO following the bidirectional Glenn and Fontan operations; however, clinical benefits have been variable.105–107 A systematic review by Bizarro and colleagues concluded that routine iNO administration in the postoperative period did not show

any significant benefit to treat pulmonary hypertension in children with congenital heart disease.108 These authors found it difficult to ascertain valid conclusions based on methodological quality, sample size, bias, and heterogeneity of the four studies included within the review.108 Despite the lack of FDA approval for this indication, the use of iNO to mitigate the effects of pulmonary vascular reactivity and postoperative pulmonary hypertension in patients with congenital heart disease is relatively frequent, and has become the standard of care in many centers for patients with suspected or documented pulmonary hypertension. iNO is contraindicated in infants who are dependent on right-to-left ductal shunt (e.g., unrepaired hypoplastic left heart syndrome or interrupted aortic arch), as lowering PVR may result in pulmonary overcirculation and decreased systemic perfusion. Further, iNO should be used cautiously with left ventricular dysfunction or obstructed total anomalous pulmonary venous return, since increasing pulmonary blood flow in this scenario may result in pulmonary edema formation and may not improve cardiac output.109,110 Initial iNO doses between 2 to 80 parts per million (ppm) have been studied; however, most randomized clinical trials support 20 ppm as a routine starting dose.79,80,111 Increased iNO doses above 40 ppm have not demonstrated improved oxygenation in subjects who have failed to respond at 20 ppm, and sustained treatment at 40 to 80 ppm have been associated with adverse effects.112 A short trial of iNO is recommended (e.g., 30 minutes) to evaluate improvement of oxygenation and/or hemodynamic parameters. If a considerable clinical improvement is demonstrated, a stepwise reduction in iNO dose is typically used for titration down to the lowest dose, which maintains that response. If no response is observed, then iNO should be titrated down and discontinued quickly.111

Weaning After clinical benefit and stability has been demonstrated, then a weaning strategy must be determined to minimize both expense and potential side effects. Typically, iNO is weaned by a series of stepwise dose reductions (e.g., decrease dose: 20 to 10 to 5 to 2.5 to 1 ppm, then off). Weaning protocols vary considerably from duration of treatment, dose reductions, time between iNO decreases, and adjuncts (e.g., increasing FIO2 or medications) to facilitate discontinuation. Waiting 4 hours in

between weaning steps has been reported as a safe duration of iNO titration.77,113 Allowing transient increases in FIO2 during the discontinuation of iNO from 1 ppm has also been reported as an adjunct to weaning. In neonates with congenital heart disease who had previously failed weaning of iNO, sildenafil (Revatio, Viagra) has been shown to ameliorate rebound pulmonary hypertension.114,115

Limitations of Inhaled Nitric Oxide The primary disadvantages of iNO are the high cost and the complex delivery system required with this therapy.116–118 iNO has a very short half-life, which requires continuous administration and is not feasible for a patient who requires long-term therapy. It is very important to optimize alveolar recruitment during iNO administration, as poorly ventilated alveoli impede iNO from passing through the alveolar–capillary membrane, thus limiting the dilation effect. Synergistic improvements in oxygenation have been observed when iNO was combined with recruitment measures, increased PEEP, and high-frequency ventilation.119–123

Hazards/Complications Exposure to iNO may be complicated by rebound pulmonary hypertension upon discontinuation. Transient increases in pulmonary artery pressure and decreases in PaO2 have been observed shortly following discontinuation, and last approximately 30 minutes before a new steady state is achieved. The phenomenon of rebound is largely attributed to longer duration of therapy and a resultant downregulation of endogenous NO production. During this transitional period from 1 ppm to off, alternatives including sildenafil and increased FIO2 have demonstrated efficacy in preventing rebound after iNO withdrawal.114,124 High concentrations of NO are associated with potential toxic effects including methemogloblinemia, nitrogen dioxide (NO2) formation, and decreased platelet aggregation.125,126 Methemoglobin (MetHb) is formed when iNO binds with hemoglobin (Hb), which reduces the availability of Hb to transport O2, consequently decreasing systemic delivery. The main risk factors for the development of methemoglobinemia are concurrently using high concentrations of both iNO and FIO2. iNO doses > 20 ppm have been associated with increased MetHb formation, and the majority of clinical trials reported the maximum MetHb level peaking at

around 8 hours of therapy. It is suggested that initial MetHb levels be analyzed by co-oximetry 4 to 8 hours after start of therapy, and every 24 hours thereafter.77,79,111 MetHb concentrations in excess of 10% have been associated with cyanosis and hypoxia. However, levels exceeding the clinically accepted threshold of 5% are unlikely to occur if using iNO doses ≤ 20 ppm. MetHb levels ≤5% may be of little clinical significance and are often lower on followup measurement, regardless of intervention (e.g., discontinuation or dose reduction).127 The combination of O2 and NO forms a toxic byproduct NO2, which has been associated with airway damage and inflammation.128 NO2 production increases exponentially when high FIO2 and iNO concentrations are used simultaneously. The quantity of NO2 formed can also be influenced by the delivery system (e.g., selfinflating resuscitator) and the amount of time left for iNO to oxidize within the circuit (e.g., partial rebreathing anesthesia circuit).

Subambient Oxygen and Inhaled Carbon Dioxide Although not routinely practiced, the use of subambient oxygen concentrations and inhaled CO2 has been used in the past and is sometimes indicated in select neonatal and pediatric patients, particularly those with congenital heart disease. The pulmonary vasculature is sensitive to acidosis and hypoxia; both can be manipulated to increase pulmonary vascular resistance (PVR), thus limiting pulmonary blood flow. Based on these principles, inspired nitrogen and carbon dioxide promote potent pulmonary vasoconstriction, and have been used as perioperative management strategies in infants with single ventricle physiology to limit pulmonary blood flow. The use of inspired nitrogen (N2) to achieve oxygen dilution or subambient gas mixtures (14% to 20% FIO2) have been used to increase PVR by inducing hypoxic vasoconstriction.129,130 Inducing hypercarbia using supplemental inspired carbon dioxide (2% to 5% FICO2) has also been used to increase PVR and limit pulmonary blood flow in neonates with hypoplastic left heart syndrome.129,130 Small interventional studies used a randomized crossover design in neonates with single ventricle physiology to compare 17% inspired O2 vs. ~3% inspired CO2 was unchanged during hypoxia (N2), and increased during hypercarbia (inspired CO2).131 A second study by these authors employing similar treatment protocols found that

inspired CO2 improved cerebral oxygenation and mean arterial blood pressure, whereas hypoxic gas mixture (17% FIO2) did not have similar hemodynamic benefits.132 In the structurally normal heart, the pulmonary and systemic circuits are connected in series and managed by two pumps, the right and left ventricles. In patients with hypoplastic left heart syndrome, a single right ventricle manages cardiac output and the distribution of blood flow is parallel, divided between the systemic and pulmonary circuits. Preoperatively, one of the primary challenges in this patient population is maintaining a balance between pulmonary (Q̇p) and systemic blood flow (Q̇s). The distribution Q̇p:Q̇s is dependent upon the relative vascular resistances of both the pulmonary and systemic circulations. Patients with hypoplastic left heart syndrome are dependent on the patent ductus arteriosus to provide systemic perfusion. Following birth, PVR gradually decreases, with a concomitant increase in systemic vascular resistance (SVR). This decrease in PVR may result in too much pulmonary blood flow (overcirculation), at the expense of systemic perfusion. Decreased systemic perfusion results in decreased coronary artery perfusion, multisystem organ failure, metabolic acidosis, and eventually cardiopulmonary collapse.133 Medical management focuses on maintaining an adequate balance of Q̇p:Q̇s and maximizing ḊO2 to the tissues. Mechanical ventilation is generally avoided preoperatively with some exceptions, including apnea related to prostaglandin infusion, transport, or impending respiratory failure. Mechanical ventilation strategies typically employ low FIO2 (0.21 to 0.25), hypoventilation, and mild respiratory acidosis (e.g., CO2 45 to 55) to achieve pulmonary vasoconstriction and improve systemic perfusion Q̇s.134,135 When conventional strategies fail to limit high Q̇p:Q̇s, subambient oxygen or CO2 may be used as temporizing adjuncts in patients with hypoplastic left heart syndrome who are at risk for hemodynamic decompensation prior to surgery. While the use of both gases has been reported postoperatively, early surgical correction and placement of a restrictive shunt are the optimal means of controlling pulmonary blood flow.136,137 Usage of either adjunct is uncommon, and the decision to use subambient oxygen or supplemental CO2, depends largely on institutional preference. Patients receiving supplemental N2 or CO2, require cardiorespiratory monitoring,

capnography, and pulse oximetry. Blood gases should be followed to access pH, PaO2, mixed venous O2, CO2, and lactate. During subambient oxygen delivery it is imperative to set the alarms on the O2 analyzer for a tight range to avoid potential disastrous swings in Q̇p:Q̇s resulting from a delivery error. If no beneficial changes in hemodynamics are noted (e.g., improved cardiac output), hypoxic gas administration should be discontinued. Patients receiving supplemental CO2 must be monitored closely via capnography to ensure appropriate fraction of inspired CO2 (FICO2) is delivered. Both subambient oxygen delivery and inspired CO2 are temporizing measures used on a short-term basis to limit overcirculation in the preoperative period. The efficacy of either therapy is supported by limited evidence, and some controversy exists about the long-term effects and impact on cerebral blood flow.138–140 Using inspired CO2 to induce vasoconstriction requires the patient to be intubated, sedated, and paralyzed to avoid stimulation of the patient’s respiratory drive. Furthermore, a compensatory metabolic alkalosis will develop over time in response to exogenous CO2 supplementation.

Anesthetic Gas Mixtures Many asthmatics can be effectively managed with conventional therapies including bronchodilators and corticosteroids or adjuvants such as terbutaline, magnesium sulfate, and heliox. However, between 10% to 30% of those with acute, severe asthma exacerbation may require intubation and mechanical ventilation and this subset of patients can be very challenging to manage safely.141 Volatile anesthetics such as isoflurane (Forane), halothane (Fluothane), and sevoflurane (Ultane) have been used as rescue therapy for children and adults with life-threatening status asthmaticus. These anesthetic agents are thought to produce bronchodilation through stimulation of beta-adrenergic receptors and subsequent increases in cyclic adenosine monophosphate concentration, which results in direct bronchial smooth muscle dilating effect.142 The use of volatile anesthetics has been primarily reported in case series as a treatment option for status asthmaticus; there have been no randomized control studies to compare the efficacy between agents, outcomes, safety, or optimal timing of initiation. Isoflurane is generally used in the PICU setting,

based upon its safety profile compared with other volatile anesthetic agents. The existing studies suggest that delivering isoflurane to intubated asthmatics improved pH and PCO2, lowered peak inspiratory pressure requirements, and rendered little to no renal toxicity.143 In one of the largest retrospective studies, isoflurane was found to improve pH and PaCO2 clearance within 4 hours in a series of patients with severe bronchospasm. This review described hypotension, arrhythmias, and temporary neurologic changes as the most common side effects.144

Delivery Basic anesthesia delivery machines have two gas sources: a pipeline supply and a compressed gas cylinder supply. These gases are typically oxygen, air, and/or nitrous oxide (N2O).145 A central piping system from bulk storage is a hospital’s main supply for anesthesia machines usually at 50 to 55 psi through Diameter Index Safety System fittings. Compressed gas cylinders are reserved for emergency use in the event of central pipeline system failure. Fresh gases enter the ventilator’s internal pipeline and travel to the vaporizer where the anesthetic agent is mixed with the fresh gas. It then leaves through a low-pressure system via the common gas outlet and enters the breathing circuit. Exhaled gases travel to a reservoir bag and exit into the scavenging system where waste gases are removed. Anesthesia machines have vaporizers that are specifically labeled, color coded, and calibrated for a specific anesthetic agent. Included on a standard vaporizer is a filling level sight glass to allow the operator to monitor the amount of liquid agent remaining during delivery, a control dial with numerical markers measured in volume percentage for agent titration, and a filling container to pour the liquid agent into. Isoflurane dose is incrementally increased to attain an exhaled concentration between 0.5% to 1.5% and clinical or laboratory improvement has been observed.146,147 A sample line placed into the inspiratory limb during agent delivery allows the clinician to monitor FIO2, minimum alveolar concentration, FICO2, agent volume percentage, and ETCO2. As a reference point, minimum alveolar concentration is based upon the alveolar concentration of an inhaled anesthetic in which 50% of patients will no longer respond to painful or surgical stimuli.

Complications

Hypotension is the most commonly reported side effect of anesthetic gas delivery, but this can be managed with vasoactive medications and fluid boluses.143,144 Although rare, malignant hyperthermia is a disorder brought upon by an excess of calcium release by the body’s skeletal muscles, associated with volatile anesthesia delivery.148 Patients experiencing malignant hyperthermia will be in a hypermetabolic state as a result of increased oxygen consumption and anaerobic metabolism and may experience tachycardia, respiratory acidosis, and hyperthermia.149 Clinically, one of the earliest signs of malignant hyperthermia is a sudden rise in ETCO2. All patients being treated with anesthetic gases should have their temperature constantly monitored as part of malignant hyperthermia surveillance. In cases of malignant hyperthermia, the initial response would be to shut off the vaporizer and disconnect the patient from the breathing circuit and manually ventilate with 100% oxygen. The sole treatment of malignant hyperthermia is dantrolene sodium (Dantrium), which should be readily available as a safety precaution. Isoflurane administration in the intensive care unit poses many logistical issues, primarily those in which clinicians assume responsibility for filling the vaporizer, titration, and anesthetic delivery? The geographic location may limit respiratory therapists’ scope of practice and license to manage anesthetic delivery under the direction of a physician. The lack of clinical practice guidelines, combined with infrequent use of this therapy in the ICU, warrants developing a comprehensive infrastructure in which roles and responsibilities are clearly defined. Furthermore, volatile anesthetics should be used with caution in the ICU, and under the support and guidance of anesthesiologists. Clinicians handling volatile anesthetics must employ precautions to protect themselves and their patients. Many hazards are associated with anesthetic gas delivery that can result in operator and/or patient decompensation. As far as operator exposure is concerned, volatile liquid spills can be harmful in poorly ventilated workplace environments. Spills must be well contained and covered with towels or other absorbents immediately, and the area must be evacuated until properly trained personnel can clean up the spill.145 Equally important, operators must be knowledgeable of the signs, symptoms, and associated complications of anesthesia delivery. The delivery of anesthetics in the context of children with life-threatening asthma

remains somewhat controversial. Considering the rarity of use, potential complications, and cost, it is imperative to develop institutional systems for medication delivery, respective responsibilities, and staff education. Further, a retrospective cohort demonstrated increased length of stay, mechanical ventilation duration, and hospital charges for children treated at centers using volatile anesthetics for severe asthma when compared with centers that did not offer volatile anesthetics. There was no statistical difference in mortality between center types.150

Extracorporeal Membrane Oxygenation Advanced life support typically consists of mechanical ventilation, inotropes, dialysis, and a host of other treatments to support the critically ill while their disease or condition improves. When conventional therapies fail, interventions including highfrequency ventilation, inhaled nitric oxide, and extracorporeal membrane oxygenation (ECMO) are considered. ECMO is an invasive technique in which blood is drained from the venous system, mechanically pumped through an artificial lung (membrane oxygenator), and reinfused to the patient through either the pulmonary or systemic circulation. The primary objectives of ECMO are to support organ function in patients with respiratory or cardiac failure in order to provide time for the disease process to reverse or to further evaluate the underlying condition and determine if medical or surgical treatment options are available.151 ECMO was originally derived using components of cardiopulmonary bypass equipment. The first successful ECMO case was reported in 1972 on an adult with severe respiratory failure.152 During this time period, ECMO was considered a last ditch effort, and perhaps not surprisingly, survival outcomes from early reports were discouraging.153 As a result, much advancement in technology, strategy, and management has been made over the years. Since, it has been used successfully to support infants, children, and adults with life-threatening cardiorespiratory failure that is refractory to conventional treatment.154–156 ECMO circuits have evolved considerably over the past 30 years, with advancements in accessibility, safety, circuit composition, and size. There are two primary modes of ECMO support, venoarterial (VA) and venovenous (VV). Both modalities employ the same basic circuitry consisting of contiguous polyvinylchloride tubing, a pump, and an artificial lung or membrane oxygenator. Additional components include drainage and reinfusion cannulas, pressure monitoring, arterial bubble detector, ports for blood sampling, gas flow meters, and devices to control temperature. Deoxygenated blood is drained from the venous system via vascular cannula and proceeds to the mechanical pump (roller head or centrifugal), where it is propelled through a membrane oxygenator. As the blood traverses the oxygenator, carbon dioxide is removed, and oxygen is titrated in to effectively achieve gas exchange. Oxygenated blood is then adjusted to the desired temperature and leaves the membrane returning to the patient via a reinfusion cannula. The fundamental

difference in physiologic support (VA or VV) is determined by the location of the vascular cannula through which blood is returned to the body (Figure 15-9).

FIGURE 15-9 Schematic of ECMO. (A) Venovenous ECMO, for pulmonary support. (B) Venoarterial ECMO, for

cardiopulmonary support, and respective patient circulations. Reproduced from Lin JC. Extracorporeal membrane oxygenation for severe pediatric respiratory failure. Respir Care. 2017;62(6):732–750.

Description Venoarterial (VA)-ECMO is the most predominant form, indicated for patients with cardiorespiratory failure as it provides both gas exchange and circulatory support while bypassing the heart and lungs. This is accomplished by draining blood from a venous source, and reinfusing into the arterial circulation (Figure 15-9B).158 In neonates and infants, the drainage cannula is surgically inserted into the right internal jugular vein, and the arterial cannula is placed in the right common carotid artery.159 Alternately, VA-ECMO can be established in larger children using a peripheral cannulation technique (femoral vein and artery) or a transthoracic approach where cannulas are placed directly into the heart (right atrium and aorta), which is a common configuration in postoperative cardiac surgery patients.160 Venovenous (VV)-ECMO is utilized in the setting of respiratory failure with acceptable cardiac function. The aims of VV-ECMO include removing CO2, subsequently raising the oxygen content of blood returning to the right atrium, thereby allowing lung-protective strategies to be continued. In this configuration, blood is drained and returned to the venous circulation at the same rate, bypassing the lungs and providing pulmonary support (Figure 15-9A). Double-lumen venous cannulas have historically been employed to provide VV support for neonates and small children. Older children and adults were primarily cannulated using two separate cannulas; for example, drainage was accomplished using a femoral vein, and then reinfused into the right internal jugular vein. Technological advancement in VV cannulas led to a new bicaval cannula with improved blood flow profiles and less recirculation, a phenomenon that occurs when oxygenated blood is syphoned into the drainage cannula, thereby reducing the efficiency of gas exchange between the circuit and patient. This type of cannula drains from both the superior and inferior vena cava, and reinfuses through a separate channel within the cannula, directing oxygenated blood toward the tricuspid valve (Figure 15-10).161 These cannulas have several advantages, including single site insertion, the use of less sedation, and the ability for older patients to undergo rehabilitation while on ECMO.162

FIGURE 15-10 Illustration of an ECMO Cannula Inserted in a Pediatric Patient. Two drainage areas—one situated in the superior vena cava and the other in the inferior vena cava—return venous blood (blue) to the pump. The inner lumen or reinfusion (red arrow) is oriented so that arterialized blood is directed toward the tricuspid valve and right atrium.

A detailed discussion with regard to cannulation strategy, types of cannulas, and other technical issues is outside the scope of this chapter. However, a few major benefits and limitations of VA-compared with VV-ECMO should be understood. The

benefits of VA include increased control over both gas exchange and hemodynamics; however, this comes with a greater risk for thromboembolic events and likelihood of central nervous system injury. In contrast, VV-ECMO provides only pulmonary support, and the lungs act as a filter to microemboli that may have directly entered the systemic circulation on VA-ECMO.

Indications Indications for ECMO include respiratory failure refractory to conventional treatment and certain cardiac applications to optimize hemodynamics and systemic oxygen delivery.

Respiratory Failure The majority of evidence supporting the efficacy of ECMO originally stemmed from randomized control trials in neonates with respiratory failure. This group generally includes diagnoses of persistent pulmonary hypertension of the newborn, meconium aspiration syndrome, respiratory distress syndrome, sepsis, and air-leak syndromes. The results of these trials were summarized in a Cochrane review, in which the authors concluded that ECMO use in mature neonates with potential reversible respiratory failure significantly improved survival.164 In contrast, infants with congenital diaphragmatic hernia often require ECMO as a result of severe lung hypoplasia and pulmonary hypertension, which may not always be reversible. The diagnosis of congenital heart disease is associated with prolonged ECMO courses, and survival following ECMO is stagnant around 50%.165 The oxygenation index (OI) is a calculation that incorporates mean airway pressure (Paw), FIO2, and arterial oxygenation (PaO2) where: [OI = Paw × (FIO2/PaO2) × 100] has been the most widely accepted metric. Ortega et al. found that when the OI exceeded 40 during conventional mechanical ventilation, the risk of mortality exceeded 80%.166 These results have been repeatedly demonstrated, and OI remains a widely accepted predictor of mortality in neonates and children with respiratory failure. As such, monitoring hemodynamic stability, the trajectory of illness, and indicators such as the OI, Pediatric Risk of Mortality [PRISM] score,

PaO2/FIO2 ratio, and pH may aid the decision process for using ECMO.167 In an analysis of newborns receiving mechanical ventilation, Bayrakci et al. determined an OI of 33.2 was a suitable threshold for ECMO utilization.167 Additionally, these authors identified greater risk of chronic lung disease when OI ≥ 40 and ECMO was not used, which suggests a benefit to earlier deployment. Absolute contraindications to ECMO are sparse, with lethal chromosomal abnormalities, irreversible brain injury, and low gestational age being major factors. Relative contraindications include moderate intraventricular hemorrhage, bleeding disorders, and certain types of congenital heart disease (particularly if in conjunction with a congenital heart disease diagnosis).168 Unlike the neonatal experience, pediatric ECMO lacks randomized control trials and consists of a more heterogeneous assortment of disease processes, including infectious or aspiration pneumonias, septic shock, and ARDS associated with trauma, surgery, or complex medical conditions. Additionally, VV-ECMO has been used for extended periods as a bridge to lung transplantation.162 Despite the lack of randomized control trials in children, ECMO utilization and the related body of literature has grown exponentially. ECMO has evolved from being a last resort to an accepted standard of care for pediatric patients failing lung-protective ventilation strategies.169 In the early ECMO epoch, indications for support were strictly limited to reversible respiratory failure, since utilization patterns and indications for ECMO have continued to expand while contraindications have become less clear. Prior to the adoption of protective lung ventilation strategies, respiratory failure patients requiring mechanical ventilation for > 7 days were not considered “ECMO candidates” based upon lower survival rates and the potential for irreversible lung injury. While there is a distinct relationship between ventilator duration prior to ECMO and reduced survival, a review by Domico et al. demonstrated no statistically significant decrease in survival until > 14 days of pre-ECMO mechanical ventilation was reached, regardless of underlying diagnosis.170 The paucity of evidence-based selection criteria for determining ECMO candidacy, or exclusion, means clinicians must compare outcomes data from available observational trials and Extracorporeal Life Support Organization (ELSO) datasets. The Pediatric Acute Lung Injury Consensus Conference Group has provided

recommendations for using ECMO in the setting of severe pediatric ARDS. This group recommended ECMO should be considered if the underlying disease process has a high likelihood of being reversed. Additionally, there was strong agreement that it is not possible to apply strict inclusion criteria for ECMO candidacy. Further, ECMO should be considered when lung-protective strategies cannot resolve deficiencies in gas exchange. To facilitate inclusion, serial structured evaluations including case history should be used to determine candidacy for ECMO. Clinicians should also consider the likelihood of benefit: long-term outcomes in relation to comorbidities, quality of life, and potential financial burdens. While definitive criteria on when ECMO should be initiated in pediatric respiratory failure are not universal, early implementation is increasing in attempts to minimize lung injury and multisystem organ failure.171

Cardiac Applications ECMO is an integral component in the perioperative management of infants and children undergoing complex heart surgeries related to congenital heart disease. Cardiac ECMO applications can be parsed into two categories based upon the presence or absence of congenital heart disease. The most common postoperative indications include failure to separate from cardiopulmonary bypass, low cardiac output syndrome, and the rapid deployment of ECMO as an adjunct to cardiopulmonary resuscitation (aka ECPR). Additionally, children with medical conditions including myocarditis, cardiomyopathy, shock, intractable arrhythmias, and pulmonary hypertension have been effectively supported with ECMO.168 ECMO and ventricular assist devices can also be used to provide circulatory support in patients who are awaiting heart transplantation. The primary goals of cardiac ECMO are to optimize hemodynamics and systemic oxygen delivery and mitigate end-organ dysfunction. For these reasons, VA-ECMO is the predominant mode of support in pediatric cardiac patients’ refractory to conventional management strategies.172 Similar to the respiratory failure cohort, careful patient selection and timely ECMO initiation before the manifestation of endorgan dysfunction or circulatory collapse is paramount to avoid increased morbidity and mortality.168

Complications ECMO is a lifesaving therapy that is employed when conventional medical management fails; however, infants and children who are supported with ECMO require significant clinical resources and account for considerable financial burdens. Patients managed with ECMO require intensive care, systemic anticoagulation, frequent laboratory sampling, and neurologic imaging. Additionally, considerable amounts of blood products are administered to account for complications from bleeding and maintain the function of the ECMO circuit. Further, given the complexity of managing the ECMO circuit and its components, a dedicated ECMO specialist and a minimum of one nurse are required at the bedside. Moreover, the median inpatient cost for ECMO exceeds $500,000/per survivor, making it nearly twice as costly as other intensive therapies such as pediatric bone marrow and liver transplantation.173

Patient Transport Intrahospital transport refers to the movement of critically ill patients from the ICU to another location for diagnostic studies and procedures in the catheterization lab or operating room. Despite the potential benefits of transports, there are inherent risks that must be identified and mitigated through diligent planning to ensure patient safety. Patient safety during intrahospital transport has not been well described in the pediatric literature as most literature in this context focused on adults.174 Infants and children often present to the nearest clinic or emergency department for initial assessments and stabilization. If specialized services or an advanced level of care is warranted, interhospital transport to a tertiary pediatric hospital is arranged. In the United States, over 200,000 infants and children are transported from community or regional hospitals for specialized neonatal or pediatric care annually.175 Current guidelines suggest transferring critically ill children to level I PICUs; however, objective criteria to identify which children may benefit most, and when transport should occur, remain elusive. Respiratory failure and sepsis are the most common reasons for interhospital transfer as specific treatment modalities including vasopressors, high-frequency ventilation, iNO, and ECMO may be required. Other common reasons for interhospital transfer include congenital heart disease, brain injury, bronchiolitis, asthma, renal failure, and cancer.176 Transport to the accepting medical center is facilitated by hospital, community, or emergency medical services (EMS)-based transport teams, or by a combination of these systems. While the decision-making process insofar as triage, logistics, and mode of transportation are outside the scope of this chapter, it is important to differentiate that fewer resources are available for transporting critically ill children compared with their adult counterparts. For example, nonspecialized teams may be more readily available; however, these lack extensive pediatric experience or training. In contrast, pediatric critical care transport teams are less common, but specialize in transporting only children and have extensive training and experience. Evidence supports the utilization of specialized pediatric transport teams when available, as markedly lower mortality and risk of adverse events has been demonstrated compared with nonspecialized teams.177,178 There are no mandatory federal accreditation requirements for transport programs, although state or regional accreditation may apply, which leaves many

aspects of team composition and functionality to the discretion of each institution. Pediatric critical care transport teams are essentially an extension of the ICU and typically consist of nurses, respiratory therapists, doctors, and paramedics. Team composition varies considerably between institutions, and is affected by perceived patient needs, available resources (e.g., unit based vs. dedicated teams), transport volume, and mode.179 The overall focus is the timely initiation of advanced therapies to stabilize the patient and taking preemptive measures to ensure life-threatening events are minimized in transit.180 It is generally prudent to optimize stabilization prior to transport as clinical interventions are more difficult to perform in transit, and may present additional risks.

Adverse Events Adverse events have been associated with any type of transport and can be parsed into risk factors relating to the patient, transport organization, technical or human error, and collective factors. The physiologic impact of transport affects the patient via two primary mechanisms, movement and environmental variations.181 Acceleration, deceleration, vibration, and positional changes are common, and magnified when transport occurs in ambulances, helicopters, or other aircraft. Additionally, once removed from the protective and controlled intensive care unit environment, patients are increasingly more vulnerable to adverse events. While many transports are uneventful, the occurrence of serious adverse events has been reported between 5% to 20%.177,182 Literature in this area is limited and varies considerably in terms of how these events are categorized and reported. Further, it is difficult to separate causal linkages between adverse events, and if the physiological changes are related to the transport or the underlying instability and pathology of the patient. In a large retrospective review, Singh et al. described the incidence of transport-related events occurring in one of eight children—with hypotension, tachycardia, and bradycardia being the most common. Moreover, these authors identified age, pretransport mechanical ventilation, cardiovascular instability, transport duration, crew levels, and scene calls were independently associated with risk of in-transit-related events.183

Mechanical Ventilation during Transport

In the early transport epoch, manual ventilation was commonly employed given the limitations and performance of the available transport ventilators. It is important to note that manual ventilation introduces considerable variability in airway pressures, which may have a clinically significant impact on gas exchange, and contribute to lung injury and hemodynamic compromise. Moreover, it is recommended that routine manual ventilation be avoided and reserved for ventilator failure or emergency use.58 Fortunately, technologic advances in portable ventilators have provided clinicians with more viable options for transport. High-performance transport ventilators with the capability of delivering smaller tidal volumes, multiple modes, advanced monitoring, and appropriate trigger sensitivity should be used in critically ill children. Additionally, the functions, monitoring, and alarms of the ventilator should be adapted based upon the patient condition and underlying physiology.184 Further, continuous capnography is recommended in all mechanically ventilated children during transport.185

Safety Implications A systematic approach for stabilizing the child prior to transport is prudent. Roles and responsibilities of team members should be clearly delineated and a plan for any anticipated complications established. Review of the patient’s history, physical exam, and trajectory are considered to determine which interventions or procedures may improve outcomes and should be completed prior to transport and which should be postponed as not to delay transfer and more definitive care. Many institutions have developed checklists identifying essential staff, equipment, medications, monitoring, and patient-specific physiologic targets.186

Key Points Infants born before 37 weeks of gestation are premature or preterm. Infants born at 37 or 38 weeks are sometimes considered early term; infants born after 42 weeks are considered post-term. As the fetal lung matures, surfactant begins to be secreted by type II alveolar cells beginning at about 20 weeks of gestation; mature surfactant does not appear until about week 35. The Dubowitz and new Ballard scoring systems provide methods to determine newborn gestational age. Respiratory distress syndrome of the neonate is caused by inadequate surfactant production associated with gestational age < 37 weeks. Signs of respiratory distress in children include tachypnea, nasal flaring, retractions, grunting, paradoxical chest movement, and head bobbing. Common neonatal respiratory conditions include respiratory distress syndrome (RDS), transient tachypnea of the newborn (TTN), and meconium aspiration syndrome (MAS). There are many types of cyanotic congenital heart disease, including coarctation of the aorta, Ebstein’s anomaly, hypoplastic left heart syndrome, pulmonary atresia, tetralogy of Fallot, transposition of the great vessels, tricuspid atresia, and truncus arteriosus. Acyanotic congenital heart disease includes atrial septal defect, aortic stenosis, patent ductus arteriosus, and ventricular septal defect. Bronchopulmonary dysplasia is a chronic lung condition associated with prematurity. Apnea of prematurity is defined as a spontaneous cessation of breathing for a period ≥ 20 seconds. Retinopathy of prematurity is associated with excessive oxygen therapy in neonates. Pediatric ARDS is similar to adult ARDS; however, the criteria have been modified to account for differences between adults and children. Approximately 60% of children with asthma have at least one exacerbation per year. Neuromuscular disorders sometimes seen in children include Duchenne muscular dystrophy, spinal muscular atrophy, myasthenia gravis, Guillain-Barré syndrome, and botulism. Bronchiolitis is the most common cause of hospitalization for children younger than 2 years old. Cystic fibrosis is a genetic exocrine gland disorder that causes excessive lung secretions, repeated pulmonary infections, pancreatic enzyme insufficiency, and other symptoms. High-flow nasal cannula oxygen therapy is a rapidly expanding modality for

infants and children in respiratory distress. Nasal intermittent positive-pressure ventilation (NIPPV) has been increasingly used in infants as a method of augmenting the beneficial effects of nasal CPAP. Conventional mechanical ventilation in neonatal and pediatric settings includes pressure-control and volume-targeted modes of ventilation. High-frequency jet ventilation and high-frequency oscillatory ventilation have been used often in neonates. Nitric oxide (NO) has been used to treat persistent pulmonary hypertension of the newborn. Volatile anesthetics have been used as rescue therapy for children with lifethreatening status asthmaticus. Extracorporeal membrane oxygenation (ECMO) may improve survival in neonates with certain types of severe respiratory failure. Interhospital transport of neonatal and pediatric patients should be performed by a trained transport team that includes nurses, physicians, and respiratory therapists.

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CHAPTER

16 Ventilator Discontinuance Kevin Proud, David Shelledy, and Jay Peters

© Anna RubaK/ShutterStock, Inc.

OUTLINE Introduction Ventilator Discontinuation Factors That Contribute to Ventilator Dependence Ventilatory Capacity Versus Ventilatory Requirements Patient Evaluation Reversal or Improvement of Disease or Condition Assessment of Oxygenation Assessment of Ventilation and Acid-Base Balance Assessment of Cardiovascular and Hemodynamic Status Assessment of Medical Condition Assessment of the Airway Weaning Indices Methods IMV/SIMV Pressure-Support Ventilation Spontaneous Breathing Trials Newer Methods Selection and Approach Monitoring Extubation Monitoring Following Extubation Management of Postextubation Upper Airway Obstruction Extubation Failure Long-Term Ventilator Dependence Terminal Weaning

OBJECTIVES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Explain why mechanical ventilation should be discontinued as quickly and safely as possible. Contrast the risks of mechanical ventilation with the risks of premature ventilator discontinuation. Explain the primary criterion for discontinuing ventilatory support. Contrast the terms ventilator discontinuance and ventilator weaning. Describe factors that contribute to ventilator dependence. Explain the balance between ventilatory capacity and ventilatory requirements with respect to the patient’s ability to spontaneously breathe. Describe factors that may reduce ventilatory capacity or increase ventilatory requirements. Explain how to evaluate if there is sufficient patient improvement to warrant ventilator discontinuance. Evaluate a patient’s oxygenation, ventilation, acid-base balance, and cardiovascular/hemodynamics status. Describe measurement and use of the maximum inspiratory pressure (MIP), vital capacity (VC), and rapid shallow breathing index (RSBI). Describe assessment of the patient’s medical condition. Determine readiness for discontinuation of mechanical ventilation. Identify and discuss weaning parameters. Contrast different methods of weaning and discontinuation of mechanical ventilation. Explain the importance of airway assessment prior to extubation. Describe the “cuff-leak test” to include values associated with the development of stridor and laryngeal edema. Discuss causes and assessment of extubation failure. Contrast methods of discontinuing mechanical ventilation in the acute setting with ventilator liberation in chronically ventilated patients. Describe the role for long-term care facilities regarding chronic ventilator patients. Explain the rationale for terminal weaning.

KEY TERMS closed-loop ventilator modes cuff-leak test extubation failure liberation from mechanical ventilation long-term acute care (LTAC) maximum inspiratory pressure (PImax or MIP) maximum expiratory pressure (PEmax or MEP) negative inspiratory force (NIF) prolonged mechanical ventilation (PMV) rapid shallow breathing index (RSBI) respiratory drive (aka ventilatory drive) spontaneous breathing trial (SBT) stridor terminal weaning ventilatory capacity ventilator discontinuance ventilatory requirements ventilatory reserve vital capacity (VC) weaning weaning parameters or indices

Introduction Complications and hazards associated with mechanical ventilation include barotrauma (e.g., pneumothorax, pneumomediastinum, subcutaneous emphysema), airway injury, infection, ventilator-associated pneumonia, pulmonary embolus, gastrointestinal bleeding, and ventilatory muscle dysfunction. Catastrophic failure of the ventilator or artificial airway can cause life-threatening complications, including death. Because of the many risks and complications associated with mechanical ventilation, patients should have the ventilator discontinued as quickly and safely as possible. Once the underlying cause that led to mechanical ventilation has sufficiently improved, and the patient has adequate spontaneous breathing and gas exchange, liberation from the ventilator should occur. On the other hand, premature discontinuation of ventilatory support exposes the patient to additional risks including severe hypoxemia, acute hypercapnia and acidosis, ventilatory muscle fatigue, and increased cardiovascular stress. Premature discontinuation of the ventilator may require reinstitution of ventilatory support, further delaying the patient’s recovery. Patients who are prematurely extubated are also exposed to the risks associated with reintubation. Thus, careful patient evaluation is essential to successful ventilator discontinuance. The primary criterion for discontinuing ventilatory support is improvement or reversal of the disease state or condition that required the need for mechanical ventilation. Once the problem requiring mechanical ventilation is resolved, most patients can be quickly removed from the ventilator. Some patients may require a structured process of gradual discontinuation of ventilatory support sometimes referred to as ventilator weaning. In this chapter, we will discuss the process of discontinuing mechanical ventilation. A stepwise approach for determining readiness for extubation will be provided, starting with a general assessment of the patient’s overall condition and then focusing on specific respiratory parameters. Several methods of discontinuing mechanical ventilation will be discussed. The chapter will end with discussions regarding failed extubations, terminal extubation, and liberation from long-term mechanical ventilation. RC Insight

Liberation from mechanical ventilation is desirable as soon as the underlying cause has sufficiently improved and the patient is hemodynamically stable and able to maintain adequate spontaneous breathing and gas exchange.

Ventilator Discontinuation The process of discontinuing mechanical ventilation has undergone significant change over the last several decades and continues to evolve today. In the past, determining readiness for ventilator discontinuance and extubation was a variable and sometimes unstructured process. Today, while the process of discontinuing mechanical ventilation is far from perfect, there is more science to help guide the clinician to determine which patients may be successfully removed from the ventilator and what methods are most effective. For most patients, the process has evolved from a gradual decrease in mechanical support known as ventilator weaning to more abrupt spontaneous breathing trials (SBTs). With this evolution has come a change in the terminology employed. Although the terms ventilator weaning and ventilator discontinuance are commonly (and often interchangeably) used, the gradual reduction in ventilatory support provided may be best described as “weaning” the patient from ventilator. Most patients, however, do not require a gradual reduction in the level of ventilatory support provided, and the term ventilator weaning has become a misnomer. For more contemporary methods of somewhat abrupt discontinuation of ventilatory support (e.g., SBTs), the terms liberation from mechanical ventilation and discontinuation of mechanical ventilation are probably more appropriate. A gradual reduction in ventilatory support may be useful in difficult-to-wean patients and the term weaning is appropriate in these cases; more abrupt methods, however, are mislabeled when described as weaning. That said, both terms are in common use and we refer to both, while highlighting the distinction. For many patients, the process for ventilator discontinuance is rapid. For example, a patient requiring mechanical ventilation due to an opioid drug overdose can often be rapidly liberated from the ventilator as soon as the effects of the drug are reversed or the drug has been sufficiently metabolized. In a similar fashion, patients receiving mechanical ventilatory support following surgery and general anesthesia may be rapidly removed from the ventilator and extubated, once the anesthesia has worn off. Other patients may require a more systematic approach, incorporating careful evaluation and the use of SBTs; ventilator discontinuance can generally be achieved in these patients soon after resolution of the problem that precipitated the need for support. A small number of ventilator patients may require an extended period of ventilator

weaning, which may occur over a period of days or weeks. These patients may be weak, debilitated, and require long-term acute care. Finally, some patients are ventilator dependent and may require mechanical ventilation for an indefinite period; these patients are sometimes described as “unweanable.” RC Insight Patients who have been receiving mechanical ventilatory support for short periods of time (e.g., < 72 hours) can often be quickly removed from the ventilator when their primary problem has resolved.

Factors That Contribute to Ventilator Dependence Success with ventilator discontinuance is dependent on the patient’s oxygenation status, cardiovascular function, and the relationship between ventilatory requirements and ventilatory capacity. Oxygenation problems contributing to ventilator dependence include decreased ventilation/perfusion ratio (V̇/Q̇) (e.g., asthma, COPD), mild to moderate congestive heart failure, increased intrapulmonary shunt (e.g., atelectasis, pneumonia, ARDS), diffusion problems (e.g., interstitial lung disease), hypoventilation (resulting in decreased alveolar oxygen tension), and decreased oxygen delivery to the tissues (e.g., anemia, decreased cardiac output). Cardiovascular problems that may contribute to ventilator dependence include myocardial ischemia, myocardial infarction, arrhythmias, coronary artery disease, heart failure, hypotension, and hemodynamic instability. Neurologic problems that may contribute to ventilator dependence include an abnormal respiratory drive (e.g., decreased or absent drive to breathe or significantly increased drive to breathe), or problems with nerve transmission (e.g., neuromuscular disease, spinal cord injury, tetanus, botulism, neuromuscularblocking agents). Sedatives, narcotics, or brain injury may cause central nervous system (CNS) depression and reduced or absent ventilatory drive. Many intensive care unit (ICU) patients develop delirium, which is associated with increased length of mechanical ventilation, longer ICU stays, increased cost, long-term cognitive impairment, and increased mortality. Psychological factors that may contribute to ventilator dependence include fear and anxiety, confusion, altered mental status, and psychological depression. Poor nutritional status or multiple comorbid conditions may also delay ventilator discontinuance. Finally, inappropriate ventilator settings (e.g., improperly set trigger sensitivity, inadequate inspiratory flow) may contribute to patient–ventilator asynchrony and increased work of breathing. Optimization of factors that contribute to ventilator dependence should improve patient outcomes and success with ventilator discontinuance (Box 16-1).

BOX 16-1 Factors Contributing to Ventilator Dependence The following factors may contribute to ventilator dependence. ∎ Ventilatory requirements exceed ventilatory capacity

Ventilatory requirements may exceed ventilatory capacity due to: • Decreased ventilatory capacity ○ Ventilatory muscle fatigue, weakness, or dysfunction ○ Decreased or absent central respiratory drive to breathe ○ Disordered lung function (e.g., obstruction, bronchospasm, secretions, alveolar filling, atelectasis) • Increased ventilatory requirements or demand ○ Increased stimulus to breathe (acidosis, hypoxemia, lung receptor stimulation, pain, anxiety) ○ Increased ventilatory requirements (e.g., increased metabolic rate, increased CO2 production, [V̇CO2], increased physiologic dead space) ∎

Oxygenation problems Oxygenation problems may be due to: • Decreased V̇/Q̇ (i.e., V̇/Q̇ < 1.0 but > 0) • Increased shunt (i.e., V̇/Q̇ = 0) • Diffusion problems • Hypoventilation • Decreased tissue O2 delivery (↓ḊO2) due to decreased hemoglobin (Hb), decreased CaO2, or decreased cardiac output ∎

Cardiovascular problems Cardiovascular problems may be due to: • Myocardial ischemia • Myocardial infarction • Cardiac valvular disease • Arrhythmias • Coronary artery disease (CAD) • Heart failure (HF) • Hypotension • Hemodynamic instability ∎ Neurologic problems Neurologic problems affecting ventilation include: • Abnormal central respiratory drive (e.g., increased or decreased drive to breathe) • Decreased nerve transmission (e.g., tetanus, botulism, spinal cord injury, use of neuromuscular-blocking agents)

Delirium associated with increased duration of mechanical ventilation ∎ Psychological factors Psychological factors that may affect ventilation and ventilator discontinuance include: • Fear and anxiety • Confusion • Altered mental status • Psychological depression • CNS depression (e.g., depressant drugs, severe hypoxia) ∎ Poor nutritional status ∎ Multiple comorbidities ∎ Mechanical factors Mechanical factors that may affect ventilation include: • Inappropriate ventilator settings (tidal volume, mode, FIO2, positive endexpiratory pressure [PEEP]) • Ventilator circuits • Demand flow systems • Inadequate ventilator inspiratory flow rate setting • Inappropriate ventilator trigger sensitivity setting • Small diameter endotracheal tubes • Patient–ventilator asynchrony

•

Ventilatory Capacity Versus Ventilatory Requirements Ventilatory capacity refers to the amount of air that can be moved into and out of the lungs by the ventilatory pump, while ventilatory requirements refers to the volume of ventilation required to achieve adequate oxygenation and carbon dioxide removal. Put another way, ventilatory capacity is how much the patient can breathe while ventilatory requirements are the level of ventilation required to meet the patient’s needs. Normally, ventilatory capacity exceeds ventilatory requirements and the difference represents the patient’s ventilatory reserve. If ventilatory capacity is less than ventilatory requirements, no ventilatory reserve is present and mechanical ventilatory support may be required. Ventilatory capacity may be decreased due to reduced respiratory drive (e.g.,

sedative drugs, CNS problems), increased ventilatory workload (e.g., increased airway resistance, decreased compliance), or reduced ventilatory muscle strength (e.g., ventilatory muscle fatigue due to increased workload or neuromuscular disease). Box 16-2 summarizes causes of decreased ventilatory capacity sometimes seen in the ICU, which may impede liberation of the patient from the ventilator. Box 16-3 summarizes causes of increased ventilatory requirements or demand that may increase ventilatory workload, further stress the cardiopulmonary system, and impede liberation from the ventilator.

BOX 16-2 Causes of Decreased Ventilatory Capacity Problems or conditions that decrease ventilatory capacity may make it difficult or impossible for patients to breathe spontaneously at a level sufficient to support their physiologic needs. Common causes of decreased ventilatory capacity include decreased ventilatory drive and ventilatory muscle fatigue, dysfunction, or weakness. Decreased ventilatory capacity may be due to: Decreased or absent ventilatory drive (aka respiratory drive) ∎ Overventilation during mechanical ventilation (induced hypocapnia) ∎ Severe hypoxia (e.g., cerebral hypoxia) ∎ Metabolic or respiratory alkalosis ∎ Electrolyte disorders ∎ Acute, severe hypercapnia (PaCO > 75 to 80 mmHg; ↑ drive to breathe 2 followed by ↓ drive to breathe) ∎ Cardiopulmonary collapse (cardiac arrest, acute myocardial infarction [MI], shock, trauma) ∎ Neurologic disease (e.g., head trauma, major stroke, brainstem tumor, cerebral hemorrhage, meningitis, encephalitis, hepatic encephalopathy, brainstem ischemia, brain death) ∎ Hypothermia ∎ Poisoning (carbon monoxide poisoning, cyanide poisoning) ∎ CNS depressants (opioids, barbiturates, benzodiazepines, tricylic antidepressants) ∎ General anesthesia ∎ COPD patients with CO retention 2 ∎ ∎

Severe hypothyroidism Severe malnutrition, starvation

∎

Decreased metabolic rate, ↓ V̇CO2

∎

Central or obstructive sleep apnea ∎ Obesity hypoventilation ∎ Central hypoventilation syndrome (Ondine’s curse) Ventilatory muscle fatigue, dysfunction, or weakness ∎ Increased work of breathing leading to fatigue • Decreased lung compliance ○ Atelectasis, pneumonia, pulmonary edema, acute respiratory distress syndrome (ARDS), pulmonary fibrosis, surfactant disruption ○ Pleural effusion, hemothorax, empyema, pneumothorax, dynamic hyperinflation (air trapping) • Decreased thoracic compliance ○ Obesity, ascites, pregnancy, thoracic deformity (kyphoscoliosis, ankylosing spondylitis) • Increased airway resistance ○ Bronchospasm, mucosal edema, increased secretions (asthma, emphysema, chronic bronchitis), epiglottitis, croup, epiglottitis, tumor, foreign body obstruction ○ Small diameter endotracheal tubes • Increased level of ventilation demanded ○ Increased ventilatory drive (e.g., hypoxemia, pain, anxiety, lung receptor stimulation, hyperventilation needed to offset metabolic acidosis) ○ Increased metabolic rate (e.g., fever, hypermetabolic state) and increased CO2 production

∎

○ Increased pulmonary dead space (e.g., pulmonary embolus, chronic obstructive pulmonary disease [COPD]) • Imposed work of breathing due to artificial airways (endotracheal tubes, tracheostomy tubes) • Imposed work of breathing due to the ventilator itself (inappropriate ventilator sensitivity or flow settings, inadequate demand flow, patient– ventilator asynchrony) Ventilatory muscle weakness or dysfunction • Neuromuscular disease ○ Amyotrophic lateral sclerosis (ALS) ○ Duchenne muscular dystrophy ○ Guillain-Barré syndrome

• • • • • •

• •

○ Multiple sclerosis (MS) ○ Myasthenia gravis ○ Poliomyelitis and acute flaccidmyelitis (AFM) Critical illness myopathy or polyneuropathy Inadequate nutrition or starvation Poor health Electrolyte disturbances Chronically elevated work of breathing (e.g., severe COPD) Toxins ○ Botulism ○ Tetanus ○ Tick paralysis Neuromuscular-blocking agents (pancuronium [Pavulon], vercuronium [Norcuron], atracurium [Tracrium], cistracurium [Nimbex]) High spinal cord injury

BOX 16-3 Causes of Increased Ventilatory Requirements or Demand Conditions that increase ventilatory requirements or increase ventilatory demand may further stress the cardiopulmonary system and delay patients’ liberation from the ventilator. Causes of increased ventilation and associated ventilatory workload include: ∎ Hypoxemia/tissue hypoxia ∎ Metabolic acidosis ∎ Pain and anxiety ∎ Increased V̇CO (trauma, infection, sepsis, fever, shivering, agitation, fighting 2 the ventilator, struggling against restraints) ∎ Increased physiologic dead space (emphysema, pulmonary embolus with complete vessel obstruction) ∎ Lung receptor stimulation (e.g., rapid shallow breathing)

Patient Evaluation Most patients receiving mechanical ventilatory support should be evaluated daily to assess their potential to achieve liberation from the ventilator. In addition to improvement or resolution of the disease state or condition requiring ventilatory support, successful ventilator discontinuance is dependent on the patient having adequate oxygenation, ventilation, and circulation. Assessment for ventilator discontinuance should include review of the patient’s acid-base balance, cardiovascular and hemodynamic status, and overall medical condition. The respiratory care clinician should also review the patient’s ventilatory capacity while considering the patient’s ventilatory requirements. Prior to extubation, assessment of the patient’s natural airway should occur. Certain weaning indices may also be of value in predicting success. It should be noted, however, that clinicians often underestimate the capability of their patients to breathe spontaneously without the ventilator.

Reversal or Improvement of Disease or Condition The first step in deciding if a patient no longer requires mechanical ventilation is to evaluate the status of the disease or condition that required ventilatory support in the first place. Because there are many causes of respiratory failure requiring mechanical ventilatory support, obtaining a definitive answer regarding whether the patient has improved sufficiently to warrant ventilator discontinuance may not be possible. In general, however, improvement in the underlying condition to a stable state that would not otherwise require mechanical ventilation is an appropriate goal. For example, if the patient required intubation and mechanical ventilatory support due to severe pneumonia, signs of clinical improvement would include a favorable response to antibiotics, resolution of fever, and improvement in leukocytosis. Improvement in oxygenation is also a key sign associated with resolution of pneumonia. If the patient was intubated and ventilated because of septic shock, improvement in hemodynamic status and reduction in vasopressor requirements would be positive signs. In the case of intubation for airway protection due to angioedema, signs of resolution would include improvements in swelling noted during physical examination indicating that extubation would not result in loss of a

patent airway. In the case of decreased mental status, assessment that the patient is now awake and able to follow commands may suggest further evaluation to determine if patient can be liberated from the ventilator.

Assessment of Oxygenation Once it has been determined that there is improvement in the underlying condition that resulted in the need for mechanical ventilation, the next step is to assess the patient’s oxygenation status. Pulse oximetry, arterial blood gas analysis, and calculation of the PaO2/FIO2 ratio (P/F ratio) should be performed. The main goal is to confirm that any existing hypoxia can be adequately treated with noninvasive supplementation (e.g., oxygen mask or nasal cannula). While no definitive cut-off exists, most clinicians use a requirement of 40% to 50% oxygen (FIO2 ≤ 0.40 to 0.50) or less with 5 to 8 cm H2O or less of positive endexpiratory pressure (PEEP) while on the ventilator as a typical threshold.1 Some national guidelines recommend using a partial pressure of oxygen to fraction of inspired oxygen (P/F) ratio of ≥ 150 while administering 5 cm H2O (or less) of PEEP, while others recommend a P/F ratio ≥ 200 in the setting of 5 cm H2O of PEEP.2 It must be noted, however, that when used alone, oxygenation status is a poor predictor of weaning success and some patients may do well with SBTs with relatively poor P/F ratios. For example, patients with chronic hypoxemia (e.g., PaO2 of 50 to 60 mmHg) may do well with a lower P/F ratio (< 150 but > 120). Severe oxygenation problems (e.g., refractory hypoxemia) may preclude ventilator discontinuance. RC Insight Assessment of weaning parameters and SBTs should be deferred in patients who require greater than 50% oxygen (FIO2 > 0.50) and greater than 5 to 8 cm H2O of PEEP.

Assessment of Ventilation and Acid-Base Balance Successful liberation from the ventilator is dependent on the ability of the patient to adequately breathe spontaneously. This, in turn, depends on the patient’s ventilatory capacity versus ventilatory demand. Ventilatory capacity requires adequate

respiratory muscle strength, an intact central respiratory drive to breathe, and adequate lung function. Physical assessment can provide clues as to the patient’s ventilatory status. For example, tachypnea (f ≥ 30 breaths/min in adults) is a sensitive marker of respiratory distress. Irregular or asynchronous breathing, periods of apnea, and rapid shallow breathing are all associated with difficulty in ventilator discontinuance. Palpable scalene muscle contraction during inspiration is associated with an increased inspiratory work of breathing (WOB). Abdominal muscle tensing during expiration is associated with increased expiratory work and obstruction to expiratory gas flow. Patient–ventilator asynchrony is also associated with difficulty in ventilator discontinuance. However, it is important to recognize that subjective assessment of readiness for ventilator discontinuance can underestimate the patient’s ability to successfully breathe spontaneously without support. RC Insight Palpable scalene muscle contraction during inspiration suggests increased inspiratory work of breathing; palpable abdominal muscle tensing during expiration suggests increased expiratory work of breathing associated with obstruction.

Bedside measures of patients’ spontaneous breathing are readily available. These include measurement of spontaneous tidal volume (VT), respiratory frequency (f), and minute ventilation (V̇E). Normal adult spontaneous VT is about 400 to 700 mL, depending on the patient’s size, gender, and overall condition. Normal adult respiratory rate is about 12 to 18 breaths/min while normal V̇E is approximately 5 to 10 L/min. Abnormal values may suggest the need for continued ventilatory support. Respiratory rate should be in the range of 6 to 30 breaths/min with a tidal volume of at least 5 mL kg/IBW (ideal body weight, adults). Rapid shallow breathing (f > 30 breath/min with a tidal volume < 300 mL in adult patients) is associated with the continuing need for ventilatory support. Markedly elevated spontaneous breathing rates (e.g., > 35 breaths/min), air hunger, diaphoresis, and accessory muscle use suggest severe distress. Minute ventilation may be abnormally high in the presence of metabolic acidosis, hypoxemia, increased dead space, fever, hypermetabolic states, or increased central respiratory drive to breathe. CNS depressants, head trauma, neurologic disease,

severe hypoxemia, and alkalosis may decrease the respiratory drive to breathe resulting in a decreased spontaneous V̇E and hypoventilation. Minute ventilation should be in the normal range (e.g., 5 to 10 L/min); decreased V̇E may be due to respiratory drive depression, while markedly increased minute ventilation is associated with respiratory distress. Maximum voluntary ventilation (MVV) can be measured at the bedside with a hand-held respirometer. MVV ≥ twice the patient’s baseline minute ventilation is associated with adequate ventilatory reserve. Comparison of the patient’s tidal volume to vital capacity at the end of an SBT estimates the ventilatory reserve. Most patients are capable of at least doubling their tidal volume. Other measures sometimes used to assess a patient’s ability to adequately spontaneously breathe include bedside measurement of maximum inspiratory pressure (MIP) and vital capacity (VC). MIP provides a measure of ventilatory muscle strength while VC provides some indication of the patient’s ability to take a deep breath and cough. MIP values > –20 to –30 cm H2O and/or VC < 15 to 20 mL/kg (or VC < 1.0 L) have been associated with impending or actual ventilatory failure and the need for mechanical ventilation. Maximum expiratory pressure (PEmax or MEP) provides a measure of expiratory muscle strength. MEP ≥ + 60 cm H2O is associated with the ability to adequately cough and clear secretions. Measures of ventilatory workload include static total compliance (CST) and airway resistance (RAW) measured while the patient is on the ventilator. Normal CST and RAW are 60 to 100 cm H2O and 1 to 2 cm H2O/L/sec plus endotracheal tube (ETT) resistance, respectively. Work of breathing can be estimated based on tidal volume and esophageal pressure measurement, though acceptable values for ventilator discontinuance have not been delineated. Oxygen cost of breathing provides another surrogate measure for WOB. Normal, spontaneous WOB is 0.5 to 1.0 joules/L; values ≥ 1.5 joules/L may be excessive. Normal oxygen cost of breathing is less than 5% of O2 consumption (V̇O2); values up to 15% are thought to be compatible with weaning success. Measures of respiratory drive include pulmonary occlusion pressure (P0.1) and P0.1/MIP. P0.1 is defined as the pressure generated upon inspiration in the first onetenth of a second following complete airway occlusion. Normal P0.1 is less than 2 cm H2O and values in the range of less than 4 to 6 cm H2O have been considered

acceptable. P0.1/MIP has greater predictive power for ventilator discontinuance than P0.1 alone.

Rapid Shallow Breathing Index Perhaps the most widely used and studied measure of patients’ readiness for ventilator discontinuance is the rapid shallow breathing index (RSBI), where: RSBI = f/VT. Rapid shallow breathing is a common finding in patients with respiratory failure. Normal RSBI is < 50. For example, a normal adult tidal volume of 500 mL (0.5 L) and respiratory rate of 15 breaths/min would result in a calculated RSBI of 30 breaths/min/L (f/VT = 15/0.5 L = 30). RSBI ≥ 105 is associated with the need for continued mechanical ventilatory support. As originally described, RSBI was measured using a hand-held respirometer and T-piece connected to the ETT. Used in this fashion, RSBI provides a measure of spontaneous breathing with no mechanical ventilatory support. Today, RSBI is often measured while the patient is breathing using the ventilator system’s spontaneous ventilation mode. Thus, RSBI may be measured with no ventilatory support, with continuous positive airway pressure (CPAP) only, or with inspiratory pressure augmentation (e.g., pressure-support ventilation [PSV] or automatic tube compensation [ATC]) with or without CPAP. The addition of pressure augmentation or CPAP may result in a lower calculated RSBI. Caution should also be used when using the ventilator display for respiratory rate, as the ventilator may not count untriggered breaths, resulting in a lower-than-actual calculated RSBI. This is most likely to occur in patients with dynamic hyperinflation (e.g., COPD patients). Factors that may increase RSBI include fever, sepsis, anxiety, and recent suctioning. It should also be recognized that ETTs increase imposed work of breathing (e.g., WOBI) and small diameter ETTs can increase RSBI. Based on likelihood ratios, RSBI < 105 is a relatively poor predictor of weaning success, although the predictive value of RSBI ≥ 105 for weaning failure is better. Current clinical practice guidelines suggest that for acutely hospitalized patients ventilated for more than 24 hours, SBTs be conducted with inspiratory pressure augmentation rather than without. Guidelines further suggest that RSBI lacks sufficient positive and

negative predictive value for routinely predicting weaning success and is less predictive in patients over 65 years of age or those mechanically ventilated for ≥ 7 days. Other factors that may affect ventilation such as compliance, airway resistance, and ventilatory dead space are discussed further in other portions of this book (see Chapter 5, Indications for Mechanical Ventilation and Chapter 8, Critical Care Patient Assessment and Monitoring). While compliance, resistance, and dead space can be measured at the bedside, none of these measures when used alone have been shown to be predictive of readiness for ventilator discontinuance. Severe derangements, however, could preclude further steps to achieve ventilator discontinuance. The assessment of ventilation to evaluate readiness for discontinuation of mechanical ventilation regarding other specific parameters is discussed later in this chapter.

Acid-Base Balance and Ventilation Arterial carbon dioxide tension (PaCO2) provides the single best clinical measure of adequate ventilation. Normal PaCO2 is 35 to 45 mmHg and normal arterial pH is 7.35 to 7.45. An elevated PaCO2 with a corresponding decrease in pH defines acute ventilatory failure. Arterial pH should be > 7.25 for ventilator discontinuance to proceed. Failure to recognize acute or chronic acid-base abnormalities may result in failure to achieve liberation from the ventilator. Arterial blood gases may identify acid-base abnormalities such as metabolic acidosis or alkalosis, which may make weaning more difficult. For example, severe metabolic acidosis will stimulate the central respiratory drive to breathe. Patients in metabolic acidosis with sufficient ventilatory reserve will increase spontaneous V̇E to achieve a compensatory decrease in PaCO2. This increased minute ventilation may worsen ventilatory muscle fatigue and make SBTs more difficult to interpret. On the other hand, metabolic alkalosis may result in a decreased central respiratory drive to breathe and carbon dioxide (CO2) retention. Common causes of metabolic acidosis seen in the ICU include kidney failure, lactic acidosis, and ketoacidosis. Common causes of metabolic alkalosis seen in the ICU include low potassium (K+), low chloride (Cl–), nasogastric tube stomach acid (HCl) loss, and vomiting. Gastric mucosal acidosis is associated with gastric mucosal

ischemia and may be useful in predicting success with ventilator discontinuance. Specifically, a lower gastric mucosal pH has been associated with weaning failure. Measurement of gastric mucosal pH requires a special nasogastric tube. Chronic derangements in acid-base balance must also be considered when contemplating liberation from mechanical ventilation. These changes can often be more difficult to identify, particularly if patients have been intubated for a long period of time and baseline renal compensation has occurred. This is particularly true of patients with chronic CO2 retention. In these situations, it is ideal to review prior baseline blood gases and metabolic panels to estimate a target PaCO2. Often, however, baseline blood gases are not available. The next best test to review is baseline serum bicarbonate (HCO3–) level, if available. If the patient has chronic elevation in serum HCO3–, baseline PaCO2 can be estimated by the following formula: Estimated PaCO2 = 40 + (0.7 × [measured baseline serum HCO3– – 24]) With this equation, a target PaCO2 can be estimated and ventilator adjustments made accordingly. For example, a patient with an elevated baseline serum HCO3– of 38 mEq/L would have an estimated target PaCO2 of about 50 mmHg: Estimated PaCO2 = 40 + (0.7 × [38 – 24]) = 50 mmHg It is unrealistic to expect a patient with chronic PaCO2 retention to have a normal PaCO2 after extubation. Elevated baseline serum HCO3– levels can sometimes be masked in the setting of an acute metabolic acidosis. If a patient with chronic hypercapnia presents with acute metabolic acidosis (e.g., septic shock), the serum HCO3– may be 24 mEq/L, yet the patient’s normal baseline HCO3– could be significantly higher. RC Insight Chronic changes in acid-base status and baseline carbon dioxide levels must be taken into consideration when attempting to liberate a patient from mechanical ventilation.

Assessment of Cardiovascular and Hemodynamic Status Assessment of the patient’s cardiovascular and hemodynamic status prior to

considering liberation from mechanical ventilation focuses on identifying cardiac or cardiovascular factors that could jeopardize success. Heart rate and blood pressure should be in the normal range; tachycardia, bradycardia, hypotension, or severe hypertension should be evaluated carefully. The electrocardiogram should be assessed for the presence of arrhythmia and (if available) cardiac output, cardiac index, and other hemodynamic variables should be examined. Severe hypertension or hypotension will generally preclude ventilator discontinuance. In cases of severe hypertension, SBTs or other attempts at weaning could further stress the heart and worsen the hypertension. Alternatively, hypertension may cause pulmonary edema due to increased afterload (the resistance of left ventricular outflow), which may further delay ventilator discontinuance. The development of an elevated pulmonary capillary wedge pressure during SBTs has been well documented, even in patients with no history of heart failure.3 It should be noted that hypertension can be caused or worsened by the ETT. This should be suspected when hypertension is absent when the patient is calm or slightly sedated but develops during an awake SBT. Hypertension due to the ETT may not limit further assessment for ventilator discontinuance. However, some patients become anxious during SBTs and develop autonomic hyperactivity manifested as hypertension and tachycardia. The addition of pressure support or automatic tube compensation (ATC) may be helpful to relieve respiratory distress during SBTs, although pressure support and ATC may affect RSBI calculations. As noted earlier, measured RSBI may be lower in the presence of PSV, ATC, or CPAP as compared to unsupported spontaneous breathing. Heart rate, rhythm, and the presence (or absence) of specific cardiac arrhythmias should be taken into consideration. For example, atrial fibrillation has been shown to be an independent risk factor for weaning failure.4 Severe tachycardia, severe bradycardia, and other abnormal rhythms should be identified and addressed prior to any attempts at SBTs or weaning. Evidence of myocardial ischemia, cardiovascular instability, or left ventricular dysfunction are all associated with increased difficulty with ventilator discontinuance. In addition to the evaluation of heart rate and blood pressure, hemodynamic assessment should include evaluation for signs of hypervolemia. Hypervolemia is

likely to include some degree of pulmonary edema, which may be enough to cause weaning failure. It is well documented that in certain conditions, such as acute respiratory distress syndrome (ARDS), simply maintaining a negative fluid balance (even in the absence of cardiac dysfunction) facilitates weaning.5 Significant hypotension should also preclude further assessment of readiness for ventilator discontinuance. Weaning or SBTs can be harmful to patients already in a shock or pre-shock state, and the risk of weaning failure is high. Patients with significant hypotension are likely to require additional fluid administration, which often results in pulmonary edema. Patients in shock often develop alterations in mental status (e.g., confusion, obtundation, coma) and may require continued intubation to secure and protect the airway. While no definitive blood pressure cutoff for ventilator weaning or SBTs exists, the need for ongoing vasopressors precludes extubation in most cases. Box 16-4 summarizes the key points in the assessment of patient readiness for ventilator discontinuance.

BOX 16-4 Factors Associated with Readiness for Ventilator Discontinuance Readiness for ventilator discontinuance is suggested by the presence of improvement or reversal of the disease state or condition requiring mechanical ventilatory support, adequate oxygenation and acid-base status, medical and hemodynamic stability, and the presence of adequate spontaneous breathing. The respiratory care clinician should: ∎ Determine if the disease state or condition requiring mechanical ventilatory support has significantly improved or resolved. ∎ Assure that the patient’s oxygenation and acid-base status are adequate. • PaO2/FIO2 ≥ 150 mmHg or

•

PaO2 ≥ 60 mmHg and/or SaO2 ≥ 90% and FIO2 ≤ 0.40 and PEEP ≤ 5 cm H2O

pH > 7.25 No lactic acidosis ∎ Assure that the patient is medically and hemodynamically stable. • Hemodynamic/cardiovascular stability ○ Heart rate 60 to 100 bpm ○ Adequate blood pressure (BP > 90/60 but < 180/110 mmHg; mean

• •

arterial pressure ≥ 65 mmHg) ○ Low-dose or no vasopressors to maintain BP ○ Q̇T (if measured) ≥ 4 L/min but ≤ 8 L/min ○ Cardiac index (if measured) ≥ 2.1 ○ No major arrhythmias (e.g., tachycardia, bradycardia, multiple premature ventricular contractions [PVCs], heart block) ○ Signs and symptoms of myocardial ischemia absent (e.g., angina, dyspnea, chest pain or discomfort, nausea, diaphoresis, ST segment changes, tachycardia, hypertension) • Adequate hemoglobin levels (e.g., ≥ 7 g/dL) • Absence of fever ∎ Assure that the patient can breathe spontaneously and has adequate CNS drive to breathe. Ideally, the patient will be awake and alert or easily arousable.

RC Insight Both very high and very low blood pressure may preclude starting SBTs.

Assessment of Medical Condition In addition to assessment of factors that may affect the patient’s oxygenation, ventilation, acid-base balance, and hemodynamic status, the respiratory care clinician should review renal function, electrolytes, neurologic status, nutritional status, metabolic factors, and overall medical condition prior to attempting ventilator discontinuance. Assessment of patients’ overall medical condition for readiness for discontinuation of mechanical ventilation is focused on identification and correction (if possible) of problems that may result in failure. The central nervous system (CNS) is probably the most common, nonpulmonaryrelated organ system to limit discontinuation of mechanical ventilation. Neurologic function should be assessed to ensure a stable and adequate respiratory drive, protection of the airway, and secretion clearance. Ideally, the patient will be awake, alert, and able to follow instructions. Neurologic control of ventilation may be impaired by sedation, narcotic drugs, neuromuscular-blocking agents, electrolyte disturbances, or brainstem strokes. CNS depressants alter mental status and may

suppress respiratory drive; they should be minimized or discontinued prior to SBTs or ventilator weaning and extubation. Daily cessation of sedation may improve SBT success and protocols or nursing algorithms to minimize sedation should be employed, where appropriate. Upper airway obstruction, aspiration, and secretion retention following extubation may occur in patients with reduced levels of consciousness. Up to 80% of patients on mechanical ventilation develop delirium at some point.6 Significant delirium inhibits the patient’s ability to participate in measurement of weaning parameters, and often raises concern about the patient’s ability to protect the airway. Delirium can be driven by many factors, but sedative medications (particularly benzodiazepines) are the single largest risk factor for the development of delirium. If agitation occurs when sedation is decreased, sedative medications are often increased, leading to a vicious cycle of agitation followed by oversedation, which can make attempts at ventilator discontinuance challenging. Malnutrition is a common complication of critical illness that can affect respiratory muscle strength. The clinician should review the patient’s nutritional status and type of nutritional support provided (enteral or parenteral) to include formula composition (amino acids, fat, carbohydrates, vitamins, and minerals). Excessive carbohydrate feeding can increase CO2 production and increase ventilatory requirements. Electrolyte disturbances, especially K+, Ca++, Mg++, and HPO42– may also impair ventilatory muscle function. Blood glucose levels and liver function tests should also be reviewed. Hyperglycemia is associated with poorer clinical outcomes in critically ill patients and hypoglycemia may cause seizures, brain damage, and cardiac arrhythmias. Liver failure may cause volume overload or other hemodynamic abnormalities, which further complicate efforts to achieve ventilator discontinuance. Acute liver failure may result in hepatic encephalopathy and cerebral edema. Somnolence, confusion, unconsciousness, and hepatic coma may occur. Bilirubin level is one measure of hepatic function included in calculation of Sequential (Sepsis-related) Organ Failure Assessment (SOFA) scores and other scoring systems (e.g., APACHE IV, SAPS II) sometimes used to predict ICU outcomes. Additional factors that may increase oxygen consumption (V̇O2), CO2 production (V̇CO2), and metabolic rate include fever, shivering, sepsis, agitation, and seizures.

Renal function and urine output should be adequate (≥ 0.5 mL/kg/h), and inappropriate weight gain or peripheral edema associated with fluid retention should be noted. As described above, fluid overload can lead to heart failure, pulmonary edema, and oxygenation problems. The timing of upcoming procedures should be taken into consideration when planning for discontinuation of mechanical ventilation and extubation. Certain procedures increase the risk of failure, while other procedures may help optimize the chances of a success. For example, in a patient with renal failure and volume overload, performing dialysis prior to attempting ventilator discontinuance will likely improve the chance of success. On the other hand, procedures that require conscious sedation will likely increase the risk of failure, especially in higher-risk individuals. Patients liberated from mechanical ventilation are at the highest risk for extubation failure and reintubation in the first 24 hours following extubation. Procedures that require sedation or studies that require transport out of the monitored ICU are best done prior to extubation. Psychological factors including anxiety, depression, and motivation can affect success in liberating the patient from the ventilator. Patients who have been receiving mechanical ventilatory support for long periods of time may become extremely anxious regarding the prospect of having the ventilator removed. Frequent and supportive communication with the patient and the patient’s family can be helpful in reducing fear, anxiety, and distress. Pain should be adequately controlled prior to attempts at weaning or extubation. Uncontrolled pain can result in increased respiratory rate and increased blood pressure, interfere with SBTs, and lead to hemodynamic instability. Similarly, the uptitration of pain medications should be avoided (if possible) during weaning trials or in the acute postextubation period because oversedation can result in failure. Careful titration of medications before and after extubation is critical in optimizing the chances of success. Box 16-5 summarizes factors that should be optimized (if possible) prior to ventilator weaning and discontinuance.

BOX 16-5 Optimizing the Patient’s Condition Prior to Ventilator Discontinuance

The following checklist includes items that should be reviewed and optimized (where possible) to improve success in liberating the patient from the ventilator. ∎ Ensure adequate oxygenation (PaO , SpO , SaO , CaO , ḊO ). 2 2 2 2 2 Treat acute pulmonary disease (e.g., infection, pneumonia, atelectasis). Hemoglobin (treat anemia if present). ∎ Optimize ventilation. • Correct patient–ventilator asynchrony, if present. • Provide adequate humidification. • Ensure secretion clearance by providing bronchial hygiene (e.g., suctioning, turning, chest physiotherapy). • Provide bronchodilator therapy to treat or prevent bronchospasm. • Avoid artificially hyperventilating the patient and creating a respiratory alkalosis. • Reduce imposed work of breathing (provide adequate ventilator inspiratory flow rate and trigger sensitivity). • Rest ventilatory muscles and avoid respiratory muscle fatigue or atrophy. ∎ Review acid-base balance and electrolytes. • Treat metabolic acidosis (e.g., kidney failure, lactic acidosis, ketoacidosis). • Treat metabolic alkalosis (e.g., treat low potassium, low chloride, nasogastric tube HCI loss, vomiting). • Treat low phosphate or magnesium; treat other electrolyte disorders. ∎ Assess cardiac and cardiovascular status. • Maintain blood pressure and cardiac output. • Treat arrhythmias, if present. • Assess for myocardial ischemia. • Optimize left ventricular function. ∎ Review renal function. • Assess kidney function and fluid balance. ∎ Treat fever, infection, or sepsis. ∎ Treat pain (minimize without oversedation). ∎ Avoid sleep deprivation. ∎ Increase exercise tolerance (early mobilization, up in chair, physical therapy). ∎ Assess medications that may affect ventilation. • Narcotics, sedatives, tranquilizers, hypnotics • Aminoglycosides

• •

Neuromuscular-blocking agents ∎ Assess psychological status. • Level of consciousness (delirium, coma) • Agitation, anxiety • Motivation ∎ Assess for hypothyroidism. ∎ Consider nutritional factors. • Avoid overfeeding (which may cause increased carbon dioxide production). • Adjust for malnutrition, protein loss. • Consider high-fat, low-carbohydrate diet to minimize carbon dioxide production. ∎ Assess gastrointestinal or abdominal factors. • Assess for bleeding or obstruction. • Assess for abdominal distension, ascites. ∎ Optimize procedural factors. • Optimize time of day (avoid evenings, nights, shift change). • Assure adequate staffing. • Avoid interruptions and disruptions. ∎ Assess technical factors. • Compensate for ETT resistance (e.g., pressure support [PSV] or automatic tube compensation [ATC]). • Assessment of intrinsic PEEP and use of PEEP/CPAP to “balance” intrinsic PEEP.

•

ABCDEF Bundle The ABCDEF bundle has been suggested for optimizing ICU patient outcomes in ventilated patients. The ABCDEF bundle includes steps to address factors that may affect success in liberating the patient from the ventilator: Assess, prevent, and manage pain Both spontaneous awakening trials (SAT) and spontaneous breathing trials (SBT) Choice of analgesia and sedation Delirium: assess, prevent, and manage Early mobility and exercise

Family engagement and empowerment Box 16-6 summarizes the ABCDEF bundle.

BOX 16-6 The ABCDEF Bundle for ICU Patients Successful liberation of the patient from the ventilator can be delayed due to oversedation, delirium, and immobility. The ABCDEF bundle provides a multidisciplinary approach to speed the liberation of the patient from the ventilator and includes the following components: ∎ Assess, prevent, and manage pain. Pain assessment may be done through use of a numerical rating scale (NRS) using the patient’s self-reported pain on a scale of 1 to 10. Other pain assessment tools include the Behavioral Pain Scale (BPS) and the Critical-Care Pain Observation Tool (CPOT). Pain medications may be administered to patients with NRS > 4, BPS > 5, or CPOT > 3. Parenteral opioids for non-neuropathic pain are first-line agents; acetaminophen, nonsteroidal anti-inflammatory drugs (NSAID), or ketamine may be used to reduce opioid requirements. ∎ Both spontaneous awakening trials (SAT) and spontaneous breathing trials (SBT). The nurse and respiratory therapist should coordinate daily SATs and SBTs. Narcotics and sedatives should be stopped or minimized each day. Daily interruption of sedation and respiratory care–driven protocolized SBTs can shorten time to ventilator discontinuance and extubation. ∎ Choice of analgesia and sedation. Sedation and analgesics should be reviewed, and changes or reductions in doses considered. Minimizing sedation may also reduce the incidence of delirium. ∎ Delirium: assess, prevent, and manage. A standardized delirium assessment program (e.g., CAM-ICU or Intensive Care Delirium Screening Checklist) including treatment and prevention options should be included. Delirium is associated increased length of mechanical ventilation, increased ICU stay, increased cost, long-term cognitive impairment, and increased mortality. Risk factors for delirium include narcotics, benzodiazepines, administration of other psychoactive drugs, mechanical ventilation, advanced age, prior cognitive impairment, untreated pain, sleep deprivation, sepsis, and other medical conditions (e.g., heart failure, abnormal blood pressure, anemia). Early and progressive mobilization, promotion of sleep hygiene, and prevention of sleep disruption may help prevent or reduce ICU delirium. ∎ Early mobility and exercise. Early mobilization and ambulation of ventilated ICU patients and physical therapy may help reduce peripheral muscle weakness.

∎

∎

Family engagement and empowerment. Family and surrogate decision makers should be included in decision making and treatment planning. The family’s wishes, concerns, questions, and participation will enable them to become active partners in the patient’s care and may improve outcomes. The ABCDEF bundle may reduce ventilator days, ICU length of stay, and mortality.

CAM–ICU, Confusion Assessment Method for the ICU delirium monitoring instrument. Data from Marra A, Ely EW, Pandharipande PP, Patel MB. The ABCDEF bundle in critical care. Crit Care Clin. 2017;33(2):225–243. doi:10.1016/j.ccc.2016.12.005.

RC Insight As many as 60% to 80% of patients requiring mechanical ventilation develop delirium during their ICU stay.

Assessment of the Airway While ETTs allow for protection of the lower airway and facilitate positive-pressure ventilation, they may also increase airway resistance and imposed work of breathing (WOBI). This is especially true in patients with high spontaneous minute ventilations or when small internal diameter (ID) ETTs are in place (e.g., ID < 7 mm in adults). Without proper humidification, ETTs may become partially occluded by dried secretions; this can dramatically increase airway resistance and WOBI. ETTs may also cause reflex bronchospasm, and bronchodilator therapy for intubated patients may be appropriate. Pressure-support ventilation (PSV) or other forms of support (e.g., automatic tube compensation [ATC]) can compensate for WOBI and low levels of PSV (5 to 8 cm H2O) or ATC are used during SBTs at many institutions. It is interesting to note that there is some evidence that tracheostomy tubes may reduce the work of breathing as compared to ETTs. Placement of a tracheostomy tube may also reduce anatomic dead space slightly (as compared to ETTs), which, in theory may be beneficial in borderline patients. Extubation will remove any imposed work of breathing (WOBI) due to the ETT. Ventilator discontinuance and patient extubation are separate, but closely linked decisions (see Clinical Focus 16-1). The decision to extubate should be based on an objective review of specific criteria (Box 16-7). Following extubation, the patient must be able to maintain an adequate natural airway; inability to protect the natural

airway is a contraindication to extubation. It must also be noted that measures of readiness for ventilator discontinuation are not predictive of airway patency or the need for airway protection.

CLINICAL FOCUS 16-1 Assessment for Spontaneous Breathing Trial (SBT) Readiness A 40-year-old male is intubated for increased work of breathing, hypoxia, and altered mental status in the setting of septic shock from pneumonia. Forty-eight hours later, his mental status has improved, and the ventilator is now set to assist/control with a tidal volume of 500 mL, and a respiratory rate of 16. FIO2 requirement has decreased from 0.60 to 0.40 (60% to 40%) and PEEP is 5 cm H2O. Since admission, the patient has required norepinephrine (Levophed) and vasopressin (Vasostrict) because of hypotension, and in the last 12 hours the dose of norepinephrine had to be increased. His plasma lactate (i.e., lactic acid) level is 5 mmol/L. Question 1: How would you describe this patient’s clinical status and readiness for discontinuation of mechanical ventilation? Answer: The patient has shown some clinical improvement in the condition that resulted in the intubation, regarding oxygenation and mental status. Oxygen requirements are reduced given that his FIO2 is less than 0.50 (50%) and PEEP is 5 cm H2O. From the hemodynamic standpoint, the patient does not meet the criteria for performing an SBT or extubation. Normal plasma lactate is 0.5 to 1.5 mmol/L; values > 4 mmol/L generally define lactic acidosis. Lactic acidosis is associated with impaired tissue oxygenation due to poor tissue perfusion. Given the lactic acidosis in the setting of escalating vasopressor doses, performing an SBT could result in increased physiologic stress on the patient and further worsen hemodynamics. Despite improvement in the patient’s pulmonary status, there are ongoing nonpulmonary issues that would preclude extubation. The patient is given 1.5 L of intravenous fluid and 24 hours later is no longer requiring vasoactive medications (norepinephrine and vasopressin have been weaned off). Additionally, his lactic acid level has normalized. His blood pressure is 130/80 mmHg, and heart rate is 90. His renal function and serum HCO3– are normal. His ventilator requirements are unchanged. Question 2: What would be the next step to assess his readiness for extubation? Answer: At this point, the primary reason for intubation has improved and he now appears

to be stable from a hemodynamic standpoint. There are no identified nonpulmonary factors that would inhibit discontinuation of mechanical ventilation. As mentioned above, the patient’s ventilator requirements are acceptable. The next step would be to specifically assess the respiratory system by measuring weaning parameters. If weaning parameters are acceptable, an SBT may then be performed.

BOX 16-7 Extubation Criteria* Ventilator discontinuance and extubation are two separate, but often linked, decisions. Following successful discontinuance of the ventilator, the patient must have adequate oxygenation and ventilation during spontaneous breathing. Patients must be able to maintain a patent airway and protect the airway from aspiration. Extubation criteria include the following. 1. Mechanical ventilatory support is no longer necessary. a. Reasons (indications) for mechanical ventilation initiation have resolved or significantly improved. b. Procedures requiring intubation (e.g., general surgery) are not planned. c. Positive ventilator weaning indices can be reassuring (although predictive power is limited): i. Reversal or improvement of the problem requiring ventilatory support. ii. Adequate oxygenation is present. iii. Patient is hemodynamically stabile. iv. No evidence of myocardial ischemia. v. pH > 7.25. vi. f/VT ≤ 105. vii. MIP < –20 to –30 cm H2O. 2. Adequate oxygenation and ventilation during spontaneous breathing can be achieved. a. Ensure adequate oxygenation can be achieved using conventional oxygen therapy (e.g., facemask, air entrainment device, nasal cannula, or highflow nasal cannula). b. Ensure adequate spontaneous ventilation is present. i. Spontaneous VT, f, and V̇E are adequate. ii. Ventilatory pattern is stable. iii. Rapid shallow breathing is not present.

iv. Minute ventilation is not abnormally elevated or depressed. v. Respiratory distress is not present (e.g., dyspnea, tachypnea, fatigue, dyspnea, diaphoresis, accessory muscle use, intercostal retractions, or abdominal paradox). 3. Patient is able to protect the airway. a. Minimal risk of aspiration. b. Adequate level of consciousness. i. Patient is awake and alert. ii. Patient is not unconscious or obtunded (e.g., Glasgow Coma Scale [GCS] ≥ 8). c. Neuromuscular function is good. 4. Adequate pulmonary secretion clearance is likely following extubation. a. Adequate cough (e.g., peak expiratory flow rate > 60 L/min). b. Sputum volume and consistency allows for natural clearance (e.g., ≤ 2.5 mL/h). c. Need for suctioning is minimal (e.g., not more than q 2 to q 3 h). 5. Assess for likelihood of upper airway obstruction or airway compromise (e.g., laryngeal edema). a. Adequate level of consciousness is present. b. Oral and upper airway anatomy are normal; no evidence of facial or oral edema (e.g., angioedema). c. Gag reflex is present. d. Minimal risk of aspiration. e. Cough is adequate to clear secretions. f. Gastric contents are minimized by discontinuation of tube feedings for 4 to 6 hours before extubation. g. Cuff-leak test is passed and suggests low risk for postextubation stridor due to laryngeal edema. *Note: Many patients who do not meet specific “weaning” criteria may still be successfully extubated— careful assessment and good clinical judgment are essential. Data from Hyzy RC. Extubation management. In: Manaker S, Finlay G, eds. UpToDate; 2014.

The importance of airway assessment when considering extubation of the patient cannot be overstated for two reasons. First, prior to extubation, it is important to

appreciate the probable level of difficulty of replacing the ETT, if it becomes necessary. The note in the medical record documenting the initial intubation is often a good source to assess the likely difficulty of reintubation. The intubation note should document the grade view of the vocal cords, number of attempts required, and the tools used for intubation. Unless factors creating difficulty with the initial intubation have resolved, it is likely that reintubation will be more difficult. Second, to the extent possible, it is important to anticipate in advance airway problems that may cause extubation failure. Some laryngeal edema occurs in most intubated patients. Laryngeal edema is caused by compression of the tissue of the larynx by the ETT. Laryngeal edema is generally transient and self-limiting; however, it can cause partial or complete airway obstruction following extubation. The primary clinical marker for the presence of laryngeal edema following extubation is stridor; about 15% of reintubations are performed because of laryngeal edema. That said, stridor alone is not a very sensitive marker for the need for reintubation. Other possible causes of upper airway obstruction following extubation include soft-tissue obstruction due to decreased levels of consciousness, angioedema, vocal cord paralysis, laryngospasm, and exacerbation of obstructive sleep apnea. On inspection, the presence of facial or oral edema may signal possible airway swelling due to angioedema. However, with the ETT in place, it is difficult or impossible to visually inspect deeper portions of the upper airway. A cuff-leak test can be performed to assess for signs of airway edema and estimate the risk of postextubation stridor (Box 16-8). A cuff-leak test is performed by leaving the ETT in place and using a syringe to deflate the ETT cuff balloon. During a ventilatorsupported positive-pressure breath, the presence of leak can be detected by the audible sound of air exiting around the ETT during inspiration while the cuff remains deflated. Inspiratory and expiratory tidal volumes (VT) measured by the ventilator during a positive-pressure breath can be compared to determine the size of the leak around the cuff. Leak volume can be calculated by subtracting the expiratory tidal volume from the inspiratory tidal volume. For example, if the inspiratory VT was 500 mL and the measured expiratory VT was 300 mL, the volume of gas lost around the ETT because of the deflated cuff would be 200 mL. The percent leak can be calculated as follows:

BOX 16-8 Cuff-Leak Test for Laryngeal Edema in Intubated Patients Prior to extubation, a cuff-leak test may be performed to assess for the presence of laryngeal edema. To perform a cuff-leak test, the respiratory clinician should: 1. Ensure the patient can adequately breathe without mechanical ventilatory support. 2. Suction the patient’s mouth and airway. 3. Deflate the ETT cuff. 4. Briefly occlude the ETT and assess ventilation. 5. Suspect laryngeal edema if the patient is unable to breathe around the occluded ETT with the cuff deflated. 6. As an alternative, the percent leak around the ETT can be calculated by comparing inspired tidal volume to expired tidal volume with the cuff deflated during a ventilator-supported breath: Percent leak = ([inspiratory VT – expiratory VT]/inspiratory VT) × 100% Leaks < 110 cc (adults) or < 25% have been associated with increased risk of postextubation stridor due to laryngeal edema.

Percent leak = ([inspiratory volume – expiratory volume] ÷ inspiratory volume) × 100% Percent leak = ([500 mL – 300 mL] ÷ 500 mL) × 100% = 40% Although the cuff-leak test can be affected by tube position and results may vary, leaks of less than 100 cc (adults) or less than 25% have been associated with increased risk of postextubation stridor.7 Postextubation stridor has been associated with increased risk for extubation failure and reintubation. The administration of systemic corticosteroids prior to extubation in patients at increased risk of postextubation stridor has been associated with lower rates of postextubation failure requiring reintubation. The optimal dose and duration of steroids has yet to be determined, and there is significant variation in practice. Previously studied regimens are presented in Table 16-1.

TABLE 16-1 Commonly Used Regimens to Prevent Postextubation Airway Edema Medication

Dose

Schedule*

Methylprednisolone (Medrol)

20 mg

Every 4 hours starting 12 hours prior to extubation

Methylprednisolone

40 mg

Once, 4 hours prior to extubation

Dexamethasone (Ozurdex)

5 mg

Every 6 hours starting 24 hours prior to extubation

Dexamethasone

8 mg

Once, 1 hour prior to extubation

Hydrocortisone (Cortef)

100 mg

Once, 1 hour prior to extubation

* Some protocols extend steroids 24 hours after extubation.

Extubation failure is associated with impaired cough effort, increased sputum volume, and impaired neurologic function. Cough effort can be assessed by measurement of peak expiratory flow rate. Sputum volume can be estimated, and suctioning frequency can be used to estimate whether secretions may pose a problem following extubation. As noted above, patients should be awake, alert, and able to follow instructions. Glasgow Coma Score (GCS) provides an estimate of level of consciousness and neurologic function. RC Insight The presence of a cuff leak of greater than 100 cc (adults) or 25% of the tidal volume is associated with a lower incidence of postextubation stridor.

Weaning Indices After the conditions that resulted in ventilator initiation are improved or resolved, oxygen requirements are reduced, and other medical conditions are not prohibitive for ventilator liberation, an assessment more specific to the respiratory system may be performed. Weaning indices or weaning parameters are maneuvers performed at the bedside with the ETT in place after 1 to 2 minutes of spontaneous breathing without ventilatory support. Tests of spontaneous breathing that may be helpful in evaluating patients for ventilator discontinuance include measurement of the patient’s spontaneous tidal volume (VT), respiratory rate (f), minute ventilation (V̇E),

maximum inspiratory pressure (MIP), maximum expiratory pressure (MEP), vital capacity (VC), rapid shallow breathing index (RSBI), and assessment of respiratory drive (e.g., P0.1). Some of these maneuvers provide measurement of respiratory muscle strength, while others are quantitative assessments of the patient’s ventilation and respiratory function (see Clinical Focus 16-2).

CLINICAL FOCUS 16-2 Weaning Indices After 7 days of mechanical ventilation for ARDS, a female patient has significant improvement in her oxygenation and ventilatory status and is now hemodynically stable and cleared for further assessment of readiness for ventilator discontinuance and extubation. Weaning indices or parameters are assessed as follows. Maximum inspiratory pressure (MIP, aka negative inspiratory force [NIF]): –30 cm H2O Vital capacity (VC): 1 L Rapid shallow breathing index (RSBI): 80 breaths/min/L Question 1: How do you interpret the obtained weaning parameters? Answer: MIP of –30 cm H2O suggests acceptable inspiratory respiratory muscle strength. A value < –20 cm H2O would suggest significant muscle weakness and risk of extubation failure. MIP is somewhat effort dependent, and when used alone is a relatively poor predictor of how a patient will do following extubation. Keeping this in mind, the patient’s value is in a reassuring range. VC alone is also a poor predictor of risk of extubation failure and there is no well-established threshold below which extubation is unsafe, especially in ARDS patients. There is a small amount of data that suggests VC > 10 mL/kg may be compatible with successful extubation in patients with neuromuscular weakness. RSBI is the most well-established weaning parameter in the medical literature. RSBI < 105 is associated with about an 80% chance of successful extubation. This patient’s RSBI is suggestive of a favorable outcome. Question 2: Given favorable weaning parameters, what would be the next step in assessing readiness for extubation? Answer: After obtaining favorable weaning parameters, an SBT may be performed. The SBT can be performed with inspiratory pressure augmentation by allowing the patient to breathe through the ventilator circuit with CPAP at 5 cm H2O and 5 cm

H2O of pressure support. As an alternative, automatic tube compensation (ATC) could be used. Should the clinician desire to perform the SBT without inspiratory pressure augmentation, a T-piece trial could be performed. For most patients, a 30-minute SBT is sufficient. At the end of 30 minutes, if no derangements in heart rate, blood pressure, respiratory rate, or oxygen saturation have developed, extubation may be performed (assuming the patient is able to maintain a patent natural airway and no other contraindications to extubation are present).

Maximum Inspiratory Pressure Maximum inspiratory pressure (MIP or PImax) provides a direct measure of inspiratory muscle strength, whereby the patient is instructed to exhale to residual volume, and then maximally inhale against a closed airway. Concurrent manometry is performed to measure the maximal negative inspiratory pressure achieved. MIP may be measured as a part of pulmonary function testing or at the bedside using a simple manometer. Clinically, MIP measurements when performed on intubated patients are sometimes referred to as negative inspiratory force (NIF). The first use of this measurement is credited to Sahn and Lakshiminarayan, who published an early report on using bedside parameters to predict weaning success. Among other findings, they reported that all patients who could generate an MIP of at least negative 30 cm H2O (MIP ≤ –30 cm H2O) were successfully extubated, while those who could not generate at least negative 20 cm H2O (MIP ≤ –20 cm H2O) failed.8 This maneuver, however, requires patient participation and is somewhat effort dependent; values can be abnormally low due to oversedation, delirium, or suboptimal patient effort. While the use of MIP as a sole predictor of successful extubation is somewhat limited, it continues to be commonly taught, measured, and reported.

Rapid Shallow Breathing Index (RSBI) As described above, RSBI is a commonly used weaning parameter that is simply the ratio of breaths/min to tidal volume (in liters). Often patients in respiratory failure who cannot generate adequate tidal volumes will breathe rapidly to compensate. Patients who exhibit rapid shallow breathing may develop ventilatory muscle fatigue and are likely to fail ventilator weaning. In the original study assessing RSBI, Yang and Tobin

found that if the index was less than 105 (RSBI < 105), the rate of successful extubation was approximately 78%; if the index was greater than 105 (RSBI > 105), the rate of failed extubation was 95%.9 These values were found to be most predictive in younger patients (< 65 years old) and when the period of intubation was less than 1 week. Because the RSBI is more representative of the patient’s physiology than measures requiring patient cooperation, it may be less prone to errors and has demonstrated reliability in numerous studies. Despite its advantages over the maximum inspiratory pressure (MIP or NIF), the RSBI is not immune to confounding factors such as oversedation, anxiety, or pain. The RSBI can also be calculated at the beginning, during, and at the end of an SBT. Stability of the RSBI throughout the SBT (usually 3 to 120 minutes) suggests a higher likelihood of success. To summarize, RSBI ≥ 105 is moderately useful in predicting weaning failure. RSBI < 105, however, is only a weak predictor of weaning success.

Minute Ventilation Minute ventilation (V̇E) is often assessed when evaluating readiness for SBTs. Studies have looked at various cut-off points, such as less than 10 L/min, less than 12 L/min, or less than 15 L/min. The variability in study results demonstrates the limited reliability of V̇E as a single measure for prediction of readiness for ventilator discontinuance. However, most clinicians are hesitant to proceed with SBTs in patients with high-baseline minute ventilation and high ventilatory frequency, as these patients will likely not pass an SBT based on the starting value of their respiratory rate. While there are no studies documenting a specific cut-off point, our experience suggests sustained V̇E > 20 L/min is associated with failure in ventilator discontinuance and extubation.

Vital Capacity Vital capacity (VC) can be measured in intubated, spontaneously breathing patients at the bedside to assess the patient’s ability to spontaneously deep breathe. VC can be measured with a hand-held respirometer or using the ventilator’s monitoring system. The patient is asked to maximally inhale and then exhale to residual volume. There is little data to suggest that VC is a reliable predictor of successful ventilator discontinuance in medical ICU patients. However, assessing the difference between

tidal volume and vital capacity at the beginning and the end of an SBT provides an estimate of the patient’s ventilatory reserve after a period of spontaneously breathing; this rough assessment of ventilatory reserve continues to be used by some clinicians. Most of the existing data using VC as a predictor of the need for mechanical ventilation is from patients with Guillain-Barré syndrome. Even in these patients, there is a large range of values reported (from 4 mL/kg to 10 mL/kg), and sensitivity and specificity are relatively poor.10,11

Integrated Indexes Integrated indexes have been developed in an attempt to improve prediction of successful ventilator weaning and discontinuance. The CROP index combines measures of compliance, respiratory rate, oxygenation, and pressure (MIP). Other integrated indices include the inspiratory effort quotient (IEQ), the CORE index (Compliance, Oxygenation, Respiration, Effort), the weaning index (WI), and the integrative weaning index (IWI). These integrative indices use various combinations of measures including compliance, MIP, tidal volume, P/F ratio, f/VT, and/or pressure–time index. Specific values for these integrated indices predictive of weaning success or failure have been recommended. For example, IEQ > 0.15 has been associated with weaning failure. Although promising, none of these integrated indices have been confirmed as having the high level of accuracy initially suggested. In summary, readiness testing may be used to help determine if a patient should undergo the next step for ventilator discontinuance, often an SBT. Indices for assessing readiness for ventilator discontinuance should be used sparingly, and each has strengths and limitations. Despite some variability in the literature, the RSBI remains the most commonly used readiness test in the ICU and holds the most reproducibility in various studies. It must be stressed that many patients are successfully liberated from mechanical ventilation despite suboptimal results on specific readiness tests. Reliance on “getting the right numbers” may inappropriately delay ventilator discontinuance. Box 16-9 summarizes commonly used weaning indices.

BOX 16-9 Indices for Predicting Readiness for Ventilator Discontinuance

Many indices for weaning and ventilator discontinuance have been suggested and the respiratory care clinician should be aware of values associated with readiness for liberation from the ventilator. Unfortunately, the predictive power of any single index is minimal. ∎ Measures of oxygenation. Specific measures of oxygenation when used alone tend to be poor predictors of weaning success. However, clinicians must assess adequacy of oxygenation and values that are reassuring include: • PaO2/FIO2 ≥ 150 mmHg

• • • •

○ PaO2/FIO2 ≥ 120 mmHg and PaO2 of 50 to 60 mmHg may be acceptable in patients with chronic hypoxemia. PaO2 ≥ 60 mmHg SaO2 ≥ 90% FIO2 ≤ 0.40 to 0.50 PEEP ≤ 5 to 8 cm H2O

∎

Measures of acid-base balance • Arterial pH > 7.25. • Gastric mucosal acidosis (e.g., gastric mucosal ischemia) has been associated with weaning failure, but requires a special, nasogastric tube for measurement. ∎ Measures of ventilation • f < 30 and > 6 breaths/min • VT > 5 mL/kg • f/VT < 105 • V̇E < 10 L/min • MVV ≥ 2 × V̇E (as a measure of ventilatory reserve) • VC > 10 to 15 mL/kg (to ensure the ability to cough and deep breathe) ∎ Measures of ventilatory muscle strength • MIP < –20 to –30 cm H2O MEP ≥ 60 cm H2O (suggests the ability to adequately cough and clear secretions) Measures of ventilatory workload • Static total compliance and airway resistance measured while on the ventilator provide an estimate of ventilatory workload. ○ Total static compliance approaching normal range (CST 60 to 100 cm H2O)

•

∎

○ Airway resistance (Raw) approaching normal (e.g., Raw 1 to 2 cm H2O/L/sec + ETT resistance)

•

∎

Work of breathing (WOB) can be estimated based on tidal volume and esophageal pressure measurement, though acceptable values for weaning have not been delineated. Oxygen cost of breathing (OCB) provides another surrogate measure for WOB. WOB and OCB approaching normal values would be considered positive findings. ○ Normal spontaneous WOB is 0.5 to 1.0 joules/L; values ≥ 1.5 joules/L may be excessive. ○ Normal OCB is < 5% of V̇O2; OCB ≤ 15% may be acceptable as a goal for weaning.

Measures of respiratory drive. Respiratory drive can be assessed by measurement of the pulmonary occlusion pressure (P0.1), which is the pressure generated upon inspiration in the first tenth of a second (0.10 sec) following complete airway occlusion. • P0.1 < 4 to 6 cm H2O (normal P0.1 < 2 cm H2O).

•

P0.1/MIP has greater predictive power than P0.1 alone.

Indices for predicting readiness for ventilator discontinuance should be used sparingly. Many patients are successfully liberated from mechanical ventilation despite suboptimal results on specific tests. Reliance on “getting the right numbers” may inappropriately delay ventilator discontinuance and patient recovery.

Methods Traditional methods for ventilator discontinuance include SBTs, pressure-support ventilation (PSV), and intermittent mandatory ventilation (IMV). The SBT is conducted by placing the patient on a system that provides minimal or no support from the ventilator. SBTs may be accomplished by use of a T-piece for entirely unsupported spontaneous breathing or through the ventilator with only minimal inspiratory support (e.g., PSV at 5 to 7 cm H2O or automatic tube compensation [ATC]). Assuming the patient tolerates the procedure, the initial SBT generally lasts 30 minutes and is used to determine if the ventilator can be discontinued. A longer period (e.g., 120 minutes) may be used for patients who been receiving mechanical ventilation for an extended period (e.g., > 7 to 10 days) or in patients who fail their initial SBT. PSV provides an alternative weaning method for patients unable to tolerate SBTs. For PSV weaning, ventilator discontinuation is accomplished by gradually decreasing the level of pressure support provided (e.g., decrease of 2 to 4 cm H2O per day). With IMV, the frequency of mandatory breaths provided by the ventilator is gradually decreased, allowing the patient to assume a larger and larger portion of his or her minute ventilation. Prior to the mid-1990s, outcomes studies to guide practice were limited and the process of ventilator discontinuation varied based on provider preferences and training. Commonly used methods gradually decreased the level of ventilator support over time until the patient required either no support or very low levels of support and was then extubated. This was accomplished by a schedule of gradually increasing periods of spontaneous T-piece tube breathing, often starting with only 5 min/h off the ventilator and gradually increasing the time off. IMV became popular in 1970s and 1980s, in which the IMV rate was gradually decreased in increments of approximately two breaths/min. Over the last 20 years, there has been a transition from these “weaning trials” to a more “abrupt discontinuation” of mechanical ventilation, also now frequently referred to as “liberation” from mechanical ventilation. The rationale for this transition largely stems from a study comparing different methods, in which SBTs with interval full ventilatory support for “rest” was shown to decrease time to extubation compared to traditional weaning.12 Here we will review several of these methods and describe some more contemporary modes of “weaning.”

IMV/SIMV One traditional method of weaning utilizes intermittent mandatory ventilation (IMV) or synchronized intermittent mandatory ventilation (SIMV). IMV was initially developed as a method to speed ventilator weaning. With IMV or SIMV, the ventilator delivers only the set number of supported “mandatory” breaths, leaving all additional spontaneous breaths unsupported (although pressure support and/or CPAP may be provided for the spontaneous breaths). A typical approach was to initially adjust the ventilator to achieve full ventilatory support. This level of support was then continued until the patient’s disease state or condition sufficiently improved to warrant a reduction in support. An alternative partial ventilatory support strategy was sometimes used with IMV. With this strategy, following ventilator initiation the mandatory respiratory rate was immediately decreased and then titrated up and down to provide a level of partial support compatible with the patient’s changing clinical status. To use this mode to wean the patient, the number of supported breaths is decreased in a stepwise fashion as tolerated, usually by two breaths/min until complete spontaneous breathing is achieved. Each reduction in mandatory rate is followed by an assessment, which may include arterial blood gas analysis. This weaning is continued until the patient can tolerate breathing without support or at a low level of support (e.g., mandatory rate ≤ five supported breaths/min) for 2 hours; the patient is then extubated. It must be noted that early claims that IMV resulted in rapid ventilator weaning have not been substantiated. Current research suggests that IMV may prolong the need for ventilatory support and that it is the least effective method of weaning (as compared to SBTs or pressure support). Further, it has been shown that low levels of IMV support (e.g., machine cycling rate ≤ 50% of full ventilatory support values) may result in a work of breathing comparable to unsupported spontaneous breathing. This may be due to patients uncoupling their breathing efforts from the support provided by the machine. Moderate levels of pressure support (e.g., 5 to 10 cm H2O) can be used to overcome this additional work. Automatic tube compensation (ATC) may also be added to SIMV with certain ventilators (e.g., Evita 4, Evita XL, Puritan-Bennett 840, Puritan-Bennett 980) to provide inspiratory pressure augmentation to overcome the resistance of the artificial airway.

Pressure-Support Ventilation Pressure support is a form of ventilatory support in which inspiration is patient triggered and the inspiratory pressure rapidly rises to a preset value; the ventilator is then flow cycled to expiration. Pressure-support ventilation (PSV) may be used in combination with IMV/SIMV or as a standalone mode. For pressure-support ventilation (as standalone mode), the ventilator may be initially set up to provide a level of inspiratory pressure resulting in an appropriate tidal volume (e.g., 4 to 8 mL/kg IBW) that allows the patient to breathe comfortably at a rate of less than 25 breaths/min. Assuming the patient meets readiness criteria, the amount of pressure is gradually decreased, by 2 to 4 cm H2O at least twice per day (as tolerated). This is continued until the patient tolerates a pressure support of 5 cm H2O for 1 to 2 hours, then the patient is extubated. Pressure-support weaning is summarized in Box 1610.

BOX 16-10 Pressure-Support Weaning For initial ventilator setup as a standalone mode, the pressure-support level is typically set to achieve an acceptable tidal volume (e.g., 4 to 8 mL/kg IBW) resulting in a respiratory rate of 25 breaths/min or less. Typically, this requires pressure-support levels of 20 cm H2O or less. Following readiness testing, the pressure-support level is then decreased in a stepwise fashion as described below. 1. Verify readiness for ventilator discontinuance. a. Reversal or significant improvement in the disease state or condition requiring mechanical ventilatory support. b. Satisfactory oxygenation (PaO2/FIO2 ≥ 150 or SpO2 ≥ 90% on FIO2 ≤ 0.40 to 0.50). c. Stable spontaneous breathing pattern. d. Satisfactory acid-base status (pH > 7.25; no lactic acidosis). e. Hemodynamic stability (HR 60 to 100, BP > 90/60 but < 180/110 mmHg, low dose or no vasopressors to maintain blood pressure, no major arrhythmias or signs of myocardial ischemia). f. Overall medical condition stable (absence of fever; patient awake and alert or easily arousable).

Reduce the pressure-support level 2 to 4 cm H2O in an incremental fashion 2. followed by assessment of the patient’s respiratory rate, heart rate, blood pressure, SpO2, and overall condition. Tolerance of the reduction in pressure support is suggested by: a. Absence of signs of distress (e.g., no agitation, anxiety, diaphoresis, accessory muscle use). b. Respiratory rate (f) < 25 breaths/min. c. Heart rate and blood pressure are stable (increase or decrease < 20% of baseline). 3. Return pressure support to previous value if signs of intolerance occur and reassess. Signs of intolerance include: a. Respiratory distress, agitation, anxiety, sweating, accessory muscle use. b. f > 25 to 30 breath/min. c. HR increase > 20% or > 12 to 140 bpm. d. BP increase or decrease > 20% or systolic pressure < 90 mmHg or > 180 mmHg. e. Continue to decrease pressure support as tolerated at least twice a day (more frequently if tolerated). f. When PSV is reduced to 5 to 8 cm H2O for approximately 2 hours without distress, consider extubation.

The rationale behind these methods is that being on mechanical ventilation has induced respiratory muscle weakness, and patients subsequently need to “exercise” the respiratory muscles until the full workload can be managed. This is somewhat different from the more abrupt approach that is done with an SBT.

Spontaneous Breathing Trials An SBT is performed after acceptable weaning parameters are demonstrated and the criteria suggesting the patient is ready for extubation are met. The SBT is often the last step in determining readiness for extubation and is performed by leaving the ETT in place but removing or minimizing ventilator support for a more extended period, typically 30 to 120 minutes. The SBT itself has also evolved over time. The initial clinical trial assessing the rapid shallow breathing index performed SBTs using

a conventional T-piece attached to the ETT, which allows for unsupported spontaneous breathing. The T-piece does provide oxygen at the same FIO2 the patient was receiving from the ventilator, but no PEEP, CPAP, or pressure support. Common practice today uses the ventilator in a spontaneous breathing mode, which allows for the addition of pressure support (e.g., 5 cm H2O) and/or CPAP (e.g., 5 cm H2O). As an alternative, most modern ventilators can provide automatic tube compensation (ATC). With ATC, the patient breathes spontaneously, and only receives enough inspiratory support from the ventilator to overcome the calculated resistance of the endotracheal (or tracheostomy) tube. To use ATC, the ETT diameter is entered into the ventilator’s control system. The system then calculates and applies the appropriate amount of inspiratory pressure augmentation needed based on the diameter of the endotracheal or tracheostomy tube and the patient’s spontaneous inspiratory flow. Whichever method of SBT is performed, the duration is usually 30 minutes but may be extended to 120 minutes in patients who have minimally acceptable weaning parameters or those with other risk factors of extubation failure. It should be noted, however, that 30-minute trials have been shown to have similar predictive power as 120-minute trials in patients who have not required prolonged mechanical ventilatory support.12 Patients who fail an SBT are placed back on full ventilatory support and “rested” for 24 hours before a repeat SBT is performed. This contrasts with traditional weaning in which patients have a gradual decrease in support over a more extended period of time. Performing several SBTs per day has not been shown to significantly reduce ventilator days compared to once-daily SBTs.13 At our institution, we generally only repeat an SBT on the same day if there is a suspected confounder that caused the patient to fail the earlier SBT (e.g., residual sedation-limiting respiration or inadequately controlled pain during the SBT). Evidence-based guidelines for liberation from mechanical ventilation are summarized in Box 16-11.

BOX 16-11 Liberation from Mechanical Ventilation in Critically Ill Adults Evidence-based guidelines for acutely hospitalized patients ventilated for > 24

hours recommend the following. 1. Prior to ventilator discontinuance, protocols minimizing sedation should be implemented. 2. The preferred approach for ventilator discontinuance is the spontaneous breathing trial (SBT). 3. Specific weaning predictors (e.g., MIP, CRS [aka CST], RSBI) lack sufficient predictive value for routine use and independent clinician judgment tends to underestimate the capacity of patients to spontaneously breathe when disconnected from the ventilator. Specific readiness criteria that should be met are described in Box 16-4 and Box 16-8. 4. Once patients meet several readiness criteria, the SBT may be conducted. 5. The initial SBT may include 5 to 8 cm H2O of inspiratory pressure augmentation (e.g., pressure support or automatic tube compensation [ATC]) or be performed without inspiratory pressure augmentation (e.g., T-piece or CPAP). a. Some clinicians believe that successful SBTs performed without inspiratory pressure augmentation provide more convincing evidence of readiness for ventilator discontinuance. b. Some patients failing an SBT without pressure augmentation might pass with pressure augmentation and then be safely extubated. c. There is little consensus regarding how to conduct SBTs (e.g., with or without pressure augmentation); however, evidence-based guidelines suggest the use of 5 to 8 cm H2O of inspiratory pressure augmentation during an initial SBT. 6. If signs of respiratory failure appear during the SBT, mechanical ventilatory support is resumed. 7. If signs of respiratory failure do not appear during the SBT, the clinician should take steps towards achieving extubation. 8. Extubation to preventative NIV should be considered in patients with high risk of extubation failure (e.g., hypercapnia, COPD, congestive heart failure, or other serious comorbidities). CRSS, static respiratory system compliance; MIP, maximum inspiratory pressure; NIV, noninvasive ventilation; RSBI, rapid shallow breathing index (f/VTT); SBT, spontaneous breathing trial. Data from Ouellette DR, Patel S, Girard TD, et al. Liberation from mechanical ventilation in critically ill adults: an official American College of Chest Physicians/American Thoracic Society Clinical Practice Guideline. Chest. 2017;151(1):166–180.

Newer Methods With advancements in computer technology, newer methods of weaning from mechanical ventilation have been developed. These methods use artificial intelligence incorporated into the ventilator’s software to adjust ventilator settings based on specific algorithms and monitored data. These methods are often referred to as closed-loop ventilator modes. Many of these modes go by different names depending on the ventilator manufacturer but are largely based on the same principles. Examples include adaptive support ventilation (ASV), proportional assist ventilation (PAV), Smartcare/PS, AutoMode, and mandatory minute volume (MMV). While these modes can be used in various situations, the theoretic advantage for ventilator weaning is related to the system’s automated and continuous assessment of the patient. These modes are designed to continuously adjust the level of ventilatory support provided based on the patient’s needs. In theory, this should enable more rapid liberation of the patient from the ventilator. Two relatively recent reviews and meta-analyses have been conducted. These studies were unable to draw clear conclusions about which (if any) newer method is especially beneficial; however, no overt harm in using closed-loop methods was identified.14,15 One study suggested closed-loop or “automated” weaning may be useful in settings with more limited clinician availability. However, evidence to suggest these modes are superior to daily SBTs is minimal. RC Insight Performing an SBT with 5 cm H2O of pressure support and 5 cm H2O of CPAP is equivalent to providing the patient with BiPAP of 10/5.

Selection and Approach As noted, methods for ventilator discontinuance include SBTs, pressure-support ventilation (PSV), and intermittent mandatory ventilation (IMV). While the best method of ventilator discontinuation is somewhat controversial and there is substantial variation in practice, the most widely accepted approach is the daily SBT. In at least one study, SBTs showed a decreased time to extubation and were less labor intensive than traditional IMV or PSV weaning.11 As noted above, closed-loop methods may be acceptable; however, further research with more direct head-tohead trials is needed to determine if closed-loop ventilation is preferable. SBT methods are also variable. SBTs may be conducted using the ventilator in spontaneous mode (with or without pressure augmentation) or T-piece attached to the ETT. As noted above, T-piece trials give the least support to the patient and may raise the threshold for passing the test. More commonly, SBTs using 5 to 8 cm H2O of pressure support are completed; 5 cm H2O of CPAP may be added. We usually perform SBTs with ATC or pressure support (5 cm H2O) and CPAP (5 cm H2O). In patients at high risk of extubation failure or risk factors for difficulty with reintubation, a more rigorous, unsupported trial is conducted (e.g., no PSV or CPAP, or CPAP only). An unsupported trial may also be conducted in patients with pulmonary edema, to assess whether removal of positive pressure results in a reaccumulation of pulmonary edema and difficulty with spontaneous breathing. Ultimately, the selection of weaning method must consider individual patient factors as well as available clinical resources.

Monitoring During the SBT, the patient should be closely monitored to assure patient safety and adequately assess the patient’s response to the SBT. During the SBT, much or all ventilatory support is withdrawn, and patients may experience significant decreases in oxygen saturation and hemodynamic instability. Because SBTs are usually conducted in the ICU, continuous telemetry for cardiac rhythm and rate and continuous pulse oximetry are provided. Blood pressure (BP) monitoring is also common, but no standard of frequency during SBTs exists. We suggest that BP be assessed, as a minimum, whenever other signs of intolerance occur (e.g., significantly increased heart rate, increased respiratory rate, respiratory distress, anxiety). Both the nurse and respiratory therapist should monitor the patient closely for vital sign derangements. The assessment of performance during the SBT is generally based on vital signs, though reassessment of RSBI may also be done. Typical criteria for terminating an SBT are increased heart rate to > 120 to 140 bpm or ≥ 20% increase from baseline, decrease in oxygen saturation < 90%, increased respiratory rate to ≥ 35, systolic blood pressure of >180 mmHg, or a decline in systolic blood pressure by 20% or more. Other signs of distress, such as agitation, anxiety, or significant diaphoresis, should also result in the termination of an SBT.11 If patients show more modest vital sign derangements, clinical judgement and context must be used to determine if the patient should be placed back on the ventilator, or if they are now ready for extubation. RC Insight Patients should be closely monitored during SBTs because they are at high risk of developing unstable vital signs.

Extubation The last step in liberating the patient from mechanical ventilation is extubation. Airway patency and protection are required for success. Patients should have an effective cough, be able to manage their secretion clearance, and have a sufficient level of consciousness and neurologic function. To achieve extubation, the patient is placed in an upright position. Oral and tracheal secretions are removed by suctioning. The ETT cuff is then deflated and the tube is removed in a rapid and smooth fashion. We prefer to extubate most patients as soon as possible following a successful SBT. Extubation during daytime hours is preferable; however, extubation may be performed at other times when the risk of reintubation is minimal. Following extubation, oxygen therapy is provided, usually by aerosol facemask or low to moderate flow nasal cannula. There is some evidence that a high-flow nasal cannula (HFNC) may reduce the rate of respiratory failure and reintubation, but current evidence does not support the routine use of HFNC following extubation. HFNC may be indicated in patients who are severely hypoxemic following extubation. Current guidelines do suggest that certain patients at high risk for extubation failure receive preventative noninvasive ventilation (NIV). Rapid institution of NIV should be performed as soon as it becomes apparent that the patient may be failing extubation. Aggressive oxygen therapy and techniques to promote airway clearance can also help prevent reintubation in at-risk patients. This may include suctioning and airway care and bronchodilator therapy. A small percentage of patients will self-extubate. These unplanned extubations generally require immediate reintubation, unless the patient is clinically stable, has a patent airway, can clear secretions, and has satisfactory oxygenation and spontaneous ventilation.

Monitoring Following Extubation Following extubation, patients should be monitored for signs of extubation failure. Patients at greatest risk for reintubation include those with a weak cough and those requiring frequent suctioning. Other risk factors include older patients with severe chronic cardiac or respiratory disease, pneumonia as the cause of respiratory failure, and those with a positive fluid balance in the 24 hours preceding extubation.

Currently, there are no national guidelines regarding duration or type of monitoring that should be performed following extubation. The patient should be directly observed for at least the first several minutes following extubation for any signs of distress. Auscultation for stridor, wheezing, and secretions should occur. The patient should be asked to cough to assess the ability to clear secretions. Assuming the patient does well immediately postextubation, routine ICU level monitoring with telemetry and continuous pulse oximetry should continue, and frequent nursing and respiratory care assessments should be performed. The duration of ICU monitoring required is debatable; factors such as duration of mechanical ventilation, risk of extubation failure, postextubation oxygen requirements, mental status, and comorbidities should be taken into consideration. As a general rule, the longer the patient was intubated, the longer he or she should be monitored in the ICU following extubation. For patients intubated less than 24 hours with no comorbidities and who are low risk for extubation failure, ICU monitoring for 6 hours is probably adequate. For patients with longer durations of mechanical ventilation or other risk factors, at least 12 to 24 hours of ICU observation is suggested. As noted, national guidelines do recommend that hospitalized patients who pass an SBT, who are at high risk for extubation failure, and have been receiving mechanical ventilation for more than 24 hours be extubated directly to noninvasive ventilation (NIV).16 Box 16-12 provides a protocol for SBTs.

BOX 16-12 Spontaneous Breathing Trials Spontaneous breathing trials (SBT) have been suggested for liberation of most critically ill adult patients from mechanical ventilation. Readiness testing provides clinical criteria to determine if the patient is ready to begin the SBT. Satisfactory readiness criteria include: ∎ Resolution or sufficient improvement in the cause of respiratory failure ∎ Adequate oxygenation ∎ Arterial pH > 7.25 ∎ Hemodynamic stability without myocardial ischemia ∎ Spontaneous inspiratory effort present Additional, optional readiness criteria include absence of severe anemia (e.g., Hb ≥ 7 to 10 g/dL), absence of fever (core temperature ≤ 38° to 38.5°C), and

absence of depressed mental status (e.g., patient should be awake and alert or easily arousable). RSBI ≥ 105 is moderately useful in predicting the probability of weaning failure. Steps in completing an SBT include: 1. Assess readiness for SBT (see above). 2. Prepare the patient. a. Minimize sedation. For patients receiving mechanical ventilation for more than 24 hours, a sedation protocol should be employed. b. Ensure that no other major activities or planned procedures will interfere with the SBT. c. Explain the procedure to the patient. Assure that you will be present to monitor his or her condition and reinstitute mechanical ventilatory support, as needed. d. Suction the airway, if needed. e. Position the patient, sitting up if possible. 3. Begin the SBT. a. Adjust the ventilator to provide spontaneous breathing. The initial SBT should be conducted with inspiratory pressure augmentation (e.g., 5 to 8 cm H2O of pressure support [PSV] or automatic tube compensation [ATC]). b. Be aware that the use of inspiratory pressure augmentation will tend to improve SBT results. For example, PSV, ATC, and CPAP tend to lower measured RSBI values and give the impression that the patient may be better able to breathe spontaneously than will be possible without support. As an alternative, the patient may be placed on a T-piece for spontaneous breathing without pressure augmentation. 4. Monitor the patient carefully. 5. Reinitiate mechanical ventilation if any of the following occur: a. Anxiety, agitation, sweating, respiratory distress. b. Respiratory rate increases to ≥ 35 breaths/min. c. SpO2 decreases to < 90%. d. Heart rate i. Increases ≥ 20% above baseline or HR > 120 to 140 bpm. ii. Decreases more than 20% below baseline. e. Systolic blood pressure i. Increases to > 180 mmHg. ii. Decreases to < 90 mmHg or decreases 20% or more from baseline. 6. If SBT is well tolerated and no adverse changes occur (see steps 4 and 5

above), continue the trial for at least 30 minutes but not more than 2 hours. 7. If the patient does well during the SBT for 30 to 120 minutes, consider extubation. 8. For patients failing their first SBT, SBTs are repeated, generally once each day. Ventilator settings should be adjusted to allow for ventilatory muscle rest between SBTs. 9. Some patients may require three or more SBTs to succeed or more than 7 days to pass an SBT. These patients are considered difficult to wean and efforts should be made to identify and correct the cause of continued ventilator dependence. Data from Epstein SK. Weaning from mechanical ventilation: the rapid shallow breathing index. In: Parsons PE, Finlay G, eds. UpToDate; September 12, 2017; Weaning from mechanical ventilation: readiness testing. In: Parsons PE, Finlay G, eds. UpToDate; November 2018; and Management of the difficult-towean adult patient in the intensive care unit. In: Parsons PE, Finlay G, eds. UpToDate; January 19, 2018.

RC Insight Patients who been ventilated > 24 hours and are high risk for extubation failure should be extubated to NIV.

Management of Postextubation Upper Airway Obstruction One of the most dreaded complications encountered following extubation is postextubation stridor and airway obstruction. Postextubation airway obstruction with stridor is associated with narrowing of the airway after removal of the ETT, usually because of swelling at or around the vocal cords. Signs of postextubation airway obstruction include stridor, respiratory distress, trouble with phonation, and elevations in arterial carbon dioxide. Surprisingly, signs are often not present immediately following extubation but can develop acutely several hours after extubation. Postextubation stridor is particularly worrisome because it can develop very rapidly and lead to respiratory failure. Postextubation upper airway obstruction can also make reintubation very difficult. Systemic corticosteroid administration is the mainstay in treatment of postextubation stridor. If possible, treatment should be started prior to extubation. If treatment is not initiated prior to extubation, the onset of action will be too slow to provide immediate improvement. In such cases, temporizing measures such as nebulized racemic epinephrine, BiPAP, and heliox therapy may be attempted,

although there is little evidence guiding the use of these alternative therapies. The need for reintubation depends on the severity of the obstruction and the patient’s clinical status; however, delays in reintubation should be avoided if the patient is showing signs of worsening. Plans for reintubation should include ready access to small (≤ 6.5 mm ID) ETTs, given the increased likelihood of airway narrowing. Surgical backup for an emergent surgical airway insertion (e.g., percutaneous tracheostomy) should be arranged. Following reintubation for postextubation stridor, there is little in the literature to guide the approach to repeat extubation. Typically, systemic steroids are given for 24 to 48 hours. Repeat cuff-leak tests are often performed, though the reliability of this test in this setting is unknown. Often, the ETT is removed over an ETT exchange device with otolaryngology service (aka ear-nose-throat, or ENT) backup available. In high-risk patients, the two safest options include proceeding directly to tracheostomy or a controlled extubation performed in the operating room under the guidance of anesthesiology with an otolaryngologist ready to perform a tracheostomy, if needed. Endoscopy can also be performed at that time to further gauge the risk for recurrence.

Extubation Failure Extubation failure is generally defined as the need for reintubation within 48 hours. Despite careful assessment for extubation readiness, there will be a significant rate of extubation failure. Given the associated risks, attempts should be made to discontinue mechanical ventilation as soon as possible. Most authors and clinicians feel that the risk of extubating too soon (resulting in extubation failure) must be balanced against the risk of extubating too cautiously and prolonging mechanical ventilation unnecessarily. Exact numbers vary, but most reports suggest an extubation failure rate of 10% to 20% represents an acceptable balance between proactive and conservative ventilator discontinuation. RC Insight A failed extubation occurs when reintubation is needed within 48 hours.

When extubation failure does occur, it is essential to assess factors that led to the

failure. It is important to discern if the failure was related to inadequate reversal of the primary problem initially causing respiratory failure, or if a new process is contributing. If the primary process had inadequately improved, more time may be the main treatment. If new issues, such as volume overload, nosocomial infection, delirium, or postextubation airway obstruction are to blame, then treatment should focus on those issues. Last, it should be noted that extubation failure identifies the patient as having a higher risk of adverse outcome. Specifically, extubation failure is independently associated with an approximate 8-fold increase in nosocomial pneumonia and a 6- to 12-fold increase in mortality.17 Factors associated with extubation failure are summarized in Box 16-13.

BOX 16-13 Factors Associated with Extubation Failure Extubation failure is generally defined as the need for reintubation within 48 hours. The risk of extubating too soon resulting in extubation failure must be balanced against the risks of extubating too cautiously and prolonged and unnecessary mechanical ventilation. Factors associated with extubation failure include: ∎ Insufficient improvement in the underlying condition requiring intubation and mechanical ventilatory support ∎ Weak cough ∎ Increased sputum volume requiring frequent suctioning ∎ RSBI > 58 ∎ Impaired neurologic function (GSC < 8) ∎ Upper airway obstruction (e.g., postextubation stridor, soft tissue obstruction) ∎ Positive fluid balance during the 24 hours prior to extubation ∎ Pneumonia as the primary diagnosis requiring mechanical ventilatory support ∎ Older patients (≥ 65 years) with severe chronic respiratory or cardiac disease Data from Hyzy RC. Extubation management. In: Manaker S, Finlay G, eds. UpToDate; 2014.

RC Insight Extubation failure requiring reintubation is associated with an 8-fold increase in nosocomial pneumonia and up to a 12-fold increase in mortality.

Long-Term Ventilator Dependence Long-term ventilator dependence, more aptly termed prolonged mechanical ventilation (PMV), has been defined variably in the literature and no clear consensus definition is currently available. To better define PMV, the National Association for Medical Direction of Respiratory Care convened a conference in 2005 that proposed that PMV should be defined as the need for mechanical ventilation for ≥ 21 consecutive days for at least 6 hours per day.18 Due to the variable definition of PMV, its true incidence and prevalence remain unknown, but it is estimated that between 6% and 14% of mechanically ventilated patients require PMV.19–21 Numerous studies have sought to identify predictors of the need for PMV; however, due to the heterogeneity of this population, no clear predictors have been identified thus far. Traditionally, patients requiring PMV have been cared for in the ICU; however, changes in reimbursement strategies in the 1990s favored transition of care from the acute care hospital to long-term acute care (LTAC) facilities for weaning of PMV. RC Insight Prolonged mechanical ventilation can be defined as the need for mechanical ventilation ≥ 21 consecutive days for at least 6 hours per day.

PMV is associated with an increased risk in morbidity and mortality. The decision to pursue PMV should be a shared one between the patient and his or her designated medical decision maker(s) and the treating physician. Particular focus should be placed on the patient’s preferences and anticipated outcomes. Early involvement of the palliative care team should be considered, if it appears that accomplishment of the patient’s goals is unlikely. Most patients in whom PMV is pursued should undergo tracheostomy placement to facilitate comfort, communication, secretion management, and transfer to an LTAC facility. RC Insight The patient’s preferences and anticipated outcomes should be reviewed and discussed with patient and/or designated decision maker(s) prior to pursuing prolonged mechanical ventilation.

The need for PMV is often related to incomplete resolution of acute illness (e.g., ARDS, sepsis) and/or development of new problems. Given the complex nature of weaning failure, Heunks and van der Hoeven proposed an “ABCDE” approach for systematic review and rapid correction of barriers to weaning (not to be confused with the ABCDEF bundle described earlier).22 These potential barriers to ventilator liberation include: Airway/lung dysfunction Brain dysfunction Cardiac dysfunction Diaphragm dysfunction Endocrine dysfunction Evaluation of the airway should include assessment of airway resistance, lung compliance, tracheal disease, and gas exchange. Attention should be placed on lung compliance and gas exchange, as these factors may improve over time allowing for more rapid weaning. Delirium is the primary driver of brain dysfunction in this patient population. The Confusion Assessment Method for the ICU (CAM-ICU) is now widely used to screen for delirium. This bedside test assesses alteration in mental status and disorganized thinking. CAM-ICU positive implies the patient is experiencing delirium. Therapy focuses on minimizing sedation and sleep disturbances. Cardiac dysfunction is common in this patient population, and as many as 25% of patients requiring PMV have underlying congestive heart failure or ischemic heart disease. Weaning trials often increase metabolic demand and may uncover underlying cardiac dysfunction. Electrocardiography, transthoracic echocardiography, and brain natriuretic peptide (BNP) may be useful in identifying patients with a cardiac component of weaning failure. Therapy should focus on optimizing heart disease management, volume status, and arrhythmia management.22,23 Diaphragm or respiratory muscle weakness often exists in the setting of general muscle weakness. Critical illness neuromyopathy is a significant contributor in this area. Definitive diagnosis is often elusive. Assessment of MIP, as previously described, may be useful in identifying patients with overt respiratory muscle weakness, but MIP does not assess respiratory muscle endurance and is therefore

limited in its utility in this patient population. The contribution of endocrine and electrolyte disturbances to weaning failure is less clearly defined; optimization of thyroid function and electrolytes, however, is good medical practice. Clinical Focus 16-3 includes the ABCDE approach.

CLINICAL FOCUS 16-3 Failure to Achieve Ventilator Liberation A 76-year-old male with a history of hypertension and diabetes is admitted to the ICU with acute respiratory distress syndrome (ARDS) requiring mechanical ventilation. After 10 days, he is hemodynamically stable and requires minimal ventilatory support. Over the next week, he undergoes a spontaneous awakening trial followed by a spontaneous breathing trial (SBT) every morning. His rapid shallow breathing index (RSBI) ranges from 50 to 150. The respiratory therapist notes that the patient appears anxious and diaphoretic at times. Question 1: What factors may be contributing to this patient’s poor performance on spontaneous breathing trials (SBTs)? Answer: The ABCDE approach is a systematic algorithm to identify barriers to ventilator liberation. The mnemonic stands for: Airway and lung dysfunction Brain dysfunction Cardiac dysfunction Diaphragm dysfunction Endocrine dysfunction Rapid correction of any of these factors may allow for more rapid liberation from the ventilator. Question 2: What are some airway factors that limit successful liberation the patient from the ventilator? Answer: Increased airway resistance, decreased compliance, and impaired gas exchange can all contribute to failure. Causes of increased airway resistance include the narrow diameter endotracheal or tracheostomy tubes, mucus plugs, tracheal disease, and bronchospasm. Therapies should focus on optimization of tube size and positioning, adequate bronchodilator administration, aggressive pulmonary toilet, and visualization of the trachea by bronchoscopy. Decreased compliance may be caused by limited distensibility of the chest wall (e.g., edema, ascites, pregnancy, obesity) or lungs (e.g., ARDS, pneumonia, interstitial lung disease). Lung compliance may change over time as the

underlying lung pathology changes; thus, frequent reassessment of static and dynamic compliance may allow for more rapid ventilator discontinuance. Question 3: What are some brain factors that limit weaning? Answer: Delirium and other psychological disturbances frequently occur in patients on mechanical ventilation. The Confusion Assessment Method for the ICU (CAMICU) is a readily available screening tool to assess for delirium at the bedside. Therapy should focus on limiting pharmacologic contributors (especially benzodiazepines), frequent reorientation of the patient, providing glasses and hearing aids, and regularzation of the patient’s sleep–wake cycle. Question 4: What are some cardiac factors that limit weaning? Answer: SBTs often increase metabolic demand and can precipitate hemodynamic instability, particularly in patients with underlying ischemic heart disease or congestive heart failure. Electrocardiogram (ECG), brain natriuretic peptide (BNP), and transthoracic echocardiography (TTE) may be useful in identifying this subset of patients. Question 5: What are some diaphragm factors that limit weaning? Answer: SBTs and other methods of ventilator weaning often place increased demand on the inspiratory muscles. Patients requiring prolonged mechanical ventilation often have muscle weakness and limited compensatory reserve. Critical illness polyneuropathy and myopathy are increasingly being recognized as contributors to respiratory muscle impairment; however, they are difficult to diagnosis definitively. Therapeutic strategies are limited but frequently focus on early mobility. Question 6: What are some endocrine factors that limit weaning? Answer: There has been limited research in this area, but optimization of thyroid function and electrolytes (particularly potassium, magnesium, and phosphorus) is potentially beneficial.

RC Insight An ABCDE (Airway, Brain, Cardiac, Diaphragm, Endocrine) dysfunction approach can systematically identify and rapidly correct barriers to weaning.

The optimal weaning strategy in PMV remains unclear. Several approaches including gradual reduction in pressure-support ventilation, SBTs, and capping of the

tracheostomy tube with noninvasive ventilation have been utilized. More recently, multiple studies have suggested that protocolized care (particularly utilizing respiratory therapists) with frequent reassessment may shorten the duration of PMV and that this standardized care may be more important than the specific weaning strategy utilized.24,25 Weaning rates from PMV have varied significantly. A meta-analysis of 30 multinational studies showed a rate of successful liberation from PMV of around 50% (range 47% to 53%).26 The duration of weaning has also been variable, likely related to the heterogeneity of patients requiring PMV. Pooled data of nine observational studies suggest that these patients spend, on average, 36 days in the ICU followed by 31 days of weaning at a post-ICU facility. Because of this, patients should not be considered permanently ventilator dependent until at least 3 months of weaning attempts are unsuccessful.27 RC Insight As many as 50% of patients requiring prolonged mechanical ventilation will be successfully liberated from the ventilator.

Terminal Weaning Terminal weaning refers to the process of withdrawing ventilator support from a patient who is not expected to survive. With few exceptions, most religions, societies, and ethicists support the notion that it is acceptable and moral to remove artificial life support if it is no longer desired by the patient and the patient’s medical decision maker, especially with the support of the treating clinician. This is generally done in patients with a very poor prognosis, and in whom additional mechanical ventilation would artificially extend their lifespan with an unacceptably low quality of life. Terminal weaning is somewhat of a misnomer and is probably better described as terminal extubation. Preparation for such an extubation depends on the patient’s condition as well as predetermined goals. Sedatives and analgesic medications are usually given to the patient prior to extubation to minimize suffering. In some cases, this must be balanced with the patient’s wishes to be alert enough to communicate with family following the extubation. Practice varies significantly, but other methods of life support, such as vasoactive medications, are often withdrawn prior to the discontinuance of mechanical ventilation. There is typically no need for measuring weaning parameters as sustained respiration after extubation is not the goal. The exception to this rule occurs if other medical conditions are fairly stable, but it has been made clear by the patient or designated medical decision makers that if the patient fails extubation, he or she would not want to undergo repeat intubation. In these cases, the patient is optimized for extubation success as much as possible. However, conventional extubation criteria are often not achievable or achievement would require an unacceptably long duration of mechanical ventilation. RC Insight Terminal extubation refers to the discontinuation of mechanical ventilation as part of withdrawing life support in a patient who is not expected to survive, to decrease suffering and allow for a more peaceful death.

Key Points Because of the associated risks, mechanical ventilation should be discontinued as quickly and safely as possible. The primary criterion for ventilator discontinuance is improvement or reversal of the disease state or condition that required the need for mechanical ventilation. Ventilator discontinuance is a broad term that includes SBTs and ventilator weaning, which involves a gradual decrease in the level of ventilatory support. Premature discontinuation of the ventilator may require reinstitution of ventilatory support, further delaying the patient’s recovery. Factors that contribute to ventilator dependence include oxygenation problems, cardiovascular problems, neurologic problems, psychological factors, poor nutrition, and multiple comorbidities. Mechanical factors can contribute to ventilator dependence and these include inappropriate ventilator settings, patient–ventilator asynchrony, and increased work of breathing due to the artificial airway. If ventilatory requirements exceed the patient’s spontaneous ventilatory capacity, ventilator discontinuance may not be possible. Reduced or absent respiratory drive to breathe, ventilatory muscle fatigue, and ventilatory muscle dysfunction or weakness may cause decreased ventilatory capacity. Hypoxemia, metabolic acidosis, pain and anxiety, increased CO2 production, increased physiologic dead space, and lung receptor stimulation may cause an increase in ventilatory requirements or demand. Factors associated with readiness for ventilator discontinuance include adequate oxygenation (P/F ratio ≥ 150) and acid-base status (pH > 7.25). Oxygen requirements ≤ 50% and ≤ 5 cm H2O of PEEP are generally acceptable for proceeding with SBTs. Hemodynamic stability should be achieved before further assessment of the readiness for discontinuation of mechanical ventilation is performed. Very high or very low blood pressure could preclude starting SBTs. Bedside assessment of patients’ spontaneous breathing may include measurement of spontaneous tidal volume (VT), respiratory rate (f), minute ventilation (V̇E), rapid shallow breathing index (RSBI), maximum expiratory pressure (MIP), and vital capacity (VC). MIP provides a measure of inspiratory muscle strength, while maximum expiratory pressure (MEP) provides a measure of expiratory muscle strength. Measurement of PaCO2 provides the single best clinical indicator of adequate ventilation. Failure to recognize acute or chronic acid-base abnormalities may result in failure to achieve liberation from the ventilator.

The rapid shallow breathing index (RSBI) is the ratio of respiratory rate (breaths/min) to tidal volume (L). RSBI < 105 is associated with about an 80% chance of successful extubation in patients requiring mechanical ventilation for more than 24 hours. Methods of ventilator weaning and discontinuance include IMV/SIMV, pressuresupport ventilation (PSV), and SBTs. Once per day SBTs may result in earlier extubation than SIMV or pressuresupport weaning. Daily cessation of sedation may improve SBT success. The ABCDEF bundle includes Assess, treat, and manage pain; Both spontaneous awakening trials (SATs) and SBTs; Choice of analgesia and sedation; Delirium (assess, prevent, manage); Early mobility and exercise; and Family engagement and empowerment. Newer “closed-loop” modes of mechanical ventilation have not yet been shown to result in early extubation when compared to once daily SBTs. Malnutrition is a common complication of critical illness that can affect respiratory muscle strength. Anxiety, depression, and poor motivation can affect success and liberating the patient from the ventilator. Indices for predicting readiness for ventilator discontinuance include measures of oxygenation, measures of acid-base balance, measures of ventilation, measures of ventilatory muscle strength, measures of ventilatory workload, and measures of respiratory drive. Initial SBTs should generally include inspiratory pressure augmentation in the form of pressure support or automatic tube compensation (ATC). A failed SBT is defined by the development of significant tachycardia, tachypnea, drop in oxygen saturation, or other signs of distress. Assessment of the patient’s ability to protect the airway and achieve adequate pulmonary secretion clearance should be performed prior to extubation. The cuff-leak test is sometimes used for assessment of laryngeal edema in intubated patients. Absence of a cuff leak is neither a sensitive nor specific marker for postextubation airway obstruction, but a cuff leak of less than 110 cc or 25% of the tidal volume has been associated with a higher chance of postextubation stridor. Corticosteroids are the mainstay of therapy for postextubation stridor. Extubation failure requiring reintubation is associated with an 8-fold increase in nosocomial pneumonia and a 6- to 12-fold increase in mortality. Prolonged mechanical ventilation (PMV) can be defined as the need for mechanical ventilation ≥ 21 consecutive days for at least 6 hours per day. Approximately 10% of mechanically ventilated patients may require PMV.

Weaning from prolonged mechanical ventilation frequently takes place in longterm acute care (LTAC) facilities. The decision to implement or continue PMV should include a discussion with the patient and/or his or her designated medical decision maker(s) to identify the patient’s preferences and discuss the anticipated outcomes. The ABCDE algorithm (Airway dysfunction, Brain dysfunction, Cardiac dysfunction, Diaphragm dysfunction, Endocrine dysfunction) can help identify barriers to weaning. Approximately 50% of patients who require prolonged mechanical ventilation are successfully weaned. Patients should not be considered permanently ventilator dependent until at least 3 months of weaning efforts have failed. Withdrawing mechanical ventilation in a patient who no longer wishes to undergo life-sustaining therapy is a difficult but ethical and acceptable practice.

References 1. Boles J-M, Bion J, Connors A, et al. Weaning from mechanical ventilation. Eur Respir J. 2007;29:1033– 1056. 2. McConville J, Kress JP. Weaning patient from the ventilator. N Engl J Med. 2012;367:2333–2339. 3. Lemaire R, Teboul JL, Cinotti L, et al. Acute left ventricular dysfunction during unsuccessful weaning from mechanical ventilation. Anesthesiology. 1988;69:171–179. 4. Tseng YH, Ko HK, Tseng YC, et al. Atrial fibrillation on intensive care unit admission independently increases the risk of weaning failure in nonheart failure mechanically ventilated patients in a medical intensive care unit. Medicine. 2016;95:3744–3753. 5. The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Comparison of two fluidmanagement strategies in acute lung injury. N Engl J Med. 2006;354:2564–2575. 6. Ely EW, Inouye SK, Bernard GR, et al. Delirium in mechanically ventilated patients: validity and reliability of the confusion assessment method for the intensive care unit (CAM-ICU). JAMA. 2001;286:2703–2710. 7. Wittekam B, Van Mook W, Tjan D, et al. Clinical review: postextubation laryngeal edema and extubation failure in critically ill adult patients Crit Care. 2009;13:233. 8. Sahn SA, Lakshiminarayan S. Bedside criteria for discontinuation of mechanical ventilation. Chest. 1973;63:1002–1005. 9. Yang K, Tobin M. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med. 1991;324:1445–1450. 10. Chevrolet JC, Deleamont P. Repeated vital capacity mesurements as a predictive parameters for mechical ventilation need and weaning success in Guillain-Barré syndrome. Am Rev Respir Dis. 1991;144:814–818. 11. Nguyen T, Badjatia N, Malhotra A, et al. Factors predicting extubation success in patients with GuillainBarre syndrome. Neurocrit Care. 2006;5(3):230–234. doi:10.1385/NCC:5:3:230. 12. Estaban A, Frutos F, Tobin M, et al. A comparison of four methods of weaning patients from mechanical ventilation. N Engl J Med. 1995;332:345–350. 13. Esteban A, Alía I, Tobin MJ, et al. Effect of spontaneous breathing trial duration on outcome of attempts to discontinue mechanical ventilation. Am J Respir Crit Care Med. 1999;159:512–518. 14. Rose L, Schultz M, Cardwell C, et al. Automated versus non-automated weaning for reducing the duration of mechanical ventilation for critically adults and children: a Cochrane systemic review and meta-analysis. Crit Care. 2015;19:48. doi 10.1186/s13054-015-0755-6. 15. Burns K, Lellouche F, Lessard M, Friedrish J. Automated weaning and spontaneous breathing trial systems versus non-automated weaning strategies for discontinuation time in invasively ventilated post-operative adults. Cochrane Database Syst Rev. 2014; (2):CD008639. doi: 10.1002/14651858.CD008639.pub2. 16. Ouillette DR, Patel S, Girard T, et al. Liberation from mechanical ventilation in critically ill adults: an official American College of Chest Physicians/American Thoracic Society Clinical Practice Guideline. Chest. 2017;151:166–180. 17. MacIntyre N. Evidence-based assessments in the ventilator discontinuation process. Respir Care. 2012;57:1611–1618. 18. MacIntyre NR, Epstein SK, Carson S, et al. Management of patients requiring prolonged mechanical ventilation: report of a NAMDRC consensus conference. Chest. 2005;128(6):3937–3954. 19. Lone NI, Walsh TS. Prolonged mechanical ventilation in critically ill patients: epidemiology, outcomes, and modeling the potential cost consequences of establishing a regional weaning unit. Crit Care. 2011;15(2):R102. doi:10.1186/cc10117. 20. Estenssoro E, Gonzalez F, Laffaire E, et al. Shock on admission day is the best predictor of prolonged mechanical ventilation in the ICU. Chest. 2005;127(2):598–603. 21. Cox CE, Carson SS, Lindquist JH, et al. Differences in one-year health outcomes and resource utilization by definition of prolonged mechanical ventilation: a prospective cohort study. Crit Care. 2007;11(1):R9. 22. Heunks LM, van der Hoeven JG. Clinical review: the ABC of weaning failure—a structured approach. Crit Care. 2010;14(6):245. 23. White AC. Long-term mechanical ventilation: management strategies. Respir Care. 2012;57(6):889–897. 24. Scheinhorn DJ, Chao DC, Stearn-Hassenpflug M, Wallace WA. Outcomes in post-ICU mechanical ventilation: a therapist weaning protocol. Chest. 2001;119(1):236–242. 25. Chao DC, Scheinhorn DJ. Determining the best threshold of rapid shallow breathing index in a therapistimplemented patient-specific weaning protocol. Respir Care. 2007;52(2):159–165.

26. Damuth E, Mitchell JA, Bartock JL, et al. Long-term survival of critically ill patients treated with prolonged mechanical ventilation: a systematic review and meta-analysis. Lancet Respir Med. 2015;3(7):544–553. 27. MacIntyre NR, Cook DJ, Ely EW Jr, et al. Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American Association for Respiratory Care; and the American College of Critical Care Medicine. Chest. 2001;120(6 Suppl):375S–395S.

Appendix

A Mechanical Ventilation and Critical Respiratory Care and the National Board for Respiratory Care (NBRC) Examinations1 © Anna RubaK/ShutterStock, Inc.

The National Board for Respiratory Care (NBRC) currently administers several different examinations which include content related to critical respiratory care and mechanical ventilation. These include the Therapist Multiple-Choice Examination, the Clinical Simulation Examination, the Adult Critical Care Specialty (ACCS) Examination and the Neonatal/Pediatric Specialist (NPS) Examination. In addition, the NBRC administers specialty examinations in the areas of pulmonary function technology (i.e. certification examination for entry-level pulmonary function technologist [CPFT] and registry examination for advanced pulmonary function technologist [RPFT]) and a sleep disorders specialty examination. The admission policies for each of these examinations can be found at the NBRC website (see: www.NBRC.org). The Therapist Multiple-Choice Examination and Clinical Simulation Examination are broken down into three major areas: 1) Patient Data, 2) Troubleshooting and Quality Control of Devices, and Infection Control, and 3) Initiation and Modification of Interventions. The Adult Critical Care Specialty Examination is broken down into two

broad areas: 1). Respiratory Critical Care and 2.) General Critical Care. What follows is a brief summary of the content areas of these examinations directly related to mechanical ventilation and critical respiratory care along with the corresponding book chapters for this text listed.

Therapist Multiple Choice Examination and Clinical Simulation Examination Patient I. Data (chapters 1, 2, and 8) The review of the patient’s medical record should include the written patient history and physical examination; review of physician’s orders relative to the cardiopulmonary system; lines, drains, and airways; laboratory results; blood gas analysis and/or hemoximetry (co-oximetry) results; pulmonary function testing results and six minute walk test results; imaging study results; maternal and perinatal/neonatal history; sleep study results; trends and monitoring results; and determination of the patient’s pathophysiologic state. Clinical assessment should include the patient interview, and physical examination. In addition, the respiratory therapist must be able to perform procedures to gather additional clinical information and evaluate procedure results. Specific information tested by the NBRC exams includes each of the following areas:1

Data in the Patient Record (see chapters 1, 2, and 8) 1. Patient history, to include diagnosis, admission notes, history of the present illness, orders, medication, progress notes, DNR status/advanced directives, and social, family, and medical history (see Chapters 1, 8). 2. Physical examination with an emphasis on the cardiopulmonary system (see Chapter 1, 8). 3. Laboratory results found in the medical record, to include CBC, electrolytes, coagulation studies, sputum culture and sensitivities, and cardiac biomarkers (see Chapters 1, 8). 4. Blood gas analysis and/or hemoximetry (CO oximetry) results (see also Chapters 1, 7, 8). 5. Pulmonary function testing results (see Chapter 8). 6. The results of imaging studies to include chest radiographs, CT scans, ultrasonography and/or echocardiography, PET scan, ventilation/perfusion

7. 8. 9.

10.

scan (see also Chapters 1, 8, 13). Maternal and perinatal/neonatal history scan (see Chapter 15). Sleep study results (see also Chapter 3 and 10). Trends in monitoring results (fluid balance, vital signs, intracranial pressure, ventilator liberation parameters, pulmonary mechanics, noninvasive monitoring, ECG, hemodynamics) (see also Chapters 1, 7-9). Determination of patient’s pathophysiologic state (see also Chapters 1, 2, 5-8, 12-13).

Clinical Assessment (Chapters 1, 2, 8) 1. Patient interview to include level of consciousness (LOC) and orientation, emotional state, ability to cooperate, pain, shortness of breath, sputum production, exercise tolerance, smoking history, environmental exposures, activities of daily living (ADLs), and learning needs (see also Chapters 1, 8). 2. Inspection to assess general appearance, airway characteristics, cough, sputum production, and character, status of the neonate (e.g. APGAR, gestational age) and skin integrity(e.g. pressure ulcers, stoma site) (see also Chapters 1, 8, 15). 3. Palpation to assess pulse, accessory muscle activity, asymmetrical chest movements, tactile fremitus, crepitus, tactile rhonchi, and/or tracheal deviation (see Chapters 1, 8). 4. Trends in monitoring data to include fluid balance, pulmonary mechanics (see Chapter 7-9). 5. Perform diagnostic chest percussion (see also Chapters 1, 8). 6. Auscultate to assess breath sounds, heart sounds, heart rhythm, blood pressure (see Chapters 1, 8). 7. Review chest radiograph for quality (patient position, penetration, lung inflation), airways, lines, and drains, presence of foreign bodies, heart size and position, and presence or change in cardiopulmonary abnormalities (e.g. pneumothorax, consolidation, pleural effusion, pulmonary edema, pulmonary artery size), the diaphragm, mediastinum, and/or trachea (see also Chapters 1, 8).

Perform Procedures to Gather Clinical Information and Evaluate Procedure, Results (Chapters 1, 2, 7-9, 12) 1. ECG (12 lead) (see also Chapters 1, 7, 8). 2. Noninvasive measures of cardiopulmonary function to include pulse oximetry, capnography, transcutaneous monitoring (see also Chapters 1, 2, 7-9). 3. Peak expiratory flow measurement (see also Chapter 8). 4. Spontaneous ventilation (tidal volume, minute volume, maximum inspiratory

5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

pressure, and vital capacity) (see Chapters 8, 9). Blood gas sample collection (see also Chapters 8, 9, 16). Blood gas analysis and/or hemoximetry co-oximetry (see also Chapters 1, 7, 8). Cardiopulmonary calculations to include P(A-a) O2, VD/VT, P/F, and oxygenation index (OI) (see Chapters 2, 8, 9, 15). Hemodynamic monitoring (see Chapters 2, 7, 9). Pulmonary compliance and airways resistance (see Chapters 7-9). Plateau pressure (see Chapters 3, 7-9). Auto-PEEP determination (see Chapters 6, 7). Spontaneous breathing trial (SBT) (see also Chapters 8, 16). Apnea monitoring (see also Chapter 15). Apnea test for brain death determination (see also Chapter 16). CPAP/NPPV titration (see also Chapters 3, 6, 10). Cuff management (see also Chapter 9). Sputum induction (see also Chapter 1, 9). Tests of respiratory muscle strength (MIP and MEP) (see Chapters 5, 8, 16). Therapeutic bronchoscopy (see also Chapters 1, 12).

Recommend Diagnostic Procedures (Chapters 1–2, 7–9, 12–13) 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Laboratory Tests (see Chapters 1, 2, 8). Imaging studies (see Chapters 1, 2, 8). Bronchoscopy (see Chapters 1, 11, 12). Bronchoalveolar Lavage (BAL) (see also Chapter 12). Pulmonary Function Testing (see Chapters 2, 5, 8). Noninvasive Monitoring (see Chapter 9). Blood Gases (see Chapters 1, 2, 7, 8). ECG (see Chapters 1, 8, 9). Exhaled gas analysis (CO2, CO, FENO) (see Chapters 2, 8, 9). Hemodynamic monitoring (see Chapters 2, 7-9). Sleep studies (see Chapters 3, 10). Thoracentesis (see Chapters 1, 12).

II. Troubleshooting, and Quality Control of Devices, and Infection Control (Chapters 3, 4, 7–10, 15) Respiratory therapists must be able to assemble and troubleshoot devices; ensure infection prevention; and perform quality control procedures. This includes medical gas delivery interfaces; the use of long-term oxygen therapy; medical gas delivery

systems; CPAP, and NPPV; humidifiers, nebulizers, metered dose inhalers, spacers, dry powder inhalers; resuscitation equipment; mechanical ventilators; intubation equipment, artificial airways, suctioning equipment; blood gas analyzers; patient breathing circuits; hyper inflation devices; secretion clearance devices; Heliox delivery devices; portable spirometers; pleural drainage; noninvasive monitoring; bronchoscopes; and hemodynamic monitoring equipment. Infection control should include infection prevention policies and procedures. Quality control procedures should include blood gas analyzers, other gas analyzers and pulmonary function equipment; mechanical ventilators and noninvasive monitors. Specific items tested by the NBRC in these areas directly related to critical respiratory care include: 1. Use of medical gas delivery interfaces (e.g. oxygen devices, high flow nasal cannula) (see Chapter 1, 9, 16). 2. CPAP (see Chapters 3, 5-7). 3. NPPV (see Chapters 3, 6, 7, 10, 16). 4. Humidifiers, and nebulizers (see Chapters 1, 6, 8, 9, 16). 5. Medical aerosol delivery devices (see Chapter 1, 9) 6. Manual resuscitator bag (see Chapters 8, 9). 7. Mechanical ventilators (see Chapters 1, 3-10). 8. Intubation equipment (see Chapters 8, 9). 9. Artificial airways (see Chapter 9). 10. Suctioning equipment (see Chapters 8, 9). 11. Blood gas analyzers (see Chapter 8). 12. Co-oximeters (see Chapter 8). 13. Patient breathing circuits (see Chapters 3, 10). 14. Secretion clearance devices (see Chapters 3, 9). 15. Heliox (see Chapters 1, 2, 15). 16. Portable spirometers (see Chapter 8). 17. Pleural drainage systems (see Chapter 9). 18. Noninvasive monitoring (e.g. oximeters, capnometers, transcutaneous monitoring devices) (see Chapters 8, 9). 19. Bronchoscopy equipment (see Chapter 12). 20. Hemodynamic monitoring equipment (e.g. transducers, catheters) (see Chapters 7, 9). 21. Perform quality control procedures for blood gas analyzers, medical gas analyzers, mechanical ventilators, and noninvasive monitors (see Chapters 8, 9).

III. Initiation and Modification of Interventions (Chapters 1–2, 5–7, 10–16) Respiratory therapists must be able to maintain a patent airway including the insertion and care of artificial airways; perform tracheostomy care; exchange artificial airways; maintain adequate humidification; and initiate protocols to prevent ventilator-associated infections. In addition, the respiratory therapist should be able to perform extubation. Respiratory care sometimes provided in the intensive care unit includes airway clearance and lung expansion and use of methods to support oxygenation and ventilation. The respiratory therapist should also be able to administer medications and specialty gases (e.g., antimicrobials, pulmonary vasodilators, bronchodilators, mucolytics/proteolytics, steroids, Heliox, iNO) and perform endotracheal installations. Finally, the respiratory therapist must be able to ensure that appropriate modifications are made to the respiratory care plan including termination of treatment (if needed), recommendations for therapy, treatment of pneumothorax, adjustment of fluid balance and electrolyte therapy, insertion or change of artificial airway, liberation from mechanical ventilation, extubation, and discontinuing treatment based on patient responses. Specific items tested by NBRC related to critical respiratory care and mechanical ventilation include: 1. Stopping treatment in the face of a life-threatening adverse event (see Chapters 1, 2, 5-9). 2. Starting or discontinuing treatment based on patient response (see Chapters 1, 2, 5-9). 3. Treatment of pneumothorax (see Chapters 1, 2, 7-9). 4. Adjustment fluid balance (see Chapters 1, 2, 7). 5. Adjustment of electrolyte therapy (see Chapters 1, 2, 7). 6. Insertion or change of an artificial airway (see Chapters 1, 2, 6-9). 7. Liberation from mechanical ventilation (see Chapter 16). 8. Extubation (see Chapter 16). 9. Seeking consultation from the physician specialist (see Chapters 1-2, 7-9, 1116). The respiratory therapist must also be able to make recommendations for specific pharmacologic interventions. Items tested on the NBRC examinations related to critical respiratory care include:

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.

Bronchodilators (see Chapters 1, 2, 7, 9). Anti-inflammatory drugs (see Chapters 1, 2, 7, 9). Mucolytics and proteolytics (see Chapters 1, 2, 9). Aerosolized antibiotics (see Chapters 1, 2, 9). Inhaled pulmonary vasodilators (see Chapters 1, 2, 9). Cardiovascular medications (see Chapters 1, 2, 7, 9). Antimicrobial medications (see Chapters 1, 2, 7, 9). Sedatives and hypnotics (see Chapters 1, 2, 7, 9). Analgesics (see Chapters 1, 2, 7, 9). Narcotic antagonists (see Chapters 1, 2, 7, 9). Benzodiazepine antagonists (see Chapters 1, 2, 7, 9). Neuromuscular blocking agents (see Chapters 1, 2, 7, 9). Diuretics (see Chapters 1, 2, 7, 9). Surfactants (see Chapter 15). Changes to drug, dosage, administration, frequency, mode or concentration (see Chapters 1, 2, 7, 9).

The respiratory therapist must also provide respiratory care in life threatening situations, assist the physician/provider performing specific procedures, and conduct patient and family education. Items tested on the NBRC examinations related to critical respiratory care include: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Interprofessional communication (see Chapter 1). Patient transport (see Chapters 3, 4, 11, 15). Intubation (see Chapters 7-9). Bronchoscopy to include endobronchial ultrasound (EBUS) and navigational bronchoscopy (ENB) (see Chapter 12). Thoracentesis (see Chapter 12) Tracheostomy (see Chapters 7-9). Chest tube insertion (see Chapters 9). Insertion of arterial or venous catheters (see Chapter 8). Moderate (conscious) sedation (see Chapters 7-9). Cardioversion (see Chapters 2, 7-9). Withdrawal of life support (see Chapter 16).

The respiratory therapist should also be able to apply disease management principles to asthma, COPD, cystic fibrosis, tracheostomy care, and ventilatordependent patients. The NBRC examinations address specific patient conditions including:

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22.

Asthma (see Chapters 2, 5-9). COPD (see Chapters 2, 5-9). Heart failure (see Chapters 2, 5-9). Post-surgical patients (see Chapters 2, 5-9). Geriatric patients (see Chapters 2, 5-9). Cardiovascular patients (see Chapters 2, 5-9). Patients with infectious disease (see Chapters 2, 5-9). Patients with pulmonary vascular disease (see Chapters 2, 5-9). Trauma patients (see Chapters 2, 5-9). Neurologic disease (see Chapters 2, 5-9). Neonatal patients (RDS, disorders of prematurity, congenital defects, apnea of prematurity) (see Chapter 15). Pediatric patients (bronchiolitis, cystic fibrosis) (see Chapter 15). Pulmonary embolism (see Chapter 2, 5-9). Shock (see Chapters 2, 5-9). Neuromuscular disease (see Chapters 2, 5-9). Burns/inhalation injury (see Chapters 2, 5-9). Lung transplantation (see Chapters 2, 5-9). Interstitial lung disease (see Chapters 2, 5-9). Drug overdose (see Chapters 2, 5-9). Traumatic brain injury (TBI) (see Chapters 2, 5-9). Sepsis (see Chapters 2, 5-9). Lung cancer (see Chapters 2, 5-9).

Adult Critical Care Specialty Examination With respect to the Adult Critical Care Specialty Examination, the advanced level adult critical care specialist must be able to perform respiratory critical care and general critical care. Specific areas covered on the ACCSE include:

Airway Management (see Chapters 6–9) 1. Apply airway clearance techniques (see Chapters 1, 9). 2. Recognize difficult airways (see Chapters 7-9). 3. Apply advanced techniques during intubation (cricoid pressure, tube changers, specialty visualization devices) (see Chapters 7-9). 4. Exchange endotracheal tubes (see Chapters 7-9). 5. Apply specialty tracheostomy tubes (see Chapter 9).

Administration of Specialty Gases (see Chapters 1, 2, 9, 11)

1. nitric oxide (see Chapters 2, 9, 11, 15). 2. helium – oxygen mixtures (see Chapters 1, 2, 9, 15).

Manage Ventilation and Oxygenation (see Chapters 2, 5–9) 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.

Initial ventilator settings (see Chapters 3, 5, 6). Advanced ventilator modes (see Chapters 3, 5, 6). Noninvasive ventilation (mask CPAP, NPPV) (see Chapters 3, 5, 6, 10). High flow nasal cannula (see Chapter 9). Waveform analysis (see Chapters 8, 9). Rescue techniques (recruitment maneuvers, inhaled vasodilators [iNO, prostacyclin) (see Chapters 7, 9, 11, 12, 14). High-frequency ventilation (see Chapters 3, 6, 11, 15). Prone positioning (see Chapters 7, 9). ECMO (see Chapter 14). Ventilator discontinuance (liberation/weaning) (see Chapter 16). Lung protective ventilation (see Chapters 2, 6, 7). Management of ARDS (see Chapters 2, 3, 5-7). Treatment of patients with traumatic injuries (see Chapters 2, 3, 5-7). Exercise, and rehabilitation while receiving ventilatory support (see Chapter 9). PEEP management (see Chapters 3, 6-7). Differential/independent lung ventilation (see Chapters 2, 6, 7, 9). Intrahospital transport (see Chapter 4, 15). Optimizing patient – ventilator interaction (see Chapter 7).

Deliver Pharmacologic Agents (see Chapter 1, 2, 5-9) 1. Aerosolized medications, other than bronchodilators (e.g. vasodilators, antimicrobials) (see Chapter 9). 2. Airway installations (e.g. epinephrine, lidocaine, cold saline, topical thrombin) (see Chapter 9). 3. Optimization of aerosol delivery during mechanical ventilation, NPPV, high flow nasal cannula (see Chapter 9).

Assess the Patient Status and Changes in Status (see Chapters 1, 2, 5–9) 1. Assess difficult airway issues (patency, Mallampati classification, airway protection, thyromental distance) (see Chapters 6, 8) 2. Assess chest imaging (radiographs, CT scans, echocardiograms, ultrasound, ventilation/perfusion scan) (see Chapters 1, 2, 6, 8, 13). 3. Assess indices of respiratory physiology and mechanics (oxygenation,

4. 5. 6. 7. 8.

9. 10. 11. 12. 13. 14. 15. 16. 17.

ventilation, capnography, capnometry, work of breathing) (see Chapters 2, 8, 9). Assess neurologic status (EEG, level of consciousness, respiratory function, brain death criteria, neuromuscular function, seizures, stroke) (see Chapter 9). Assess cardiovascular status (physical assessment, coronary artery disease, diagnostic testing, dysrhythmias, hypertension, CHF) (see Chapters 2, 8, 9). Assess hemodynamics (preload, afterload, contractility, rate, cardiac output, oxygen delivery) (see Chapters 2, 8, 9). Assess different types of shock (anaphylactic, cardiogenic, septic, hypovolemic, neurogenic) (see Chapters 2, 8, 9). Recognize mechanisms of respiratory failure (ARDS, aspiration, atelectasis, drug induced respiratory failure, hypoventilation syndrome, neuromuscular disease, obstructive lung disease, pneumonia, postsurgical respiratory failure, pulmonary contusion, pulmonary edema [cardiac and noncardiac], pulmonary embolism, restrictive lung disease, sleep apnea, transfusion related lung injury, upper airway obstruction) (see Chapter 1, 2, 8, 9). Assess renal function (see Chapter 9). Assess acid-base balance (see Chapters 2, 5, 8, 9). Assess nutrition/feeding (see Chapter 9). Assess endocrine disorders (see Chapter 9). Assess respiratory quotient (see Chapters 2, 3, 9). Assess gastrointestinal function (abdominal compartment syndrome, ileus, feeding tube placement, G.I. bleeding/endoscopy) (see Chapter 8, 9). Assess coagulation and risk for deep vein thrombosis (see Chapters 8, 9). Assess the musculoskeletal system (ICU myopathy, muscle atrophy, spinal cord injury, rhabdomyolysis) (see Chapters 1, 2, 8, 9). Apply therapeutic hypothermia (see Chapter 9).

Anticipate Care Based on Laboratory Results (see Chapters 1, 2, 5-9) 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Albumin (see Chapter 8). CBC (transfusion, trigger, transfusion refusal) (see Chapter 8). Cardiac markers (troponin, BNP) (see Chapters 2, 8, 9). Noncardiac biomarkers (D-dimer, lactate, procalcitonin) (see Chapter 8). Electrolytes, magnesium, calcium, and phosphate (see Chapter 8). Acid-base status, anion gap, ketones, and lactate level (see Chapters 2, 8, 9). Coagulation studies (see Chapters 2, 8, 9). Culture and sensitivities (blood, stool, sputum, urine) (see Chapters 2, 8, 9). Sputum Gram stain (see Chapters 2, 8, 9). Hemoximetry (carboxyhemoglobin, methemoglobin) (see Chapters 2, 8, 9).

11. 12. 13. 14.

Endocrine assessment (cortisol, glucose, thyroid function) (see Chapter 9). BUN and creatinine (see Chapter 9). Liver function (bilirubin, ammonium, AST, ALT) (see Chapter 2, 9). Fluid analysis (plural, urine, CSF, peritoneal) (see Chapters 8, 9).

Anticipate Care Based on Imaging And/or Reports of Imaging (see Chapters 1, 2, 5–9, 13) 1. 2. 3. 4.

Radiographs (chest, spine, abdominal) (see Chapters 2, 8, 9). CT scan (brand, chest, abdomen) (see Chapters 2, 8). MRI (see Chapters 2, 8). Ultrasound (lung, plural, abdominal, vascular, echocardiography) (see Chapter 13). 5. Nuclear scans (V/Q, cerebral blood flow) (see Chapter 8). 6. Angiography (pulmonary, coronary, bronchial, gastrointestinal, cerebral) (see Chapter 8).

Anticipate Effects of Pharmacologic Agents (see Chapters 1, 2, 5-9) 1. Sedatives/hypnotics (continuous or intermittent, dexmedetomidine, benzodiazepine) (see Chapters 1, 2, 7-9). 2. Analgesia (continuous or intermittent, regional or systemic, opioids, ketamine) (see Chapters 1, 2, 7-9). 3. Neuromuscular blocking agents (vercuronium, cisatracurium, succinylcholine, rocuronium) (see Chapters 1, 2, 7-9). 4. Reversal agents (naloxone, flumazenil, sugammadex, neostigmine, edrophonium) (see Chapter 1, 2, 5). 5. Vasoactive and inotropic agents (see Chapters 1, 2, 7-9). 6. Drugs that may induce methemoglobinemia (lidocaine, dapsone, nitric oxide, nitroprusside, benzocaine) (see Chapters 1, 2, 7-9, 15). 7. Prophylaxis for deep vein thrombosis (see Chapters 1, 2, 8). 8. Prophylaxis for stress ulcers (see Chapters 1, 2, 8). 9. Prophylaxis for delirium (see Chapters 1, 2, 7). 10. Diuretics (see Chapters 1, 2 7-9). 11. Drug interactions (see Chapters 1, 2, 7-9). 12. The effect of comorbid conditions on drug metabolism and excretion (renal failure, hepatic failure) (see Chapters 1, 2, 7-9).

Anticipate Care Based on Nutritional Status (see Chapters 9, 12) 1. Complications of malnutrition (protein wasting, hypoglycemia, respiratory muscle catabolism) (see Chapter ).

2. Complications of nutritional support (aspiration, central line infection, defeating syndrome, outplacement of feeding to) (see Chapter 9). 3. Enteral and parenteral nutrition ((see Chapter 9). 4. Morbid obesity (see Chapter 9). 5. Metabolic study for caloric requirements (see Chapters 8, 9). 6. Metabolic study for exhaled gas analysis (see Chapters 8, 9).

Prevent Ventilator Associated Events (see Chapters 1, 2, 5–9) 1. 2. 3. 4. 5.

Oral care (see Chapter 9). Bed position (see Chapter 9). Minimize intubation time (aggressively weaning, NPPV) (see Chapter 16). Ventilator circuit care (see Chapter 3). Specialty airways (polyurethane cuff, subglottic suction, endotracheal tube) (see Chapters 8, 9). 6. Assessment of cuff integrity and pressure (see Chapters 8, 9).

Recognize and Manage Patients with Infections and/or Sepsis (see Chapters 1, 2, 5–9) 1. Recognition of clinical and laboratory signs consistent with infection, and severe sepsis (catheter associated infection, culture, data, CBC) (see Chapters 1, 2). 2. Management of patients with infections and sepsis (pneumonia, catheter associated infection) (see Chapters 2, 6, 7). 3. Prevention of infection, and sepsis (isolation procedures, skin integrity, personal protective equipment, catheter care) (see Chapters 8, 9).

Manage End-Of-Life Care (see Chapters 2, 5, 16) 1. 2. 3. 4.

Palliative care, hospice care and advance directives (see Chapter 16). Determination of brain death (see Chapter 16). Withdrawal of life support (see Chapter 16). Care of organ donors (see Chapter 16).

Prepare for Disaster and Mass Casualty Events (see Chapter 4) 1. Patient movement and protection, equipment and supply management (see Chapter 4).

Interact with Members of an Interdisciplinary Team (see Chapter 1).

Perform Specific Procedures (see Chapters 1 and 2) 1. Arterial line insertion and monitoring (see Chapter 8). 2. Mini-BAL (see Chapter 12). 3. Esophageal probe (NAVA, transpulmonary pressure monitor) (see Chapters 69).

Troubleshoot Systems (see Chapters 1, 2, 5-9) 1. 2. 3. 4.

Chest tube drainage (see Chapter 9). Bronchoscopy (see Chapters 1, 12). Hemodynamic monitoring (arterial pressure, CVP) (see Chapters 1, 2, 7-9). Inhaled vasodilators therapy (nitric oxide, prostaglandins) (see Chapters 1, 11, 15).

1 Adapted from: NBRC: Document Library. Credentialing Examinations Detailed Content Outlines. The National Board for Respiratory Care Inc: Olathe, KS; 2019. See: https://www.nbrc.org/resources/#document-library

Appendix

B Abbreviations © Anna RubaK/ShutterStock, Inc. A/C assist-control mode ABG arterial blood gas ACLS advanced cardiovascular life support AIDS acquired immunodeficiency syndrome AP anteroposterior APC adaptive pressure control APRV airway pressure release ventilation ARDS acute respiratory distress syndrome ARF acute respiratory failure ASV adaptive support ventilation ATC automatic tube compensation BAL bronchoalveolar lavage BD base deficit BE base excess BiPAP bi-level airway pressure BLS basic-life support BNP brain natriuretic peptide BSA body surface area BTPS body temperature and pressure saturated BUN blood urea nitrogen

CAD coronary artery disease CAP community acquired pneumonia CBC complete blood count CHF congestive heart failure CI cardiac index CK-MB creatinine kinase MB fraction CMV continuous mandatory ventilation CNS central nervous system COPD chronic obstructive pulmonary disease CPAP continuous positive airway pressure CPT chest physiotherapy CSF cerebral spinal fluid CT computed tomography CVA cerebrovascular accident CVP central venous pressure CXR chest x-ray DNR do not resuscitate DPI dry powder inhaler DVT deep vein thrombosis EBUS endobronchial ultrasound ECG electrocardiograph ECMO extracorporeal membrane oxygenation EEG electroencephalogram EMG electromyogram EPAP expiratory positive airway pressure ETT endotracheal tube FET forced expiratory technique HAP hospital-acquired pneumonia Hb hemoglobin HCAP healthcare-associated pneumonia HCO3– bicarbonate Hct hematocrit HFJV high frequency jet ventilation

HFOV high frequency oscillatory ventilation HFPPV high frequency positive pressure ventilation HFPV high-frequency percussive ventilation HFV high frequency ventilation HIV human immunodeficiency virus HME heat and moisture exchanger IBW ideal body weight (predicted body weight) ICP intracranial pressure IMV intermittent mandatory ventilation iNO inhaled nitric oxide IPAP inspiratory positive airway pressure IPF interstitial pulmonary fibrosis IPPB intermittent positive pressure breathing IPV intrapulmonary percussive ventilation IS incentive spirometry LABA long acting B2 –agonist LMA laryngeal mask airway MAP mean arterial pressure MDI metered dose inhaler mEq milliequivalent MI myocardial infarction MMV mandatory minute ventilation MRI magnetic resonance imaging MVV maximal voluntary ventilation NAVA neutrally adjusted ventilatory assist NIH ARDSnet Acute Respiratory Distress Syndrome Network of the National Institutes of Health NIV noninvasive ventilation NIV noninvasive ventilation NREM nonrapid eye movement NSCLC non-small-cell lung cancer OSA obstructive sleep apnea PA posteroanterior PAH pulmonary arterial hypertension

PAP pulmonary artery pressure PAV proportional assist ventilation PC pressure control PC-CMV pressure control continuous mandatory ventilation PC-CSV pressure control continuous spontaneous ventilation PC-IMV pressure control intermittent mandatory ventilation PC-IRV pressure control inverse ratio ventilation PCV pressure control ventilation PCWP pulmonary capillary wedge pressure PEEP positive end-expiratory pressure PEEPi intrinsic PEEP (auto-PEEP) PEP positive expiratory pressure PFT pulmonary function test PIE pulmonary interstitial emphysema PIP peak inspiratory pressure PND paroxysmal nocturnal dyspnea PPHN persistent pulmonary hypertension of the newborn Pplat plateau pressure PRVC pressure regulated volume control PS pressure support PSV pressure support ventilation PVC premature ventricular contraction PVR pulmonary vascular resistance RDS respiratory distress syndrome REE resting energy expenditure RSBI rapid shallow breathing index RSI rapid sequence intubation SABA short-acting β2-agonist SCLC small cell lung cancer SIMV synchronized intermittent mandatory ventilation SOB shortness of breath SPN solitary pulmonary nodule SVN small-volume nebulizer

TB tuberculosis UAO upper airway obstruction VAP ventilator-associated pneumonia VC volume control VC-CMV volume control-continuous mandatory ventilation VC-IMV volume control intermittent mandatory ventilation VS volume support WOB work of breathing WOBI Imposed work of breathing

Pulmonary and Blood Gas Abbreviations CC chest wall compliance CL lung compliance CT total compliance Crs respiratory system compliance DLCO diffusing capacity of lung for carbon monoxide Ḋo2 oxygen delivery f respiratory rate FVC forced vital capacity FVL flow-volume loop FRC functional residual capacity FEV1 forced expiratory volume in one second of expiration FEV25–75% forced expiratory flow, midexpiratory phase, from 25% to 75% of vital capacity FIo2 fractional concentration of inspired oxygen Pao2 partial pressure of oxygen, arterial PAo2 partial pressure of oxygen, alveolar Po2 partial pressure of oxygen, pulmonary capillary P(A – a)o2 alveolar–arterial Po2 difference PV̅o2 mixed venous Po2 Patm atmospheric pressure Paw airway pressure P̅aw mean airway pressure

PB barometric pressure Pco2 partial pressure of carbon dioxide Paco2 partial pressure of carbon dioxide, arterial Pco2 partial pressure of carbon dioxide, mixed venous PEF peak expiratory flow MEP maximum expiratory pressure MIP maximum inspiratory pressure P0.1 mouth occlusion pressure at 100 msec R respiratory quotient Raw airway resistance sGaw specific airway conductance Spo2 oxygen saturation as measured by pulse oximetry SVC slow vital capacity TLC total lung capacity A alveolar ventilation

V̇E vinute ventilation VC vital capacity V̇co2 carbon dioxide production VD dead space volume VD/VT dead space to tidal volume ratio V̇o2 oxygen consumption V̇o2max maximum oxygen consumption V̇/Q̇ or V̇A/Q̇ ventilation-perfusion VT tidal volume Q̇T cardiac output per minute TE expiratory time TI inspiratory time TTOT total respiratory cycle time V̇A minute alveolar ventilation V̇E minute ventilation

Appendix

C Equations © Anna RubaK/ShutterStock, Inc.

Minute ventilation: V̇E = VT × f Physiologic Dead Space: VD/VT = (Paco2 – PĒco2)/Paco2 VD = VD/VT × VT Alveolar Po2 (abridged alveolar gas equation): PAo2 = FIo2 × (PB – 47) – 1.25 × Paco2 Oxygenation Index: OI = [P̅aw × Fio2)/Pao2] × 100 Shunt: Q̇s/Q̇t = (Cc'o2 – Cao2)/(Cc'o2 – Cv̅o2) Arterial Oxygen Content: Cao2 = (Hb × 1.34 × Sao2) + (0.003 × Pao2) Henderson-Hasselbalch Equation: pH = 6.1 + log[HCO3-])/(0.03 × Paco2)] Anion Gap:

AG = ([Na+] + [K+]) – ([Cl+] + [HCO3-]) (Because its concentration is small, [K+] is often omitted from this calculation) Respiratory System Compliance on Ventilator (aka Total Compliance): Crs = VT/(Pplat – PEEP) Airway resistance (on ventilator): Raw = (PIP – Pplat)/inspiratory flow (L/sec) Ideal Body Weight (aka predicted body weight [PBW]): Males: IBW = 50 + 2.3 × [Height (inches) – 60] Females: IBW = 45.5 + 2.3 × [Height (inches) – 60] Mean Arterial Blood Pressure (estimate): MAP = [systolic + (2 × diastolic)]/3 Cardiac Output: Q̇T = HR × SV Fick Equation: Q̇T = V̇o2/C(a – v̅)o2 Cardiac Index: CI = Q̇T/BSA Systemic Vascular Resistance: SVR = [(MAP – CVP)/CO] × 80 Pulmonary Vascular Resistance: PVR = [(MPAP – PCWP)/CO] × 80 Cerebral Perfusion Pressure: CPP = MAP – ICP Work of Breathing: WOB = ΔP × ΔV (1 joule = 10 cm H2O × L) Alveolar to Arterial Oxygen Difference:

P(a – a)o2 = PAo2 – Pao2 Oxygen Delivery: Ḋo2 = Cao2 (mL O2/100 mL blood) × Q̇T (mL/min)

Glossary © Anna RubaK/ShutterStock, Inc.

A Acidosis An abnormally low pH in body tissues. Acidosis is typically identified via an arterial pH < 7.35. Acute alveolar hyperventilation A sudden decrease in PaCO2 with a corresponding increase in pH (i.e., uncompensated respiratory alkalosis). Acute asthma An active flare-up (exacerbation) of asthma symptoms, often in response to a specific trigger, in a patient with asthma. Acute lung injury (ALI) A noncardiogenic form of hypoxemic respiratory failure, now called mild ARDS. Features include bilateral pulmonary infiltrates on chest x-ray and a pulmonary capillary wedge pressure (PCWP) < 18 mmHg but distinguished by the presence of a PaO2/FIO2 < 300 but > 200. See also acute respiratory distress syndrome (ARDS). Acute physiology and chronic health evaluation (APACHE) scoring system A system developed to predict severity of illness and mortality in intensive care unit (ICU) patients using specific patient parameters to assess overall status. Acute respiratory distress syndrome (ARDS) Respiratory disorder characterized by the abrupt onset of respiratory distress; associated with severe hypoxemia and diffuse pulmonary opacities on chest radiograph. ARDS may be caused by pneumonia, aspiration of gastric contents, inhalation of toxic gases, or pulmonary contusion. Severity is based on the PaO2/FIO2 ratio while PEEP ≥ 5 cm H2O: mild (200 mmHg < PaO2/FIO2 ≤ 300 mmHg), moderate (100 mmHg < PaO2/FIO2 ≤ 200 mmHg), and severe (PaO2/FIO2 < 100 mmHg). In addition to PaO2/FIO2 < 100 mmHg, severe ARDS criteria include CST ≤ 40 mL/cm H2O, PEEP ≥ 10 cm H2O, V.E ≥ 10 L/min, and radiographic severity. Acute respiratory failure (ARF) A sudden decrease in arterial oxygenation with or without carbon dioxide retention. Acute ventilatory failure (AVF) A sudden increase in PaCO2 with a corresponding decrease in pH (i.e., uncompensated respiratory acidosis). Acute ventilatory failure superimposed on chronic ventilatory failure An episode of acute ventilatory failure in a patient who has existing chronic ventilatory failure. It represents a patient with a chronically elevated Paco2 (e.g., COPD with chronic CO2 retention) who experiences an acute additional increase in Paco2 with a corresponding decrease in pH. Adaptive pressure control (APC) An adaptive feedback mechanism that automatically adjusts the pressure level from breath to breath to achieve the targeted tidal volume. This allows the ventilator to maintain a relatively stable tidal volume in the face of changes in compliance, resistance, or patient effort. Adaptive pressure ventilation See adaptive support ventilation. Adaptive support ventilation (ASV) A ventilator mode that makes automatic adjustments in respiratory rate and inspiratory pressure based on measurements of respiratory mechanics to deliver the desired minute ventilation

and minimize the work of breathing. Adaptive targeting (a) A targeting scheme that allows the ventilator to automatically adjust targets between breaths in response to varying patient input. Adverse events Incidents that negatively affect a patient’s health. Adverse events may be spontaneous (e.g., an allergic response to a substance encountered in routine daily activities) or may be an unwanted outcome of an intervention (e.g., a medication side effect or surgical complication). Afterload The resistance against which the ventricle must eject blood during contraction; the load that opposes myocardial shortening. Airway pressure-release ventilation (APRV) A ventilator mode that is a form of pressure-control ventilation that is designed to allow unrestricted spontaneous breathing throughout the breath cycle. I:E ratios greater than 1:1 are generally used, allowing short expiratory times to maintain end-expiratory lung volume. Functionally, APRV sets two levels of continuous positive airway pressure (CPAP), which are time triggered and time cycled. APRV allows spontaneous breathing at both levels. Airway resistance (Raw) An assessment of lung function that can be estimated by the pressure difference between peak inspiratory pressure (PIP) and the plateau pressure (Pplateau) per unit of gas flow into the lungs. During mechanical ventilation airway resistance can be calculated where Raw = (PIP – Pplat)/inspiratory gas flow. Altitude hypoxia A form of ambient hypoxia due to reduced barometric pressure at high altitude. Alveolar dead space Alveoli that are ventilated but not perfused. Alveolar ventilation Volume of gas moving into and out of the alveoli. Alveolar volume (VA) The volume of gas in the alveoli. Alveoli Air sacs in the lung where gas exchange takes place between alveolar gas and capillary blood. Ambient hypoxia Hypoxia due to a reduction in inspired oxygen (↓PIO2 or ↓FIO2). Amyotrophic lateral sclerosis (ALS) A chronic, progressive motor neuron disease of both upper and lower motor neurons resulting in progressive voluntary muscle weakness, which eventually leads to respiratory failure. Anaphylactic shock A form of distributive shock, usually caused by an allergic reaction (e.g., bee sting), which leads to inappropriate peripheral vasodilation that results in decreased systemic vascular resistance and low blood pressure as well as (in some instances) bronchospasm. Anatomic dead space The volume of gas in the conducting airways that does not participate in gas exchange. Anatomic shunt Passage of blood from the right side of the heart to the left side of the heart via anatomic structures that bypass the alveoli. Normally, a small amount of venous blood is carried from the bronchial veins, Thebesian veins, and pleural veins to the left side of the heart where it mixes with oxygenated blood from the pulmonary circulation. Anemic hypoxia Inadequate blood oxygen content (CaO2) due to decreased hemoglobin (Hb) or alteration in the ability of the hemoglobin to carry oxygen (e.g., elevated carboxyhemoglobin or methemoglobinemia). Anion gap A measure of the difference in concentration of positively charged serum electrolytes (Na+) and negatively charged serum electrolytes (Cl– and HCO3-). A normal ion gap is 8 to 16 mEq/L, depending on the laboratory instrumentation in place. Anteroposterior (AP) In radiology, a view in which the x-ray machine is set up in front of the patient and the film is located behind the patient so that the image is a view looking from the front to the back of the patient’s body. APACHE score See Acute Physiology and Chronic Health Evaluation (APACHE) scoring system. Apnea The complete cessation of breathing, which represents a severe form of ventilatory failure requiring mechanical ventilatory support if the patient is to survive. Apnea backup A ventilator setting in which the ventilator resumes ventilation with pre-set mandatory breaths if no spontaneous patient breaths are detected within a set time period.

Arrhythmia An abnormal heart rhythm, which can be related either to the rate of heart beats (inappropriately fast or slow) or the regularity of beats, or a combination of inappropriate rate and regularity. Arterial oxygen content (Cao2) Amount of oxygen present in arterial blood, expressed in mL or volumes %. Arterial oxygen tension. The partial pressure of oxygen (PaO2) in the arterial blood. Ascites Abnormal accumulation of fluid in the abdomen. It usually occurs in association with inhibited venous return and liver dysfunction. Assist/control (A/C) A ventilator mode that provides time- or patient-triggered continuous mandatory ventilation, which can be volume controlled or pressure controlled. Assist/control pressure control ventilation (PC A/C) A ventilator mode that provides time- or patient-triggered continuous mandatory ventilation with a set pressure. Assist/control volume control ventilation (VC A/C) A ventilator mode that provides time- or patient-triggered continuous mandatory ventilation with a set volume. Asthma A chronic inflammation of the bronchi that leads to obstruction and difficulty breathing. Asthma exacerbation An acute episode of cough, dyspnea, and related symptoms triggered by allergens, environmental exposures, infection, or emotional upset in patients with asthma. Asynchrony In mechanical ventilation, incorrect timing of the ventilator’s activity in relation to the timing of the patient’s spontaneous breathing. Atelectasis Collapse of alveoli. Atelectotrauma Lung injury due to cyclic alveolar expansion and collapse, often caused by mechanical ventilation. Atrial natriuretic peptide (ANP) A peptide hormone secreted by heart muscle cells in the atria that helps maintain homeostasis of fat, water, sodium, and potassium. Automatic positive airway pressure (autoPAP) Feature on some devices for continuous positive airway pressure (CPAP) that actively monitors one or more airway variables and responds to upper airway changes automatically by adjusting the pressure delivered during each breath. Automatic servo ventilation (autoSV) A noninvasive ventilator mode similar to bilevel positive airway pressure, spontaneous timed (BPAP S/T), which is commonly used for patients with sleep apnea. Automatic tube compensation (ATC) Automated form of pressure support designed to reduce the imposed work of breathing due to endotracheal or tracheostomy tubes. Automode A dual-control mode available on some ventilators, which can automatically titrate the level of support provided between control and support modes, dependent on the patient’s level of spontaneous ventilation. AutoPEEP Unintentional positive end-expiratory pressure (PEEP) due to incomplete airway emptying during expiration. Autotriggering Initiation of inspiration by the ventilator without a corresponding patient effort due to inappropriate ventilator trigger-sensitivity settings.

B Barotrauma Lung injury due to inappropriate pressures, often caused by mechanical ventilation. Barrel chest A broadening of the rib cage that occurs because of airway obstruction and pulmonary over inflation in patients with obstructive lung disease; commonly seen in emphysema. Baseline (bias) flow A continuous flow of gas through the ventilator circuit. Baseline pressure The pressure during mechanical ventilatory support at end expiration. Basophils White blood cells that respond to specific inflammatory stimuli, such as allergy or wounds.

Bicarbonate (HCO3-) An electrolyte found in the blood; pH of the body is determined by the ratio of HCO3- to carbonic acid (H2CO3). Bilevel positive airway pressure (BiPAP) A noninvasive ventilator mode that supports spontaneously breathing patients by providing two pressures, one on inspiration and one on expiration. Biovariable targeting (b) A ventilation targeting scheme in which the ventilator automatically sets the inspiratory pressure or tidal volume randomly to mimic the variability observed during normal breathing. Blood urea nitrogen (BUN) A measurement that helps determine how well the kidneys are functioning. Botulism A neurologic disorder caused by ingestion of neurotoxins produced by Clostridium botulinum bacteria. Bowel sounds Sounds that are heard on auscultation of the abdomen, caused by bowel contents moving through the intestines. Their presence or absence is an important indicator of overall gut health. Bradycardia Inappropriately slow heart rate, typically < 60 beats per minute. Bradypnea Abnormally slow respiratory rate. Brain natriuretic peptide (BNP) A peptide hormone secreted by cardiac muscle cells in response to stretching. Higher than normal BNP levels may indicate heart failure. Breath An inspiration followed by an expiration would be a single breath. A breath may be further defined as the positive change in airway flow (inspiration) paired with a negative change in airway flow (expiration) associated with ventilation of the lungs. Breath cycle The breath cycle is made up of an inspiratory and expiratory phase and can be described by the inspiratory time, expiratory time, and total cycle time. Breath trigger Method by which inspiration begins, either by time or patient effort, which is sensed by a change in pressure or flow. Bronchial hygiene Techniques that improve oxygenation in ventilated patients, including suctioning and airway care, provision of adequate humidification, and administration of bronchodilators and inhaled anti-inflammatory agents. Bronchiolitis Inflammation of the bronchioles. Bronchoalveolar lavage (BAL) A technique in which saline is introduced into the bronchi via a bronchoscope and then collected for analysis as a means of diagnosing lung disease. Bronchoscopy A procedure in which a bronchoscope is passed through the upper airway into the trachea and bronchial tree for diagnostic or therapeutic purposes.

C Capillary shunt Movement of blood via the pulmonary capillaries past alveoli that are not ventilated. Carbon monoxide poisoning Inhalation of carbon monoxide forms carboxyhemoglobin in the blood, which inhibits normal oxygen binding to hemoglobin and causes hypoxia. Carboxyhemoglobin Hemoglobin that binds to carbon monoxide in place of oxygen. Cardiac output (CO) The volume of blood ejected from the heart’s ventricles, equal to the stoke volume multiplied by the heart rate (in beats per minute). Cardiogenic pulmonary edema (CPE) Fluid buildup in the lungs caused by heart failure (specifically the left ventricle). Cardiogenic shock Condition occurring when the heart is unable to pump an adequate amount of blood and oxygen to the tissues. Cardiopulmonary bypass An extracorporeal circuit used to move blood into a reservoir where blood is heated, oxygenated, and returned to the arteries to maintain circulation during heart surgery.

Central venous catheter (CVC) A catheter placed into a vein and guided to the vena cava and right atrium in patients requiring central venous pressure (CVP) measurement and frequent administration of medications or fluids. Cerebral infarction Loss of a blood supply to the brain resulting in tissue death. Also known as ischemic stroke. Chest radiographs Images of the chest taken with x-rays. Chest tubes A hollow and flexible plastic tube inserted into the chest to drain unnecessary contents, such as air, fluid, or blood that may have accumulated inside the pleural cavity. Chief complaint The principal problem or symptom set that causes a patient to seek medical care. Chronic alveolar hyperventilation A chronically decreased PaCO2 with a normal or near-normal pH (i.e., compensated or partly compensated respiratory alkalosis). Chronic obstructive pulmonary disease (COPD) Progressive, irreversible condition characterized by dyspnea and difficulty exhaling; may include a chronic cough. Chronic respiratory failure A condition where the respiratory system is unable to properly oxygenate and/or remove carbon dioxide for an extended length of time. Chronic ventilatory failure A chronically elevated Paco2 , with a normal or near-normal pH owing to metabolic compensation. Circulatory hypoxia A condition that results in low tissue oxygen levels due to low cardiac output, low blood pressure, or inadequate circulation. Closed-loop ventilator modes Ventilator modes in which a target parameter is set by the operator and the ventilator automatically adjusts other parameters to reach the target. Coma A state of extended unconsciousness and inability to arouse or respond to stimuli. Community-acquired pneumonia (CAP) An infection acquired outside of a hospital, resulting in pneumonia. Congestive heart failure (CHF) A clinical syndrome in which there is impairment of ventricular filling or impairment of injection of blood, resulting in inadequate blood flow to body tissues and organs. Continuous mandatory ventilation (CMV) A mode of ventilation in which every breath is a mandatory breath. Mandatory breaths may be time or patient triggered. Continuous positive airway pressure (CPAP) A ventilator mode that supports a spontaneously breathing patient by providing continuous pressure during inspiration and expiration. CPAP may be used on ventilated patients during IMV/SIMV and as a method of weaning. CPAP may also be used for patients who experience sleep apnea. Continuous renal replacement therapy (CRRT) A treatment used to remove waste products, optimize fluid balance, and provide hmodynamic stability for patients with kidney injury. Continuous spontaneous ventilation (CSV) A breath sequence for which all breaths are spontaneous. Continuous venovenous hemodialysis (CVVHD) A form of continuous renal replacement therapy in which venovenous access enables diffusive filtration of the blood. Continuous venovenous hemofiltration (CVVH) A form of continuous renal replacement therapy in which venovenous access enables convective filtration of the blood. Controlled ventilation A mode of ventilation in which every breath is time triggered. Coronary artery disease (CAD) Narrowing or blockage of the coronary arteries that causes reduced blood flow, resulting in reduced oxygen availability to the heart muscle. Crackles Brief, high-pitched lung sounds associated with bronchitis and other lung disorders. Crackles are characterized as fine (high-pitched, short-lasting), medium, or coarse (low-pitched, longer-lasting). Critical care Health services for critically ill patients who require continuous monitoring and care. Critical care ventilators Mechanical ventilators used for support of critically ill patients in respiratory failure.

Cuff-leak test A method for determining whether airway inflammation is present prior to extubation. Cyanosis The bluish appearance of the skin, lips, gums, or finger nails, indicative of hypoxemia. Cycle Completion of a full breath, from the beginning of inspiration to the end of expiration. Cycle asynchrony Poor coordination between the patient’s respiratory drive and the ventilator. Cystic fibrosis (CF) A genetic disorder that results in abnormally thick secretions of mucus, which progressively impairs the patient’s ability to breathe and causes recurrent infections in the lungs.

D Dead space Gas in the lungs that does not participate in gas exchange. Dead space ventilation See Dead space. Dead space volume (VD) is the total volume of gas that does not participate in gas exchange. Decremental PEEP Gradual reduction of PEEP to identify the optimal PEEP following a lung recruitment maneuver. Deep vein thrombosis (DVT) Formation of a blood clot in a deep vein, usually of the legs, resulting in leg pain, swelling, immobility, and damage to the blood vessel wall; DVT may also occur in a major vein of the pelvis, arms, or other vessels. If the clot detaches, it may travel to the heart and then lungs, causing a pulmonary embolus. Diabetes A metabolic disorder caused by pancreatic failure to produce adequate amounts of insulin. Dialysis Passage of blood across a semipermeable membrane to filter toxic materials and maintain electrolyte balance, fluid, and pH when the kidneys are impaired and unable to maintain normal processes. Diaphragmatic dysfunction Inability of the diaphragm to adequately support lung function. Patients with diaphragmatic weakness or dysfunction may require mechanical ventilatory support. Diffusion limitations Impaired oxygen diffusion across the alveolar–capillary membrane due to a variety of causes, including ventilation–perfusion mismatch, reduced surface area, or increased diffusion distance. Disconnect Removal of a patient from the ventilator. Distributive shock Forms of shock in which inappropriate peripheral vasodilation results in decreased systemic vascular resistance and low blood pressure. Double cycling Ocurs when the ventilator’s set inspiratory time is less than the patient’s neuro-inspiratory time. Double triggering An asynchrony of the ventilator that occurs when the ventilator cycles into expiration while the patient is still making an inspiratory effort, resulting in two consecutive breaths before the patient exhales. Dual targeting (d) A targeting scheme that allows the ventilator to automatically switch between pressure control and volume control during a single breath. Ductus arteriosus The channel that connects the main pulmonary artery to the descending aorta of the fetal heart, allowing blood to bypass the lungs. This opening normally closes shortly after birth, but in some infants, it remains open (i.e., patent ductus), which causes hypoxia and failure to thrive. Dull percussion notes A non-resonant, flat sound produced when the clinician taps his or her fingers against a patient’s chest. Dynamic autoPEEP Amount of end-expiratory pressure remaining in the lower airways during a breath.

E Echocardiography Use of ultrasound imaging to examine heart structures and function. Ejection fraction The percentage of blood pumped by the ventricle during a single cardiac contraction.

Electrical activity of the diaphragm (EAdi) Neural output from the respiratory center in the brain that is sent to the diaphragm during breathing. Placement of an esophageal catheter allows for measurement of the activity. Electrical discharge of the diaphragm (Edi) See Electrical activity of the diaphragm. Electrocardiogram A recording of the eletrical activity of the heart. Electrolytes Minerals in the body that have an electrical charge, e.g., Na+, K+, Cl–, Ca2+, HCO3-, Mg2+. Encephalitis Inflammation of the brain most commonly caused by a viral infection. Endobronchial ultrasound (EBUS) High-frequency sound waves are used in combination with a bronchoscope to observe tissues of he respiratory system. Endotracheal tube (ETT) An artificial airway that is passed through the nose or mouth and advanced into the trachea. Enteral nutrition Delivery of liquid food mixtures given through a tube into the stomach or small bowel (i.e., tube feeding). Eosinophils Immune cells that tend to increase in the presence of parasitic infection, allergy, or cancer. Exacerbation Sudden worsening of respiratory symptoms, including increased dyspnea, cough, and changes in the quality or quantity of sputum. Expected maximal renal compensation Occurs when a chronic increase in Paco2 of 10 mmHg causes the kidneys to increase H+ secretion resulting in an increase in plasma HCO3-3 of about 4 to 5 mEq/L. Expiratory positive airway pressure (EPAP) Pressure applied to the airway during the expiratory phase. Expiratory time (TE) The time interval from the start of expiratory flow to start of inspiratory flow. Components include expiratory flow time and expiratory pause time. Extracorporeal CO2 removal (ECCO2-R) Technique used to remove carbon dioxide from the blood artificially. Extracorporeal life support organization (ELSO) A non profit organization established supporting health care professionals and scientists who are involved in extracorporeal membrane oxygenation. Extracorporeal lung support (ECLS) See extracorporeal membrane oxygenation (EMCO). Extracorporeal membrane oxygenation (ECMO) Artificial method of oxygenating blood in which blood is removed from the body and circulated through a machine. While inside the machine, the blood passes a semipermeable membrane where the blood becomes oxygenated and ventilated, and then is returned to the body. Extrinsic PEEP Positive end-expiratory pressure applied to the airway at the end of expiration used for therapeutic purposes. Extubation failure Inability of a patient to spontaneously breath and protect her or his airway following removal of the endotracheal tube or tracheostomy tube. Exudate Fluid rich in cellular and proteinaceous material that oozes from pores, wounds, or other openings in membranes or skin. Exudative pleural effusion Collection of an abnormal volume of fluid in the pleural space suggestive of inflammation or malignancy. See Exudate.

F Facial pressure ulcer Damaged skin and tissue as a result of pressure on the face for an extended period of time. Family history A record of disease states in parents and other immediate family members relevant to a patient’s health status. Fine crackles See crackles.

Flail chest Paradoxical motion of the chest resulting from three or more rib fractures in two or more places. Flow asynchrony Poor coordination between the patient’s flow demand and the flow provided by the ventilator. Flow cycled The ending of inspiration due to inspiratory flow decay below a preset threshold. Flow trigger The ventilator begins inspiration when a change in flow is detected. Fluid overload Excess fluid in the blood vessels; hypervolemia. Foramen ovale A small opening between the left and right atria of the fetal heart that usually closes at birth. Failure of the foramen ovale to close creates a shunt and hypoxia. Fraction of inspired oxygen (FIO2) The concentration of oxygen found in the inspired gas. Frequency Repetition of a specific event over a measured span of time. Respiratory frequency is the same as respiratory rate. Full ventilatory support When the mechanical ventilator provides 100% of the work of breathing required to meet the patient’s ventilatory needs. Full-face mask Interface used during noninvasive ventilation, which covers the entire face, spanning from the top of the head to underneath the chin, and is attached with straps across the back of the head. Functional residual capacity (FRC) The volume of air remaining in the lungs after completion of a passive expiration.

G Glasgow coma scale A rating of patient mental status that is based on his or her motor function, ability to respond to stimuli, and open his or her eyes, and is used to determine the status of brain function in the ICU. Guillain-Barré syndrome A progressive, nonpermanent form of muscle weakness and flaccid paralysis of the arms and legs. If the diaphragm is affected, mechanical ventilatory support may be required.

H Head bobbing Forward motion of a child’s head on each inhalation, suggesting difficulty breathing and is a sign of respiratory distress. Head, eye, ear, nose, throat (HEENT) A portion of a physical examination that assesses the upper airway and adjacent structures. Hematocrit (Hct) The proportion of blood that is composed of red blood cells. Hemoglobin (Hb) The protein in red blood cells that transports oxygen. Hepatomegaly An abnormally large liver. Hertz (Hz) One cycle per second or 60 cycles per minute. High-altitude cerebral edema (HACE) Collection of fluid that results in swelling of the brain, as a result of being exposed to high altitudes. HACE is a form of severe altitude sickness associated with elevations greater than 10,000 feet. Symptoms of HACE include trouble walking (i.e., ataxic gait), irritability, confusion, drowsiness, lethargy, and progressive decline of mental function followed by coma. Urgent treatment of HACE should include oxygen therapy and moving the patient to a lower altitude as soon as possible. High-altitude pulmonary edema (HAPE) Collection of fluid in the lung that may interfere with gas exchange and result in respiratory failure, caused by exposure to high altitude. HAPE is a form of severe altitude sickness associated with elevations greater than 10,000 feet. Treatment of HAPE includes rest, warmth, oxygen therapy, and descent, particularly from very high altitude (> 13,000 feet). High-flow nasal cannula Oxygen modality used to deliver high flows (40 to 60 L/min) of humidified oxygen to the patient via nasal cannula.

High-frequency jet ventilation (HFJV) HFJV uses a jet of air delivered through a special endotracheal tube adapter. Constant gas flow interrupters are incorporated, which are time cycled and pressure limited. Tidal volume is dependent on amplitude, jet driving pressure, jet orifice size, length of inspiratory jet time on, and the patient’s compliance and resistance. High-frequency oscillatory ventilation (HFOV) A ventilator that delivers vibrations to the airway via piston pumps or a vibrating diaphragm. The ventilator delivers very small tidal volumes at high frequencies. Both inspiratory and expiratory phases are active. HFOV uses frequencies in the range of 180 to 900 breaths/min (3 to 15 Hz; 1 Hz = 60 breaths/min) and very small tidal volumes (50 to 250 mL) to create a rapidly oscillating bias flow that affects gas transport through complex nonconductive mechanisms. HFOV is the most commonly used form of high-frequency ventilation in neonates and adults. High-frequency percussive ventilation (HFPV) A form of HFV that combines time-cycled pressure-control ventilation with a phasitron to provide oscillatory or percussive ventilation throughout inspiration and expiration. HFPV may improve secretion clearance, improve oxygenation and ventilation, and lower airway pressures. High-frequency positive-pressure ventilation (HFPPV) Use of a conventional positive-pressure ventilator to deliver low tidal volumes at a very rapid rate. High-frequency ventilation (HFV) General term to describe mechanical ventilation that delivers small tidal volumes at a very high respiratory frequency. Possible indications for HFV include ARDS, bronchopleural fistula, and air leaks, but HFV is not recommended as a first choice for mode of ventilation and should be avoided in patients with obstructive lung disease. Forms of HFV include HFJV, HFOV, HFPV, and HFPPV. History of present illness (HPI) A patient’s report of the complaint(s) and symptoms that led her or him to seek treatment. Histotoxic hypoxia Reduced oxygen concentrations in the tissues due to the inability of the tissues to utilize oxygen (e.g., cyanide poisoning). Hypercapnia Abnormally elevated PaCO2 due to hypoventilation. Hypercapnic respiratory failure Acute and chronic hyperventilation, also known as “pump failure” or “ventilatory failure.” Hypercarbic respiratory failure See hypercapnic respiratory failure. Hyperechoic Material that produces ultrasound signals of higher amplitude or density because it is highly soundwave reflective. Hyperresonance Lower-pitched percussion noises present on percussion indicative of overinflation of the lung. Hyperthermia Higher than normal body temperature. Hyperventilation An abnormally reduced PaCO2 caused by excessive movement of air into and out of the alveoli. Hypoechoic Material that produces low-amplitude or low-density ultrasound signals because it absorbs sound waves. Hypotension Abnormally low blood pressure. Hypothermia Lower than normal body temperature. Hypoventilation Inadequate ventilation resulting in increased PaCO2. Hypovolemic shock Reduced blood flow to the body due to blood or fluid loss resulting in organ dysfunction. Hypoxemia Low arterial blood oxygen levels. Hypoxemic respiratory failure A form of respiratory failure where the primary problem is inadequate oxygenation of arterial blood. Also known as “lung failure.”

I

Iatrogenic injury Damage caused by a procedure or medication. Immunocompromised patient Individual who has a weakened immune system that has difficulty fighting an infection or is easily susceptible to infection. Impending ventilatory failure A term used in cases where an elevated Paco2 is not yet present but is likely to occur in the immediate future if no action is taken. Inotropes Medications that increase the force of cardiac muscle contraction. Inspiratory flow The rate at which gas moves into the lungs during inspiration; typically recorded in liters per minute (L/min) or liters per second (L/sec). Inspiratory positive airway pressure (IPAP) Positive pressure applied during inspiration but not expiration. Inspiratory pressure The airway pressure exerted during inspiration. Inspiratory time (TI) The period from the start of inspiratory flow to the start of expiratory flow. Inspiratory to expiratory (I:E) ratio Expresses the relationship between inspiratory time and expiratory time. A typical I:E ratio is 1:2. Inspiratory waveform One of several flow patterns during inspiration associated with mechanical ventilation. Intelligent targeting (i) Artificial intelligence algorithms adjust the ventilator based on changing lung mechanics or patient effort. Intensive care unit (ICU) A hospital unit that provides continual care to severely ill patients who need close observation and rapid response to changes in their condition. Interface The transition point between one surface and another; the object that connects the patient to the therapeutic device or ventilator (e.g., face mask, nasal mask). Intermittent mandatory ventilation (IMV) Mode of ventilation in which a mandatory respiratory rate is set but the patient is still able to spontaneously breathe in between mandatory breaths. The most common form of IMV is spontaneous intermittent mandatory ventilation (SIMV). Interprofessional education (IPE) Training individuals from different health disciplines together so that collaborative practice can be encouraged. Intra-aortic balloon pump (IABP) A mechanical device that inflates a balloon in the aorta during diastole and deflates during systole to support cardiac output and increase perfusion. Intracranial pressure (ICP) Measurement of the pressure of the brain and cerebrospinal fluid. Increases in ICP can occur due to traumatic injury. Intrapulmonary shunt A condition in which alveoli are perfused but not ventilated. Intrinsic PEEP See AutoPEEP. Invasive ventilation Mechanical ventilation that requires an artificial airway, such as an endotracheal tube or tracheostomy tube. Iron lung A negative-pressure device that ventilates patients, commonly known for its use during the polio epidemics in the United States. The patient’s body is enclosed inside a chamber with only the head remaining outside of the chamber. Ischemic hypoxia Reduced oxygen concentration in the tissues due to an inadequate blood supply. Isoechoic Material that produces ultrasound signals equivalent to surrounding tissues or structures.

L Laryngeal mask airway (LMA) Supraglottic airway that consists of a tube with an inflatable cuff at the end, which rests in the larynx when properly inserted. The cuff is inflated to seal the airway to allow direct flow into the lungs.

Leak Refers to an air leak during mechanical ventilation. Common leaks include cuff leaks or leaks in a ventilator circuit. Left ventricular assist device (LVAD) A mechanical device surgically inserted to support left ventricular function. Liberation from mechanical ventilation The process of removing a patient from mechanical ventilatory support. Long cycling Inspiratory times are longer than what the patient requires, which delays ventilator cycling. Long-term acute care (LTAC) A facility that provides ongoing care for patients with serious illness who do not require intensive care or recurrent diagnostic testing but are too ill to be placed in a nursing home. Lower inflection point (LIP) The point on a pressure–volume curve at which an increasing linear relationship begins. This point has been identified as the pressure level at which alveolar collapse ceases and alveolar recruitment begins. Lung compliance (LC) The ability of lung tissue to stretch in response to increased volume of air, normally reported as the volume change per unit pressure change. Lung injury prediction score (LIPS) Assigns points for the presence of specific factors associated with the development of ARDS. These include the presence of shock, aspiration, sepsis, pneumonia, orthopedic spine surgery, acute abdominal surgery, cardiac surgery, aortic vascular surgery, traumatic brain injury, smoke inhalation, near-drowning, lung contusion, multiple fractures, alcohol abuse, obesity, hypoalbuminemia, chemotherapy, Fio2 > 0.35 or more or O2 therapy > 4 L/min, tachypnea > 30 breaths/min, Sao2 or Spo2 < 95%, and diabetes mellitus. LIPS > 4 is predictive for the development of ARDS. Lung-protective conventional ventilation (LPCV) Ventilation strategy that takes a conservative approach to delivery of tidal volume, reducing plateau pressure, and positive end-expiratory pressure in order to prevent lung injury while still maintaining appropriate alveolar recruitment. Lung-protective ventilatory strategy See lung-protective conventional ventilation. Lymphocytes A type of white blood cell that is involved in an immune response.

M Mandatory breaths Breaths initiated and/or cycled by the ventilator. Mandatory minute ventilation (MMV) A ventilator mode in which the ventilator monitors the exhaled minute ventilation as a target variable. If the exhaled minute ventilation falls below the operator set parameter, the ventilator will trigger mandatory breaths or increase inspiratory pressure until the target is reached. Maximum expiratory pressure (Pemax or MEP) A measurement used to assess expiratory respiratory muscle strength, in which the patient exhales against a closed system and the pressure generated is measured. Maximum inspiratory pressure (Pimax or MIP) A measurement used to assess inspiratory respiratory muscle strength that measures the pressure generated by a forced inhalation against an occluded airway. Also known as “negative inspiratory force (NIF).” Mean airway pressure (Paw or MAP) The average pressure within the airway during mechanical ventilation. Mechanical circulatory support (MCS) Use of an artificial pump to mechanically circulate blood. Mechanical dead space Volume of rebreathed gas due to a mechanical device. Mechanical ventilation Refers to the use of a mechanical ventilator to support or replace the action of the normal ventilatory pump. Mechanical ventilatory support See mechanical ventilation. Meconium Earliest stool in an infant, excreted before, during, or immediately after birth. Meningitis Inflammation of the spinal cord or cerebral membranes as a result on an infection. Metabolic acidosis A decrease in the pH associated with a reduced concentration of plasma bicarbonate

(HCO3-). Metabolic alkalosis An increase in the pH associated with an increased concentration of plasma bicarbonate (HCO3-). Methemoglobinemia A condition in which the blood contains an increased level of oxidized hemoglobin, resulting in reduced oxygen binding to hemoglobin. Minimum PEEP The least amount of PEEP that maintains adequate arterial oxygenation with a safe FiO2. Minute alveolar ventilation (V̇A) The volume of gas exhaled from the alveoli per minute. Minute ventilation (V̇E) The volume of gas exhaled from the lungs per minute, also known as “minute volume.” Missed triggering A form of trigger asynchrony that develops when the patient’s inspiratory effort does not trigger a ventilator breath. Mode asynchrony Asynchrony that develops when the mode selected does not match the patient’s spontaneous ventilatory efforts. Modified Allen test Test performed at the bedside before a radial arterial puncture or cannulation to determine whether there is adequate ulnar artery perfusion (i.e., adequate collateral blood flow). Monocytes White blood cells that are the primary defense during an immune response. Musculoskeletal disease Any disorder that affects the functioning of muscles and bones. Myasthenia gravis Autoimmune disorder characterized by impaired transmission of neural impulses across the neuromuscular junction, caused by the destruction of the postsynaptic acetylcholine receptors. Myocardial infarction (MI) Death of the cardiac muscle cells due to impaired blood flow and/or hypoxia. Also known as “heart attack.”

N Nasal flaring Widening of the nostrils during inspiration, indicating increased work of breathing. Nasopharyngeal airway A hollow, airway device inserted into the nose and directed along the floor of the nose, parallel to the hard palate. This device helps maintain patency of the upper airway and allows for suctioning. Nebulizer A device that produces an aerosol, or suspension, of particles in a gas. Negative inspiratory force (NIF) See maximal inspiratory pressure (MIP). Negative-pressure ventilation Negative-pressure ventilators enclose the chest and exert a negative pressure around the thorax to cause lung inflation. See iron lung. Neonatal intensive care unit (NICU) Unit in the hospital designed for patients who require continual monitoring and care, specifically for newborn infants up to 1 month old. Neonate A newborn from birth to 1 month old. Neural–ventilatory coupling Synchrony between the ventilator and the neurological signals from the respiratory center. Neurally adjusted ventilatory assist (NAVA) A mode of mechanical ventilation that relies on electrical signaling from the diaphragm to trigger the ventilator’s action. Neuro-inspiratory time The time from the initiation of diaphragmatic activity to the deactivation of the diaphragm during inspiration, as set by the patient’s respiratory center. Neurogenic shock Damage to the brain or spinal cord may cause neural transmission problems resulting in vasodilation and hypotension, leading to hypotension and shock. Neurologic disease Any disorder that impairs the functioning of the nervous system, particularly the central nervous system (CNS).

Neuromuscular blockade Pharmacologic inhibition of transmission of impulses from motor nerves to skeletal muscles, which results in paralysis. Neuromuscular disease Any disorder that impairs the functioning of the nerves involved in muscle function and movement. Neutrophils White blood cells primarily engaged in fighting bacterial infections. Non-ST segment elevation MI (NSTEMI) A form of myocardial infarction in which the ECG is characterized by ST segment depression and/or T-wave inversion in two or more leads without Q-wave development. Noninvasive intermittent positive-pressure ventilation (NIPPV) NIPPV provides ventilatory support by mask or other interface that does not require tracheostomy or endotracheal tube intubation. Also known as noninvasive ventilation (NIV). Noninvasive ventilation (NIV) Mechanical ventilation that does not require insertion of an invasive artificial airway, such as an endotracheal tube or tracheostomy tube.

O Obesity hypoventilation syndrome A condition affecting individuals who are unable to adequately ventilate due to being obese, resulting in elevated carbon dioxide levels in the blood. Also known as “Pickwickian syndrome.” Obstructive lung disease Lung disease characterized by airway inflammation and obstruction. Obstructive sleep apnea (OSA) A sleep disorder caused by obstruction of the upper airway. It is characterized by repeated pauses in breathing during sleep (apneas) and associated reduction in blood oxygen saturation. Obtunded Low level of consciousness. Occupational history List or description of a patient’s current and previous places of employment that is used for evaluation of environmental exposure and working conditions. Open lung ventilation A mechanical ventilation strategy that combines low tidal volumes with PEEP to maximize alveolar recruitment and avoid overdistention. Also known as “open lung strategy.” Optimal PEEP The positive end-expiratory pressure that provides for maximal tissue oxygen delivery, best compliance, or maximal lung recruitment without risking barotrauma. Optimal targeting (o) Ventilation in which the ventilatory pattern is automatically adjusted to optimize work of breathing in the face of changing lung mechanics or patient effort. Organ transplantation Procedure in which a failing or damaged organ is surgically removed and replaced with a functioning organ. Oronasal mask Interface used during noninvasive ventilation that covers the nose and mouth and is attached with straps across the back of the head. Oropharyngeal airway A curved airway device inserted into the mouth and hypopharynx. This device maintains patency of the upper airway to allow movement of air and passage of other suction catheter devices. Overdistention Excessive stretching of the alveoli because of increased pressures. Oxygen consumption (V̇O2) The volume of oxygen consumed by body tissues in 1 minute. Oxygen content in arterial blood (CaO2) The amount of oxygen present in arterial blood. Oxygen content in mixed venous blood (Cv̄O2) The amount of oxygen present in mixed venous blood. Oxygen delivery (ḊO2) Rate of oxygen transport to the peripheral tissues determined by the cardiac output and arterial oygen content. Oxygen saturation in mixed venous blood (Sv̄O2) Amount of oxygen bound to hemoglobin in mixed venous blood.

P Palliative care Care for patients with terminal conditions that focuses on increasing patient comfort without necessarily offering treatment for the condition. Paradoxical chest movement Chest movement characterized by outward movement on expiration and inward movement on inspiration. Parameters Ventilator settings or variables (e.g., tidal volume, respiratory rate, inspiratory peak flow, inspiratory time, PEEP). Parenteral nutrition Nutritional support provided via intravenous route. Parietal pleural Serous membrane of mesothelial cells and connective tissue that lines the chest wall, diaphragm, and mediastinum. Partial pressure of alveolar oxygen (PaO2) Alveolar oxygen tension; normally reported in mmHg. Partial pressure of arterial oxygen (PaO2) Arterial oxygen tension; normally reported in mmHg. Partial pressure of mixed venous oxygen (Pv̄O2) Mixed venous oxygen tension of blood returning to the right side of the heart from all parts of the body. Pv̄O2 is usually measured using a sample of blood from the pulmonary artery. Partial ventilatory support The ventilator and the respiratory muscles each provide some of the work of breathing. Patient-triggered breaths Ventilator breaths are initiated by patient effort. Patient–ventilator asynchrony Lack of coordination in the timing of spontaneous breathing and breaths provided by the ventilator. Peak airway pressure (Paw) The maximum airway pressure during a mechanically assisted inspiration, measured relative to atmospheric pressure. Peak flow In ventilated patients, the peak flow refers to the inspiratory peak flow of gas during a mandatory or spontaneous breath. Peak inspiratory pressure (PIP) The maximum pressure achieved during inspiration. Percussion notes The sounds made when tapping upon the chest or the abdomen. Percutaneous Passing through the skin. Pericardial effusion An abnormal accumulation of fluid in the pericardial cavity. Peritoneal fluid Fluid produced within the abdominal cavity to lubricate the abdominal organs. Excess accumulation of this fluid is called ascites. pH A measurement of hydrogen ion concentration [H+] in solution. Physical assessment A review of a patient’s condition following a physical examination. Physiologic dead space The sum of anatomic dead space and alveolar dead space, representing the presence of gas in the lungs that does not participate in gas exchange. Physiologic PEEP Low levels of PEEP (e.g., 3 to 5 cm H2O) to replace the “natural” PEEP provided by the glottis. Plasma bicarbonate Amount of HCO3- in the blood plasma (see HCO3-). Plateau pressure (Pplat) Pressure recorded during an end-inspiratory breath hold following a mandatory breathe from the ventilator. Pleural effusion An abnormal collection of excess fluid in the pleural space. Pleural friction rub An abnormal sound that is heard on auscultation of the chest, which occurs when pleurae are inflamed or when fluid accumulates in the pleural cavity.

Pneumonia Inflammation and consolidation of lung tissue caused by respiratory infection. Symptoms include cough, fever, pain in the chest, and dyspnea. Pneumothorax An collection of air between the lung and the chest wall that causes collapse of the lung. PaO2/FIo2 ratio (P/F ratio) Simply PaO2 divided by FIO2. Point-of-care ultrasonography Bedside ultrasound imaging that uses high-frequency sound waves to evaluate tissues for diagnostic purposes or therapies. Polycythemia Elevated red blood cell count. Portable chest x-rays Device that can be transported and used at the bedside to obtain a radiographic image of a patient’s thorax and lungs. Positive end-expiratory pressure (PEEP) Positive pressure applied at the end of expiration. In mechanical ventilation, PEEP is sometimes used to “recruit” collapsed alveoli and thereby improve oxygenation. Positive-pressure ventilation A type of ventilation where pressures greater than atmospheric pressure are applied to the lungs to support or effect inspiration. Posteroanterior (PA) images In radiology, a view in which the x-ray machine is set up behind the patient and the film is located in front of the patient so that the image is a view looking from the back to the front of the patient’s body. Postextubation The time frame immediately following removal of an endotracheal tube thath requires careful monitoring of oxygenation and ventilatory status, ability to maintain a clear airway, and patient comfort. Preintubation The time frame immediately preceding insertion of an endotracheal tube. Preload The volume of blood within the ventricle at the end of diastole (end-diastolic volume). Pressure amplitude of oscillation (∆P) Trough oscillatory pressure subtracted from peak oscillatory pressure; “power” setting for high-frequency oscillatory ventilation that affects tidal volume and carbon dioxide removal. Pressure assist Patient-triggered continuous mandatory ventilation with a set pressure. Pressure assist/control Time- or patient-triggered continuous mandatory ventilation with a set inspiratory pressure. Pressure control (PC) Time-triggered continuous mandatory ventilation with a set inspiratory pressure. Pressure control-continuous mandatory ventilation (PC-CMV) A ventilator mode in which breaths are time or patient triggered, pressure limited, and time cycled. Pressure control-continuous spontaneous ventilation (PC-CSV) A ventilator mode in which spontaneous breaths are patient triggered, pressure limited, and flow cycled. Pressure control-intermittent mandatory ventilation (PC-IMV) A pressure-control mode in which spontaneous breaths are interspersed with mandatory breaths. Pressure control-synchronized intermittent mandatory ventilation (PC-SIMV) See pressure control intermittent mandatory ventilation. Pressure-control ventilation (PCV) See pressure control. Pressure cycled Inspiration ends when airway pressure reaches a set pressure threshold. Pressure-regulated volume control (PRVC) A ventilator mode in which the pressure automatically varies breath to breath to achieve the target tidal volume. Pressure-support ventilation (PSV) A ventilator mode in which all breaths are patient triggered, pressure targeted, and flow cycled. Pressure–time scalar Used to identify the mode of ventilation as well as PIP, Pplateau, and baseline pressure (e.g., PEEP or CPAP). Observation of the pressure–time scalar can also provide a visual representation of the inspiratory time, expiratory time, and I:E ratio. Pressure trigger The ventilator detects a pressure drop at the proximal airway due to the inspiratory effort of the

patient and the ventilator begins the inspiratory phase. Primary breaths Mandatory breaths during continuous mandatory ventilation and intermittent mandatory ventilation, or spontaneous breaths during continuous spontaneous ventilation. Prolonged mechanical ventilation (PMV) Extended use of mechanical ventilation due to failure of the patient to improve sufficiently to resume spontaneous breathing. Prone positioning Positioning of a patient lying horizontal and face down, used for patients with acute respiratory distress syndrome (ARDS) who are unresponsive to other oxygenation efforts. Proportional assist ventilation (PAV) Mode of ventilation that uses a servo targeting scheme to provide ventilatory support in which airway pressure is proportional to the patient’s inspiratory effort. Pulmonary drive pressure (ΔP) The difference between plateau pressure and positive end-expiratory pressure (PEEP). Pulmonary edema Accumulation of excess fluid in the interstitial and alveolar spaces in the lung. Pulmonary vascular resistance (PVR) Measurable resistance in the pulmonary blood vessels against which the right ventricle must eject blood. Pulse oximetry The process of rapidly determining the saturation of hemoglobin with oxygen using an oximeter.

R Rapid sequence intubation (RSI) Technique used for emergency airway intubation. Rapid shallow breathing index (RSBI) A measure of spontaneous breathing with no mechanical ventilatory support: RSBI= . Recruitment maneuvers (RMs) Techniques used to open and maintain collapsed alveoli to improve oxygenation. Red blood cell (RBC) count The total number of red blood cells in 1 mL of blood. Renal failure Inadequate kidney function. Respiratory acidosis A decrease in the pH associated with an elevated PaCO2; may also be described as hypoventilation, hypercapnia, hypercapnic respiratory failure, and ventilatory failure. Respiratory alkalosis An increase in blood pH associated with a decrease in PaCO2; also known as hyperventilation. Respiratory care A field or subject area within medical practice that encompasses diagnostic, therapeutic, and support services involved in the care of patients with disorders that affect the respiratory system. Patient services may be performed by a range of healthcare professionals, including physicians, nurses, and respiratory therapists. Respiratory distress syndrome (RDS) Condition of a newborn characterized by dyspnea with cyanosis. Respiratory drive The stimulus to breathe provided by the patient’s respiratory center. Also known as “ventilatory drive.” Respiratory failure General term indicating the inability of the heart and lungs to adequately oxygenate and ventilate. Respiratory mechanics The properties and behavior of muscles and tissues that determine respiratory capability. Common measures of respiratory mechanics include compliance or resistance. Respiratory rate (f) The frequency of breaths per unit of time (usually per minute). Respiratory system compliance (Crs) The elastic properties of the respiratory system. Respiratory therapist A healthcare provider specifically trained and educated to deliver respiratory care to patients across multiple settings, including acute care hospitals and ICUs.

Retinopathy Damage to the retina. Retractions An abnormal breathing pattern in which the intercostal and suprasternal spaces sink in during inspiration. Retractions can be caused by respiratory distress and/or upper airway obstruction. Reverse triggering A form of asynchrony that occurs when a time-triggered breath stimulates the diaphragm, resulting in diahragmatic contraction, which then triggers the next breath. Right ventricular failure Inability of the right ventricle to adequately pump blood to the lungs. Rise time The rate at which flow increases from baseline to peak during pressure-supported or pressure-control breaths.

S Secondary breaths Breaths that occur in addition to the primary breaths during intermittent mandatory ventilation. Sensitivity Threshold value set so when triggered, inspiration will begin. Sepsis A life-threatening condition in which an infection produces immune system responses that cause injury to organs and tissues (e.g., extremely high fever). Septic shock Response to an infection resulting in hypotension and reduced blood flow to the organs. Vasoconstriction occurs in an attempt to maintain appropriate blood flow to vital organs and may result in tissue hypoxia or organ dysfunction. Sequential organ failure assessment (SOFA) score An assessment of organ failure. Serum bicarbonate See Plasma bicarbonate. Serum creatinine A measure of kidney function. Servo targeting (r) A targeting scheme in which ventilator output automatically adjusts based on varying input measures. Set-point targeting (s) A targeting scheme in which the operator sets all waveform parameters. Severe oxygenation problems Extreme hypoxemia while breathing increased oxygen concentrations that does not improve significantly using conventional oxygen therapy. Shock Shutdown of organs and tissues due to inadequate blood flow. Short cycling Premature ventilator cycling caused by inspiratory times not long enough to meet the patient’s needs. Simplified acute physiology score (SAPS) A scoring system using 17 variables to assess the probability of mortality in seriously ill patients. Skin breakdown Damage to skin and tissues as a result of continued pressure on a specific area for an extended period of time. Slow, extended daily dialysis (SLEDD) A form of renal replacement therapy used in critical care. SOFA score See Sequential Organ Failure Assessment (SOFA) score. Splenomegaly Abnormal enlargement of the spleen. Spontaneous breathing trial (SBT) An assessment of a patient’s ability to breath on their own prior to extubation. Spontaneous breaths The patient controls the start and end of inspiration, independent of any ventilator settings for inspiratory time and expiratory time. Spontaneous ventilation Ventilation achieved through spontaneous breathing. ST segment elevation MI (STEMI) A form of myocardial infarction characterized by ECG findings of ST segment elevation followed by T-wave inversion and then Q wave development over a period of several hours if the heart

muscle is not reperfused. Static autoPEEP Positive end-expiratory pressure remaining in the lower airways during an expiratory pause. Step-down unit Secondary care facilities in a hospital intended for patients who have been in ICU who continue to need long-term acute care but no longer need intensive care. Stridor A harsh inspiratory sound caused by inflammation and edema of the larynx. Stuporous Having low level of consciousness; inability to arouse or respond. Surfactant A solution of lipids and proteins produced by epithelial cells in the lung that lowers alveolar surface tension. Sustained low-efficiency dialysis (SLED) A form of dialysis to support renal function. Synchronized intermittent mandatory ventilation (SIMV) See intermittent mandatory ventilation. Synchrony Correspondence between ventilator breaths and patient effort.

T Tachycardia An abnormally rapid heart rate. Tachypnea Abnormally increased respiratory rate. Targeting scheme A targeting scheme describes the relationship between operator inputs and ventilator outputs to achieve a specific ventilatory pattern. Targeting schemes may be set point, dual, biovariable, servo, adaptive, optimal, or intelligent targeting schemes. Terminal flow During flow-cycled mechanical ventilation, terminal flow is the decline in flow during inspiration required to end inspiration and cycle into expiration. Terminal weaning Withdrawal of ventilatory support for patients who may be unable to spontaneously breathe or protect their airway. Withdrawal may result in end of life and is sometimes used for patients who have advanced disease with no hope of significant improvement. Tetanus A neurologic disorder caused by neurotoxins produced by certain gram-positive Clostridium tetani bacteria, which results in muscular spasms, muscular rigidity, and may lead to respiratory failure. Thermodilution A technique for measuring cardiac output by injecting a cold or cool indicator and sampling with a thermistor. Thoracentesis Removal of fluid from the pleural space with a needle or small catheter. Tidal volume (VT) The volume of gas moved into the lungs during inspiration. Exhaled tidal volume is the volume of gas exhaled following inspiration. Time cycled Inspiratory time ends after a preset time interval has elapsed. Time trigger Starting of inspiratory flow due to a preset time interval. Time-triggered breaths See time trigger. Titrate To gradually increase or decrease a level of medication or substance until optimal results are achieved. Total artificial heart (TAH) A surgically installed mechanical pump that circulates blood for patients with inadequate ventricular function. Total cycle time (Ttot) The amount of time needed to complete one breath cycle; the sum of inspiratory time and expiratory time. Total face mask A device used during noninvasive ventilation that covers the entire face spanning from the forehead to the chin and is attached with straps across the back the head. Total parenteral nutrition (TPN) Provision of nutrition via intravenous fluids in patients unable to obtain food normally due to unconsciousness or damage to the GI tract.

Tracheostomy An artificial opening in the trachea performed to maintain an open airway in patients with disorders affecting the upper airway. Tracheostomy tube Artificial airway inserted surgically or percutaneously through an opening in the neck into the trachea. Tracheostomy tubes protect the lower airway and may be cuffed or uncuffed. Transducer A device that converts pressure or a similar physiologic phenomenon into an electrical signal to allow measurement. Transmural wall pressure The difference in pressure across two sides of a wall of an organ. Transudate A fluid that passes through a membrane and contains few cells or proteins; certain forms of edema are caused by accumulation of transudate that is an ultrafiltrate of plasma. Fluid overload can be one source of transudate. Trauma Serious, acute injury to the body. Trauma center A facility specializing in treating patients who have experienced a major traumatic injury. Trigger A parameter that initiates a breath; can relate to spontaneous effort by the patient, time, or sensormeasured flow of gas. Trigger asynchrony Lack of correspondence between the patient’s inspiratory effort and the beginning of the ventilator-supported breath. Trigger delay A delay between the time the patient initiates inspiration and when the ventilator actually delivers the breath. Trigger sensitivity A setting on the ventilator that is adjusted to allow for minimal work of breathing while avoiding autotriggering. Trigger work The amount of patient effort required to trigger the machine breath; inappropriate trigger sensitivity settings and autoPEEP can increase trigger work. Tumor A collection of abnormal cells that grow inappropriately in a mass. Tumors may be cancerous (e.g., carcinoma) or benign (e.g., adenoma). Tympanic Quality of the loud, drum-like, high-pitched sound typically heard on percussion of the abdomen when gas is present or over the chest when a pneumothorax has occurred.

U Upper airway obstruction Blockage of air flow through the pharynx, larynx, or trachea with potential lifethreatening consequences. Obstruction may be partial or complete. Upper inflection point (UIP) The point on a pressure–volume curve at which the increasing linear relationship begins to flatten out. This point has been identified as the pressure at which alveolar overdistention begins.

V Vasopressors Medications that constrict blood vessels and raise blood pressure. Venoarterial ECMO (VA-ECMO) An extracorporeal membrane setup that removes blood from a major vein (e.g., femoral vein), oxygenates it, and returns it via a major artery (e.g., femoral artery). This method provides respiratory and hemodynamic support. Venoarterial (VA) A technique in which blood is removed from a vein and returned via an artery. Venovenous (VV) A technique in which blood is removed from a vein and then returned to a vein. Venovenous ECMO (VV-ECMO) An extracorporeal membrane setup that removes blood from a major vein (e.g., femoral vein), oxygenates it, and returns it to another major vein (e.g., jugular vein). This method provides respiratory support only.

Ventilator asynchrony See asynchrony. Ventilator discontinuance Removal or cessation of mechanical ventilation. See also weaning. Ventilator mode The method for mechanically ventilating a patient with pressure or volume targets or support. Partial or full ventilatory support modes are available. Ventilator-associated lung injury (VALI) Pulmonary damage or dysfunction that occurs in association with mechanical ventilation; this term is used when the ventilator is suspected to be the cause of lung injury, but this cannot be conclusively proven. Ventilator-associated pneumonia (VAP) Pneumonia in patients that has developed at least 48 hours after initiation of mechanical ventilation. Ventilator-induced lung injury (VILI) An injury to the lung that occurs because of mechanical ventilation. Ventilatory capacity General term indicating the amount of air that can be moved into and out of the lungs by the natural ventilatory pump. Ventilatory discontinuance The process of discontinuing mechanical ventilation. Ventilatory failure An elevated PaCO2, which may be acute or chronic. Ventilatory muscle fatigue Fatigue in the muscles that support ventilation. Ventilatory requirements The volume of ventilation required to achieve adequate oxygenation and ventilation. Also known as “ventilatory demand” or “ventilatory load.” Ventilatory reserve The difference between the patient’s ventilator capacity and ventilatory requirements. Ventilatory workload The effort performed by the respiratory muscles to maintain adequate ventilation. Also known as “work of breathing (WOB)”. Visceral pleura The membrane that covers the external lung surface. Vital capacity The maximum volume of gas that a patient is able to expel from the lungs after a maximal inspiration or inhaled from a point of maximal exhalation. Volume assist Patient-triggered continuous mandatory ventilation with a set volume. Volume assist/control Time- or patient-triggered continuous mandatory ventilation with a set volume. Volume-assured pressure support (VAPS) A dual control mode of ventilation that monitors gas flow and volume during inspiration and adjusts pressure to ensure the preset tidal volume is delivered. Volume control (VC) Time-triggered continuous mandatory ventilation with a set volume that will not change if the patient condition changes. Volume control-continuous mandatory ventilation (VC-CMV) A ventilator mode in which all breaths are mandatory and may be patient or time triggered, time cycled, and volume limited. Volume control-intermittent mandatory ventilation (VC-IMV) A volume-control mode in which spontaneous breaths are interspersed with mandatory breaths. Volume controlled-synchronized intermittent mandatory ventilation (VC-SIMV) See volume controlintermittent mandatory ventilation. Volume cycled Inspiration ends when inspired volume reaches the set threshold. Volume of carbon dioxide production (V̇CO2) The amount of carbon dioxide produced by the body per minute. Volume of oxygen uptake (V̇O2) The amount of oxygen taken up by the body per minute. Volume-support ventilation (VS) A ventilator mode used for spontaneously breathing patients where ventilation is patient triggered and flow cycled. Pressure support automatically adjusts to deliver the target tidal volume. Volutrauma Overdistention of alveoli due to excessively high volume in mechanically ventilated patients.

W Wavelength The distance from the peak of one wave to the peak of the next wave in measuring sound or electromagnetic impulses. Weaning A gradual reduction in the level of ventilatory support provided. Weaning parameters or indices A set of measurements that suggest that a mechanically ventilated patient is a good candidate for successful weaning from the ventilator. Work of breathing (WOB) The effort required for a person to inhale and exhale to achieve adequate oxygenation and ventilation.

Index © Anna RubaK/ShutterStock, Inc. Note: Locators followed by the letter b, f, t refers to box, figures, and tables respectively

A ABCDEF bundle, 648 abdominal examination, 413 abdominal ultrasound, 585–586 anatomic landmarks, 586 ascites and paracentesis, assessment for, 586 general concepts, 585–586 acid-base balance, respiratory failure and, 58–66, 392–394 causes of, 66b combined and mixed acid-base disorders, 65–66 metabolic acidosis, 62–65 causes of normal anion gap and increased anion gap, 64b metabolic alkalosis, 62–65 causes of, 65b respiratory acidosis, 61–62 respiratory alkalosis, 61–62 acidosis, 120 acute alveolar hyperventilation, 62 superimposed on chronic ventilatory failure, 62 acute asthma exacerbation, respiratory failure and, 74–75, 75b–76b acute exacerbation of COPD, respiratory failure and, 31, 76–79 acute hypercapnic respiratory failure, 426

acute kidney insufficiency (AKI), 421 acute lung injury (ALI), 144 acute myocardial infarction, respiratory failure and, 83 Acute Physiology and Chronic Health Evaluation (APACHE), 70 acute respiratory distress syndrome (ARDS), 5, 28–29, 30b, 115, 128, 286, 570 Berlin definition, 80 high-frequency oscillatory ventilation for, 545–558 adjuncts for, 549–548 aerosol medication delivery, 550 algorithm for severe, 556t–558t bronchoscopy during, 552–553 endotracheal tube misplacement or obstruction and, 553–554 fluctuation of mPaw and ΔP, 551–552 infection control and, 554 inhaled nitric oxide, 550–551 introduction, 546 lung-protective conventional ventilation, transition from, 552 lung recruitment maneuvers, 548–549 oxygenation, 546–548 pneumothorax and, 553 prone positioning, 550 tracheostomy, 551 transition to extracorporeal membrane oxygenation, 551 transport of patients, 552 troubleshooting, 553–554 ventilation, 549 noninvasive ventilation, 530 pediatric critical care, 609–611, 622 PEEP and recruitment maneuvers, 476–477 respiratory failure and, 80–81 acute respiratory failure (ARF), 6, 28 conditions associated with the development, 12b defined, 31b

acute ventilatory failure (AVF), 19, 30, 62, 282, 294, 296, 297–298, 297b, 306 superimposed on chronic ventilatory failure, 32, 62 adaptive pressure control, 342 adaptive pressure ventilation (APV), 131–132, 160 adaptive support ventilation (ASV), 313, 343–344 adaptive targeting, 315 adverse events, 621 afterload, 146 Airon pNeuton, 241–242 airway clearance therapies, ICU and, 22–23 airway management and monitoring, 497–509 artificial airway, 501–503, 504f–505f, 506b–507b bronchial hygiene, 509–510 cuff pressure and volume, 501 endotracheal tube characteristics, 500–501 tracheostomy tubes, 503, 508–509 airway pressure release ventilation (APRV), 108, 127, 320b, 344–345, 373 airway pressures, 458–460 airway resistance, 103, 461–462, 463b alarms, mechanical ventilation and, 139–140 alkalosis, 120 ALS. See amyotrophic lateral sclerosis alveolar dead space, 42, 456 alveolar ventilation, 99b, 283b alveolar volumes, 103 alveoli, 602 alveoloar overdistention, 379 amyotrophic lateral sclerosis (ALS), 29, 98 anaphylactic shock, 51, 52b anatomic dead space, 55, 456 anatomic shunt, 43 anemia, 426 anemic hypoxia, 426

anion gap, 429 anion gap (AG), 62 APACHE. See Acute Physiology and Chronic Health Evaluation apnea, 30, 282, 294, 295–296, 295b, 306, 531 backup ventilation, 162 of prematurity, pediatric critical care, 609 APV. See adaptive pressure ventilation ARDS. See acute respiratory distress syndrome ARF. See acute respiratory failure arrhythmia, 51 ascites, 413, 585–586 assist/control pressure-control ventilation, 368 assist/control volume ventilation, 327, 368. See also volume control-continuous mandatory ventilation (VC-CMV) asthma, 604 acute, 529 exacerbation, 285 noninvasive ventilation, 528 pediatric critical care, 611–612 ASV. See adaptive support ventilation asynchrony cycle, 373–374 flow, 372–373 mode, 374–375 patient-ventilator, 369 trigger, 371 ventilator, 81 ventilator system monitoring and, 513–516 atelectasis, 12, 29 atelectrauma, 144 atrial natriuretic peptide (ANP), 147 auscultation, 415–416 automatic positive airway pressure (autoPAP), 107 automatic-servo ventilation, 107

automatic tube compensation (ATC), 108, 127–128 automode, 131, 347 autoPAP. See automatic positive airway pressure autoPEEP, 104, 371 autotriggering, 353, 372

B BAL. See bronchoalveolar lavage barotrauma, 303, 370 barrel chest, 414 baseline (bias) flow, 371 baseline pressure, 531 basophils, 427 bicarbonate, 428 bilevel positive airway pressure (BiPAP), 106, 528 Bio-Med Devices Crossvent 4+, 242–244 biovariable targeting, 315 BiPAP. See bilevel positive airway pressure blood gases, patient assessment and, 422–426 arterial blood gas interpretation, 426 arterial line insertion and sampling, 424 arterial sampling, 422 brachial artery, 423 complications of arterial punctures, 423–424 femoral artery, 423 indications for radial artery cannulation, 424 radial arterial puncture, 422–423 sample analysis, 426 venous blood gases, 425 blood urea nitrogen, 403 botulism, 69 bowel sounds, 402

bradycardia, 51 bradypnea, 54, 56, 410 brain natriuretic peptides (BNP), 431 breath, components of, 98b breath cycles, 157 mechanical ventilation and, 113–115 breath trigger, mechanical ventilation and, 111–113, 157 bronchial hygiene, 376 bronchiolitis, 604 pediatric critical care, 614–615 bronchoalveolar lavage (BAL), 20, 561 bronchoscopy, 6, 560 high-frequency oscillatory ventilation and, 552–553 in ICU, 560–563 diagnostic bronchoscopy, 560–561 noninvasive ventilation and, 531 Bunnell Life Pulse, 230–232

C CAD. See coronary artery disease capillary shunt, 40 capnography, 480–484 capnometry, 480 carbon monoxide poisoning, 33 carboxyhemoglobin (HbCO), 49 cardiac arrhythmia, 6 cardiac examination, 412 cardiac output, 402, 450 cardiac ultrasound, 579–582 apical four-chamber view, 581 assessment of volume responsiveness, 582 general concepts, 579–580

parasternal long-axis view, 580 parasternal short-axis view, 580–581 subcostal view, 581 cardiogenic pulmonary edema (CPE), 528–529 noninvasive ventilation, 528–529 cardiogenic shock, 51, 52b, 83 cardiopulmonary bypass, 570 cardiovascular system, mechanical ventilation and, 146–147 complications, 150 CC. See chief complaint CCU. See coronary care units central nervous system, mechanical ventilation and, 148 central venous catheter, 579 cerebral infarction, 6 Chatburn’s 10 maxims, modes of ventilation and, 112b Chest Cuirass Ventilator, 100f chest radiographs, 422 chest tubes, drainage, and management, 420 CHF. See congestive heart failure chief complaint (CC), 403, 405 chronic alveolar hyperventilation, 62 chronic hypercapnic respiratory failure, 426 chronic lung disease, pediatric critical care, 608–609 chronic obstructive pulmonary disease (COPD), 5, 29 noninvasive ventilation, 528 chronic respiratory failure, 31 chronic ventilatory failure, 32, 62, 284 closed-loop ventilator modes, 657 coma, 6 comatose patients, 417 community-acquired pneumonia, noninvasive ventilation, 531 compliance, 461 conduction disorders, 6

congenital heart disease, pediatric critical care, 622 congestive heart failure (CHF), 12, 31 continuous mandatory ventilation, 117–122, 306 continuous positive airway pressure (CPAP), 30, 125–126, 157, 292, 313, 341, 341f, 528 noninvasive ventilation, 125–126 obstructive sleep apnea and, 125, 126b recruitment maneuvers, 125 continuous renal replacement therapy (CRRT), 566 continuous spontaneous ventilation (CSV), 307, 339 continuous venovenous hemodialysis (CVVHD), 567 continuous venovenous hemofiltration (CVVH), 567 control breath, 330 controlled ventilation, 329 conventional mechanical ventilation, pediatric critical care, 618–620 COPD. See chronic obstructive pulmonary disease coronary artery disease (CAD), 12, 82 coronary care units (CCU), 4 Covidien Puritan Bennett 840 ventilator, 185–189 Covidien Puritan Bennett 980 ventilator, 189–194 CPAP. See continuous positive airway pressure crackles, 416 critical care defined, 2 neonatic and pediatric. See pediatric intensive care units (PICU) point-of-care ultrasound. See point-of-care ultrasound critical care ventilators, 156–228, 535 Covidien Puritan Bennett 840, 185–189 Covidien Puritan Bennett 980, 189–194 Dräger Evita Infinity V500, 211–217 Dräger Evita XL, 217–221 GE Healthcare CARESCAPE R860, 221–226 Getinge Servo-i, 174–179 Getinge Servo-u, 179–184

HAMILTON–C1, 169–174 HAMILTON-C3, 163–169 HAMILTON-G5, 156–163 Newport e360 Ventilator, 194–198 Philips Respironics V60 Ventilator, 226–228 Vyaire AVEA, 198–205 Vyaire VELA, 205–211 critical respiratory care assessment. See patient assessment description, 2–12 intensive care units, 4b–5b, 4–6, 15b–16b. See also individual entry airway clearance therapies, 22–23 assessment of patient in, 12–21 design of, 10–11 medications ordered in, 15b interprofessional practice, 8–9 long term acute care, 11 monitoring. See patient monitoring other units, 11 overview, 2 personnel, 6–7 skilled nursing facilities, 12 specialty hospitals, 11–12 types of, in ICU, 3t–4t, 21–22 CRRT. See continuous renal replacement therapy CSV. See continuous spontaneous ventilation cuff-leak test, 651 CVVH. See continuous venovenous hemofiltration CVVHD. See continuous venovenous hemodialysis cyanosis, 412 cycle asynchrony, 373–374 cycle variables, mechanical ventilation and, 113, 315 cystic fibrosis, pediatric critical care, 615

antibiotics, 615 pharmacologic airway clearance therapies, 615 physiologic airway clearance therapies, 615

D dead space, 452 units, 39 ventilation, 55–58, 283b volume, 132 decremental PEEP trial, 382 deep vein thrombosis, 578 respiratory failure and, 86 DeVilbiss IntelliPAP AutoBilevel, 266–267, 268t DeVilbiss IntelliPAP Bilevel S, 265–266, 267t dialysis, 560 diffusion limitation, 43 distributive shock, 51, 52b double cycling, 373 double triggering, 372 Dräger Babylog VN500, 272–276, 276t–277t Dräger Carina, 251–253, 254t Dräger Evita Infinity V500, 211–217 Dräger Evita XL, 217–221 Dräger Oxylog 3000 Plus, 253–256, 257t dual targeting, 315 ductus arteriosus, 603 dynamic autoPEEP, 383

E EBUS. See endobronchial ultrasound echocardiography, 571

ECMO. See extracorporeal membrane oxygenation ejection fraction, 573 electrical discharge from the diaphragm, 372 electrolytes, 403 ELSO. See Extracorporeal Life Support Organization emphysema, 76 encephalitis, 69 endobronchial ultrasound (EBUS), 20 endotracheal intubation, 321–323, 506b–507b endotracheal suctioning, 518b–519b endotracheal tube selection and management, pediatric critical care, 616–617 enteral nutrition, 72, 568 eosinophils, 427 EPAP. See expiratory positive airway pressure equation of motion, 129b expected maximal renal compensation, 61 expiratory positive airway pressure (EPAP), 125, 535 expiratory time, 98 Extracorporeal Life Support Organization (ELSO), 570 extracorporeal membrane oxygenation (ECMO), 546, 560, 570–573 discontinuance, 571–573 indications, 570 mechanical ventilation during, 591–599 approaches, 598 decision to transition, 597 Fio2 and PEEP, 593–594 goals, 592–595 mode, 594 monitoring, 594 special respiratory care issues, 597 targets for oxygenation, Paco2, and hemoglobin, 593 transitioning, 596–597 methods, 570–571

monitoring during, 571 pediatric critical care and, 609, 625–629 cardiac applications, 628 complications, 628–629 indications, 627–628 respiratory failure, 627–628 extrauterine life, pediatric critical care, 603–604 extrinsic PEEP, 104 extubation criteria, 649b failure, 646, 661b exudates, 21 exudative pleural effusions, 562

F facial pressure ulcers, 540 family history, 403, 406–407 fetal circulation, pediatric critical care, 602–603 fetal lung development, pediatric critical care, 602 fine crackles, 416 flail chest, 379 flow asynchrony, 372–373 flow cycling, mechanical ventilation and, 115, 315 flow–time scalar, 137 flow trigger, 371 mechanical ventilation and, 112 flow waveforms, mechanical ventilation and, 137–138 fluid overload, 490 foramen ovale, 603 fraction of inspired oxygen, 138–139 FRC. See functional residual capacity full-face mask, 533

full ventilatory support, 313 functional residual capacity (FRC), 528

G gastrointestinal system, mechanical ventilation and, 147 GE Healthcare CARESCAPE R860, 221–226 Getinge Servo-i, 174–179 Getinge Servo-u, 179–184 Glasgow Coma Scale, 69b Guillain-Barré syndrome, 31

H HACE. See high-altitude cerebral edema HAMILTON–C1, 169–174 HAMILTON-C3, 163–169 HAMILTON-G5, 156–163 HAMILTON-MR1, 236–240 HAMILTON-T1, 232–236 HAPE. See high-altitude pulmonary edema head bobbing, 604 head trauma, respiratory failure and, 85–86 heart failure, 6, 12 respiratory failure and, 81–83 heart sounds, normal and abnormal, 412b–413b HEENT examination, 411–412 helmet, 534t hemoglobin (Hb), 411 hepatomegaly, 413 hertz (Hz), 546 heterogeneous ventilation, pulmonary system, 145–146 diaphragmatic dysfunction, 145–146

immune system, 146 mucociliary motility, 146 respiratory muscles, 145 ventilation/perfusion mismatch, 145 work of breathing, 146 HFV. See high-frequency ventilation high-altitude cerebral edema (HACE), 36 high-altitude pulmonary edema (HAPE), 36 high-flow nasal cannula, 606 high-frequency jet ventilation (HFJV), 132, 321b high-frequency oscillatory ventilation (HFOV), 133, 320b, 545–558 adjuncts for, 549–548 aerosol medication delivery, 550 algorithm for severe, 556t–558t bronchoscopy during, 552–553 endotracheal tube misplacement or obstruction and, 553–554 fluctuation of mPaw and ΔP, 551–552 infection control and, 554 inhaled nitric oxide, 550–551 introduction, 546 lung-protective conventional ventilation, transition from, 552 lung recruitment maneuvers, 548–549 oxygenation, 546–548 pneumothorax and, 553 prone positioning, 550 tracheostomy and, 551 transition to extracorporeal membrane oxygenation, 551 transport of patients, 552 troubleshooting, 553–554 ventilation, 549 high-frequency percussive ventilation (HFPV), 132–133, 321b high-frequency positive pressure ventilation (HFPPV), 132, 321b high-frequency ventilation (HFV), 132–134, 320b, 348–349

high-frequency ventilators, 228–232 Bunnell Life Pulse, 230–232 Percussionaire VDR-4, 230 Vyaire 3100B High-Frequency Oscillator, 228–230 history and physical examinations, results of, 13b–14b history of present illness (HPI), 403, 405–406 HPI. See history of present illness humidification, mechanical ventilation and, 140–141 hypercapnea, 30 hypercapnia, 282, 452 clinical manifestations of, 33t hypercapnic respiratory failure, 30–31, 282, 528 hyperechoic structure, 578 hyperresonance, 510 hyperresonant percussion, 415 hyperventilation, 30, 126, 282 hypoechoic structure, 578 hypotension, 32, 68 hypothermia, 411, 479, 565 hypoventilation, 32b, 120, 282 hypovolemic shock, 51, 52b, 84 hypoxemia, 404 assessment of severity of, 31t hypoxemic respiratory failure, 29, 282, 528, 570 hypoxia altitude, 36 ambient, 36 anemic, 33 circulatory, 51, 52–53 clinical manifestations of, 33t histotoxic, 33 ischemic, 33 types of, 34t–35t

I IABP. See intra-aortic balloon pump iatrogenic injury, 535 ICU. See intensive care units imaging, patient assessment portable chest radiographs, 431 ultrasound imaging, 431–432 immunocompromised patients, noninvasive ventilation, 529 impending ventilatory failure, 62, 282, 296, 298–300 imposed work of breathing, 338 IMV. See intermittent inventory ventilation; intermittent mandatory ventilation inhaled gas mixtures, pediatric critical care, 620–625 anesthetic gas mixtures, 624–625 hazards/complications, 623 helium–oxygen mixtures, 620–621 limitations of, 623 nitric oxide, 621–623 subambient oxygen and inhaled carbon dioxide, 623–624 weaning, 623 initial ventilator settings, 306–308 inotropes, 489 inspiratory flow, 159 waveform, 373 inspiratory pause, mechanical ventilation and, 138–139 inspiratory positive airway pressure (IPAP), 106, 535 inspiratory pressure, 158 inspiratory time, 98, 158 inspiratory-to-expiratory ratio, 98 intelligent targeting, 315 intensive care units (ICU), 2 airway clearance therapies, 22–23 assessment of patient in, 12–21

bronchoscopy, 20–21 cardiac monitoring, 21 imaging in, 20 laboratory studies, 19–20 medical record, reviewing of, 12–14, 13b–14b, 16 patient history, 16–17 physical examination, 17–19 thoracentesis, 20–21 bronchoscopy, 560–563 diagnostic bronchoscopy, 560–561 design of, 10–11 diagnostic and supportive procedures, 559–575 dialysis in the ICU, 566–567 extracorporeal membrane oxygenation, 570–573 discontinuance, 571–573 indications, 570 methods, 570–571 monitoring during, 571 mechanical circulatory assistance, 573–575 discontinuance of, 575 indications, 573 methods, 573–574 monitoring, 574–575 medications ordered in, 15b nutrition in the ICU, 567–569 enteral nutrition, 568–569 parenteral nutrition, 569–570 special considerations, 570 predictive scoring tools used in, 70b–71b pulmonary history in, 17b respiratory care in, 4b–5b, 15b–16b types of, 4–6, 21–22 temperature regulation in, 563–566

evaporation techniques, 564 immersion techniques, 564–565 management of environmental hyperthermia, 564 management of environmental hypothermia, 565 therapeutic hypothermia, 565–566 thoracentesis, 562–563 intermittent inventory ventilation, 307 intermittent mandatory ventilation (IMV), 122–124, 316 interprofessional education (IPE), 8 interprofessional practice (IPP), 8 intra-aortic balloon pump (IABP), 573 intracranial hemorrhage, 6 intracranial pressure, 104 intrapulmonary shunt, 476 intrinsic PEEP, 104 invasive ventilation, 107–108, 321 IPAP. See inspiratory positive airway pressure IPE. See interprofessional education IPP. See interprofessional practice iron lung, 96, 97f isoechoic structure, 586

L laboratory studies, patient assessment and, 426–431 blood glucose and diabetes, 429–430 cardiac markers, 431 clinical chemistry, 427–428 complete blood count, 427 electrolytes, 428–429 hemoglobin and hematocrit, 426–427 kidney function tests, 430–431 platelets, 427

red blood cell count, 427 white blood cell count and differential, 427, 428b laryngeal mask airway (LMA), 498 left ventricular assist devices (LVADs), 573 leukocytosis, 427 liberation from mechanical ventilation, 638 LIPS. See Lung Injury Prediction Score long cycling, 373 long-term acute care (LTAC), 11 long-term applications, 532 lower inflection point (LIP), 381 LPCV. See lung-protective conventional ventilation LTAC. See long-term acute care lung compliance, 101 lung failure. See hypoxemic respiratory failure Lung Injury Prediction Score (LIPS), 71 lung-protective conventional ventilation (LPCV), 546 lung-protective ventilatory strategy, 313 lung ultrasound, 583–585 characteristics of pleural effusion, 584 detection of pneumothorax, 583 evaluation of pleural effusion, 584 general concepts, 583 pleural drainage procedures, 584–585 respiratory failure, determining the etiology of, 585 LVADs. See left ventricular assist devices lymphocytes, 427

M mandatory breaths, 315 cycling, mechanical ventilation and, 114 mandatory minute ventilation, 320b

maximal expiratory pressure (MEP), 434, 458, 464–465, 643 maximal inspiratory pressure (MIP), 432–434, 458, 464–465, 651, 652 mean airway pressure, 104–105, 106b mean airway pressure (mPaw), 546 mechanical circulatory assistance, ICU and, 573–575 discontinuance of, 575 indications, 573 methods, 573–574 monitoring, 574–575 mechanical circulatory support (MCS), 573 mechanical dead space, 456 mechanical ventilation, 2, 21–22, 96–153. See also mechanical ventilatory support; ventilation baseline pressure, 103–104 cardiovascular system and, 146–147 complications, 150 central nervous system and, 148 complications, 150 complications of, 149–151, 304b–305b airway complications, 149 cardiac/cardiovascular, 150 CNS/psychological, 150 equipment failure, 149 gastrointestinal, 151 immune system, 151 lung injury due to pressure, 149 neuromuscular, 150–151 nutritional, 151 oxygen toxicity, 150 renal, 150 ventilator-associated pneumonia, 149–150 contraindications of, 303–304 during extracorporeal membrane oxygenation, 591–599 approaches, 598

decision to transition, 597 Fio2 and PEEP, 593–594 goals, 592–595 mode, 594 monitoring, 594 special respiratory care issues, 597 targets for oxygenation, Paco2, and hemoglobin, 593 transitioning, 596–597 gastrointestinal system and, 147 complications, 151 goals of, 313 indications for, 294–303 acute ventilatory failure, 294, 296, 297–298, 297b apnea, 294, 295–296, 295b impending ventilatory failure, 296, 298–300 severe oxygenation problems, 300–303 introduction of, 96–98 invasive ventilation, 107–108 mean airway pressure, 104–105, 106b modes. See also ventilator modes monitoring, 458–465 airway pressures, 458–460 airway resistance, 461–462 compliance, 461 maximum expiratory pressure, 464–465 maximum inspiratory pressure, 464–465 peak and mean airway pressure, 459 PEEP and AutoPEEP, 460 plateau pressure, 459–460 rapid shallow breathing index, 464 vital capacity, 464–465 work of breathing, 462–464 negative pressure breathing, 99–100

noninvasive ventilation, 106–107 parameters, 137–142 alarms, 139–140 flow waveforms, 137–138 humidification, 140–141 inspiratory pause, 138–139 PEEP/CPAP, 139 sigh breaths, 141–142 peak inspiratory pressure, 103 plateau pressure, 103 positive end-expiratory pressure, 103–104 autoPEEP, 104 optimal, 104 positive pressure breathing, 100–103 principles, 109–117 breath cycle, 113–115 breath trigger, 111–113 cycle variables, 113 flow cycling, 115 flow trigger, 112 input power and control systems, 109–111 mandatory breath cycling, 114 operator interface, 115–116 patient cycling, 113–114 pneumatically powered ventilators, 109 pressure cycling, 114 pressure trigger, 112 time cycling, 114 time trigger, 112–113 ventilator classification or taxonomy, 116–117 ventilator terminology, 111 volume cycling, 114–115 pulmonary system and, 142–146

airway pressures, 144–145 heterogeneous ventilation, 145–146 oxygenation, 142–143 ventilation, 143–144 renal system and, 147 complications, 150 sleep and, 148 spontaneous breathing, 99 ventilator initiation, 108–109 mechanical ventilators, 155–280 Airon pNeuton, 241–242 Bio-Med Devices Crossvent 4+, 242–244 Bunnell Life Pulse, 230–232 manufacturer’s specifications, 232t Covidien Puritan Bennett 840 ventilator, 185–189 accessories, 189 assist/control pressure control, 187 assist/control (volume control), 185–186 bilevel, 188 leak compensation, 189 manufacturer’s specifications, 189t–190t modes, 185–188 neomode, 189 noninvasive ventilation, 188 proportional assist ventilation, 188 SIMV (pressure control), 187 SIMV (volume control), 186 SIMV volume control+, 187–188 special features, 188–189 spontaneous volume support, 188 tube compensation, 188–189 volume control+, 187 Covidien Puritan Bennett 980 ventilator, 189–194

accessories, 194 apnea backup ventilation, 193 assist/control (volume control), 190 bilevel, 192–193 Leak Sync, 193 manufacturer’s specifications, 193t–194t modes, 189–193 NeoMode 2.0, 193 noninvasive ventilation, 193 proportional assist ventilation, 193 SIMV pressure control, 191–192 SIMV (volume control), 190–191 SIMV volume control+, 192 special features, 193 spontaneous pressure support, 192 spontaneous volume support, 192 tube compensation, 193 volume control+, 192 DeVilbiss IntelliPAP AutoBilevel, 266–267, 268t DeVilbiss IntelliPAP Bilevel S, 265–266, 267t Dräger Babylog VN500, 272–276, 276t–277t Dräger Carina, 251–253, 254t Dräger Evita Infinity V500, 211–217 accessories, 217 apnea backup ventilation, 216 AutoFlow, 216 automatic tube compensation, 216 low-flow PV loop, 216 manufacturer’s specifications, 217t–218t modes, 211–216 nebulizer, 216 noninvasive ventilation, 217 pressure control A/C, 214

pressure-control-airway pressure-release ventilation, 215 pressure-control-continuous mandatory ventilation, 213–214 pressure-control-pressure-support ventilation, 215 pressure-control-synchronized intermittent mandatory ventilation, 214 pressure-control-synchronized intermittent mandatory ventilation+, 215 special features, 216–217 spontaneous-continuous positive airway pressure, 216 spontaneous-continuous positive airway pressure/ volume support, 215 spontaneous-continuous positive pressure/ pressure support, 215 spontaneous-proportional pressure support, 216 variable pressure-support ventilation, 216 volume control–A/C, 212 volume-control–continuous mandatory ventilation, 212 volume-control-mandatory minute volume ventilation, 213 volume-control–synchronized intermittent mandatory ventilation, 212–213 Dräger Evita XL, 217–221 accessories, 221 airway pressure-release ventilation, 220 apnea ventilation, 220 AutoFlow, 220 automatic tube compensation, 220 continuous mandatory ventilation, 217 low-flow PV loop, 220 mandatory minute volume ventilation, 219 manufacturer’s specifications, 220t–221t modes, 217–220 nebulizer, 220 neonatal ventilation, 220 noninvasive ventilation, 220 PCV+ Assist, 219–220 pressure-controlled ventilation+/pressure- supported spontaneous breathing, 219 pressure-control ventilation+, 219 special features, 220

synchronized intermittent mandatory ventilation, 218 synchronized intermittent mandatory ventilation/ pressure support, 218–219 Dräger Oxylog 3000 Plus, 253–256, 257t GE Healthcare CARESCAPE R860, 221–226 accessories, 226 A/C pressure control, 223 A/C pressure-regulated volume control, 223 A/C volume control, 222 apnea backup ventilation, 225 BiLevel airway pressure ventilation, 224 BiLevel airway pressure ventilation volume guaranteed, 224 continuous positive airway pressure/pressure support, 223 FRC procedure, 225 indirect calorimetry, 225 leak compensation, 225 manufacturer’s specifications, 225t–226t modes, 222–224 noninvasive ventilation, 224 special features, 224–225 SpiroDynamics, 225 spontaneous breathing trial, 225 synchronized intermittent mandatory ventilation pressure control, 223 synchronized intermittent mandatory ventilation pressure-regulated volume control, 223–224 synchronized intermittent mandatory ventilation volume control, 222–223 tube compensation, 225 volume support, 224 Getinge Servo-i, 174–179 accessories, 179 apnea backup ventilation, 178 automode, 177–178 Bi-Vent, 178 Heliox, 179 leak compensation, 178–179

manufacturer’s specifications, 179t–180t modes, 175–178 nasal CPAP, 178 neurally adjusted ventilatory assist, 178 noninvasive ventilation, 178 open lung tool, 178 pressure control, 176 pressure-regulated volume control, 176–177 pressure support, 176 SIMV (pressure control), 176 SIMV (PRVC), 177 SIMV (volume control), 175–176 special features, 178–179 spontaneous/CPAP, 176 stress index, 179 volume control, 175 volume support, 177 Getinge Servo-u, 179–184 accessories, 184 apnea backup ventilation, 184 automode, 183 Bi-Vent/APRV, 183 leak compensation, 184 manufacturer’s specifications, 184t–185t modes, 180–184 nasal CPAP, 184 neurally adjusted ventilatory assist, 183 noninvasive ventilation, 184 pressure control, 181 pressure-regulated volume control, 182 pressure support/CPAP, 182 SIMV (pressure control), 181–182 SIMV (PRVC), 182

SIMV (volume control), 180–181 special features, 184 volume support, 182–183 HAMILTON–C1, 169–174 accessories, 174 adaptive support ventilation, 172 airway pressure-release ventilation, 172 apnea backup ventilation, 173 duo positive-pressure airway pressure, 171 dynamic lung panel, 173 manufacturer’s specifications, 173t–174t modes, 169–173 nasal continuous positive airway pressure, 172–173 nasal continuous positive airway pressure-pressure control, 173 nebulizer, 173 noninvasive ventilation, 172 pressure-controlled ventilation+, 171 pressure synchronized intermittent mandatory ventilation +, 171 special features, 173 spontaneous/CPAP, 171 spontaneous/timed noninvasive ventilation, 172 synchronized controlled mandatory ventilation plus, 169–170 synchronized intermittent mandatory ventilation plus, 170–171 HAMILTON-C3, 163–169 accessories, 169 adaptive pressure ventilation with controlled mandatory ventilation, 165–166 adaptive pressure ventilation with synchronized intermittent mandatory ventilation, 166 adaptive support ventilation, 167 airway pressure-release ventilation, 166 apnea backup ventilation, 168 duo positive-pressure airway pressure, 166 dynamic heart/lung panel, 168 high-flow oxygen therapy, 168

INTELLiVENT-ASV, 168 manufacturer’s specifications, 168t–169t modes, 164–167 nasal continuous positive airway pressure, 167 nebulizer, 168 noninvasive ventilation, 167 pressure-controlled ventilation+, 165 pressure synchronized intermittent mandatory ventilation+, 165 pressure/volume tool, 167–168 special features, 167–168 spontaneous mode, 165 spontaneous/timed noninvasive ventilation, 167 synchronized controlled mandatory ventilation, 164–165 synchronized intermittent mandatory ventilation, 165 HAMILTON-G5, 156–163 accessories, 163 adaptive pressure ventilation with controlled mandatory ventilation, 160 adaptive pressure ventilation with synchronized intermittent mandatory ventilation, 160 adaptive support ventilation, 161 airway pressure-release ventilation, 160–161 apnea backup ventilation, 162 duo positive-pressure ventilation, 160 dynamic heart/lung panel, 162 Intellicuff®, 162 INTELLiVENT-ASV, 162 manufacturer’s specifications, 162t–163t modes, 157–162 nasal continuous positive airway pressure, 161–162 noninvasive ventilation, 161 pressure-controlled mandatory ventilation, 158 pressure-synchronized intermittent mandatory ventilation, 158–159 pressure/volume tool, 162 special features, 162

spontaneous/timed noninvasive ventilation, 161 spontaneous ventilation, 159 synchronized controlled mandatory ventilation, 157 synchronized intermittent mandatory ventilation, 157–158 volume support, 159–160 HAMILTON-MR1, 236–240 accessories, 240 adaptive support ventilation, 239 airway pressure-release ventilation, 239 apnea backup ventilation, 240 DuoPAP, 238–239 dynamic lung panel, 240 manufacturer’s specifications, 240t–241t modes, 236–240 nasal continuous positive airway pressure, 240 nasal continuous positive airway pressure-pressure control, 240 nebulizer, 240 pressure-controlled ventilation+, 238 pressure synchronized intermittent mandatory ventilation+, 238 special features, 240 spontaneous mode, 238 spontaneous/timed noninvasive ventilation, 239–240 synchronized controlled mandatory ventilation+, 236, 238 synchronized intermittent mandatory ventilation+, 238 HAMILTON-T1, 232–236 adaptive support ventilation, 235 airway pressure-release ventilation, 234–235 apnea backup ventilation, 235 CO2 monitoring, 236 DuoPAP, 234 manufacturer’s specifications, 236t–237t modes, 232–235 nebulizer, 235

noninvasive ventilation, 235 oxygen, 235 pressure-controlled ventilation+, 233–234 pressure synchronized intermittent mandatory ventilation+, 234 special features, 235–236 spontaneous mode, 234 spontaneous/timed noninvasive ventilation, 235 synchronized controlled mandatory ventilation+, 233 synchronized intermittent mandatory ventilation+, 233 introduction, 155 Medtronic Newport HT70 Plus, 256–259, 259t–260t neonatal ventilators, 272–279 Newport e360 ventilator, 194–198 biphasic pressure-release ventilation/assist/ control mandatory ventilation, 197 biphasic pressure-release ventilation/ synchronized intermittent mandatory ventilation, 197–198 Flex Cycle, 198 leak compensation, 198 manufacturer’s specifications, 198t–199t modes, 195–198 noninvasive ventilation, 198 pressure-control assist/control mandatory ventilation, 196 pressure-control SIMV, 196 pressure control/spontaneous, 196 special features, 198 volume-control/assist/control mandatory ventilation, 195 volume-control SIMV, 195 volume control/spontaneous, 196 volume-target pressure-control/assist/control mandatory ventilation, 196 volume-target pressure control/spontaneous, 197 volume-target pressure-control/synchronized intermittent mandatory ventilation, 197 Percussionaire VDR-4, 230 Philips Respironics Trilogy Ventilator, 263–265, 266t Philips Respironics V60 Ventilator, 226–228

apnea backup ventilation, 228 Auto-Trak Sensitivity, 228 average volume-assured pressure support, 227–228 continuous positive airway pressure mode, 227 leak adaptation, 228 manufacturer’s specifications, 229t modes, 227–228 noninvasive ventilation, 228 pressure-control ventilation, 227 proportional pressure ventilation, 228 special features, 228 spontaneous/timed mode, 227 pNeuton mini, 242, 243t pNeuton Models A and S, 242 ResMed Astral 100/150, 269–272, 272t–273t ResMed Lumis Tx, 267–269, 270t Smiths Medical Pneupac babyPAC 100, 276–278 Vyaire AVEA, 198–205 accessories, 205 advanced settings, 203–205, 204t airway pressure-release ventilation/biphasic, 202 apnea backup ventilation, 203 artificial airway compensation, 203 CPAP/pressure support, 200–201 leak compensation, 205 maneuvers, 205 manufacturer’s specifications, 205t–206t modes, 199–203 nasal continuous positive airway pressure/ intermittent mandatory ventilation, 203 pressure A/C, 200 pressure A/C with volume guarantee, 202 pressure-regulated volume control (assist/control), 201 pressure-regulated volume control SIMV, 201

pressure SIMV, 200 pressure SIMV with volume guarantee, 202–203 special features, 203, 205 time cycled pressure limited A/C, 202 time cycled pressure limited SIMV, 202 time cycled pressure limited with volume guarantee, 203 volume A/C, 199 volume SIMV, 199 Vyaire 3100B High-Frequency Oscillator, 228–230 manufacturer’s specifications, 230t mode, 228–229 special features, 229 Vyaire Infant Flow SiPAP, 278–279 Vyaire LTV 1200, 248–251, 251t–252t Vyaire ReVel, 244–248 A/C + pressure, 246 A/C + pressure-regulated volume control, 246 apnea backup ventilation, 247 CPAP + pressure-support ventilation, 246 manufacturer’s specifications, 248t–249t mode, 244–247 nebulizer, 248 noninvasive positive-pressure ventilation A/C, 247 noninvasive positive-pressure ventilation/CPAP/ pressure support, 247 optional pulse oximetry, 248 oxygen, 247 pressure-regulated volume support, 247 SIMV + pressure, 246 SIMV + PRVC, 246–247 SIMV + volume, 245–246 special features, 247–248 spontaneous breathing trial, 247 Vyaire VELA, 205–211

accessories, 211 advanced settings, 209, 210t, 211 airway pressure-release ventilation/biphasic, 208 apnea backup ventilation, 209 CPAP/pressure support, 208 maneuvers, 211 manufacturer’s specifications, 211t–212t modes, 206–209 noninvasive positive-pressure ventilation A/C, 209 noninvasive positive-pressure ventilation/CPAP/ pressure support, 209 noninvasive positive-pressure ventilation/SIMV, 209 NPPV leak compensation, 211 pressure A/C, 207 pressure-regulated volume control, 208 pressure-regulated volume control SIMV, 208 pressure SIMV, 207–208 special features, 209–211 volume A/C, 206 volume SIMV, 206–207 ZOLL Eagle II, 259–262, 262t–263t mechanical ventilatory support, 2. See also mechanical ventilation adjustment of. See ventilatory support, adjustment of goals of, 293–294 indications for, 32 initial ventilator settings, 306–308. See also ventilator initiation pressure control-continuous mandatory ventilation, 307 pressure control-continuous spontaneous ventilation, 307–308 pressure control-intermittent mandatory ventilation, 307 volume control-continuous mandatory ventilation, 307 volume control-intermittent mandatory ventilation, 307 patient assessment for, 305–306 respiratory failure and, 291–293 meconium aspiration syndrome (neonatal), 605, 608

medical history, components of, 404b medical intensive care units (MICU), 4 medical record review, 402–403 Medtronic Newport HT70 Plus, 256–259, 259t–260t meningitis, 69 mental status, assessment of, 416–417, 418b MEP. See maximal expiratory pressure metabolic acidosis, 62 ventilatory support adjustment and, 393–394 metabolic alkalosis, 63 ventilatory support adjustment and, 394 methemoglobinenemia, 33 MI. See myocardial infarction MICU. See medical intensive care units minimum PEEP, 379 minute ventilation, 98, 99b, 282, 652 MIP. See maximal inspiratory pressure missed triggering, 371–372 mode asynchrony, 374–375 modified Allen test, 424 modified Mallampati Classification, 323f monitoring of mechanical ventilation. See under mechanical ventilation monocytes, 427 musculoskeletal disease, 12 myasthenia gravis, 31 myocardial infarction (MI), 6, 51

N nasal flaring, 604 nasal intermittent positive-pressure ventilation (NIPPV), 618 nasal mask, 534t nasopharyngeal airway, 498

nebulizer, 163 negative inspiratory force (NIF), 652 negative pressure breathing, 99–100 negative pressure ventilation, 96, 312 neonatal and pediatric critical care, 601–630 apnea of prematurity, 609 ARDS, pediatric, 609–611 asthma, 611–612 bronchiolitis, 614–615 chronic lung disease (neonatal), 608–609 conventional mechanical ventilation, 618–620 cystic fibrosis, 615 endotracheal tube selection and management, 616–617 expected values for important respiratory parameters, 616 extracorporeal membrane oxygenation, 625–629 cardiac applications, 628 complications, 628–629 indications, 627–628 extrauterine life, transition to, 603–604 fetal circulation, 602–603 fetal lung development, 602 inhaled gas mixtures, 620–625 anesthetic gas mixtures, 624–625 hazards/complications, 623 helium–oxygen mixtures, 620–621 limitations of, 623 nitric oxide, 621–623 subambient oxygen and inhaled carbon dioxide, 623–624 weaning, 623 meconium aspiration syndrome (neonatal), 608 monitored parameters, 615–616 neonatal respiratory conditions, 605–609 neurologic conditions, 612–613

neuromuscular diseases, 613–614 noninvasive support, 617–618 other congenital anomalies, 609 patient transport, 629–630 adverse events, 629 mechanical ventilation during transport, 630 safety implications, 630 persistent pulmonary hypertension, newborn, 608 recognizing respiratory distress, 604–605 respiratory distress syndrome (neonatal), 605–607 indications, 606 procedure, 606–607 surfactant replacement, 606 treatment, 606 retinopathy of prematurity, 609 transient tachypnea, newborn, 607–608 neonatal intensive care unit (NICU), 4, 6 neonatal respiratory conditions, 605–609 neonatal ventilators, 272–279 Dräger Babylog VN500, 272–276 Smiths Medical Pneupac babyPAC 100, 276–278 Vyaire Infant Flow SiPAP, 278–279 neonate, 604 neurally adjusted ventilatory assist (NAVA), 134–136, 315, 370 neural–ventilatory coupling, 372 neurogenic shock, 51, 52b neuro-inspiratory time, 373 neurologic conditions, pediatric critical care and, 612–613 neurologic diseases, respiratory failure and, 86–88, 285 infection and, 88–89 ventilatory support, 89 neurologic examination, 417, 419 neuromuscular blockade, 396

neuromuscular disease, 6, 29, 287 noninvasive ventilation, 532 pediatric critical care and, 613–614 neutrophils, 427 Newport e360 ventilator, 194–198 NICU. See neonatal intensive care unit NIPPV. See nasal intermittent positive-pressure ventilation NIV. See noninvasive ventilation noninvasive monitoring, 476–486 capnography, 480–484 capnometry, 480 pulse oximetry, 476–480, 478–480 transcutaneous O2/CO2, 484–486, 486b–487b noninvasive positive pressure ventilation (NPPV), 98 noninvasive support, pediatric critical care, 617–618 noninvasive ventilation (NIV), 106–107, 316, 527–542 complications and hazards, 539–540 facial pressure ulcers, 540–541 equipment, 533–535 application, 533 critical care ventilators, 535 interface, 533, 534f noninvasive ventilators, 535 indications, 528–532, 532b–533b acute respiratory distress syndrome, 530 asthma, 528 bronchoscopy, 531 cardiogenic pulmonary edema, 528–529 chronic obstructive pulmonary disease, 528 community-acquired pneumonia, 531 immunocompromised patients, 529 long-term applications, 532 neuromuscular disease, 532

palliative care, 531 postextubation, 529 preintubation, 529–530 sleep apnea and obesity hypoventilation syndrome, 531 trauma, 531–532 initiation, 535–539 discontinuing of NIV, 539 location of, 539 monitoring, 539 ongoing management, 538–539 recognizing failure of NIV, 539 settings, 535–538 risk factors and problems associated with, 540t special considerations, 540–541 high-flow nasal cannula, 540–541 specialty modes of NIV support, 541 non-ST segment elevation MI (NSTEMI), 68 NPPV. See noninvasive positive pressure ventilation NRS 2002. See Nutrition Risk Screening 2002 NUTRIC. See The Nutrition Risk in the Critically Ill The Nutrition Risk in the Critically Ill (NUTRIC), 71 Nutrition Risk Screening 2002 (NRS 2002), 71

O obesity hypoventilation syndrome, noninvasive ventilation and, 531 obstructive lung disease, 372 obstructive shock, 52b, 84 obstructive sleep apnea, 528 obtunded patients, 417 occupational history, 403, 407, 408b open lung strategy, 384 open lung ventilation, 376

optimal PEEP, 379 optimal targeting, 315 oronasal mask, 532, 534t oropharyngeal airway, 498 oxygenation, 35–54 alveolar ventilation, 37 blood oxygen content, 45–46 conducting airways, 37 effect of hyperventilation, 37–38 effect of hypoventilation, 38–39 factors that affect hemoglobin, 47–50 factors that affect O2 saturation, 46–47 high-frequency oscillatory ventilation and, 546–548 impaired diffusion, 43 indices of O2 transfer, 43–45 inspired oxygen, 36–37 matching of gas and blood (V/Q), 39–42, 40f–42f oxygen delivery, 50–51, 50b, 52b shunt, 43 anatomic shunt, 43 physiologic shunt, 43 steps in the process, 35b tissue oxygen uptake and utilization, 51, 53–54 ventilatory support adjustment and, 375–386 oxygen delivery, 104

P PAC. See pressure assist/control palliative care, noninvasive ventilation, 531 paradoxical chest movement, 604 parenteral nutrition, 72, 497, 569 parietal pleural, 583

partial ventilatory support, 313 past medical history (PMH), 403, 406 patient assessment, 401–446. See also patient monitoring blood gases, 422–426 arterial blood gas interpretation, 426 arterial line insertion and sampling, 424 arterial sampling, 422 brachial artery, 423 complications of arterial punctures, 423–424 femoral artery, 423 indications for radial artery cannulation, 424 radial arterial puncture, 422–423 sample analysis, 426 venous blood gases, 425 imaging portable chest radiographs, 431 ultrasound imaging, 431–432 laboratory studies, 426–431 blood glucose and diabetes, 429–430 cardiac markers, 431 clinical chemistry, 427–428 complete blood count, 427 electrolytes, 428–429 hemoglobin and hematocrit, 426–427 kidney function tests, 430–431 platelets, 427 red blood cell count, 427 white blood cell count and differential, 427 physical assessment, history and, 402–421 abdominal examination, 413 ancillary use of equipment, 420 auscultation, 415–416 back and spine, 412

bedside assessment in the ICU, 413 cardiac examination, 412 chest tubes, drainage, and management, 420 chief complaint, 405 collection chamber, 420–421 extremities, 413–414 family history, 406–407 general appearance, 407, 409 HEENT examination, 411–412 history, 403–405 history of present illness, 405–406 medical history, components of, 404b medical record review, 402–403 mental status, assessment of, 416–417, 418b neurologic examination, 417, 419 occupational history, 407, 408b pain monitoring, 419–420 palpation, 414 past medical history, 406 patient and/or family interview, 405 percussion, 415 physical assessment, 407 pulmonary history, components of, 408b–409b skin, 411 social history, 406 suction control chamber, 421 thorax and lung examination, 414–416 urine output monitoring, 421–422 vital signs, 409–411 water seal chamber, 421 pulmonary function testing, 432–444 airway occlusion pressure, 434 bedside tests of spontaneous breathing, 432

common arrhythmias, 437–441 electrocardiogram, 436–437 FVC and FEV1, 435–436 heart failure, 441–444 heart rate and rhythm, 437 myocardial infarction, 441 peak flow, 435 rapid shallow breathing index, 432 respiratory mechanics, 432 tidal volume, minute ventilation, and respiratory rate, 432 vital capacity, 434 patient cycling, mechanical ventilation and, 113–114 patient monitoring, 449–524. See also patient assessment airway management and monitoring, 497–509 artificial airway, 501–503, 504f–505f, 506b–507b bronchial hygiene, 509–510 cuff pressure and volume, 501 endotracheal tube characteristics, 500–501 tracheostomy tubes, 503, 508–509 chest tubes, drainage, and management, 496 dialysis, 496 electrocardiogram monitoring, 487–495 hemodynamic monitoring, 488–493 arterial blood pressure monitoring, 488 cardiac output/index, 492–493 cardiopulmonary calculations, 493–494 central venous pressure, 490 fluid balance, 489–490 mechanical circulatory assistance, 494–495 pulmonary artery catheters, 490–492 titrate vasopressors and inotropes, 488–489 intracranial pressure monitoring, 495 introduction, 450

mechanical ventilation, monitoring, 458–465 airway pressures, 458–460 airway resistance, 461–462 compliance, 461 maximum expiratory pressure, 464–465 maximum inspiratory pressure, 464–465 peak and mean airway pressure, 459 PEEP and AutoPEEP, 460 plateau pressure, 459–460 rapid shallow breathing index, 464 vital capacity, 464–465 work of breathing, 462–464 mental status, assessment for, 495 neurologic function, assessment for, 495 noninvasive monitoring, 476–486 capnography, 480–484 capnometry, 480 pulse oximetry, 476–480 transcutaneous O2/CO2, 484–486, 486b–487b nutritional support, 496–497 optimal PEEP, 474–476 overview, 450 patient care, 509–510 recruitment maneuvers, 474–476 renal function and urine output monitoring, 495–496 temperature monitoring and regulation in the ICU, 496 therapeutic hypothermia, 496 ventilation, monitoring, 451–452 ventilator graphics, 465–474 flow-time curves, 470–474 pressure, flow, and volume curves, 465 pressure–time curves, 465–470 pressure–volume curves, 470

ventilator system monitoring, 510–522 airway problems, 516 asynchrony and fighting the ventilator, 513–516 bronchospasm, 518–519 infection, 521–522 pneumothorax, 519–521 recognition and treatment of common complications, 512–513 secretions, 516–518 ventilatory parameters and mechanical ventilation, 452–458 alveolar ventilation and dead space, 456–457 I:E ratio and patient- or time-triggered VC-CMV, 457 I:E ratio and time-triggered VC-CMV, 457 intermittent mandatory ventilation and I:E ratio, 457 monitoring and adjustment of I:E ratio, 457–458 respiratory rate, 452 tidal volume and minute ventilation measurement and evaluation, 452–455 ventilatory requirements and ventilatory capacity, 455–456 patient transport, pediatric critical care, 629–630 adverse events, 629 mechanical ventilation during transport, 630 safety implications, 630 patient-triggered breaths, 314 patient–ventilator asynchrony, 369 patient–ventilator interaction, 370–375 autotriggering, 372 cycle asynchrony, 373–374 double triggering, 372 flow asynchrony, 372–373 missed triggering, 371–372 mode asynchrony, 374–375 reverse triggering, 372 trigger asynchrony, 371 trigger delay, 372

trigger work, 371 PAV. See proportional assist ventilation PAW. See peak airway pressure PCV. See pressure control ventilation peak airway pressure (PAW), 103b, 113 peak and mean airway pressure, 459 peak flow, 435 peak inspiratory pressure (PIP), 103 pediatric critical care. See neonatal and pediatric critical care pediatric intensive care units (PICU), 4 PEEP. See positive end-expiratory pressure Percussionaire VDR-4, 230 percussion notes, 415, 510 percutaneous endoscopic gastrostomy tube, 568 pericardial effusion, 578 peritoneal fluid (ascites), 413 persistent pulmonary hypertension of the newborn (PPHN), 608, 621 P/F ratio, 300 Philips Respironics Trilogy Ventilator, 263–265 Philips Respironics V60 Ventilator, 226–228 physical assessments, 402. See also under patient assessment physiologic dead space, 55, 283b, 456 physiologic PEEP, 377 PICU. See pediatric intensive care units PIP. See peak inspiratory pressure pitting edema, 413b plasma bicarbonate, 426 plateau pressure, 103 platelets, 427 pleural effusion, 560, 578 pleural friction rubs, 416 PMH. See past medical history PMV. See prolonged mechanical ventilation

pneumonia, 12, 29 respiratory failure and, 79–80 pneumothorax, 409, 451 high-frequency oscillatory ventilation and, 553 pNeuton mini, 242, 243t pNeuton Models A and S, 242 point-of-care ultrasound, 577–589 abdominal ultrasound, 585–586 anatomic landmarks, 586 ascites and paracentesis, assessment for, 586 general concepts, 585–586 cardiac ultrasound, 579–582 apical four-chamber view, 581 assessment of volume responsiveness, 582 general concepts, 579–580 parasternal long-axis view, 580 parasternal short-axis view, 580–581 subcostal view, 581 history and evolution of, 578 introduction, 578–579 lumbar puncture, ultrasound-guided, 587–588 lung ultrasound, 583–585 characteristics of pleural effusion, 584 detection of pneumothorax, 583 evaluation of pleural effusion, 584 general concepts, 583 pleural drainage procedures, 584–585 respiratory failure, determining the etiology of, 585 transducers holding and movement of, 579 types of, 578–579 vascular ultrasound, 586–587 deep vein thrombosis, detection of, 587

vascular access, 586–587 polycythemia, 49 portable chest x-rays, 431 portable ventilators, 232–272 Airon pNeuton, 241–242 Bio-Med Devices Crossvent 4+, 242–244 DeVilbiss IntelliPAP AutoBilevel, 266–267 DeVilbiss IntelliPAP Bilevel S, 265–266 Dräger Carina, 251–253 Dräger Oxylog 3000 Plus, 253–256 HAMILTON-MR1, 236–240 HAMILTON-T1, 232–236 Medtronic Newport HT70 Plus, 256–259 Philips Respironics Trilogy Ventilator, 263–265 pNeuton mini, 242 pNeuton Models A and S, 242 ResMed Astral 100/150, 269–272 ResMed Lumis Tx, 267–269 Vyaire LTV 1200, 248–251 Vyaire ReVel, 244–248 ZOLL Eagle II, 259–262 positive end-expiratory pressure (PEEP), 30, 103, 124–125, 160, 294, 313, 530 extrinsic, 104 intrinsic, 104 positive pressure ventilation, 97, 312, 528 posteroanterior (PA) images, 431 postextubation, noninvasive ventilation, 529 preintubation, noninvasive ventilation, 529–530 preload, 146 pressure amplitude of oscillation, 549 pressure assist, 266 pressure assist/control (PAC), 156 pressure augmentation, 132

pressure control-continuous mandatory ventilation, 332–334, 335b pressure control-continuous spontaneous ventilation (PC-CSV), 315, 339–341 pressure control-intermittent mandatory ventilation (PC-IMV), 315, 337–339, 368 pressure control ventilation (PCV), 301, 315, 373 pressure cycling, mechanical ventilation and, 114, 315 pressure-regulated volume control (PRVC), 108, 130, 313, 342, 373 pressure support (PS), 156 pressure-support ventilation (PSV), 115, 126–127, 315, 339–341, 368, 373 pressure-support weaning, 656b pressure-synchronized intermittent mandatory ventilation (P-SIMV), 156 pressure–time scalar, 137 pressure trigger, 371 mechanical ventilation and, 112 primary breath, 327 prolonged mechanical ventilation (PMV), 661 prone positioning, 376 high-frequency oscillatory ventilation and, 550 proportional assist ventilation (PAV), 129–130, 313, 345–347, 370 PRVC. See pressure-regulated volume control PS. See pressure support P-SIMV. See pressure-synchronized intermittent mandatory ventilation pulmonary edema, 6, 29 pulmonary embolus, respiratory failure and, 86 pulmonary function testing, patient assessment and, 432–444 airway occlusion pressure, 434 bedside tests of spontaneous breathing, 432 common arrhythmias, 437–441 electrocardiogram, 436–437 FVC and FEV1, 435–436 heart failure, 441–444 heart rate and rhythm, 437 myocardial infarction, 441 peak flow, 435

rapid shallow breathing index, 432 respiratory mechanics, 432 tidal volume, minute ventilation, and respiratory rate, 432 vital capacity, 434 pulmonary history, components of, 408b–409b pulmonary system, mechanical ventilation and, 142–146 pulmonary vascular resistance (PVR), 146 pulse oximetry, 450, 476–480 pump failure. See hypercapnic respiratory failure

R Ramsey Sedation Scale, 69b rapid-sequence intubation (RSI), 322 rapid shallow breathing index (RSBI), 643, 652 RBC. See red blood cell recruitment maneuvers, 376, 474 red blood cell (RBC), 427 renal failure, 12 renal system, mechanical ventilation and, 147 complications, 150 ResMed Astral 100/150, 269–272, 272t–273t ResMed Lumis Tx, 267–269, 270t respiratory acidosis, 32, 61, 292 ventilatory support adjustment and, 393 respiratory alkalosis, 61 respiratory care, defined, 2. See also critical respiratory care respiratory distress syndrome (neonatal), 605–607 indications, 606 procedure, 606–607 surfactant replacement, 606 treatment, 606 respiratory drive, 284–285, 639

respiratory failure, 2, 27–92, 282 assessment for, 33–73 acid-base balance. See acid-base balance cardiac and circulatory status, 66–68, 67b cognitive and neurologic status, 68–71 dead space, alveolar ventilation and, 55–58 nutritional status, 71–73 oxygenation. See oxygenation Paco2, alveolar ventilation and, 58 prediction of ICU outcomes, 73 ventilation, 54–55 clinical manifestations of, 32–33, 291–293 defined, 28 description of, 28–32 management principles for patients, 74–90 acute asthma exacerbation, 74–75, 75b–76b acute exacerbation of COPD, 76–79 acute myocardial infarction, 83 acute respiratory distress syndrome, 80–81 deep vein thrombosis, 86 head trauma, 85–86 heart failure, 81–83 infection, neurologic diseases caused by, 88–89 neurologic and neuromuscular disease, 86–88 pneumonia, 79–80 postoperative patients, 89–90 pulmonary embolus, 86 sepsis, 84 shock, 83–84 trauma, 85 ventilatory support, neurologic diseases and, 89 overview of, 28 physiologic causes of, 29t

types of, 28–32, 31b respiratory mechanics maneuver, 162 respiratory rate, 159, 282 respiratory system compliance, 461 respiratory therapists, 2 retinopathy of prematurity, pediatric critical care, 609 retractions, 604 reverse triggering, 372 The Richmond Agitation-Sedation Scale, 70b rise time, 373 RSBI. See rapid shallow breathing index RSI. See rapid-sequence intubation

S SAPS. See Simplified Acute Physiologic Score secondary breaths, 327 sensitivity, 159 sepsis, 6 respiratory failure and, 84 septic shock, 51, 52b Sequential Organ Failure Assessment (SOFA), 71 serum bicarbonate, 487 servo targeting, 315 set-point targeting, 315 severe oxygenation problems, 282, 300–303 shock, 6, 31 categories of, 52b respiratory failure and, 83–84 short cycling, 373 shortness of breath, 405–406 shunt, 43 anatomic shunt, 43

physiologic shunt, 43 SICU. See surgical intensive care units sigh breaths, mechanical ventilation and, 141–142 Simplified Acute Physiologic Score (SAPS), 70 SIMV. See Synchronized intermittent mandatory ventilation SLED. See sustained low-efficiency dialysis SLEDD. See slow, extended daily dialysis sleep, mechanical ventilation and, 148 sleep apnea, noninvasive ventilation, 531 slow, extended daily dialysis (SLEDD), 567 Smiths Medical Pneupac babyPAC 100, 276–278 social history, 403 SOFA. See Sequential Organ Failure Assessment splenomegaly, 413 spontaneous breathing trials (SBTs), 638 spontaneous breaths, 315 mechanical ventilation and, 99 spontaneous ventilation, 159 static autoPEEP, 383 step-down units, 6 stridor, 650 ST segment elevation MI (STEMI), 68 stuporous patients, 417 surfactant, 602 surgical intensive care units (SICU), 4 sustained low-efficiency dialysis (SLED), 567 Swan-Ganz catheter, 425 synchronized intermittent mandatory ventilation (SIMV), 115, 157, 306, 316

T tachycardia, 38 tachypnea, 38, 410, 604

targeting scheme, 315 temperature regulation, in ICU, 563–566 evaporation techniques, 564 immersion techniques, 564–565 management of environmental hyperthermia, 564 management of environmental hypothermia, 565 therapeutic hypothermia, 565–566 terminal flow, 374 tetanus, 69 thermodilution, 574–575 thoracentesis, 6, 562–563, 580 tidal volume, 97, 157, 282, 352t time cycling, mechanical ventilation and, 114, 315 time trigger, mechanical ventilation and, 112–113 time-triggered breaths, 157, 330. See also control breath titrate, 376 total artificial heart (TAH), 573 total cycle time, 98 total face mask, 534t total parenteral nutrition (TPN), 569 tracheostomy, 6, 323–325, 455 high-frequency oscillatory ventilation and, 551 tubes, 455, 508 transducers holding and movement of, 579 types of, 578–579 transient tachypnea, newborn, 607–608 transmural wall pressures, 104 transudates, 21 trauma centers, 6 noninvasive ventilation and, 531–532 respiratory failure and, 85

trigger asynchrony, 371 trigger delay, 372 trigger sensitivity, 371 trigger work, 371 tympanic percussion, 415

U ultrasound. See point-of-care ultrasound upper airway obstruction, 37 upper inflection point (UIP), 381 U.S. Food and Drug Administration (FDA), 132

V VAC. See volume assist/control VALI. See ventilator-associated lung injury VAP. See ventilator-associated pneumonia vascular ultrasound, 586–587 deep vein thrombosis, detection of, 587 vascular access, 586–587 vasopressors, 83 venoarterial (VA), 570 venoarterial (VA)-ECMO, 627 venovenous (VV), 570 venovenous (VV)-ECMO, 627 ventilation, 282–291. See also mechanical ventilation assessment of, 290–291 defined, 282 lung function, 286 modes of. See under ventilator initiation respiratory drive, 284–285 factors affecting, 285b

terms used in, 283b–284b ventilatory capacity, 284 ventilatory muscles, 287 ventilatory requirements, 288–289 workload, 286 ventilator-associated lung injury (VALI), 124, 450 ventilator-associated pneumonia (VAP), 79, 146, 450 ventilator asynchrony, 81 ventilator discontinuance, 637–665 cuff-leak test for laryngeal edema, 651b description, 638–639 extubation, 658–660 criteria, 649b failure, 659–661 management of postextubation upper airway obstruction, 659 monitoring following extubation, 658–659 factors associated with readiness for, 646b factors contributing, 640b factors that contribute to ventilator dependence, 639 ventilatory capacity versus ventilatory requirements, 639 introduction, 638 long-term ventilator dependence, 661–662 methods, 653–657 IMV/SIMV, 655 newer methods, 656–657 pressure-support ventilation, 655 spontaneous breathing trials, 655–656 monitoring, 658 optimizing the patient’s condition prior to, 647b patient evaluation, 639–657 ABCDEF bundle, 648 assessment of cardiovascular and hemodynamic status, 645 assessment of medical condition, 645–648

assessment of oxygenation, 642 assessment of the airway, 648–651 assessment of ventilation and acid-base balance, 642–644 integrated indexes, 653 maximum inspiratory pressure, 651 minute ventilation, 652 rapid shallow breathing index, 651 reversal or improvement of disease or condition, 642 vital capacity, 652–653 weaning indices, 651–653 selection and approach, 657–658 terminal weaning, 662 ventilator-induced kidney injury (VIKI), 422 ventilator-induced lung injury (VILI), 97, 474 ventilator initiation, 108–109, 311–364 choosing of appropriate ventilator, 326 choosing the mode of ventilation, 326–349 adaptive pressure control, 342 adaptive support ventilation, 343–344 airway pressure-release ventilation, 344–345 automode, 347 continuous positive airway pressure, 341 continuous spontaneous ventilation, 339 full ventilatory support, 329 high-frequency ventilation, 348–349 mandatory minute ventilation, 343 neurally adjusted ventilatory assist, 347–348 nomenclature, 327 partial ventilatory support, 300 pressure control-continuous mandatory ventilation, 332–334, 335b pressure control-continuous spontaneous ventilation, 339–341 pressure control-intermittent mandatory ventilation, 337–339 pressure-regulated volume control, 342

pressure-support ventilation, 339–341 proportional assist ventilation, 345–347 targeting schemes, 328t–329t volume control-continuous mandatory ventilation, 330–332, 333b volume-controlled intermittent mandatory ventilation, 334–337, 338b volume support, 342–343 establishment of the airway, 321–325 endotracheal intubation, 321–323 tracheostomy, 323–325 goals of mechanical ventilation, 313 introduction of, 312–313 management of specific disease states and conditions, 360–362 acute exacerbation of COPD, 361 acute respiratory distress syndrome, 361–362 asthma, 361 neuromuscular disease, 362 methods of ventilation, 313–321, 319b–321b invasive ventilation, 321 negative-pressure ventilation, 313–314 noninvasive ventilation, 316, 321 positive-pressure ventilation, 314 terminology, 314–316, 317t–318t settings, 349–360 alarms and limits, 354t, 360 breath trigger, 353 CPAP, 360 expiratory time, 353, 357–358 humidification, 360 I:E ratio, 353, 358 inspiratory pause, 357 inspiratory pressure, 351 intermittent sigh breaths, 351 mode, 350

normal tidal volume, rate, and minute ventilation, 350–351, 352t oxygen percentage, 358–360 patient assessment, 360 PEEP, 360 pressure control, 355 pressure rise time or slope, 355–357 for tidal volume and rate, 350–351, 352t volume control, 353–355 ventilator modes, 117–136 airway pressure-release ventilation, 127 automatic tube compensation, 127–128 continuous mandatory ventilation, 117–122 continuous positive airway pressure, 125–126 noninvasive ventilation, 125–126 obstructive sleep apnea and, 125 recruitment maneuvers, 125 dual modes and adaptive control, 130–132 adaptive support ventilation, 131–132 automode, 131 pressure augmentation, 132 pressure-regulated volume control, 130 volume-assured pressure support, 132 volume support, 130 high-frequency ventilation, 132–134 intermittent mandatory ventilation, 122–124 modes, 119t neurally adjusted ventilatory assist, 134–136 positive end-expiratory pressure, 124–125 lung recruitment maneuvers, 124–125 pressure-support ventilation, 126–127 proportional assist ventilation, 129–130 ventilator system monitoring, 510–522 airway problems, 516

asynchrony and fighting the ventilator, 513–516 bronchospasm, 518–519 infection, 521–522 pneumothorax, 519–521 recognition and treatment of common complications, 512–513 secretions, 516–518 ventilator weaning, 638 ventilatory capacity, 282, 284, 639 decreased, causes of, 641b increased, causes of, 642b ventilatory failure, 32b, 282. See also hypercapnic respiratory failure ventilatory muscle fatigue, 286 ventilatory requirements, 282, 639 ventilatory reserve, 284, 639 ventilatory support, adjustment of, 367–399. See also mechanical ventilatory support acid-base balance, 392–394 metabolic acidosis, 393–394 metabolic alkalosis, 394 respiratory acidosis, 393 respiratory alkalosis, 393 cardiac and cardiovascular support, 394–396 initiation of, 368–369 oxygenation, 375–386 application of PEEP, 383–384 AutoPEEP, 384 bronchial hygiene, 385–386 compliance-titrated PEEP, 380–381 Fio2, 376–377 methods, 379–383 minimum PEEP, 379 optimal PEEP for oxygen delivery, 379–380 PEEP and AutoPEEP, 382–383 PEEP/CPAP, 377–379

PEEP–Fio2 tables, 380 pressure–volume curves, 381–382 prone positioning, 385 recruitment maneuvers, 384–385 patient–ventilator interaction, 370–375 autotriggering, 372 cycle asynchrony, 373–374 double triggering, 372 flow asynchrony, 372–373 missed triggering, 371–372 mode asynchrony, 374–375 reverse triggering, 372 trigger asynchrony, 371 trigger delay, 372 trigger work, 371 sedation and neuromuscular blockade, use of, 396 ventilation, 386–392 alveolar ventilation, 386–388 assist/control ventilation, 390–391 control mode volume ventilation, 390 IMV/SIMV, 391 intentional hyperventilation, 388 Paco2 and, 387–389, 391–392 permissive hypercapnia, 388 PSV, 391–392 tidal volume, rate, and minute ventilation, 386 ventilatory workload, 284 ventricular failure, 573 VILI. See ventilator-induced lung injury visceral pleural, 583 vital capacity, 652–653 vital signs, 409–411 volume assist, 216

volume assist/control (VAC), 156 volume-assured pressure support (VAPS), 132 volume control-continuous mandatory ventilation (VC-CMV), 315–316, 330–332, 333b volume-controlled intermittent mandatory ventilation (VC-IMV), 330, 334–337, 338b volume-control ventilation, 103, 307, 315 volume cycling, mechanical ventilation and, 114–115, 315 volume of oxygen uptake, 98 volume support, 108, 319b, 342–343 ventilator modes and, 130 volutrauma, 132 Vyaire AVEA, 198–205 Vyaire 3100B High-Frequency Oscillator, 228–230 Vyaire Infant Flow SiPAP, 278–279 Vyaire LTV 1200, 248–251, 251t–252t Vyaire ReVel, 244–248 Vyaire VELA, 205–211

W wavelength, 578 WBC. See white blood cell count weaning, 638 weaning indices or parameters, 652 white blood cell count (WBC), 427, 428b WOB. See work of breathing work of breathing (WOB), 112, 286, 346b, 462–464, 528

Z ZOLL Eagle II, 259–262, 262t–263t

The table shows six columns: VA, Q, VA over Q, PO2, PCO2, and PN2. The entries in the first two columns are in inverse minutes and in the last three columns are in millimeters of mercury. Row entries correspond to the values from top to bottom of the lungs. They are as follows. Row 1: 0.24, 0.07, 3.3, 132, 28, 553. Row 2: 0.52, 0.50, 1.0, 108, 39, 556. Row 3: 0.67, 0.83, 0.80, 98, 41, 574. Row 4: 0.82, 1.29, 0.63, 89, 42, 582. Total. VA: 4.2, Q: 5.0. VA over Q: 0.84. Back to Figure In the upright position, the apices receive more ventilation and lung bases receive more perfusion. In the supine position, the anterior side receives more ventilation and the posterior side receives more perfusion. Back to Figure The relationships are as follows: V over Q equals 0, a shunt unit; low V over Q; V over Q equals 1, an ideal normal; V over Q greater than 1; V over Q equals V over 0 equals infinity, a dead space unit; and silent unit. Back to Figure In both illustrations, P subscript v bar O subscript 2 is the pressure in the channels near the entry to alveolus, P subscript uppercase A O subscript 2 is the alveolar pressure, P subscript c prime O subscript 2 is the pressure at the base of alveolus, and P subscript lowercase a O subscript 2 is the pressure in the exit channel. A. Normal ventilation. Uniform ventilation with room air. F subscript I O subscript 2 equals 0.21, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 150 millimeters of mercury. Venous admixture is 2 to 5 percent of cardiac output. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 equals 104, P subscript c prime O subscript 2 equals 104, and P subscript lowercase a O subscript 2 equals 80 to 100. Uniform ventilation with 100 percent O 2. F subscript I O

subscript 2 equals 1.0, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 713 millimeters of mercury. Venous admixture is 2 to 5 percent of cardiac output. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 equals 663, P subscript c prime O subscript 2 equals 663, and P subscript lowercase a O subscript 2 equals 500 to 550. B. Under ventilation to perfusion. There is a block to one of the alveolus, causing it to shrink. Low V over Q in room air. F subscript I O subscript 2 equals 0.21, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 150 millimeters of mercury. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 of the larger alveolus equals 104, P subscript uppercase A O subscript 2 of the smaller alveolus equals 50, P subscript c prime O subscript 2 under larger alveolus equals 104, P subscript c prime O subscript 2 under smaller alveolus equals 50, and P subscript lowercase a O subscript 2 equals 55. Low V over Q with oxygen therapy. F subscript I O subscript 2 equals 0.40, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 285 millimeters of mercury. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 of the larger alveolus equals 235, P subscript uppercase A O subscript 2 of the smaller alveolus equals 115, P subscript c prime O subscript 2 under larger alveolus equals 235, P subscript c prime O subscript 2 under smaller alveolus equals 115, and P subscript lowercase a O subscript 2 equals 95. Back to Figure In both illustrations, P subscript v bar O subscript 2 is the pressure in the channels near the entry to alveolus, P subscript uppercase A O subscript 2 is the alveolar pressure, P subscript c prime O subscript 2 is the pressure at the base of alveolus, and P subscript lowercase a O subscript 2 is the pressure in the exit channel. C. Alveolar filling. Physiologic shunt, room air. One of the alveoli is filled with fluid and labeled, consolidation, pneumonia, or pulmonary edema, V over Q equals 0. F subscript I O

subscript 2 equals 0.21, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 150 millimeters of mercury. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 of the unfilled alveolus equals 104, P subscript c prime O subscript 2 under unfilled alveolus equals 104, P subscript c prime O subscript 2 under filled alveolus equals 40, and P subscript lowercase a O subscript 2 equals 50. Physiologic shunt, 100 percent O2. One of the alveoli is filled with fluid and labeled, consolidation, pneumonia, or pulmonary edema, V over Q equals 0. F subscript I O subscript 2 equals 1.0, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 713 millimeters of mercury. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 of the unfilled alveolus equals 663, P subscript c prime O subscript 2 under unfilled alveolus equals 663, P subscript c prime O subscript 2 under filled alveolus equals 40, and P subscript lowercase a O subscript 2 equals 60. D. Atelectasis. Physiologic shunt, room air. One of the alveoli is shrunken and labeled, atelectasis, V over Q equals 0. F subscript I O subscript 2 equals 0.21, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 150 millimeters of mercury. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 of the normal alveolus equals 106, P subscript c prime O subscript 2 under normal alveolus equals 106, P subscript c prime O subscript 2 under shrunken alveolus equals 40, and P subscript lowercase a O subscript 2 equals 50. Physiologic shunt, 100 percent O2. One of the alveoli is shrunken and labeled, atelectasis, V over Q equals 0. F subscript I O subscript 2 equals 1.0, P subscript B equals 760 millimeters of mercury, and P subscript I O subscript 2 equals 713 millimeters of mercury. P subscript v bar O subscript 2 equals 40, P subscript uppercase A O subscript 2 of the normal alveolus equals 663, P subscript c prime O subscript 2 under shrunken alveolus equals 40, and P subscript lowercase a O subscript 2 equals 60. Back to Figure

Horizontal axis shows PO2 at pH equals 7.40, ranging from 0 to 100 in increments of 10. Vertical axis shows percentage of SO2, ranging from 0 to 100 in increments of 10. All data are approximate. The curve is plotted through (0, 0), (28, 50), (42, 75), (62, 90), and (100, 97). Back to Figure Horizontal axis shows PO2 at pH equals 7.40, ranging from 0 to 100 in increments of 10. Vertical axis shows percentage of SO2, ranging from 0 to 100 in increments of 10. All data are approximate. The curve is plotted through (0, 0), (28, 50), (42, 75), (62, 90), and (100, 97). The curve shifts left when there is decrease in PCO2, decrease in temperature, increase in pH, and decrease in 2 to 3 DPG. The curve shifts right when there is increase in PCO2, increase in temperature, decrease in pH, and increase in 2 to 3 DPG. Back to Figure Horizontal axis shows time in seconds and vertical axis shows flow in liters per minute. Each cycle is for 6 seconds. One half of the sinusoidal curve occurs in the first 2 seconds, followed by a sharp fall to a negative value and a gradual rise to 0 value in the next 4 seconds. The total cycle is T subscript tot, the first 2 seconds is T subscript I, and the next four seconds is T subscript E. Back to Figure Alveolar pressure is measured in centimeters of water. During inspiration, pressure falls from 0 to negative 1 and rises to 0, and during expiration, the pressure rises from 0 to positive 1 and falls to 0. Intrapleural pressure is measured in centimeters of water. During inspiration, pressure falls from negative 5 to negative 8, and during expiration, the pressure rises to negative 5. Volume change is in liters. During inspiration, the volume rises from 0 to 0.5 and during expiration, the volume falls to 0. Tidal

volume is 0.5 liters. Air flow is measured in liters per second. During inspiration, the flow falls from 0 to negative 0.5 and rises to 0, and during expiration, the pressure rises from 0 to positive 0.5 and falls to 0. Back to Figure Inspiratory circuit is through a tube through a ventilator, humidifier, and temperature ports. Expiratory circuit is through a tube through temperature ports, water trap, and ventilator. A monitoring line is attached to the ventilator. Back to Figure The region of constant pressure is PEEP. The pressure rises sharply to PIP, falls sharply by a small value, remains constant for a short period at P subscript plateau, falls further sharply, rises by a small amount, and remains constant at AutoPEEP. The region between PIP and P subscript plateau is resistance flow, between P subscript plateau and autoPEEP is compliance tidal volume, and under autoPEEP is total-PEEP. Back to Figure The fluctuations in flow increase to a crescendo, resulting in decrease in pressure support. The fluctuations then decrease to a decrescendo, resulting in increase in pressure support. At constant flow during central apnea, the pressure is constant and is the backup rate. EPAP is 7 centimeters of water, IPAP subscript min is 9 centimeters of water, and IPAP subscript max is 17 centimeters of water. Back to Figure The first graph displays Paw-V. Horizontal axis shows centimeters of water, ranging from negative 10 to 50 in increments of 10. Vertical axis ranges from 0 to 0.700 in increments of 0.100. All data are approximate. A vertical line is y equals 0. A loop is plotted through (5, 0), (10, 0.5), and

(30, 0.55). The second graph displays V-flow. Horizontal axis shows liters, 0 to 0.700 in increments of 0.100. Vertical axis ranges from negative 50 to 50 in increments of 12.5. All data are approximate. A horizontal line is x equals 0. A loop is plotted through (0, 0), (0.1, 32.5), (0.5, 32.5), and (0.5, negative 32.5). The third graph displays flow in liters per minute. Horizontal axis shows time in seconds, ranging from 0 to 16 in increments of 2. Vertical axis ranges from negative 50 to 50 in increments of 12.5. The graph shows upright and inverted triangles for each cycle. The fourth graph displays volume in liters. Horizontal axis shows time in seconds, ranging from 0 to 16 in increments of 2. Vertical axis ranges from negative 0 to 0.7 in increments of 0.1. The graph shows sawtooth peaks across 2.5 seconds at a height of 0.5. The alphanumeric data by the side are as follows. Pmean: 10, PEEP: 5, Flo2 volume in percentage: 35, MV in liters per minute: 4.5, MV subscript spn in liters per minute: 0, F subscript total in bpm: 10, and V subscript TI in liters: 0.450. Alphanumeric data at the bottom are as follows. O2: 35, V subscript T: 0.450, T subscript insp: 1.7, f: 10, PEEP: 5, and P subscript supp: 0. Back to Figure In all the graphs, horizontal axis shows time in seconds, ranging from 0 to 14 in increments of 1. All data are approximate. In the first graph, vertical axis shows flow in liters per minute, ranging from negative 50 to 40 in increments of 10. Each cycle lasts for approximately 3 seconds, and in each cycle, the flow increases to 10 and falls to 0 within a fraction of a second, rises to 30, falls to 0 and then to negative 35, and rises to 0. In the second graph, vertical axis shows pressure in centimeters of water, ranging from 0 to 24 in increments of 4. Each cycle lasts for approximately 4 seconds, and in each cycle, the pressure curves upward to 12, falls sharply 5, and then very gradually to 4. In the third graph, vertical axis shows volume in milliliters, ranging from 0 to 600 in increments of 100. Each cycle lasts for approximately 2.5 seconds, and in each cycle, the sawtooth curves peak to 400.

Back to Figure There are seven columns: order control variable, family breath sequence, genus primary breath targeting scheme, species secondary breath targeting scheme, example mode names, abbreviation, and variety operational difference. Row entries are as follows. Row 1: Volume, CMV, set-point, NA, volume control assist/control, VC-CMV subscript s, no data. Row 2: No data, no data, Dual, NA, Continuous mandatory ventilation with pressure limited, VC-CMV subscript D, no data. Row 3: No data, IMV, set-point, set-point, volume control synchronized intermittent mandatory ventilation, VC-IMV subscript S, S, no data. Row 4: No data, no data, dual, set-point, synchronized intermittent mandatory ventilation, volume control servo-I ventilator, VC-IMV subscript D, S, no data. Row 5: No data, no data, dual adaptive, set point, mandator minute volume with pressure limited ventilation, VC-IM subscript DA, S, no data. Row 6: No data, no data, dual, adaptive, automode volume control to volume support, VC-IMV subscript D, A, no data. Row 7: No data, no data, adaptive, set-point, mandatory minute volume ventilation, VC-IMV subscript A, S, no data. Row 8: Pressure, CMV, set-point, NA, pressure control assist control, PC-CMV subscript S, no data. Row 9: No data, no data, adaptive, NA, pressure-regulated volume control, PC-CMV subscript A, no data. Row 10: No data, IMV, set-pint, set-point, airway pressure release ventilation, PC-IMV subscript S, S, no data. Row 11: No data, no data, set-point, NA, high-frequency oscillatory ventilation, PCIMV subscript S, S, frequency above 150 cycles per minute negative airway pressure possible. Row 12: No data, no data, adaptive, set-point, adaptive pressure ventilation synchronized intermittent mandatory ventilation, PC-IMV subscript A,S, no data. Row 13: No data, no data, adaptive, adaptive, automode pressure regulated volume control to volume support, PC-IMV subscript A, A, no data. Row 14: No data, no data, optimal, optimal, adaptive support ventilation, PC-IMV subscript O, O, no data. Row 15: No data, no data, optimal or intelligent, optimal or intelligent, intellivent-ASC, PC-IMV subscript OI OI, no data. Row 16: No

data, SCV, set point, NA, pressure support, PC-CSV subscript S, setpoint constant. Row 17: No data, no data, biovariable, NA, variable pressure support, PC-CSV subscript B, set-point automatically adjusted at random. Row 18: No data, no data, servo, NA, proportional assist ventilation, PC-CSV subscript R, pressure proportional to diaphragmatic electromyogram. Row 19: No data, no data, servo, NA, neutrally adjusted ventilatory support, PC-CSV subscript R, pressure proportional to diaphragmatic electromyogram. Row 20: No data, no data, adaptive, NA, volume support, PC-CSV subscript A, pressure adjusted to achieve tidal volume target. Row 21: No data, no data, adaptive, NA, mandatory rate ventilation, PC-CSV subscript A, pressure adjusted to achieve rate target. Row 22: No data, no data, intelligent, NA, smart care/PS, PC-CSV subscript t, no data. The variety level of description may be needed to differentiate between modes that have same order, family, genus, and species. CMV equals continuous mandatory ventilation. NA equals not applicable. VC equals volume control. Subscripts. S equals set-point. D equals dual. A equals adaptive. O equals optimal. I equals intelligent. R equals servo. B equals biovariable. IMV equals intermittent mandatory ventilation. PC equals pressure control. CSV equals continuous spontaneous ventilation. Back to Figure Each set consists of three graphs. In all the graphs, horizontal axis shows time in seconds, ranging from 0 to 14 in increments of 1. In the first graph of each set, vertical axis shows flow in liters per minute, ranging from negative 40 to 60 in increments of 10. In the second graph, vertical axis shows pressure in centimeters of water, ranging from 0 to 16 in increments of 4. In the third graph, vertical axis shows volume in cc, ranging from 0 to 800 in increments of 100. All data are approximate. A. In the first graph, each cycle lasts approximately 6 seconds, during which the flow increases sharply to 60, remains constant for half a second, falls sharply to negative 40, and rises gradually to 0. In the second graph,

each cycle lasts approximately 3 seconds, during which the pressure increases sharply to 15.5 and curves downward to 0. In the third graph, each cycle lasts approximately 5 seconds, during which the volume rises sharply to 700, falls gradually to 0, and then very gradually to negative 50. B. In the first graph, each cycle lasts approximately 5 seconds, during which the flow increases gradually from negative 15 to 0, then sharply to 60, remains constant for half a second, falls sharply to negative 30, and rises gradually to 0. In the second graph, each cycle lasts approximately 3 seconds, during which the pressure increases sharply to 16 and curves downward to 0. In the third graph, each cycle lasts approximately 3.8 seconds, during which the volume rises sharply to 700 and falls gradually to 0. Back to Figure While lying supine, A and C, the anterior half is well ventilated and the posterior half is poorly ventilated. When lying prone, B and D, the posterior half is well ventilated and the anterior half is poorly ventilated. The organs are in the posterior region, while the heart is in the anterior region. No gas exchange occurs between the organs and the heart. Back to Figure Each set consists of three graphs. In all the graphs, horizontal axis shows time in seconds, ranging from 0 to 14 in increments of 1. In the first graph of each set, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. In the second graph, vertical axis shows pressure in centimeters of water, ranging from 0 to 20 in increments of 2. In the third graph, vertical axis shows volume in milliliters, ranging from 0 to 600 in increments of 200. All data are approximate. A. In the first graph, each cycle lasts approximately 6 seconds, during which the flow increases sharply to 55, falls to 0 and then sharply to negative 55, rises to 0, followed by two oscillating waves. In the second graph, each cycle lasts approximately 8.5 seconds, during which

the pressure remains constant at 5 for a second, rises to 16, falls to 5 and remains constant at 5 with mild fluctuations. In the third graph, each cycle lasts approximately 6 seconds, during which the volume rises sharply to 500, falls gradually to 0, followed by to smaller peaks at 50, each a second apart. B. The graphs are similar, except that the amplitude in the second cycle of second and third graphs are lower. Back to Figure The pressure rises to a maximum value, P subscript high, falls gradually with fluctuations corresponding to ATC and T subscript high, falls sharply to P subscript low, and rises sharply to a maximum value. The flow rises and falls sharply, and oscillates twice, before falling sharply and rising, corresponding to T subscript low. Back to Figure In both graphs, horizontal axis shows time in seconds, ranging from 0 to 8 in increments of 1, and vertical axis shows pressure in centimeters of water, ranging from negative 5 to 10 in increments of 5. All data are approximate. For PSV 5 centimeters of water, PEEP is constant at pressure equals 1.5, Pcirc is plotted through (0, 1.5), (2, 1.5), (2.5, 0), (3, 6), (6, 5.5), and (7, 1.5), and Ptrach is plotted through (0, 1.5), (2, 1.5), (3, negative 6), (4, 4.5), and (8, 0). For ATC, PEEP is constant at pressure equals 1.5, Pcirc is plotted through (0, 1.5), (2, 1.5), (2.2, 0), (3, 9), and (7, 1), and Ptrach is plotted through (0, 1.5), (2, 1.5), (2.2, negative 1.5), and then fluctuates at (3, 0). Back to Figure In the first graph, triangular waves of low amplitude and high frequency and square waves of high amplitude are plotted. The triangular waves and the central portion of the square waves are within the green region. In second graph, the HFOV and CMV curves rise and then fall, forming

loops. CMV curve is shifted right. The central portion of the HFOV curve and a part of CMV curve are in the green region. Back to Figure Convection: Proximal alveolar units are exposed to central airway oscillatory pressures. Direct ventilation of close alveoli. Turbulence in bronchioles. Oscillatory pressure applied at airway opening is damped by flow-dependent resistance and inertance of tracheal tube and central airways. Turbulent flow and radial mixing. Convection and diffusion: Atelectatic compartments exposed to increased oscillatory pressures. Pendelluft. Asymmetric velocity profiles. Inspiratory velocity profile. Expiratory velocity profile. High peripheral resistance increases pressure transmission to more proximal airways and nearby alveoli. Alveoli distal to a zone of increased peripheral resistance, see low pressures due to decreased flow. Diffusion: Laminar flow and radial mixing. Expanded and aerated alveoli protected from high oscillatory pressures. Collateral ventilation. Cardiogenic mixing. Back to Figure Pressure graph shows a yellow trace showing square wave, and a gray wave showing irregular peaks with fluctuation. P subscript peak is 24. Flow graph shows a repeated cycle of sharp rise, gradual dip, sharp dip, and gradual rise. RR in b per minute is 24. Volume graph shows triangular waves. VTe is 358 milliliters. Edi graph shows irregular peaks with fluctuations. Edi peak is 43 microvolts. O2 concentration is 30 percent, PEEP is 5 centimeters of water, and NAVA level is 0, 4 centimeters of water per microvolt. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 4 in increments of 1. In the first graph of each set, vertical axis shows flow

in liters per minute, listing negative 100, 0, and 100. In the second graph, vertical axis shows pressure in centimeters of water, listing 0 and 50. In the third graph, vertical axis shows volume in liters, listing 0 and 10. A. Flow curve is plotted through (0, 100), (1.5, 0), (1.5, negative 100), and (3, 0). Pressure curve is plotted through (0, 35), (1.5, 35), and (1.5, 0). Volume curve is a sawtooth curve, peaking at 0.7. B. Flow curve is plotted through (0, 20), (1.5, 20), (1.5, negative 100), and (3, 0). Pressure curve is plotted through (0, 10), (1.5, 40), and (1.5, 0). Volume curve is a triangular curve, peaking at 0.7. C. Flow curve is plotted through (0, 0), (1.5, 50), (1.5, negative 100), and (3, 0). Pressure curve is plotted through (0, 0), (1.5, 50), and (1.5, 0). Volume curve is a triangular curve, peaking at 0.7. D. Flow curve is plotted through (0, 50), (1.5, 0), (1.5, negative 100), and (3, 0). Pressure curve is plotted through (0, 20), (1.5, 35), and (1.5, 0). Volume curve is a sawtooth curve, peaking at 0.7. E. Flow curve is plotted through (0, 0), (0.7, 20), (1.5, 0), (1.5, negative 100), and (3, 0). Pressure curve is plotted through (0, 0), (1.4, 35), and (1.5, 0). Volume curve is a triangular curve, peaking at 0.7. Back to Figure The distance between PIP and P subscript plat is Raw. When there is increased airway resistance, Raw increases. When there is decreased compliance, the size of Raw decreases. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 20 in increments of 1. The sigh cycle in all graphs lasts approximately 3.5 seconds. In the first graph, vertical axis shows flow in liters per minute, ranging from negative 0.8 to 0.8 in increments of 0.4. Each cycle lasts about 3 seconds, during which the curve rises sharply to 0.8, falls sharply to negative 0.4, and rises gradually to 0. In the sigh cycle, the curve rises sharply to 1 and then falls to 0 with fluctuations. In the second graph, vertical axis shows volume in liters, ranging from 0 to 0.6 in increments of

0.2. Each cycle lasts about 2.5 seconds and shows triangular wave, peaking at 0.3. During the sigh cycle, the curve rises from 0 to 0.6 with mild fluctuations. In the third graph, vertical axis shows Paw in centimeters of water, ranging from 0 to 40 in increments of 10. Each cycle lasts approximately 3 seconds, showing a small square wave and a long region of constant. In the sigh cycle, the square wave is wider. Back to Figure Horizontal axis shows lung volume, listing RV, FRC, and TLC. Vertical axis shows pulmonary vascular resistance. The curve for total falls from RV to FRC and then rises toward TLC. The curve for alveolar rises from RV to TLC. The curve for extra-alveolar falls from RV to TLC. Back to Figure Tissue blood flow is in milliliters per gram per minute, ranging from 0 to 1 in increments of 0.2. Approximate data from the graph, presented in the format, condition: control, error value of control, induced lung injury, error value of induced lung injury, are as follows. APRV with spontaneous breathing: 0.65, 0.8, 0.75, 0.95. APRV without spontaneous breathing equal V subscript E: 0.45, 0.55, 0.42, 0.45. APRV without spontaneous breathing equal P subscript AW: 0.58, 0.65, 0.62, 0.8. The APRV with spontaneous breathing and APRV without spontaneous breathing equal V subscript E values of induced lung injury is less than 0.05. Back to Figure The buttons are select button and exit button. The panels and displays are airway pressure manometer, display window, front panel, control panel, alarm panel, and pulse oximeter panel. Back to Figure There are four classes: 1 through 4. With each progressive class, more of

the tongue protrudes outward and the gap between the base and roof of the mouth in the back reduces and closes. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 2 to 14 in increments of 1. In the first graph, vertical axis shows flow in liters per minute, ranging from negative 60 to 60 in increments of 20. Each cycle lasts for about 4 seconds and consists of a square wave followed by an inverted triangular wave. In the second graph, vertical axis shows pressure in centimeters of water, ranging from 0 to 24 in increments of 4. Each cycle lasts for about 4 seconds and consists of triangular waves between regions of flatness. Patient-triggered breath has a small bump during the initial part of the wave, while ventilator-triggered breath does not. In the third graph, vertical axis shows volume in milliliters, ranging from 0 to 600 in increments of 100. The graph shows triangular waves spanning for three seconds, reaching a peak of 600. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 2 to 14 in increments of 1. In the first graph, vertical axis shows flow in liters per minute, ranging from negative 60 to 60 in increments of 20. Each cycle lasts for about 3 seconds, during which the graph peaks at 30, falls to 0, then to negative 30, and rises to 0. In the second graph, vertical axis shows pressure in centimeters of water, ranging from 0 to 24 in increments of 4. Each cycle lasts for about 4 seconds and consists of curved sawtooth waves between regions of flatness. In the third graph, vertical axis shows volume in milliliters, ranging from 0 to 600 in increments of 100. The graph shows triangular waves spanning for three seconds, reaching a peak of 400. Back to Figure

In all graphs, horizontal axis shows time in seconds, ranging from 2 to 14 in increments of 1. In the first graph, vertical axis shows flow in liters per minute, ranging from negative 50 to 40 in increments of 10. Each cycle lasts for about 3 seconds, during which the graph peaks at 30, falls to 0, then to negative 25, and rises to 0. In the second graph, vertical axis shows pressure in centimeters of water, ranging from 0 to 24 in increments of 4. Each cycle lasts for about 4 seconds and consists of fluctuations between 4 and 8. In the third graph, vertical axis shows volume in milliliters, ranging from 0 to 600 in increments of 100. The graph shows triangular waves spanning for a second, reaching a peak of 200. Back to Figure Horizontal axis shows time and vertical axis shows pressure in centimeters of water. The curve falls sharply under the trigger threshold by a low value, rises sharply, and then falls. Between two such cycles, there are missed triggers consisting of inverted triangles under the trigger threshold. Back to Figure Horizontal axis shows time in seconds and vertical axis shows flow in liters per minute. The graph shows square waves for inspiration, which fall sharply under the base value during the initial stages of expiration. During normal respiration, the curve rises sharply to the zero value. During autoPEEP expiration, the curve rises gradually and then sharply to zero value. Back to Figure Horizontal axis shows time in seconds and vertical axis shows flow in liters per minute. The graph for rapid rise time rises sharply, falls sharply by a small flow value, remains constant for a period, and then falls

sharply. The graph for appropriate rise time rises sharply, remains constant for a period, and falls sharply. The graph for slow rise time rises gradually and falls sharply. Back to Figure Horizontal axis shows time in seconds and vertical axis shows pressure in centimeters of water. During inspiration, the pressure rises sharply and remains constant, followed by a mild dip, a sharp rise, and a sharp dip. There is no graph for expiration. The mild dip is labeled A, the region between the beginning of the cycle till the mild dip is B, and the region between beginning of the cycle and the sharp rise is C. A. Patient begins to breathe out before the ventilator’s inspiratory time has been reached causing a pressure spike at the end inspiration. B. Patient inspiratory time. C. Ventilator inspiratory time. Back to Figure In all graphs, horizontal axis shows time in seconds, listing 1 and 2. In the first set of graphs, vertical axis shows flow in liters per minute, ranging from negative 80 to 100 in increments of 20. The curve rises sharply to 80, falls to 100, then to negative 70, and gradually rises to 0. With increase in percentage, the width of the initial portion of the curve shrinks toward the right. In the second set of graphs, vertical axis shows pressure in centimeters of water, ranging from 0 to 20 in increments of 5. The curve is sawtooth peaking at 20. With increase in percentage, the width of the graph shrinks toward the right. Back to Figure In the side of the trunk, the movement is from top to bottom in a curved path. In the anterior side of the trunk, the movement is a zig-zag motion from top to bottom. Back to Figure

The photos show the insertion of radial arterial line in a patient’s arm and a closer view of the same. The graph shows that the pressure falls from systolic pressure at 128 millimeters of mercury to diastolic pressure at 82 millimeters of mercury with dicrotic notch, which rises again to systolic pressure. The period of each cycle is 0.75 seconds at the rate of 80 per minute, while the ejection time is the rises from diastolic to systolic pressure. Back to Figure The wave consists of a small bump, P, a small dip, Q, a sharp peak, R, a sharp dip, S, followed by two bumps T and U. PR interval is the region between the beginning of P and R, PR segment is between the ending of P and beginning of R, QRS interval includes Q, R, and S portions, ST interval is the region between the ending of T and S, and ST segment is between the ending of S and beginning of T. Back to Figure HR equals 65 bpm, rate is 60 to 100 beats per minute, rhythm is regular, P waves are uniform and upright in appearance, one preceding each QRS complex, PR interval is 0.12 to 0.20 seconds, and QRS is less than 0.10 seconds. Back to Figure A. The ECG shows a sharp peak between three curved and short peaks. Rate is usually 60 to 100 beats per minute but may be faster or slower, rhythm is irregular, P waves are uniform and upright in appearance, one preceding each QRS complex, PR interval is 0.12 to 0.20 seconds, and QRS is less than 0.10 seconds. B. The ECG shows a sharp peak between regions of fluctuations. Rate is atrial rate, usually greater than 400 beats per minute, ventricular rate is variable, atrial and ventricular rate is very irregular, and regular, bradycardic ventricular rhythm may

occur as a result of digitalis toxicity, there are no identifiable P waves, there is an erratic and wavy baseline, there is no PR interval, and QRS is less than 0.10 seconds. Back to Figure The ECG shows a compensatory pause of an extended regular cycle between two normal cycles. Atrial and ventricular rate depend on underlying rhythm. The rhythm is irregular because of PVC. If the PVC is interpolated or sandwiched between two normal beats, the rhythm will be regular. No P wave is associated with the PVC. There is no PR interval with the PVC because the ectopic originate in the ventricles. QRS is less than 0.12 seconds, wide and bizarre, and T wave is frequently in opposite direction of the QRS complex. Back to Figure B. The ECGs shows fluctuating dome-shaped waves. Ventricular rate equals 111 bpm. Atrial rate is not discernible and ventricular rate is 100 to 250 beats per minute. Atrial rhythm is not discernible and ventricular rhythm is essentially regular. P waves may be present or absent; if present, they have no set relationship to the QRS complexes, appearing between the QRSs at a rate different from that of the VT. There is no PR interval. QRS is usually less than 0.12 seconds and often difficult to differentiate between the QRS and the T wave. Note: Three or more PVCs occurring sequentially are referred to as a “run” of VT. C. The ECG shows fluctuating waves with an almost equal amplitude. Rate is 280 to 300 beats per minute. Rhythm is rapid and monomorphic, a form of ventricular tachycardia. P waves are generally not discernible but may alter appearance of QRS morphology. PR interval is not discernible. QRS is a monomorphic form of ventricular tachycardia with wide QRS complexes. D. The ECG shows irregular, oscillating waves of low and high frequency. Rate cannot be determined because waves or complexes are not discernible to measure. Rhythm is rapid and chaotic with no

pattern or regularity. P waves, PR interval, and QRS are not discernible. Back to Figure The ECG shows an almost straight line. Ventricular rate usually indiscernible, but may see some atrial activity. Atrial rhythm may be discernible, while ventricular rate is indiscernible. P waves are usually not discernible. PR interval is not measurable. QRS is absent. Back to Figure A. The ECG shows normal pattern with the missing U wave. Atrial and ventricular rates are within normal limits and the same. Regular atrial and ventricular rhythm. P waves are in size and configuration, one P wave for each QRS. PR interval is prolonged, greater than 0.20 seconds, but constant. QRS is less than 0.10 seconds. B. The ECG shows a regular wave with a short region of flatness, corresponding to dropped beat. Atrial rate greater than ventricular rate and both are usually within normal limits. Atrial rhythm is regular and P waves plot through, while ventricular waves are irregular. P waves are normal in size and configuration; some P waves are not followed by a QRS and there are more P waves than QRS complexes. There is a progressive increase in the PR interval with each cycle, although lengthening may be slight, until a P wave appears without a QRS, example, dropped or blocked QRS. QRS is less than 0.10 seconds but is dropped periodically. C. The ECG shows an irregular dip and a curved peak, followed by two smaller peaks. Atrial rate is greater than ventricular rate, ventricular rate determined by the origin of the escape rhythm. Atrial and ventricular rhythms are regular through atrial and ventricular rhythms are disconnected. P waves are normal in size and configuration, and are more disconnected from QRS, more P waves than QRS complexes. There is no PR interval; the atria and ventricles beat independently of each other; no relationship between the P waves and QRS complexes. QRS is narrow or wide depending on the location of the escape pacemaker and the condition of the interventricular

conduction system. Narrow QRS is junctional pacemaker, while wide QRS is ventricular pacemaker. Back to Figure A. In a normal wave, the ST segment is elevated. B. There are five ECGs depicting the evolution of an infarct on the ECG is shown with the following changes. a. Early or pre-ischemic ECG: A peak followed by a wide, curved, and flat peak. b. ST segment elevation: A peak which continues to a curved fall midway. c. Pathologic Q wave formation: A short peak which continues to a curved fall midway. d. T wave inversion: A peak followed by a tip. e. Normalization with a persistent Q wave: A short peak followed by a sharp peak. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a sharp peak, PIP and plateau. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a square peak at 50, corresponding to peak inspiratory flow and a dip to negative 30, corresponding to peak expiratory flow. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows a triangular wave with flat peak. The rise corresponds to inspired tidal volume and the fall corresponds to expired tidal volume. Back to Figure Horizontal axis shows time. Vertical axis lists 0, 25, and 30. During inspiration, the pressure rises sharply to 10, then steadily to 30, and curves downward to 25, corresponding to inspiratory pause. During

expiration, the pressure curves downward to 0. Tidal volume, V subscript T, equals 500 milliliters, inspiratory flow rate equals 60 liters per minute equals 1 liter per second. Equations under the graphs are as follows. Static total compliance, C subscript ST equals delta V over delta P equals V subscript T over P subscript plateau minus P subscript baseline equals 500 over 25 minus 0 equals 20 milliliters per centimeter of water. Dynamic compliance C subscript dynamic equals delta V over delta P equals V subscript T over PIP minus P subscript baseline equals 500 over 30 minus 0 equals 16.7 milliliters per centimeter of water. Airway resistance, R subscript aw equals PIP minus P subscript plat over inspiratory flow rate equals 30 minus 25 over 1 liter per second equals 5 centimeters water per liter per second. Back to Figure Horizontal axis shows transpulmonary pressure in centimeters of water, listing FRC and 10. Vertical axis shows volume in liters, listing 0 and 1.0. During inspiration, the loop rises from (FRC, 0) to (10, 0.8), and during expiration, the loop falls from (10, 0.8) to (FRC, 0). The region between the line dividing the curve in two halves and the inspiration curve corresponds to nonelastic work, example R subscript AW. The region enclosed within the line, vertical axis, and x equals 0.8 corresponds to elastic work, example compliance and elastance. Back to Figure Horizontal axis shows pressure in centimeters of water and vertical axis shows lung volume in liters. The curves for emphysema, normal, and fibrosis show rising curves, each shifted further right and downward than the previous one. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12

in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a sharp rise to 5, a plateau, a curved peak to 10, and a gradual fall to 0. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a sharp peak at 50, followed by a gradual and sharp dip to negative 30. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows triangular waves with curved peaks at 350. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a square peak at 20 with a notch. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a curved peak at 80, followed by a curved dip at negative 80. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows triangular waves with curved and wide peaks at 350. The curves are further apart. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. There are two square waves, one with a curved dip and the other with a gradual rise, corresponding to B. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The graph shows a peak to 70, a gradual fall to 0, corresponding to A, a sharp dip to negative 70, and a gradual rise to 0.

The first curve has a sharp peak and the second curve has a curved peak. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows triangular waves with curved and wide peaks at 500. The curves are further apart. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a square peak at 20 with a protruding notch, labeled A. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a curved peak at 80, followed by a curved and fluctuating dip at negative 80. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows triangular waves with curved and wide peaks at 500. The curves are further apart. Back to Figure In all graphs, horizontal axis shows time in seconds, listing 1 and 2. In the first set of graphs, vertical axis shows flow in liters per minute, ranging from negative 80 to 100 in increments of 20. The curve rises sharply to 80, falls to 100, then to negative 70, and gradually rises to 0. With increase in percentage, the width of the initial portion of the curve shrinks toward the right. In the second set of graphs, vertical axis shows pressure in centimeters of water, ranging from 0 to 20 in increments of 5. The curve is sawtooth peaking at 20. With increase in percentage, the width of the graph shrinks toward the right. Back to Figure

A. There are two graphs. In both graphs, the flow rises sharply, falls gradually and then sharply, and rises again, while pressure rises sharply and then gradually, and falls sharply. During pressure trigger, there is a notch in the pressure curve during the beginning of the patient effort when the curve begins rising. During flow trigger, there is a diagonal notch in the flow curve during the beginning of the patient effort when the curve begins rising. B. There are two graphs. Both show pressure subscript AW in centimeters of hydrogen in the horizontal axis and V subscript T in milliliters, ranging from 0 to 750 in increments of 250. All data are approximate. In the first graph, flow curve rises from (0, 0) to (12, 520), while the pressure curve is plotted through (0, 0), (1, 300), and (12, 520). In the second graph, flow curve rises from (0, 50) to (38, 400) and the pressure curve is plotted through (0, 50), (10, 300), and (38, 400). Back to Figure Horizontal axis shows P subscript AW in centimeters of water, ranging from negative 20 to 40 in increments of 20. Vertical axis shows V subscript T in milliliters, ranging from 0 to 750 in increments of 250. All data are approximate. The flow curve is plotted through (0, 0), (negative 2, 100), (0, 200), (5, 250), and (20, 500). The pressure curve is plotted through (0, 0), (5, 250), and (20, 500). Back to Figure Horizontal axis shows airway pressure in centimeters of water, ranging from 0 to 40 in increments of 10. Vertical axis shows volume above FRC in liters, ranging from 0.0 to 1.6 in increments of 0.4. All data are approximate. The curve for normal lungs is plotted from (0, 0.0) to (19, 1.55). The curve for ARDS is plotted from (0, 0) to (39, 0.95). Back to Figure

Horizontal axis shows P subscript AW in centimeters of water, ranging from negative 20 to 40 in increments of 20. Vertical axis shows V subscript T in milliliters, ranging from 0 to 750 in increments of 250. All data are approximate. The flow curve rises from (0, 0) to (40, 350). The pressure curve is plotted through (0, 0), (10, 350), and (20, 350). Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a square peak at 10 with fluctuations. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a sharp peak at 80, followed by a gradual fall, a sharp dip to negative 80, and a curved rise to 0. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows triangular waves with curved and wide peaks at 500. The curves are further apart. In all graphs, the width and height of the second cycle is greater than that of the first cycle. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows square waves between fluctuations. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a curved peak at 70, followed by a sharp dip at negative 80 between fluctuations. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows square waves at 700 beginning with a notch.

Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a square-shaped sawtooth curve peaking at 15. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a sharp peak at 70, a gradual dip, and a sharp dip to negative 40, followed by a rise to 0. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows wide triangular waves with curved peaks at 400. Back to Figure Horizontal axis shows pressure in centimeters of water, listing 0, 10, and 20. Vertical axis shows volume in milliliters, ranging from 0 to 200 in increments of 50. All data are approximate. The loop is plotted through (0, 10), (10, 50), (13, 160), (20, 200), (10, 180), and (0, 10). An arrow points toward (9, 15), the intersection of two tangents of the rising part of the loop. Back to Figure Horizontal axis shows wavelength in nanometers, ranging from 600 to 1000 in increments of 100. Vertical axis shows extinction coefficient, listing 0.01, 0.1, 1, and 10. All data are approximate. There are two vertical lines, corresponding to red at 660 nanometers and infrared at 940 nanometers. The curve for hemoglobin falls through (600, 8), (940, 0.3), and (1000, 0.07). The curve for oxyhemoglobin is plotted through (600, 0.9), (660, 0.1), and (100, 0.4). Back to Figure Horizontal axis shows wavelength in nanometers, ranging from 500 to

700 in increments of 50. Vertical axis shows absorbance, ranging from 0 to 25 in increments of 5. All data are approximate. The graph for Hb is plotted through (500, 4), (550, 13), (605, 2), and (700, 0). The graph for HbO2 is plotted through (500, 4), (545, 14.5), (560, 9), (575, 15.5), (600, 1.5), and (650, 0). The graph for HbCO is plotted through (500, 5), (540, 14.5), (555, 12), (565, 14.5), (600, 1.5), and (650, 0). The graph for MetHb falls from (500, 9) to (700, 0). The graph for HbS is plotted through (500, 6), (590, 9), (620, 21), (660, 3), and (700, 0). Back to Figure Horizontal axis shows PO2 at pH equals 7.40, ranging from 0 to 100 in increments of 10. Vertical axis shows percentage of SO2, ranging from 0 to 100 in increments of 10. All data are approximate. The curve is plotted through (0, 0), (28, 50), (42, 75), (62, 90), and (100, 97). Back to Figure Horizontal axis shows PO2 in millimeters of mercury, ranging from 0 to 100 in increments of 25. Vertical axis shows SO2 in percentage, ranging from 0 to 100 in increments of 25. All data are approximate. The dissociation curve rises through (0, 0), (28, 50), (42, 75), (62, 90), and (100, 97). It shifts right during hyperthermia, increase in 2,3-DPG, acidosis, and hypercarbia. It shifts left during hypothermia, alkalosis, and CO. Back to Figure Horizontal axis shows time and vertical axis shows pressure of carbon dioxide. The graph shows that when exhalation begins, the pressure is zero and corresponds to 1, rises sharply and corresponds to 2, rises gradually over a long period till the end of exhalation, corresponding to 3, and falls sharply. Back to Figure

Horizontal axis shows time and vertical axis shows pressure of carbon dioxide. The graph shows that when exhalation begins, the pressure is zero and corresponds to 1, rises sharply and corresponds to 2, rises steadily over a long period till the end of exhalation, corresponding to 3, and falls sharply. Back to Figure A. A mainstream sensor is at the junction of ventilator circuit and endotracheal tube, which is connected to capnometer by an electronic cable. B. A sample port is at the junction of ventilator circuit and endotracheal tube, which is connected to capnometer by a gas sample line. Back to Figure The process flows as follows: pulmonary veins PCWP, left atrium PCWP, left ventricle SBP, aorta SBP, arteries SBP, capillaries, veins, vena cava IVC plus SVC CVP, right atrium CVP, right ventricle PAP, pulmonary arteries PAP, and pulmonary capillaries alveoli. Back to Figure The curve rises from diastolic pressure at 82 millimeters of mercury to systolic pressure at 128 millimeters of mercury and falls back to diastolic pressure. The falling part of the curve has dicrotic notch. The total period of the waveform is 0.75 seconds at the rate of 80 per minute. The period between the rise and dicrotic notch is ejection time. Back to Figure A normal ECG waveform begins after a square waveform. A central venous pressure waveform begins after a square waveform in rising pattern, consisting of irregular patter. A wave is labeled a, its descent, x, a notch in the descent, c, a smaller wave v, and its descent, y.

Back to Figure It has four ports: proximal, distal, to the thermistor, and to the balloon. The proximal port passes through the superior vena cava. The port to the balloon passes through the right atrium and ventricle and into the pulmonary artery. Back to Figure The catheter passes through superior vena cava, right atrium and ventricle, and pulmonary artery. The waveforms in all regions show a normal ECG waveform. In addition, the waveform at right atrium shows an irregular and fluctuating waveform, the waveform at right ventricle shows square waves with a protruding notch, the waveform beginning at pulmonary artery shows curved waves between sharp fluctuations, and the waveform at the location of inflated balloon is flat, irregular wave. Back to Figure A. A photo shows metal laryngoscopes. B. A photo shows a silicone tubing attached with a cuff. C1. An illustration shows a tubing attached with a cuff, a syringe, and a pressure gauge. C2. A photo shows a pressure gauge. Back to Figure A. Three photos show the airway placed against a person's cheek. The curved end is then inserted through the mouth and positioned against the throat. B. Accompanying illustration shows the same process. After insertion, the mouth closed around the device. Back to Figure A1. Endotracheal tube with curved blade is inserted into the vallecula located above the epiglottis. A2. Endotracheal tube with straight blade is

inserted into the epiglottis. A3. An endotracheal tube with a curved blade is inserted into the vallecula and a flexible tube is inserted through the nose and positioned above the trachea with forceps. B1. A syringe is connected to the mask. B2. The syringe is removed and the tube is held by its neck. Back to Figure B3. The mask is inserted through the mouth. B4. The tip is secured at the larynx, and a finger is inserted into the mouth to push the tubing to the back. B5. The mask and tubing are secured and the finger is removed. B6. A syringe is attached to the tube inflating the mask inside. Back to Figure A. A tube with a cuff, port, and syringe. B. A tube with speech cannula, low-profile speaking valve, fenestrated tracheostomy tube, and subglottic suction cannula. Back to Figure In both sets, horizontal axis shows time in seconds, ranging from 0 to 14 in increments of 2. In the first set, there are two graphs. In the first graph, vertical axis shows flow in liters per minute, ranging from negative 50 to 40 in increments of 10. In each cycle, the curve rises steadily from negative 45 to negative 20, rises sharply to 30, remains constant with a notch in the middle, and falls sharply to negative 45. In the second graph, vertical axis shows P subscript AW in centimeters of water and P subscript ES in centimeters of water, ranging from negative 8 to 24 in increments of 4. P subscript AW shows triangular sawtooth curves, which fall gradually over time. A curve superimposed on a cycle shows a wider P subscript AW curve. In each cycle of P subscript ES, the curve rises from negative 6.5 to 4, remains constant, and falls to negative 6.4. In the second set, there are two graphs. In the first graph, vertical axis shows

flow in liters per minute, ranging from negative 50 to 60 in increments of 10. In each cycle, the curve rises steadily from negative 10 to 0, rises sharply to 45, then to 60, and falls sharply to negative 45 before rising to 0. In the second graph, vertical axis shows P subscript AW in centimeters of water and P subscript ES in centimeters of water, ranging from 0 to 40 in increments of 10. P subscript AW shows triangular curves peaking at 30 and with a notch at the base. P subscript ES is an almost flat curve with mild fluctuations. Back to Figure The graph shows rectangular curves during inhalation and inverted righttriangular curves during exhalation. During some cycle, there are two consecutive inhalation curves and an elongated exhalation curve. Back to Figure In all graphs, horizontal axis shows time in seconds, ranging from 0 to 12 in increments of 2. In the first graph, vertical axis shows pressure subscript AW in centimeters of water, ranging from negative 10 to 20 in increments of 10. The curve shows a square peak at 20 with a protruding notch. In the second graph, vertical axis shows flow in liters per minute, ranging from negative 80 to 80 in increments of 40. The curve consists of a curved peak at 70, followed by a curved dip with fluctuations at negative 70. In the third graph, vertical axis shows V subscript T in milliliters, ranging from negative 250 to 750 in increments of 250. The curve shows triangular waves with flat and wide peaks at 450. The curves are further apart. Back to Figure A. A mask covers the nose and mouth and is strapped around the head and lower jaw. B. A mask covers the nose and is strapped around the head and lower jaw. C. An interface is inserted into the nose and is

secured with straps around head and cheek. D. A helmet is over the head and is secured under the armpits. Back to Figure A. The illustration shows the following elements in the CPAP system: threshold pressure valve, expiratory limb, T-adapter connected to pressure manometer and patient, inspiratory limb, humidifier, antiasphyxia valve, one-way valve, flowmeter, reservoir bag, and blender. B. Two PEEP vales. C. A face mask with PEEP valve. Back to Figure Two photos, A and B, show Extracorporeal Membrane Oxygenation System consisting of a touchscreen interface. C. The circuit is as follows: heart, venous bladder, fluids, heparin infusion, centrifugal pump, carbon dioxide–oxygen pump, oxygenator, air bubble detector, pressure monitor displaying 100, heat exchanger, transonic flowmeter, and temperature monitor, displaying 38 degrees Celsius. Back to Figure The organs are right and left pulmonary arteries, right and left pulmonary veins, right and left lungs, foramen ovale, aorta, ductus arteriosus, pulmonary trunk, inferior vena cava, liver, ductus venosus, descending aorta, umbilical vein, and umbilical arteries. Back to Figure In both graphs, horizontal axis shows age in years, listing 0, 0.5, 1, 5, 10, and 18. The dotted lines and solid lines trace an almost similar path. In the first graph, vertical axis shows heart rate, ranging from 50 to 200 in increments of 50. The curve for 99 falls from (0, 185) to (18, 135). The curve for 95 falls from (0, 170) to (18, 125). The curve for 90 falls from (0, 165) to (18, 115). The curve for 50 falls from (0, 140) to (18, 85). The

curve for 10 falls from (0, 120) to (18, 70). The curve for 5 falls from (0, 115) to (18, 65). The curve for 1 falls from (0, 100) to (18, 50). In the second graph, vertical axis shows respiratory rate, ranging from 0 to 80 in increments of 10. The curve for 99 falls from (0, 79) to (18, 35). The curve for 95 falls from (0, 62) to (18, 28). The curve for 90 falls from (0, 58) to (18, 25). The curve for 50 falls from (0, 40) to (18, 20). The curve for 10 falls from (0, 30) to (18, 15). The curve for 5 falls from (0, 28) to (18, 13). The curve for 1 falls from (0, 21) to (18, 11). Back to Figure A. The circulation is as follows: Systemic venous circulation and ECMO pump, oxygenator, and heater, right atrium, right ventricle, left atrium, left ventricle, and systemic arterial circulation. Systemic and venous circulation also leads to ECMO pump. B. The circulation is as follows: Systemic venous circulation, right atrium, ECMO pump, oxygenator, and heater, right atrium, right ventricle, left atrium, left ventricle, and systemic arterial circulation. ECMO pump also leads to systemic arterial circulation. Back to Figure There are six columns: Value, Normal range, superscript a, mild hypoxemia, moderate hypoxemia, moderate to severe, and very severe hypoxemia. Row entries are as follows. Row 1: PaO2 in millimeters of mercury, superscript b, 80 to 100, 60 to 79, 50 to 59, 40 to 49, less than 40. Row 2: SaO2 in percent, superscript c, 96 to 98, 91 to 95, 85 to 90, 75 to 84, and less than 75. Back to Table There are six columns: VC, VA, PC, PA, PS, and SV. Row entries are as follows. Trigger variable: Time, patient effort, Time, patient effort, patient effort, patient effort. Target variable: Volume per flow, volume per flow, inspiratory pressure, inspiratory pressure, inspiratory pressure, baseline

pressure. Cycle variable: Volume, volume, time, time, flow, flow. Expiratory pressure: 0 or PEEP, 0 or PEEP, 0 or PEEP, 0 or PEEP, 0 or PEEP, 0 or CPAP. Back to Table Row entries are as follows. VAC: VC and VA. PAC: PC and PA. V-SIMV: VC, VA, PS, and SV. P-SIMV: PC, PA, PS, and SV. PSV: PS and SV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: S CMV; VAC; VC, VA; VC-CMV; no data. Row 2: SIMV; VSIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; (S)CMV. Row 3: PCMV; PAC; PC, PA; PC-CMV; no data. Row 4: P-SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; P-CMV. Row 5: Spontaneous; PS or CPAP; PS, CPAP spontaneous; PC-CSV; P-CMV. Row 6: VS; PS with a Vt setting; PS; PC-CSV; APVcmv. Row 7: APVcmv; PAC with a Vt setting; PC; PC-CMV; no data. Row 8: APVsimv; P-SIMV with a PS Vt setting; PC, PS; PC-IMV; APVcmv. Row 9: DuoPAP; P-SIMV; PC, PS; PC-IMV; PC-IMV. Row 10: APRV; P-SIMV, I:E usually inversed; PC, PS; PC-IMV; P-CMV. Row 11: ASV; P-SIMV with min vol setting; PC, PS; PC-IMV; no data. Row 12: INTELLiVENT; ASV; P-SIMV with min vol setting; PC, PS; PC-IMV; no data. Row 13: NIV; PS; PS; PC-CSV; P-CMV. Row 14: NIVST; P-SIMV; PC, PS; PC-IMV; P-CMV. Row 15: nCPAP-PS; P-SIMV; PC, PS; PC-IMV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: (S)CMV; VAC; VC, VA; VC-CMV; no data. Row 2: SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; SIMV. Row 3: PCV

positive; PAC; PC, PA; PC-CMV; no data. Row 4: P-SIMV positive; PSIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; P-SIMV positive. Row 5: Spontaneous; PS or CPAP; PS, CPAP spontaneous; PC-CSV; APVsimv. Row 6: APVcmv; PAC with a Vt setting; PC, PS; PC-CMV; no data. Row 7: APVsimv; P-SIMV with a PS Vt setting; PC, PS; PC-IMV; APVsimv. Row 9: DuoPAP; P-SIMV; PC, PS; PC-IMV; APVsimv. Row 10: APRV; PSIMV (I:E usually inversed); PC, PS; PC-IMV; APVsim. Row 11: ASV; PSIMV with minimum minute ventilation setting; PC, PS; PC-IMV; no data. Row 12: INTELLiVENT; ASV; P-SIMV with minimum minute ventilation setting; PC, PS; PC-IMV; no data. Row 13: NIV; PSV; PS; PC-CSV; PCV positive. Row 14: NIV-ST; P-SIMV; PC, PS; PC-IMV; no data. Row 15: nCPAP-PS; P-SIMV; PC, PS; PC-IMV; PCV positive. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: (S)CMV positive; PAC with a Vt setting; PC; PC-CMV; no data. Row 2: SIMV positive; P-SIMV with a PS Vt setting; PC, PA, PS, CPAP spontaneous; PC-IMV; SIMV positive. Row 3: PCV positive; PAC; PC, PA; PC-CMV; no data. Row 4: P-SIMV positive; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Row 5: Spontaneous; PS or CPAP; PS, CPAP spontaneous; PC-CSV; SIMV positive. Row 6: DuoPAP; P-SIMV; PC, PS; PC-IMV; SIMV positive. Row 7: APRV; PSIMV (I:E usually inversed); PC, PS; PC-IMV; SIMV positive. Row 8: ASV; P-SIMV with min vol setting; PC, PS; PC-IMV; no data. Row 9: NIV; PSV; PS; PC-CSV; PCV positive. Row 10: NIV-ST; P-SIMV; PC, PS; PCIMV; no data. Row 11: nCPAP; P-SIMV; CPAP spontaneous; PC-CSV; no data. Row 12: nCPAP-PC; P-SIMV; PC, CPAP spontaneous; PC-IMV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths

delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: Volume Control; VAC; VC, VA; VC-CMV; Volume Control. Row 2: SIMV (Volume Control); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; Volume Control. Row 3: Pressure Control; PAC; PC, PA; PC-CMV; Pressure Control. Row 4: SIMV (Pressure Control); PSIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Pressure Control. Row 5: Pressure Support; PS; PS; PC-CSV; Pressure Control. Row 6: Spontaneous/CPAP; CPAP; CPAP spontaneous; PC-CSV; Pressure Control. Row 7: Pressure-Regulated Volume Control (PRVC); PAC; PC, PA; PC-CMV; Pressure Control. Row 8: SIMV (PRVC); P-SIMV; PC, PA, PS; PC-IMV; Pressure Control. Row 9: Volume Support; PS with a Vt setting; PS; PC-CSV; Volume Control. Row 10: Automode (VC/VS); Variable V-SIMV; VC, VA, PS; PC-IMV; no data. Row 11: Automode (PC/PS); Variable P-SIMV; PC, PS; PC-IMV; no data. Row 12: Automode (PRVC/VS); P-SIMV; PC, PS; PC-IMV; no data. Row 13: Bi-Vent; P-SIMV (I:E usually inversed); PC, PS, CPAP; PC-IMV; Pressure Control. Row 14: NAVA; NAVA; Variable pressure; PC-IMV; Pressure Control. Row 15: NIV (Pressure Control); PAC; PC, PA; PC-CMV; Pressure Control. Row 16: NIV (Pressure Support); PS; PS; PC-CSV; Pressure Control. Row 17: Nasal CPAP; CPAP; Spontaneous; PC-CSV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: Volume Control; VAC; VC, VA; VC-CMV; Volume Control. Row 2: SIMV (Volume Control); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; Volume Control. Row 3: Pressure Control; PAC; PC, PA; PC-CMV; no data. Row 4: SIMV (Pressure Control); P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Pressure Control. Row 5: Pressure Support/CPAP; PS or CPAP; PS, CPAP spontaneous; PC-CSV; Pressure Control. Row 6: Pressure-regulated Volume Control (PRVC); PAC; PC, PA; PC-CMV; no data. Row 7: SIMV (PRVC); P-SIMV; PC, PA, PS; PC-

IMV; Pressure Control. Row 8: Volume Support; PS with a Vt setting; PS; PC-CSV; PRVC. Row 9: Automode (VC/VS); Variable V-SIMV; VC, VA, PS; PC-IMV; no data. Row 10: Automode (PC/PS); Variable P-SIMV; PC, PS; PC-IMV; no data. Row 11: Automode (PRVC/VS); P-SIMV; PC, PS; PC-IMV; no data. Row 12: Bi-Vent/APRV; P-SIMV (I:E usually inversed); PC, PS, CPAP; PC-IMV; no data. Row 13: NAVA; NAVA; Variable pressure; PC-IMV; Pressure Control. Row 14: NIV (Pressure Control); PAC; PC, PA; PC-CMV; Pressure Control. Row 15: NIV (Pressure Support); PS; PS; PC-CSV; Pressure Control. Row 16: Nasal CPAP; CPAP; Spontaneous; PC-CSV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: A/C (VC); VAC; VC, VA; VC-CMV; VC, PC. Row 2: SIMV (VC); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VC, PC. Row 3: A/C (PC); PAC; PC, PA; PC-CMV; VC, PC. Row 4: SIMV (PC); P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; VC, PC. Row 5: Pressure Support; PS; PS; PC-CSV; VC, PC. Row 6: CPAP; CPAP; CPAP spontaneous; PC-CSV; VC, PC. Row 7: VC positive; PAC; PC, PA; PCCMV; VC, PC. Row 8: SIMV (VC positive); P-SIMV; PC, PA, PS; PC-IMV; VC, PC. Row 9: Volume Support; PS with a Vt setting; PS; PC-CSV; VC, PC. Row 10: Bilevel; P-SIMV; PC, PS, CPAP; PC-IMV; VC, PC. Row 11: Proportional Assist ventilation; PA; Variable pressure; PC-CSV; VC, PC. Row 12: NIV (A/C/VC); VAC; VC, VA; VC-CMV; VC, PC. Row 13: NIV (A/C/PC); PAC; PC, PA; PC-CMV; VC, PC. Row 14: NIV (Pressure Support); PS; PS; PC-CSV; VC, PC. Row 15: NIV (SIMV/VC); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VC, PC. Row 16: NIV (SIMV/PC); P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV VC, PC. Back to Table There are five columns: mode name, generic mode, types of breaths

delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: A/C (VC); VAC; VC, VA; VC-CMV; VC, PC. Row 2: SIMV (VC); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VC, PC. Row 3: A/C (PC); PAC; PC, PA; PC-CMV; VC, PC. Row 4: SIMV (PC); P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; VC, PC. Row 5: Pressure Support; PS; PS; PC-CSV; VC, PC. Row 6: CPAP; CPAP; CPAP spontaneous; PC-CSV; VC, PC. Row 7: VC positive; PAC; PC, PA; PCCMV; VC, PC. Row 8: SIMV (VC positive); P-SIMV; PC, PA, PS; PC-IMV; VC, PC. Row 9: Volume Support; PS with a Vt setting; PS; PC-CSV; VC, PC. Row 10: Bilevel; P-SIMV; PC, PS, CPAP; PC-IMV; VC, PC. Row 11: Proportional Assist ventilation; PA; Variable pressure; PC-CSV; VC, PC. Row 12: NIV (A/C/VC); VAC; VC, VA; VC-CMV; VC, PC. Row 13: NIV (A/C/PC); PAC; PC, PA; PC-CMV; VC, PC. Row 14: NIV (Pressure Support); PS; PS; PC-CSV; VC, PC. Row 15: NIV (SIMV/VC); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VC, PC. Row 16: NIV (SIMV/PC); P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; VC, PC. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: VC/ACMV; VAC; VC, VA; VC-CMV; VC/ACMV. Row 2: VC/SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VC/SIMV. Row 3: PC/ACMV; PAC; PC, PA; PC-CMV; PC/ACMV. Row 4: PC/SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PC/SIMV. Row 5: VC/SPONT; PS; PS; PC-CSV; PC/ACMV. Row 6: PC/SPONT; PS; PS; PC-CSV; PC/ACMV. Row 7: VTPC/ACMV; PAC with a Vt setting; PC, PA; PC-CMV; PC/ACMV. Row 8: VTPC/SIMV; P-SIMV with a Vt setting; PC, PA, PS, CPAP spontaneous; PC-IMV; PC/SIMV. Row 9: VTPC/SPONT; PS with a Vt setting; PS; PC-CSV; PC/ACMV. Row 10: Volume Support; PS with a Vt setting; PS; PC-CSV; PC/ACMV. Row 11: BPRV/ACMV; PAC; PC, PS, CPAP; PC-CMV; PC/ACMV. Row 12: BPRV/SIMV; P-SIMV; PC, PA; PC-IMV; PC/SIMV. Row 13: NIV; Can be used in any of the

above modes; no data; no data; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Asterisk corresponds to neonatal ventilation. Row entries are as follows. Row 1: Volume A/C; VAC; VC, VA; VC-CMV; Volume A/C. Row 2: Volume SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; Volume SIMV. Row 3: Pressure A/C; PAC; PC, PA; PC-CMV; Pressure A/C. Row 4: Pressure SIMV; PSIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Pressure SIMV. Row 5: CPAP/Pressure Support; CPAP or PS; CPAP spontaneous or PS; PCCSV; Volume A/C, pressure A/C, TCPL A/C asterisk. Row 6: PRVC A/C; PAC; PC, PA; PC-CMV; PRVC A/C. Row 7: PRVC; SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PRVC; SIMV. Row 8: APRV/Biphasic; P-SIMV; PC, PS, CPAP; PC-IMV; Volume A/C, pressure A/C, TCPL A/C asterisk. Row 9: TCPL A/C asterisk; PAC; PC, PA; PCCMV; TCPL A/C asterisk. Row 10: TCPL SIMV asterisk; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; TCPL SIMV asterisk. Row 11: Pressure A/C plus VG asterisk; PAC; PC, PA; PC-CMV; Pressure A/C plus VG asterisk. Row 12: Pressure SIMV plus VG asterisk; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Pressure SIMV plus VG asterisk. Row 13: Pressure TCPL plus VG asterisk; PAC; VC, VA, PS, CPAP spontaneous; PCCIMV; Pressure TCPL plus VG asterisk. Row 14: Nasal CPAP/IMV asterisk; CPAP or P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Volume A/C, pressure A/C, TCPL A/C asterisk. Back to Table The features are as follows. Volume limit: Pressure A/C, pressure SIMV, CPAP/PS, PRVC A/C, PRVC SIMV, APRV/biphasic, TCPL A/C, and TCPL SIMV. Mach vol: Pressure A/C and pressure SIMV. Insp rise: Pressure A/C, pressure SIMV, PRVC A/C, and PRVC SIMV. Flow cycle: Pressure A/C, pressure SIMV, PRVC A/C, PRVC SIMV, TCPL A/C, and

TCPL SIMV. Waveform, demand flow, sigh, V sync, and V sync rise: Volume A/C and volume SIMV. Bias flow and pres trig: Volume A/C, volume SIMV, pressure A/C, pressure SIMV, CPAP/PS, PRVC A/C, PRVC SIMV, APRV/biphasic, TCPL A/C, TCPL SIMV, pressure A/C plus VG, pressure SIMV plus VG, and pressure TCPL plus VG. PSV rise, PSV cycle, and PSC T max: Volume SIMV, pressure SIMV, CPAP/PS, PRVC SIMV, APRV/biphasic, TCPL SIMV, and pressure SIMV plus VG. T high sync, T high PSV, and T low sync: APRV/biphasic. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: Volume A/C; VAC; VC, VA; VC-CMV; no data. Row 2: Volume SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VSIMV. Row 3: Pressure A/C; PAC; PC, PA; PC-CMV; no data. Row 4: Pressure SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PSIMV. Row 5: CPAP/Pressure Support; CPAP or PS; CPAP spontaneous or PS; PC-CSV; Volume A/C or Pressure A/C. Row 6: PRVC A/C; PAC; PC, PA; PC-CMV; no data. Row 7: PRVC SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PRVC-SIMV. Row 8: APRV/Biphasic; PSIMV; PC, PS, CPAP; PC-IMV; Volume A/C or Pressure A/C. Row 9: NPPV A/C; PAC; PC, PA; PC-CMV; no data. Row 10: NPPV SIMV; PSIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; P-SIMV. Row 11: NPPV/CPAP/PS; CPAP or PS; CPAP spontaneous or PS; PC-CSV; Volume A/C or Pressure A/C. Back to Table The features are as follows. Assured volume: Pressure A/C and pressure SIMV. Volume limit: PRVC A/C and PRVC SIMV. Insp rise: Pressure A/C, pressure SIMV, PRVC A/C, and PRVC SIMV. Waveform, sigh, and V sync: Volume A/C and volume SIMV. Bias flow: Volume A/C, volume SIMV, pressure A/C, pressure SIMV, CPAP/PS, PRVC A/C, PRVC SIMV,

APRV/biphasic, NPPV A/C, NPPV SIMV, and NPPV/CPAP/PS. PC flow cycle: Pressure A/C, pressure SIMV, PRVC A/C, PRVC SIMV, NPPV A/C, and NPPV SIMV. PSV cycle: Volume SIMV, pressure SIMV, CPAP/PS, PRVC SIMV, and APRV/biphasic. PSV Tmax: Volume SIMV, pressure SIMV, CPAP/PS, PRVC SIMV, APRV/biphasic, NPPV SIMV, and NPPV/CPAP/PS. Percent T high sync, T high PSV, and T low sync: APRV/biphasic. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: VC-CMV; VAC; VC; VC-CMV; no data. Row 2: VC-A/C; VAC; VC, VA; VC-CMV; no data. Row 3: VC-SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VC-SIMV. Row 4: VC-MMV; V-SIMV; VC, VA, PS; VC-IMV; no data. Row 5: PC-CMV; PAC; PC; PC-CMV; no data. Row 6: PC-A/C; PAC; PC, PA; PC-CMV; no data. Row 7: PC-SIMV; PSIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; VC-SIMV. Row 8: PCSIMV positive; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; VCSIMV. Row 9: PC-PS; P-SIMV; PC, PA, PS; PC-IMV; no data. Row 10: PC-APRV; P-SIMV; PC, PS, CPAP; PC-IMV; VC-SIMV. Row 11: SPNCPAP/PS; CPAP or PS; CPAP spontaneous or PS; PC-CSV; VC-SIMV. Row 12: SPN-CPAP/VS; PS with a Vt setting; PS; PC-CSV; VC-SIMV. Row 13: SPN-CPAP; CPAP; Spontaneous; PC-CSV; VC-SIMV. Row 14: SPN-PPS; PA; Variable pressure; PC-CSV; VC-SIMV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: CMV; VAC; VC, VA; VC-CMV; no data. Row 2: SIMV; VSIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; CMV. Row 3: SIMV/PSupp; V-SIMV; VC, VA, PS; VC-IMV; no data. Row 3: MMV; VSIMV; VC; VC-IMV; no data. Row 4: MMV-PSupp; V-SIMV; VC, PS; PC-

IMV; no data. Row 5: PSupp; PS; PS; PC-CSV; no data. Row 5: CPAP/PSupp; Spont or PS; PS, CPAP spontaneous; PC-CSV; CMV. Row 6: PCV positive; PAC; PC, PA; PC-CMV; CMV. Row 7: PCV+ positive/PSupp.; P-SIMV; PC, PA, PS; PC-IMV; CMV. Row 8: PCV positive Assist; PAC; PC, PA; PC-CMV; no data. Row 9: APRV; P-SIMV; PC, PS, CPAP; PC-IMV; CMV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: A/C VC; VAC; VC, VA; VC-CMV; no data. Row 2: SIMV; VC; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; Multiple modes. Row 3: A/C PC; PAC; PC, PA; PC-CMV; no data. Row 4: SIMV PC; PSIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Multiple modes. Row 5: CPAP/PS; CPAP or PS; CPAP spontaneous or PS; PC-CSV; Multiple modes. Row 6: A/C PRVC; PAC; PC, PA; PC-CMV; no data. Row 7: SIMV PRVC; P-SIMV with Vt set; PC, PA, PS, CPAP spontaneous; PCIMV; Multiple modes. Row 8: VS; PS with Vt set; PS; PC-CSV; Multiple modes. Row 9: BiLevel; P-SIMV; PC, PS, CPAP spontaneous; PC-IMV; Multiple modes. Row 10: BiLevel VG; P-SIMV with Vt set; PC, PS, CPAP spontaneous; PC-IMV; Multiple modes. Row 12: NIV; PS; PS; PC-CSV; A/C PC. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: PAC; PC, PA; PC-CMV; no data. Row 2: S/T mode; PSIMV; PC, PS, CPAP; PC-IMV; no data. Row 3: CPAP mode; CPAP; CPAP spontaneous; PC-CSV; no data. Row 4: AVAPS; P-SIMV; PC, PA; PC-IMV; no data. Row 5: Proportional Assist Ventilation; PA; Variable pressure; PC-CSV; PAC. Row 6: NIV (A/C/VC); VAC; VC, VA; VC-CMV; no data. Row 7: NIV (Pressure Support); PS; PS; PC-CSV; no data. Row

8: NIV (SIMV/VC); V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; no data. Row 9: NIV (SIMV/PC); P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: (S)CMV; PAC; PC, PA; PC-CMV; no data. Row 2: SIMV positive; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; SIMV positive. Row 3: PCV positive; PAC; PC, PA; PC-CMV; no data. Row 4: P-SIMV positive; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PSIMV positive. Row 5: Spontaneous; PS or CPAP; PS, CPAP spontaneous; PC-CSV; SIMV positive. Row 6: DuoPAP; P-SIMV; PC, PS; PC-IMV; SIMV positive. Row 7: APRV; P-SIMV (I:E usually inversed); PC, PS; PC-IMV; SIMV positive. Row 8: ASV; P-SIMV with min vol setting; PC, PS; PC-IMV; no data. Row 9: NIV; PSV; PS; PC-CSV; PCV positive. Row 10: NIV-ST; P-SIMV; PC, PS; PC-IMV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: (S)CMV positive; PAC with a Vt setting; PC; PC-CMV; no data. Row 2: SIMV positive; P-SIMV with a PS Vt setting; PC, PA, PS, CPAP spontaneous; PC-IMV; SIMV positive. Row 3: PCV positive; PAC; PC, PA; PC-CMV; no data. Row 4: P-SIMV positive; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Row 5: Spontaneous; PS or CPAP; PS, CPAP spontaneous; PC-CSV; SIMV positive. Row 6: DuoPAP; P-SIMV; PC, PS; PC-IMV; SIMV positive. Row 7: APRV; PSIMV (I:E usually inversed); PC, PS; PC-IMV; SIMV positive. Row 8: ASV; P-SIMV with min vol setting; PC, PS; PC-IMV; no data. Row 9: NIV; PSV; PS; PC-CSV; PCV positive. Row 10: NIV-ST; P-SIMV; PC, PS; PCIMV; no data. Row 11: nCPAP; P-SIMV; CPAP spontaneous; PC-CSV; no

data. Row 12: nCPAP-PC; P-SIMV; PC, CPAP spontaneous; PC-IMV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: CPAP; CPAP; CPAP spontaneous; PC-CSV; no data. Row 2: IMV plus CPAP; P-SIMV; PC or CPAP spontaneous; PC-IMV; no data. Row 3: IMV plus CPAP with pressure limit; P-SIMV or V-SIMV; PC, VC, CPAP spontaneous; PC-IMV, VC-IMV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: A/C; VAC; VC, VA; VC-CMV; no data. Row 2: SIMV; VSIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; no data. Row 3: CPAP; CPAP or PS; PS or CPAP spontaneous; PC-CSV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: A/C plus Volume; VAC; VC, VA; VC-CMV; VAC. Row 2: SIMV plus Volume; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VSIMV. Row 3: A/C plus Pressure; PAC; PC, PA; PC-CMV; PAC. Row 4: SIMV plus Pressure; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; P-SIMV. Row 5: CPAP plus Pressure Support; CPAP or PS; CPAP spontaneous or PS; PC-CSV; PAC. Row 6: A/C plus PRVC; PAC; PC, PA; PC-CMV; PRVC. Row 7: SIMV plus PRVC; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PRVC-SIMV. Row 8: Pressure-regulated VS; PS with a volume target; PS; PC-CSV; PAC. Row 9: NPPV A/C; PAC; PC, PA; PC-CMV; PAC. Row 10: NPPV/CPAP/PS; CPAP or PS; CPAP

spontaneous or PS; PC-CSV; Pressure A/C. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: Volume A/C; VAC; VC, VA; VC-CMV; VAC. Row 2: Volume SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; VAC. Row 3: Pressure A/C; PAC; PC, PA; PC-CMV; PAC. Row 4: Pressure SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; PAC. Row 5: CPAP/Pressure Support; CPAP or PS; CPAP spontaneous or PS; PCCSV; PAC. Row 6: NPPV; CPAP or PS; CPAP spontaneous or PS; PCCSV; PAC. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: VC-SIMV with AutoFlow; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Row 2: PC-A/C; PAC; PC, PA; PC-CMV; no data. Row 3: PC-BiPAP; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Row 4: SPN-CPAP/PS; PS; PS, CPAP spontaneous; PC-CSV; VC-SIMV. Row 5: SPN-CPAP; Spont; CPAP spontaneous; PCCSV; VC-SIMV. Row 6: SPN-CPAP/PS with a volume guarantee; PS; PS, CPAP spontaneous; PC-CSV; VC-SIMV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: VC-CMV; VAC; VC; VC-CMV; no data. Row 2: VC-A/C; VAC; VC, VA; VC-CMV; no data. Row 3: VC-SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; no data. Row 4: VC-CMV with AutoFlow; PC; PC; PC-CMV; no data. Row 5: VC-A/C with AutoFlow; PAC; PC, PA;

PC-CMV; no data. Row 6: VC-SIMV with AutoFlow; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Row 7: PC-BiPAP; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; no data. Row 8: SPN-CPAP; CPAP or PS; CPAP spontaneous or PS; PC-CSV; VC-CMV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: A/C MV VC; VAC; VC, VA; VC-CMV; A/C MV VC. Row 2: SIMV/VC; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; SIMV/VC. Row 3: A/C MV PC; PAC; PC, PA; PC-CMV; A/C MV PC. Row 4: SIMV/PC; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; SIMV/PC. Row 5: SPONT mode; CPAP or PS; PS, CPAP spontaneous; PC-CSV; SIMV/PC. Row 6: NIV; Can be used in any of the above modes; no data; no data; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: CV; VAC; VC; VC-CMV; Available. Row 2: A/C VAC; VC, VA; VC-CMV; Available. Row 3: SIMV; V-SIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; Available. Row 4: PC; PAC; PC, PA; PC-CMV; Available. Row 5: PC-SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Available. Row 6: CPAP; CPAP; CPAP spontaneous; PC-CSV; Available. Row 7: S; PS; PS; PC-CSV; Available. Row 8: S/T; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; Available. Row 9: T; PC; PC; PC-CMV; Available. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as

follows. Row 1: CPAP; CPAP; CPAP spontaneous; PC-CSV; no data. Row 2: Bilevel; PAC; PC; PC-CMV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: CPAP; CPAP; CPAP spontaneous; PC-CSV; no data. Row 2: Bilevel; PAC; PC; PC-CMV. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: CPAP; CPAP; CPAP spontaneous; PC-CSV; no data. Row 2: ASV; PS; PS; PC-CSV; PS (timed). Row 3: ASVAuto; PS; PS; PC-CSV; PS (timed). Row 4: PAC; PAC; PC, PA; PC-CMV; PAC. Row 5: S; PAC; PS; PC-CSV; no data. Row 6: ST; P-SIMV; PS; PC-IMV; PS. Row 7: T; PAC; PC; PC-CMV; PC. Row 8: iVAPS; PS; PS; PC-CSV; PS. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: (A)CV; VAC; VC, VA; VC-CMV; (A)CV. Row 2: V-SIMV; VSIMV; VC, VA, PS, CPAP spontaneous; VC-IMV; (A)CV. Row 3: P(A)CV; PAC; PC, PA; PC-CMV; (A)CV. Row 4: P-SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; (A)CV. Row 5: PS; PS; PS, PA; PC-IMV; (A)CV. Row 6: CPAP; CPAP; CPAP spontaneous; PC-CSV; (A)CV. Row 7: (S)T; PS; PS; PC-CSV; no data. Row 8: P(A)C; PAC; PC, PA; PC-CMV; no data. Row 9: iVAPS; PS; PS; PC-CSV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths

delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: PC-CMV; PAC; PC; PC-CMV; no data. Row 2: PC-A/C; PAC; PC, PA; PC-CMV; no data. Row 3: PC-SIMV; P-SIMV; PC, PA, PS, CPAP spontaneous; PC-IMV; VAC. Row 4: PC-PS; P-SIMV; PC, PA, PS; PC-IMV; no data. Row 5: PC-MMV; P-SIMV; PC, PA, PS; PC-IMV; no data. Row 6: PC-APRV; P-SIMV; PC, PS, CPAP; PC-IMV; VAC. Row 7: SPN-CPAP/PS; CPAP or PS; CPAP spontaneous or PS; PC-CSV; VAC. Row 8: SPN-CPAP/VS; PS with a Vt setting; PS; PC-CSV; VAC. Row 9: SPN-CPAP; CPAP; Spont; PC-CSV; no data. Row 10: SPN-PPS; PA; Variable pressure; PC-CSV; VAC. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: CMV, PC, PC, PC-CMV, no data. Row 2: IMV plus CPAP; P-SIMVl PC, CPAP spontaneous; PC-IMV; no data. Row 3: SPN-CPAP; CPAP; Spont; PC-CSV; no data. Back to Table There are five columns: mode name, generic mode, types of breaths delivered, ventilatory pattern, and apnea backup. Row entries are as follows. Row 1: NCPAP; CPAP; CPAP spontaneous; PC-CSV; no data. Row 2: BiPhasic; P-SIMV; PC, CPAP spontaneous; PC-IMV; VAC. Back to Table There are seven columns: Height in inches, IBW in kilograms, 4 milliliters per kilogram, 6 milliliters per kilogram, 8 milliliters per kilogram, 10 milliliters per kilogram, and 100 milliliters per kilogram or V subscript E. Row entries for males are as follows. Row 1: 60, 50, 200, 300, 400, 500, 5000. Row 2: 61, 52.3, 209.2, 313.8, 418.4, 523, 5230. Row 3: 62, 54.6, 218.4, 327.6, 436.8, 546, 5460. Row 4: 63, 56.9, 227.6, 341.4, 455.2,

569, 5690. Row 5: 64, 59.2, 236.8, 355.2, 473.6, 592, 5920. Row 6: 65, 61.5, 246, 369, 492, 615, 6150. Row 7: 66, 63.8, 255.2, 382.8, 510.4, 638, 6380. Row 8: 67, 66.1, 264.4, 396.6, 528.8, 661, 6610. Row 9: 68, 68.4, 273.6, 410.4, 547.2, 684, 6840. Row 10: 69, 70.7, 282.8, 424.2, 565.6, 707, 7070. Row 11: 70, 73, 292, 438, 584, 730, 7300. Row 12: 71, 75.3, 301.2, 451.8, 602.4, 753, 7530. Row 13: 72, 77.6, 310.4, 465.6, 620.8, 776, 7760. Row 14: 73, 79.9, 319.6, 479.4, 639.2, 799, 7990. Row 15: 74, 82.2, 328.8, 493.2, 657.6, 822, 8220. Row entries for females are as follows. Row 1: 60, 45.5, 182, 273, 364, 455, 4550. Row 2: 61, 47.8, 191.2, 286.8, 382.4, 478, 4780. Row 3: 62, 50.1, 200.4, 300.6, 400.8, 501, 5010. Row 4: 63, 52.4, 209.6, 314.4, 419.2, 524, 5240. Row 5: 64, 54.7, 218.8, 328.2, 437.6, 547, 5470. Row 6: 65, 57, 228, 342, 456, 570, 5700. Row 7: 66, 59.3, 237.2, 355.8, 474.4, 593, 5930. Row 8: 67, 61.6, 246.4, 369.6, 492.8, 616, 6160. Row 9: 68, 63.9, 255.6, 383.4, 511.2, 639, 6390. Row 10: 69, 66.2, 264.8, 397.2, 529.6, 662, 6620. Row 11: 70, 68.5, 274, 411, 548, 685, 6850. Row 12: 71, 70.8, 283.2, 424.8, 566.4, 708, 7080. Row 13: 72, 73.1, 292.4, 438.6, 584.8, 731, 7310. Row 14: 73, 75.4, 301.6, 452.4, 603.2, 754, 7540. Row 15: 74, 77.7, 310.8, 466.2, 621.6, 777, 7770. Back to Table There are seven columns: initial PaO2 with FiO2 equals 1.0, initial SpO2 with FiO2 equals 1.0, step 1 FiO2 decrease, step 2 FiO2 decrease, step 3 FiO2 decrease, step 4 FiO2 decrease, and step 5. Row entries are as follows. Row 1: Greater than 300; 100 percent; Decrease by 20 percent to 0.80 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 20 percent to 0.60 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 10 percent to 0.50 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 10 percent to 0.40 and assess SpO2, if greater than or equal to 90 percent proceed to next step; Obtain ABGs and reassess, consider decrease by 5 percent to 0.35 based on SpO2. Row 2: 200 to 300; 100 percent;

Decrease by 20 percent to 0.80 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 20 percent to 0.60 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 10 percent to 0.50 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 10 percent to 0.40 and assess SpO2, if greater than or equal to 90 percent proceed to next step; Obtain ABGs and reassess. Row 3: 150 to 199; 99 percent to 100 percent; Decrease by 20 percent to 0.80 and assess SpO2, if greater than 95 percent proceed to next step; Decrease by 20 percent to 0.60 and assess SpO2, if greater than or equal to 90 percent proceed to next step; Obtain ABGs and reassess; no data; no data. Row 4: 100 to 149; 96 percent to 100 percent; Decrease by 20 percent to 0.80 and assess SpO2, if greater than or equal to 90 percent proceed to next step; Obtain ABGs and reassess; no data, no data; no data. Row 5: Less than 100; less than 96 percent to 100 percent; Consider increase in PEEP. Back to Table There are eight columns: condition, CVP, PAP, PCWP, PVR, SVR, CO, and BP. Row entries are as follows. Row 1: Fluid overload, increase, increase, increase, increase or N, increase or N, increase or N, increase or N. Row 2: Left-ventricular failure: increase, increase, increase, increase, increase or N, decrease, decrease. Row 3: Hypovolemic shock, decrease, decrease, decrease, increase or N, increase, decrease, decrease. Row 4: Septic shock, decrease or N, decrease or N, decrease or N, decrease or N, decrease, increase, decrease. Row 5: Cardiogenic shock, increase, increase, increase, increase or N, increase, decrease, decrease. Row 6: Pulmonary embolus, increase, increase, decrease or N, increase, increase, decrease or N, decrease or N. Row 7: Lung over distension, increase, increase, decrease, increase, increase, decrease, decrease. Row 8: ARDS, decrease or N, increase, decrease or N, increase or N, increase or N, N, increase or N. Back to Table

There are 11 columns: characteristic, normal sinus, paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, first-degree AV block, second-degree AV block type 1, second-degree AV block type 2, and complete AV block type 3. Row entries are as follows. Row 1: Rate in beats per minute; 60 to 100; 150 to 250; 250 to 350 atrial while ventricular rate varies; atrial rate greater than 400, ventricular rate varies; 100 to 250 ventricular; difficult to discern; normal; atrial greater than ventricular, both usually normal; atrial greater than ventricular, both usually normal; atrial greater than ventricular, both usually normal. Row 2: Rhythm; Regular; Regular; Atrial is regular ventricular can be regular or irregular; Irregular; Regular ventricular; Rapid and chaotic; Regular; Atrial regular, ventricular pauses; Atrial regular, ventricular irregular with pauses; Regular. Row 3: P waves; Uniform, upright, one before each QRS; May be hard to see; Sawtooth P waves; No P waves identifiable; Usually not discernible; Not discernible; Prolonged, constant PR interval; Progressive widening, then dropped; Some P waves not followed by QRS; No relationship between P and QRS. Row 4: QRS; Narrow; Narrow; Narrow; Narrow; Wide; Not discernible; Narrow; Narrow, sometimes dropped; Can be wide; Narrow or wide. Row 5: Clinical severity; Normal; Mild to moderate; Usually mild to moderate; Mild to severe, depending on context; Severe to life threatening; Life threatening; Mild; Mild to moderate, depending on context; Severe to life threatening; Life threatening. Back to Table There are six columns: ventilatory modes and parameters, lung rest strategy or ultra-low tidal volume, lung-protective conventional ventilation strategy or ARDS network-like approach, high-frequency oscillatory ventilation HFOV, and emergency ventilation strategy or rapid detitration as allowed. Row entries are as follows. Row 1: PC, VC, PSV, NAVA; 20 to 25 centimeters of water; P subscript plateau less than or equal to 30 centimeters of water or P subscript ti less than or equal to 25 centimeters

of water; mPaw less than or equal to 24 centimeters of water; LRM, see text. Row 2: PEEP; 10 to 15 centimeters of water; PEEP 10 to 20 centimeters of water; N/A; PEEP 16 to 20 centimeters of water. Row 3: FIO2; less than or equal to 40 percent; less than or equal to 40 percent; less than or equal to 40 percent; 100 percent. Row 4: Delta P equals P subscript plateau minus PEEP; 10 to 15 centimeters of water; less than or equal to 18 centimeters of water; less than or equal to 90 centimeters of water; delta P less than or equal to 18 centimeters of water, P subscript plateau less than or equal to 30 centimeters of water, P subscript peak less than or equal to 35 centimeters of water. Row 5: V subscript T; less than or equal to 3 milliliters per kilogram per IBW; 4 to 6 milliliters per kilogram per IBW; less than or equal to 2 to 3 milliliters per kilogram per IBW; 4 to 6 milliliters per kilogram per IBW. Row 6: Respiratory rate; 6 to 10 breaths per minute; 10 to 35 breaths per minute; greater than 7 hertz; 15 to 35 breaths per minute. Row 7: V subscript E; lower 1 to 2 liters per minute; higher 8 to 14 liters per minute; NA; 10 to 16 liters per minute. Row 8: P subscript etCO2; lower; higher; higher; higher. Row 9: Time on ECMO; longer, lung derecruited; shorter, lung remains recruited; shorter, lung remains recruited; if abrupt discontinuation of ECMO. Back to Table There are six columns: ventilatory modes and parameters, lung rest strategy or ultra-low tidal volume, lung-protective conventional ventilation strategy or ARDS network-like approach, high-frequency oscillatory ventilation HFOV, and emergency ventilation strategy or rapid detitration as allowed. Row entries are as follows. Row 1: Drawbacks; “White-out” CXR, difficult to detect pneumonia or alveolar hemorrhage, difficult emergent lung reexpansion; Risk of volutrauma, air leaks with bronchopleural fistulas slower to heal; Deeper sedation and NMB may be required; Difficult recruitment of atelectatic lung if prior “ultralow” tidal volume used. Row 2: Comment; Favor if: Goal “off ventilator first,” air leaks with bronchopleural fistulas, or bridging to lung transplant, allows

early physical therapy and ambulation, “awake ECMO”; Favor if: Goal “off ECMO first,” bridge to recovery or decision, bleeding or thrombosis on ECMO, may be needed if low patient Sao2 on optimized VV-ECMO; Favor if: Goal “off ECMO first,” bridge to recovery or decision, not for bridge to lung transplant; Emergency ventilator settings depend on phase of disease, example, early severe ARDS versus improving, recovery phase, consider LRM, NMB, prone, HFOV. Back to Table There are six columns: disorder, age, location, pathology, findings, and treatment. Row entries are as follows. Row 1: Duchenne muscular dystrophy; 2 to 5 years; X-linked hereditary disorder; Lack of dystrophin in skeletal and smooth muscle of heart and brain muscle leads to cellular instability; Progressively worsening symmetrical skeletal muscle weakness, decline in respiratory status in second decade of life; Supportive, NIV, steroids, and secretion clearance. Row 2: Spinal muscular atrophy SMA, types 1 to 4; SMA type 1, less than 6 months, SMA type 2, 6 to 18 months; Anterior horn cell; Mutation of the survival motor neuron, SMN, gene, which produces a protein necessary for function of nerves; Dependent on type, severe respiratory weakness and progressive skeletal muscle weakness, type 1; Supportive SMA type 1 life expectancy, less than 2 years without NIV and nutritional support. Row 3: Myasthenia gravis; 1 year to adult; Neuromuscular junction; Antibodies block or destroy receptors at NMJ, which prevent muscles from contracting; Fluctuating periods of weakness, decreased muscle contraction, ocular and bulbar weakness; Acetylcholinesterase inhibitors, immunosuppression, and thymectomy. Row 4: Guillain-Barré; 1 year to adult; Neuromuscular junction; Autoimmune-mediated insult to the myelin sheath covering the peripheral nerve; Rapidly ascending paralysis, legs then arms, with areflexia, respiratory failure can occur; Supportive, may involve mechanical ventilation, plasmapheresis or IVIG. Row 5: Botulism; 1 to 6 months; Neuromuscular junction; Presynaptic binding of toxin

prevents release of AcH into NMJ; Descending paralysis with bulbar findings, weak cry, suck, ptosis, commonly progresses to respiratory failure; Supportive, may require mechanical ventilation, botulism immune globin. Back to Table There are five columns: weight and age, respiratory rate, inspiratory flow in liters per meter, V subscript E in liters, and C subscript dyn in milliliters of water. Row entries are as follows. Row 1: 1 kilogram, 35 to 55, 0.53 to 1.3, 0.175 to 0.44, 0.65 to 1.25. Row 2: 3 kilograms, 30 to 50, 1.4 to 3.6, 0.45 to 1.2, 2.4 to 3.6. Row 3: 5 kilograms, 30 to 45, 2.3 to 5.4, 0.75 to 1.6, 4 to 6. Row 4: 10 kilograms and 1 year, 30 to 40, 4.5 to 9.6, 1.25 to 2.8, 8 to 12. Row 5: 16 kilograms and 3 years, 25 to 35, 6.0 to 13.5, 2.0 to 4.5, 13 to 19. Row 6: 19 kilograms and 5 years, 20 to 30, 6.0 to 13.7, 2.0 to 4.6, 15 to 23. Row 7: 27 kilograms and 8 years, 15 to 25, 6.1 to 16.2, 2.0 to 5.4, 22 to 32. Row 8: 35 kilograms and 10 years, 15 to 25, 7.9 to 21.0, 2.6 to 7.0, 28 to 42. Row 9: 45 kilograms and 12 years, 15 to 22, 10.1 to 27.0, 3.4 to 7.9, 36 to 54. Row 10: 61 kilograms and 15 years, 12 to 18, 11.0 to 29.3, 3.7 to 8.8, 49 to 73. Row 11: 70 kilograms and 18 years, 12 to 16, 12.6 to 33.6, 4.2 to 9.0, 56 to 84. Back to Table There are four columns: newborn, infant, child, and large child or adolescent. Row entries are as follows. Ideal body weight in kilograms: less than 3, 3 to 10, 10 to 40, greater than or equal to 40. Tidal volume. Newborn: Healthy lungs, 6 to 7 milliliters per kilogram, diseased lungs, 3 to 5 milliliters per kilogram. Infant, child, and large child or adolescent: Healthy lungs: 6 to 7 milliliters per kilogram, restrictive lung disease, 5 to 7 milliliters per kilogram, and obstructive lung disease, 8 to 12 milliliters per kilogram. Peak inspiratory pressure in centimeters of water: 18 to 28 for all, adjust if in pressure-targeted mode to target tidal volume. Positive end-expiratory pressure in centimeters of water: 3 to 5, 5 to 8, 5 to 14,

and 5 to 16. Respiratory rate in breaths per minute: 20 to 40, 20 to 30, 16 to 26, 12 to 22. Inspiratory time in seconds: 0.3 to 0.4, 0.4 to 0.8, 0.8 to 1.0, 0.8 to 1.2. FIO2 in percentage: Targeted to achieve goal gas exchange, greater than or equal to 50, greater than or equal to 50, greater than or equal to 50. Back to Table There are eight columns: PEEP, Sao2, BP, CO, DO2, PCWP, C subscript ST, and C subscript a minus v O subscript 2. Row entries are as follows. Row 1: 12, 73, 104 over 60, 6.3, 649, 20, 27, 3.3. Row 2: 14, 80, 105 over 64, 6.3, 693, 18, 30, 3.6. Row 3: 16, 82, 100 over 58, 6.2, 700, 16, 36, 4.1. Row 4: 18, 92, 105 over 68, 6.0, 768, 16, 48, 5.6. Row 5: 20, 100, 95 over 55, 5.8, 806, 17, 37, 6.3. Row 6: 22, 100, 80 over 52, 5.3, 736, 20, 33, 6.0. Row 7: 24, 100, 65 over 40, 5.1, 714, 23, 23, 4.4. Back to Table There are four columns: A. Initial ABG, B. 1 week of illness, C. Respiratory failure, and D. Mechanical ventilation. Row entries are as follows. pH: 7.36, 7.39, 7.29, 7.62. Paco2: 55, 68, 86, 40. Pao2: 60, 50, 45, 60. HCO3 negative: 30, 40, 40, 40. Back to Table There are seven columns: time, FiO2, PEEP in centimeters of water, SpO2, VT in milliliters, P subscript plateau in centimeters of water, and CST in milliliters per centimeters of water. Row entries are as follows. Row 1: 1, 1.0, 5, 100%, 500, 30, 20. Row 2: 2, 1.0, 8, 100%, 500, 29, 24. Row 3: 3, 1.0, 10, 100%, 500, 28, 28. Row 4: 4, 1.0, 12, 100%, 500, 29, question mark. Row 5: 5, 1.0, 14, 100%, 500, 34, question mark. Back to Table