Mosby’s PDQ for Respiratory Care - Revised Reprint [2nd Edition] 0323100724, 9780323100724, 9780323170109, 9780323113793

Table of contents :
Front Cover......Page 1
Mosby’s PDQ for Respiratory Care......Page 2
Copyright Page......Page 3
Table of Contents......Page 4
ABBREVIATIONS......Page 5
CHAPTER 1. PULMONARY ASSESSMENT......Page 7
ANATOMY......Page 8
PULMONARY ASSESSMENT......Page 11
CHAPTER 2. PULMONARY DISEASES......Page 15
DISEASES AND DISORDERS......Page 17
CHAPTER 3. MICROBES, WMD, EQPT DISINFECTION......Page 57
MICROBIAL ORGANISMS......Page 58
BIOTERRORISM AGENTS......Page 62
EQUIPMENT DISINFECTION......Page 63
CHAPTER 4. MEDICATIONS......Page 65
GENERAL INFORMATION......Page 67
BRONCHODILATORS......Page 69
XANTHINE DRUGS......Page 78
LEUKOTRIENE INHIBITORS......Page 80
CROMOLYN AND NEDOCROMIL......Page 82
CORTICOSTEROIDS......Page 84
NEUROMUSCULAR BLOCKERS......Page 92
ADJUNCT MEDICATIONS......Page 93
CHAPTER 5. THERAPEUTIC MODALITIES......Page 97
MEDICAL GASES......Page 98
MEDICATION DELIVERY DEVICES......Page 103
THERAPIES......Page 105
CPT/PD POSITIONS......Page 107
ARTIFICIAL AIRWAYS AND SUCTIONING......Page 109
SUCTIONING......Page 110
INTUBATION......Page 111
ESOPHAGEAL OBTURATOR AIRWAY (EOA)......Page 112
PASSY-MUIR SPEAKING VALVE (PMV)......Page 113
DIAGNOSTIC TOOLS......Page 114
BREATHING RETRAINING EXERCISES......Page 127
CHAPTER 6. ABGs, LABS, AND HEMODYNAMICS......Page 129
NORMAL LABORATORY VALUES IN INTERNATIONAL SYSTEM OF UNITS......Page 130
BLOOD GAS SAMPLING ERRORS......Page 131
ARTERIAL BLOOD GASES ADULT NORMAL VALUES......Page 132
RELATIONSHIP OF PH, PACO2, AND HCO3 IN ACUTE CONDITIONS......Page 133
COPD PATIENT NORMAL VALUES......Page 134
OXYHEMOGLOBIN DISSOCIATION CURVE......Page 135
BLOOD GAS FORMULAS......Page 136
HEMODYNAMIC PARAMETERS......Page 138
MEDICAL CONDITIONS AND HEMODYNAMIC CHANGES......Page 140
URINE LABORATORY TESTING......Page 141
ADULT LABORATORY VALUES......Page 142
CEREBROSPINAL FLUID (CSF) LABORATORY TESTING......Page 146
CHAPTER 7. PFTs AND X-RAYS......Page 147
SPIROMETRY......Page 148
PFT......Page 149
CHEST X-RAYS......Page 159
CHAPTER 8. EKGs......Page 169
EVALUATION OF EKG RHYTHMS......Page 170
INTERPRETATION OF RHYTHMS......Page 173
MYOCARDIAL INFARCTION......Page 182
BUNDLE BRANCH BLOCKS......Page 184
ELECTROLYTE OR DRUG EFFECTS......Page 185
CHAPTER 9. CHEST TUBES AND BRONCHOSCOPY......Page 187
STANDARD THREE-BOTTLE SYSTEM24......Page 188
CHEST TUBES......Page 189
BRONCHOSCOPY......Page 191
CHAPTER 10. VENTILATORS, CPAP, AND BIPAP......Page 195
MECHANICAL VENTILATION......Page 197
MODES OF VENTILATION......Page 202
OTHER VENTILATOR CONTROLS......Page 211
CPAP AND BIPAP THERAPY......Page 216
COMPLICATIONS OF VENTILATION......Page 218
TROUBLESHOOTING......Page 219
CHAPTER 11. NEONATAL AND PEDIATRIC RESPIRATORY CARE......Page 223
CARDIOPULMONARY EVENTS AT BIRTH......Page 225
ASSESSMENT OF THE NEONATAL PATIENT......Page 228
NEONATAL CARDIAC AND PULMONARY DISORDERS......Page 234
CHAPTER 12. BLS AND ACLS......Page 245
SYNCHRONIZED CARDIOVERSION......Page 246
BASIC LIFE SUPPORT (BLS)......Page 247
ADVANCED CARDIAC LIFE SUPPORT (ACLS)......Page 250
TREATABLE CAUSES IN PULSELESS ARREST......Page 254
POST-CARDIAC ARREST CARE......Page 255
ACUTE CORONARY SYNDROMES......Page 256
BRADYCARDIA (ADULT WITH A PULSE)......Page 257
UNSTABLE ADULT TACHYCARDIA WITH A PULSE......Page 258
WIDE-COMPLEX STABLE ADULT TACHYCARDIA......Page 259
NARROW-COMPLEX STABLE ADULT TACHYCARDIA......Page 260
SHOCK......Page 261
PEDIATRIC ADVANCED LIFE SUPPORT (PALS)......Page 262
NEONATAL RESUSCITATION GUIDELINES......Page 266
NEONATAL FLOW ALGORITHM......Page 267
CHAPTER 13. FORMULAS AND FACTS......Page 269
CONVERSIONS......Page 271
TEMPERATURE......Page 272
FACTS......Page 273
BODY MASS INDEX (BMI)......Page 274
BASAL METABOLIC RATE (BMR) AND RESTING ENERGY EXPENDITURE (REE)......Page 275
OXYGEN INDEX (OI)......Page 276
HUMIDITY AND AEROSOL THERAPY......Page 277
ATMOSPHERIC PRESSURE......Page 279
GAS LAWS......Page 280
REFERENCES......Page 281
INDEX......Page 282

Citation preview

Mosby’s

G R V

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Helen Schaar Corning, RRT

3251 Riverport Lane Maryland Heights, Missouri 63043 Mosby’s PDQ for Respiratory Care

ISBN 978-0-323-10072-4

Copyright © 2013 by Mosby, Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215-239-3804 fax: (+1) 215-239-3805 email:[email protected]. You may also complete your request online via the Elsevier homepage (http://www.elsevier.com), by selecting “Customer Support” and then “Obtaining Permissions.”

G R V

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NOTICE Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioners, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages, to identify the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Author or Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book.

99

Managing Editor: Billie Sharp Freelance Developmental Editor: Betsey Stream McCormac Publishing Services Manager: Julie Eddy Senior Project Manager: Richard Barber Design Direction: Julia Dummitt, Jamey Almond Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

TABLE OF CONTENTS ABBREVIATIONS

1

PULMONARY ASSESSMENT

3

PULMONARY DISEASES

11

MICROBES, WMD, EQPT DISINFECTION

53

MEDICATIONS

61

THERAPEUTIC MODALITIES

93

ABGs, LABS, AND HEMODYNAMICS

125

PFTs AND X-RAYS

143

EKGs

165

CHEST TUBES AND BRONCHOSCOPY

183

VENTILATORS, CPAP, AND BIPAP

191

NEONATAL AND PEDIATRIC RESPIRATORY CARE 219 BLS AND ACLS

241

FORMULAS AND FACTS

265

REFERENCES

277

INDEX

278

Abbreviations

ABBREVIATIONS

Δ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . change

L . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . decreased K . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . increased BID. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . two times daily BSA . . . . . . . . . . . . . . . . . . . . . . . . . . . . body surface area cap. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . capsule CHF . . . . . . . . . . . . . . . . . . . . . . . congestive heart failure cm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . centimeters CNS . . . . . . . . . . . . . . . . . . . . . . . . central nervous system cont . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .continuous dL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . deciliter DPI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . dry powder inhaler exp. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . expiratory F . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . female f . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . frequency or rate f/b . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . followed by FiO2 . . . . . . . . . . . . . . . . . . . . fraction of inspired oxygen g . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . gram G⫹ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . gram positive C⫺ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . gram negative GI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . gastrointestinal hr . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .hour IM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . intramuscular in . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .inches insp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . inspiratory IV . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . intravenous kg . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . kilogram L . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . liter L/m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . liters/minute L/sec . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . liters/second lb . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . pound M . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . male m2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . meters squared maint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . maintenance max . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . maximum mcg . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . microgram MDI . . . . . . . . . . . . . . . . . . . . . . . . . . metered dose inhaler 1

Abbreviations

med . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . medication mEq . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . milliequivalent mfg . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . manufacturer mg . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . milligram min . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . minute mL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . milliliter mm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . millimeter mm Hg . . . . . . . . . . . . . . . . millimeters of mercury or Torr mol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . mole neb . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . nebulizer NS . . . . . . . . . . . . . . . . . . . . . . normal saline 2.5 to 3.0 mL NSAID . . . . . . . . . . nonsteroidal antiinflammatory drug oz . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ounces PB . . . . . . . . . . . . . . . . . . . . . . . . . . . . pressure barometric PO . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . by mouth PRN . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . as needed psi . . . . . . . . . . . . . . . . . . . . . . . . . pounds per square inch psr. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . pressure pt . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . patient q . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . every QlD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . four times daily RBC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . red blood cell resp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . respiratory sol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . solution spont . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . spontaneous SpO2 . . . . . . . . . . . . . . pulse oximeter oxygen saturation SQ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . subcutaneous tab . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . tablet TID . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . three times daily tx . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . treatment μ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . micro UTI . . . . . . . . . . . . . . . . . . . . . . . . . . urinary tract infection vent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ventilator vol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .volume w/a . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . while awake w/o . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . without WBC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . white blood cell WOB . . . . . . . . . . . . . . . . . . . . . . . . . . . . work of breathing

2

PULMONARY ASSESSMENT See references 15, 16, and 24

Pulmonary Assessment

Anatomy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Lungs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Vocal Cords . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 Laryngeal Cartilage and Trachea . . . . . . . . . . . . . 5 Respiratory Anatomy . . . . . . . . . . . . . . . . . . . . . . . 6 Pulmonary Assessment . . . . . . . . . . . . . . . . . . . . . . 7 Patient Assessment . . . . . . . . . . . . . . . . . . . . . . . . 7 Physical Assessments . . . . . . . . . . . . . . . . . . . . . . 8 Vital Signs: HR, BP, RR, Temp . . . . . . . . . . . . . . . . 8 Glasgow Coma Scale . . . . . . . . . . . . . . . . . . . . . . . 8 Auscultation and Other Assessments . . . . . . . . . 9 Patterns of Respiration . . . . . . . . . . . . . . . . . . . . . 10

3

Pulmonary Assessment

4

LUNGS21 Right Lung

Left Lung

Apical segment Apical-posterior segment Superior lobe

Middle lobe

Posterior segment

Anterior segment

Anterior segment

Superior lingular segment

Medial basal segment

Inferior lingular segment

Superior lobe

Lateral segment Superior basal segment

Inferior lobe

Superior segment Posterior basal segment Anterior basal segment

Lateral basal segment Horizontal fissure Oblique fissure

Oblique fissure

Anterior medial segment

Inferior lobe

VOCAL CORDS24 Vallecula

LARYNGEAL CARTILAGE AND TRACHEA24

Epiglottis

Epiglottis Hyoid bone

True vocal cords

Cuneiform cartilage

Corniculate cartilage Arytenoid cartilage Thyroid cartilage Cricothyroid ligament Cricoid cartilage

Trachea False vocal cords

Glottis

Corniculate cartilage

ANTERIOR VIEW

POSTERIOR VIEW

5

RESPIRATORY ANATOMY21 Opening of auditory (eustachian) tube

Pharyngeal tonsil (adenoids) Nasopharynx

Soft palate

Uvula

Palatine tonsil

Epiglottis

Oropharynx Hyoid bone Lingual tonsil

Vocal cords

Trachea Laryngopharynx Esophagus

6

PULMONARY ASSESSMENT PATIENT ASSESSMENT CHART REVIEW

INFORMATION

Dx, Sx, Medical Hx Meds

Chest x-rays Review entire patient chart

Past and present C/0, CC Medications (affecting respiratory status) Significant information Reduce the chances of medical administration error Respiratory, narcotic, renal, antibiotics, etc. Relevant pulmonary data All relevant data with emphasis on pulmonary

BEDSIDE HISTORY/INTERVIEW

INFORMATION

Progress notes Order changes MAR

First impression

Respiratory, movement, talking, what’s on bedside table Level of consciousness Confused, delirious, lethargic, (sensorium) obtunded, stuporous, comatose C/O, CC, severity Patient input Amplifying factors Exercise, allergies, fatigue, sleep, sickness, etc. Similar/previous illness Previous admissions Medications Things that help/hinder condition Environmental factors/ Dust: chemicals, smoke, plants, occupations etc. Changes in intake/output Perfusion to kidneys, CHF, etc. Oxygen Home use and need Cough Type, frequency, productivity Sx, Signs and symptoms; C/O, complaining of; CC, chief complaint; MAR, medication administration record.

7

PHYSICAL ASSESSMENTS Appearance Physical inspection

Color, warm, facial expression, accessory muscles Edema, positioning, clubbing or yellow stains, cyanosis, extremity temperatures, mucous membranes, tremors, fingernails, etc.

VITAL SIGNS: HR, BP, RR, TEMP VITAL SIGN

NORMAL VALUE

Heart rate (HR) Blood pressure (BP)

60-100 bpm

IMPORTANCE OF VALUES Bradycardia 60 Tachycardia 100 Increased  hypertension Decreased  hypotension Bradypnea 8/min Tachypnea 20/min

120/80 Systolic 90-130 Diastolic 60-90

Respiratory 8-20/minute rate (RR) (see Resp Pattern on p. 10) Temperature* Axillary 97.6º F Oral 98.6º F Tympanic 99.6º F Rectal 99.6º F

36.4º C Hypothermia  37.0º C low temp 37.6º C Hyperthermia  37.6º C high temp

*Temperature  or 1º F is considered normal. See also Hemodynamics and ABG chapters.

GLASGOW COMA SCALE

S 6 C 5 4 O 3 R 2 E 1

EYES (OPENING)

VERBAL RESPONSE

MOTOR RESPONSE

Spontaneous To speech To pain None

Oriented Confused Inappropriate Incomprehensible None

Normal Localizes pain Withdraws from pain Flexion to pain Extension to pain None

Total score 8, intubate; minimum score is 3.

8

AUSCULTATION AND OTHER ASSESSMENTS AUSCULTATION/ ASSESSMENTS Breath sounds Bronchophony Crackles

Diminished breath sounds

Egophony Pleural friction rub

Rhonchi

Tracheal sounds Vocal fremitus Wheeze Whispering pectoriloquy Accessory muscles

Percussion of chest

INFORMATION Clear over all lobes is normal. Increased tissue density, consolidation. Fine crackles (also called rales) indicate fluid in the lungs, pulmonary edema/CHF. Coarse crackles are associated with secretions. Poor air movement, fluid in lung tissue, hemothorax, pneumothorax, COPD, or other disease/disorder. e-e-e sounds like a-a-a. Creaking sound or audible crackles at pleural area that do not change with cough. Indicates secretions; sounds like very audible coarse crackles. Upper airway edema, stridor, restriction, or obstruction. Voice vibrations radiate into lungs. Bronchospasm, narrow airways, and secretions. Whisper 1-2-3 with consolidation sounds high pitched. Use of accessory muscle, including neck muscles, chest and abdominal muscles, indicates dyspnea; possibly asthma or COPD exacerbation. Low pitched and dull sounding is normal.

COPD, Chronic obstructive pulmonary disease.

9

PATTERNS OF RESPIRATION11 Normal

Regular and comfortable at a rate of 12-20 per minute

Bradypnea

Slower than 12 breaths per minute

Tachypnea

Faster than 20 breaths per minute

Hyperventilation (hyperpnea)

Faster than 20 breaths per minute, deep breathing

Sighing

Frequently interspersed deeper breath

Air trapping

Increasing difficulty in getting breath out

Cheyne-Stokes

Varying periods of increasing depth interspersed with apnea

Kussmaul

Rapid, deep, labored

Biot

Irregularly interspersed periods of apnea in a disorganized sequence of breaths

Ataxic

Significant disorganization with irregular and varying depths of respiration

10

PULMONARY DISEASES

11

Pulmonary Diseases

See references 3, 6, 23, 24, and 25 DISEASES AND DISORDERS . . . . . . . . . . . . . . . . . . . 13 Acquired Immune Deficiency Syndrome (AIDS) . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Acute Respiratory Distress Syndrome (ARDS) . . . . . . . . . . . . . . . . . . . . . . . . . 14 Adenoma (see Bronchogenic Carcinoma) Alpha1 Antitrypsin Deficiency (see Emphysema) Alveolar Proteinosis . . . . . . . . . . . . . . . . . . . . . . . . . 15 Amyotrophic Lateral Sclerosis (ALS), or Lou Gehrig’s Disease . . . . . . . . . . . . . . . . . . . . 16 Aspergillosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Asthma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Atelectasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Blastomycosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Bronchiectasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Bronchiolitis Obliterans with Organizing Pneumonia (BOOP) (see Pneumonia) Bronchitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Bronchogenic Carcinoma (Lung Cancer). . . . . . . . 26 Cancer/Carcinoma (see Bronchogenic Carcinoma) Chronic Obstructive Pulmonary Disease (COPD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Clubbing, Digital Clubbing, or Hypertropic Pulmonary Osteoroarthropathy (HPO). . . . . . . . 28 Coccidioidosis (San Joaquin Fever, Valley Fever) . . 29 Cor Pulmonale (Right Heart Failure) . . . . . . . . . . . 29 Cryptococcosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Cystic Fibrosis (Mucoviscidosis, Pancreatic Enzyme Deficiency) . . . . . . . . . . . . . . . . . . . . . . . . 30 Drowning, Near-Drowning . . . . . . . . . . . . . . . . . . . 31 Emphysema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Empyema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Fibrosis, Pulmonary . . . . . . . . . . . . . . . . . . . . . . . . . 33 Flail Chest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Guillain-Barré Syndrome (Inflammatory Demyelinating Polyneuropathy) . . . . . . . . . . . . . 35 Hemothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Histoplasmosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Influenza . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 Interstitial Lung Disease . . . . . . . . . . . . . . . . . . . . . 37 Ketoacidosis (Diabetic Ketoacidosis) . . . . . . . . . . 37

Kyphoscoliosis (Including Kyphosis and Scoliosis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 Legionnaire’s Disease . . . . . . . . . . . . . . . . . . . . . . . 38 Lou Gehrig’s Disease (see Amyotrophic Lateral Sclerosis [ALS])

Lung Cancer/Adenoma/Neoplasm (see Bronchogenic Carcinoma)

Myasthenia Gravis . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Neuromuscular Disease (see Amyotrophic Lateral Sclerosis [ALS], Guillain-Barré Syndrome, Myasthenia Gravis) Obstructive Pulmonary Diseases (see Chronic Obstructive Pulmonary Disease)

Pulmonary Diseases

Oxygen Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Pectus Carinatum (Pigeon Breast) . . . . . . . . . . . . . 40 Pectus Excavatum (Funnel Chest) . . . . . . . . . . . . . 40 Pickwickian Syndrome (Obesity Hypoventilation) . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Pleural Effusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Pleuritis (Pleurisy) . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Pneumoconiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Pneumonia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Pneumonitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Psittacosis (Chlamydia psittaci Infection, Parrot Fever, Ornithosis) . . . . . . . . . . . . . . . . . . . . 44 Pulmonary Abscess . . . . . . . . . . . . . . . . . . . . . . . . . 44 Pulmonary Edema . . . . . . . . . . . . . . . . . . . . . . . . . . 44 Pulmonary Embolism (PE), Thromboembolism . . . 45 Pulmonary Hypertension. . . . . . . . . . . . . . . . . . . . . 46 Respiratory Failure . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Restrictive Disease (see specific listings) Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Silicosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Sleep Apnea, Obstructive Sleep Apnea (OSA), Central Sleep Apnea . . . . . . . . . . . . . . . . . 48 Smoke Inhalation . . . . . . . . . . . . . . . . . . . . . . . . . . . 50 Thrush. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50 Tuberculosis (TB, Mycobacterium tuberculosis) . . . 50

SEE ALSO Neonatal and Pediatric Respiratory Care

12

PULMONARY DISEASES LEGEND D Definition E Etiology S Signs, Symptoms, Diagnostic Tests Tx Treatment

LDISEASES AND DISORDERSL ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS) D Infection with human immunodeficiency virus (HIV), along with an AIDS-defining illness. Profound immunosuppression and opportunistic infections, including Pneumocystis jirovecii (previously carinii) pneumonia (PCP), tuberculosis, Kaposi’s sarcoma, non-Hodgkin lymphoma B-cell, coccidiomycosis, histoplasmosis, and others. E HIV retrovirus causes AIDS. HIV infects T-helper (CD4) lymphocytes and other body cells, resulting in profound immunosuppression. Spread by contact with blood and body fluids, as in sexual contact, sharing needles, brood transfusions, occupational exposure, and mother to baby. Detectable antibodies develop within 6 months. Antibody tests: ELISA and Western Blot. Normal CD4 cell count is 1000 cells/cm3. Decreased immunity indicated by decreased CD4 cell count; when CD4 below 200 cells/cm3 opportunistic infections develop. Viral load increases; anything above zero indicates replication of HIV in the blood. S Severe weakness, fever, swollen glands, persistent diarrhea or bloody stools, 13

unexplained bleeding, prolonged loss of appetite, weight loss. Leukopenia, frequent opportunistic infections. Symptoms can take years to develop. AIDS develops within 10 years for most, sometimes takes longer. Tx Prophylaxis and prompt treatment of primary and secondary infections and neoplasms. Pulmonary hygiene, bronchodilators, oxygen, and mechanical ventilation if indicated. Antibiotics, antiretroviral therapy, nucleoside analog reverse transcriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors. Drugs include: zidovudine (AZT), pentamidine, delavirdine, nevirapine, efavirenz, ritonavir, saquinivir, indinavir, and nelfinavir. Cancers are treated with chemotherapy, radiation, alpha interferon, surgical resection, lobectomy, or pneumonectomy. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) D Restrictive pulmonary disease with nonspecific lung response to stresses or injuries of pulmonary or nonpulmonary nature. Also known as noncardiogenic pulmonary edema, shock lung, wet lung, white lung, and ventilator lung. E Damage to A-C membrane resulting in: inadequate surfactant activity, atelectasis, shunting, decreased compliance, decreased FRC, severe hypoxemia, pulmonary edema, pulmonary fibrosis, and respiratory failure. Associated with sepsis, viremia, thoracic trauma, hemorrhagic shock, pancreatitis, air or fat emboli, aspiration pneumonia, 14

near-drowning, acute lung injury (ALI), oxygen toxicity, and prolonged mechanical ventilation. S Respiratory distress, dyspnea, tachypnea, tachycardia, cyanosis, hypoxemia. Breath sounds: rales, wheezes. PFT: restrictive disease, decreased FRC. X-ray: diffuse pulmonary infiltrates, interstitial pattern, ground-glass or honeycomb appearance. Tx Treat underlying causes and complications. Mechanical ventilation as required to treat hypercarbia and acidosis; utilize lowest acceptable pressures to minimize adverse lung affects. PEEP/CPAP. Oxygen at lowest acceptable level to avoid O2 toxicity while maintaining adequate PaO2. Steroids, antibiotics, diuretics, ECMO, surfactant therapy (experimental), as indicated. ADENOMA: See Bronchogenic Carcinoma ALPHA1 ANTITRYPSIN DEFICIENCY: See Emphysema ALVEOLAR PROTEINOSIS D Progressive and chronic deposition of lipoprotein into alveoli. E Idiopathic. S Ranges from asymptomatic or mild illness to fatal. Dyspnea, cough, digital clubbing, and hypoxemia. X-ray: possible diffuse bilateral infiltrates. Tx Bronchial hygiene with CPT or vibratory PEP therapy, and effective cough technique. Bronchoscopy with bronchoalveolar lavage. Treat symptoms and complications. 15

AMYOTROPHIC LATERAL SCLEROSIS (ALS), OR LOU GEHRIG’S DISEASE D Degenerative neuromuscular disease causing progressive atrophy of the hands, forearms, and legs. Eventually leads to withering of muscles throughout the body, including the muscles of ventilation. Poor prognosis, with 80% of patients dying within 5 years. Pulmonary complications a frequent cause of death. E Progressive degeneration of the brain and spinal cord motor neurons. Familial cases 8% to 10%, remainder of cases sporadic. Occurrence of disease increases with age. S Muscle atrophy, muscle weakness, decreased muscle strength, hypoventilation, ineffective cough, atelectasis, pneumonia, hypoxemia, hypercapnia, and respiratory failure. PFT: restrictive disease with decreased FVC, decreased Plmax, decreased PEmax. Other tests: EMG, spinal tap, neurologic examination, and laboratory tests. Tx Prevent respiratory complications and provide ventilatory support via BiPAP or full support as required. Provide oxygen. Secretion clearance, cough techniques, and assisted cough. ASPERGILLOSIS D Disease resulting from pulmonary infection with Aspergillus fumigatus, a fungal mold found in decaying vegetation, grain, and soil. Can be inhaled or ingested. Immunosuppressed patients at higher risk. E Same. S Depends on form of Aspergillus infection. Symptoms common to all forms are cough 16

and frequent pulmonary infections. Allergic aspergillosis is the most common form, with asthma-type symptoms, eosinophilia, abnormal bronchograms, and elevated serum IgE level. Second disease form is invasive granuloma of the lungs with necrotizing pneumonia-type symptoms and hemoptysis. Third disease form is infection by fungal ball, mycetoma, or aspergilloma, in lung cavities already infected by tuberculosis. Tx Depends on type and severity. Bronchial hygiene therapy and infection control. Antifungal medication. Lung resection if other therapies fail. ASTHMA D An obstructive pulmonary disease characterized by reversible airway obstruction, hyper-reactive airways, bronchospasm, mucosal edema, inflammation, narrowed airways, increased mucous secretions, and mucous plugs. Episodes occur intermittently and can be mild, moderate, or severe. Various stimuli cause the increased airway responsiveness. Status asthmaticus is severe, life-threatening airway obstruction due to acute asthma attack that is unresponsive to optimal treatment over time. E Familial; child of asthmatic parent 3 to 6 times more likely to develop asthma. Intrinsic (nonallergic asthma): emotional states of stress, distress, or anxiety. Environmental factors include cold, change in temperature, or change in humidity. Also, exercise, infection, and aspirin. Extrinsic (allergic asthma): increased sensitivity to allergens and irritants. Smoke, air pollution, pollen, certain foods, certain animals, dust 17

mites, infection, and changes in temperature or humidity. Antigen-antibody reaction occurs, involving interaction with immunogloblin E (IgE), resulting in degranulation of mast cells. Ruptured mast cells release chemical mediators such as histamine, kinins, serotonin, and slow-reacting substance of anaphylaxis (SRS-A). Mediators have potent inflammatory effects, causing mucosal edema, bronchospasm, increased mucous production, and mucous plugs. S Repeat episodes of cough, dyspnea, tachypnea, chest congestion, and chest tightness, often brought on by specific triggers or allergens. Also, restlessness, anxiety, orthopnea, use of accessory muscles, hypoxemia, and cyanosis. Breath sounds: wheezes, rhonchi. Hypocapnea usually present early in asthmatic episode. Eucapnea in middle stage of asthmatic episode can indicate impending respiratory failure. Profound increased work of breathing can eventually lead to fatigue, hypoventilation, hypercapnia, and respiratory failure. Labs: WBC increased if infection present. Eosinophil count increased in extrinsic asthma. PFT: obstructive disease and decreased flow rates. FVC and peak flow significantly decreased and may improve post bronchodilator treatment. Tx Prevention and prophylactic treatment. Avoid known allergens and triggers. Pulmonary education and rehabilitation covering the scope of the disease: prevention, therapeutics, and medications. Fast-acting beta2 bronchodilator as needed for symptoms; or for prevention before exercise 18

or before exposure to known allergen or trigger. Other medications include longacting beta2 agonist, ipratropium bromide, corticosteroids, cromolyn, nedocromil, theophylline, and leukotriene modifier. STEPWISE APPROACH FOR MANAGING ASTHMA IN ADULTS and YOUTHS 12 YEARS OF AGE (2007 Asthma Guidelines. NHLBI)

The National Institute of Health has established guidelines for the pharmacological management, control, and prevention of asthma. The National Heart, Lung, and Blood Institute (NHLBI) can be accessed online for the most current information at www.nhlbi.nih.gov. The following is the stepwise approach for management of asthma based on the severity of symptoms. Please refer to the Abbreviations Key and Notes that follow the chart. Intermittent Asthma Step 1. Mild intermittent asthma Symptoms occur less than once per week, nocturnal symptoms occur less than twice per month, asymptomatic between exacerbations. ◆ Fast relief: SABA PRN. Fast-acting beta2specific bronchodilator PRN for symptoms (i.e., albuterol). ◆ Long-term control: No daily medications needed. Persistent Asthma—Daily Medication Step 2. Mild persistent asthma Symptoms occur two or more times per week, nocturnal symptoms occur three or more times per month. ◆ Fast relief: SABA PRN. Fast-acting beta2specific bronchodilator PRN for symptoms (i.e., albuterol). 19

Long-term control: preferred—low-dose ICS; alterative—cromolyn, nedocromil, theophylline, or LTRA. Step 3. Moderate persistent asthma Symptoms occur daily, nocturnal symptoms occur two or more times per week. Consider consultation with an asthma specialist. ◆ Fast relief: SABA PRN. Fast-acting beta2specific bronchodilator PRN for symptoms (i.e., albuterol). ◆ Long-term control: preferred—low-dose ICS plus LABA or medium-dose ICS; alternative—low-dose ICS plus either theophylline, LTRA, or zileuton. Also, consider short course of OCS. Step 4. Severe persistent asthma Continuous symptoms, frequent nocturnal symptoms, severity of symptoms limit activities of daily living. Consult with asthma specialist if Step 4 care or higher is required. ◆ Fast relief: SABA PRN. Fast-acting beta2specific bronchodilator PRN for symptoms (i.e., albuterol). ◆ Long-term control: preferred—mediumdose ICS plus LABA; alternative—mediumdose ICS plus either theophylline, LTRA, or zileuton. Also, consider OCS. Step 5. Severe persistent asthma (nonsufficient response to Step 4) ◆ Fast relief: SABA PRN. Fast-acting beta2specific bronchodilator PRN for symptoms (i.e., albuterol). ◆ Long-term control: preferred—high-dose ICS plus LABA and consider omalizumab (Xolair) for patients who have allergies. Also, consider OCS. ◆

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Step 6. Severe persistent asthma (nonsufficient response to Step 5) ◆ Fast relief: SABA PRN. Fast-acting beta2specific bronchodilator PRN for symptoms (i.e., albuterol). ◆ Long-term control: preferred—high-dose ICS plus LABA plus oral corticosteroid and mandatory OCS. Also, consider omalizumab for patients who have allergies. ABBREVIATIONS KEY EIB—Exercise-induced bronchospasm ICS—Inhaled corticosteroid LABA—Long-acting inhaled beta2 agonists (include beta2-specific bronchodilators [e.g., Serevent, Foradil, and Brovanal] with a duration of effect of around 12 hours; however, LABA have a slower onset of action than SABA and are not used for acute bronchospasms. LABA are the 12-hour maintenance bronchodilators; SABA are the emergency bronchodilators.) LTRA—Leukotriene receptor antagonist (also known as leukotriene inhibitors; include Singulair, Accolate, and ZyfIo) OCS—Oral corticosteroid SABA—Inhaled short-acting beta2 agonists (include beta2-specific bronchodilators [e.g., albuterol, Xopenex, Tornalate, Maxair, terbutaline] with a quick onset of action; provide the fastest relief of bronchospasm). NOTES • The stepwise approach is meant to assist, not replace, clinical decision making. Individual patient needs must be met. 21

• Patient response to treatments should be reviewed every 1 to 6 months. First, check adherence, environmental control, and comorbid conditions. If patient is managing symptoms with sustained control for at least 3 months, a gradual stepwise reduction in treatment may be indicated. If patient is unable to manage symptoms (as evidenced by daily use of a fast-acting beta2 bronchodilator), a step up in treatment may be necessary. • At each step: Patient education, environmental control, management of comorbidities. • At steps 2-4: Consider subcutaneous immunotherapy for patient with allergic asthma. • If alternative treatment is used and response is inadequate, discontinue it and use preferred treatment before stepping up. • Zileuton is less desirable as adjunctive therapy due to limited studies and need to monitor liver function. Theophylline requires monitoring of serum concentration levels. • Immunotherapy for steps 2-4 is based on evidence for house dust, animal danders, and pollens; evidence is still lacking for molds, cockroaches. Evidence is strongest for immunotherapy with single allergens. • Clinicians who administer immunotherapy or omalizumab (Xolair, an antibody used in allergy-related asthma and the first asthma treatment that works by blocking IgE) should be prepared and equipped to identify and treat anaphylaxis. ATELECTASIS D Poor aeration, poor expansion, and/or collapse of portion(s) of the lung. E Multiple causes include: pneumothorax, pleural effusion, tumor, decreased surfactant activity, bronchial obstruction, 22

foreign body, chest trauma, lung diseases, severely diminished ventilation. S Dyspnea, tachypnea, chest pain, tachycardia. Breath sounds: diminished over affected area. Percussion: dullness over affected area. PFT: restrictive pattern. X-ray: reveals location and severity with radiopacity, platelike or patchy infiltrates, displaced fissures, possible mediastinal shift toward affected side, possible elevated diaphragm on affected side. Tx Treat underlying cause. Improve aeration. Bronchial hygiene. BLASTOMYCOSIS D Disease caused by Blastomyces dermatitidis fungus, resulting in granulomatous systemic infection of the skin, bones, lungs, and other organs. Can produce systemic infection or respiratory infection with lesions, lobar pneumonia, pleural effusions, a miliary process, and lymph node enlargement. E Blastomyces dermatitidis, a yeastlike fungal organism. Primarily limited to North America, found in soil. Infection acquired by inhalation. S Can be an asymptomatic, self-limiting illness. Others experience fever, chest cold, cough with hemoptysis or purulent sputum, dyspnea, chest pain, and headache. X-ray: possible lobar consolidation with cavitation. Tx Antifungal medication. Bronchial hygiene therapy. BRONCHIECTASIS D Obstructive pulmonary disease with abnormal and irreversible dilation of bronchi and/or bronchioles, destructive changes 23

in bronchial wall, and loss of resiliency. Resultant chronic inflammation, fibrosis, necrosis, and impaired mucous clearance. Three types of bronchiectasis are: saccuiar (cystic), cylindrical (fusiform), and varicose. Saccular is the most severe. E Bronchopulmonary infection in early childhood is most common cause. Also: Chemical irritants, tumors, atelectasis, bacterial infection, pneumonia, bronchial asthma, cystic fibrosis, carcinoma, and immune deficiency diseases. S Chronic loose productive cough with copious amount of mucopurulent sputum. Sputum separates into three layers. Top layer, frothy and watery; center layer, turbid and mucopurulent; bottom layer, opaque and purulent. Hemoptysis, frequent pulmonary infections, cyanosis, general weakness. Breath sounds: rhonchi, rales, wheezes. X-ray: can help reveal type of bronchiectasis: saccular, widespread atelectasis; cylindrical, hazy vascular markings. Hyperinflation of unaffected areas. Bronchogram can show location and severity, with bronchi clearly outlined (air bronchograms). ABG: possible hypoxemia, and hypercapnea in advanced disease. PFT: obstructive disease pattern. Tx Bronchial hygiene, aerosol therapy, mucolytics, CPT, PD, bronchoscopy. Infection control with antibiotics. Avoid smoke. Maintain good nutrition. If other methods fail, surgical resection for severe localized bronchiectasis. BRONCHIOLITIS OBLITERANS WITH ORGANIZING PNEUMONIA (BOOP) See Pneumonia. 24

BRONCHITIS D Inflammation of bronchial mucosa that can be acute or chronic. Chronic bronchitis (blue bloater) is classified as COPD. Definition for chronic bronchitis includes cough with mucous production most days, for 3 months or longer, for 2 successive years. E Heredity factors. Acute bronchitis associated with viral or bacterial infection or inhalation of chemicals, pollutants, or irritants. Chronic bronchitis associated with long-term exposure to inhaled smoke, other pollutants, occupational exposure to chemicals, chronic asthma, and frequent pulmonary infections. Greatly increased airway resistance, with air trapping. S Acute bronchitis—Cough, initially nonproductive, later productive. Breath sounds: rhonchi, wheezes. Can lead to bronchiolitis, pneumonia, and chronic bronchitis. Chronic bronchitis—Cough with copious amount of mucopurulent sputum, dyspnea, cyanosis. Increased use of accessory muscles, pursed-lip breathing, and digital clubbing possible. Cor pulmonale can develop. Breath sounds: rhonchi, wheezes. PFT: obstructive disease pattern. ABG: possible hypoxemia, hypercapnia, compensated respiratory acidosis, and acute or chronic respiratory failure. X-ray: hyperinflation and depressed diaphragm. Tx Avoid smoke and other pollutants. Expectorants, cough suppressants, humidification of inspired air, oxygen, bronchial hygiene, bronchodilators. Antiinflammatory medication, steroids. Antibiotics for infection. Additional therapy for chronic bronchitis includes low-concentration 25

oxygen (with consideration for hypoxic drive breathing). Diuretics and digitalis as indicated. Pulmonary rehabilitation. BRONCHOGENIC CARCINOMA (LUNG CANCER) D Bronchogenic carcinoma (lung cancer) is malignant tumor(s) resulting from damage to the genetic DNA of cells, and mutations in stem cell lines of the lungs. A tumor, neoplasm, or adenoma can be malignant (cancerous) or nonmalignant. Carcinoma is cancer derived from lining cells of organs. Most common form of bronchogenic carcinoma is adenocarcinoma, representing 30% to 35% of all lung cancers. Other types are squamous cell, large cell, and small cell carcinoma. E Can be idiopathic. Many cancers linked to carcinogens. Approximately 85% of bronchogenic carcinoma cases linked to smoking. Other causative substances include arsenic, asbestos, benzo (a) pyrene, certain man-made mineral fibers, ionizing radiation, mustard gas, radon, and vinyl chloride. S Depends on type of cancer and degree of obstruction. Can be asymptomatic, especially in early stages. Obstructive tumors can cause dyspnea, cough, hemoptysis, chest pain, and frequent pulmonary infections. Percussion: dullness over affected area. Breath sounds: diminished and/or wheezes, rhonchi, and rales. PFT: varies by type and severity. X-ray: possible opaque mass, nodule(s), infiltrates, atelectasis, and mediastinal shift. Tx Depends on type of cancer. Prevention, avoid smoking, avoid exposure to 26

carcinogens. Treat symptoms and complications, supportive care. Radiation therapy, chemotherapy, surgical resection, lobectomy, or pneumonectomy as indicated. CANCER/CARCINOMA See Bronchogenic Carcinoma. CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) D In the past, COPD was used to encompass most obstructive lung disorders. Currently, the American Thoracic Society classifies COPD as follows: emphysema and chronic bronchitis (including chronic asthmatic bronchitis). Obstructive pulmonary disease is the broader term and includes emphysema, bronchitis, asthma, bronchiectasis, cystic fibrosis, and bronchopulmonary dysplasia (BPD). Information is listed individually about these obstructive diseases. (Most other pulmonary diseases are classified as restrictive.) GOLD EXPERT PANEL COPD CLASSIFICATION STAGES The Gold expert panel classified COPD into four stages (0 to 3): • Stage 0: At risk for COPD. Patient may have chronic cough and sputum production: normal spirometry readings. • Stage I: Mild COPD. FEV1 80%, FEV1/FVC 70%. Patient may or may not have chronic cough and increased sputum production. • Stage II: Moderate COPD. Worsening airflow, beyond stage I. Stage II patient often symptomatic, has shortness of breath with exertion and seeks medical attention. Stage IIA patient—FEV1 of 50% to 80%; stage IIB 27

patient—FEV1 of 30% to 50%. With FEV1 50%, patient more prone to acute exacerbations of COPD. • Stage III: Severe COPD. FEV1 30%. Stage III includes patients with right heart failure or respiratory failure. Quality of life is severely affected. Stage III patients with acute exacerbations often require hospitalization: episodes frequently are life threatening. The diagnosis of COPD should be considered in any patient with a chronic cough, sputum production, and risk factors (e.g., tobacco use, alpha1-antitrypsin deficiency and/or occupational exposure to dust and chemicals). With clinical signs of COPD, spirometry is used to confirm the diagnosis. All spirometry readings are taken after bronchodilator treatment. Findings that establish the diagnosis of COPD: FEV1 80% of predicted value and FEV1/FVC 70%. These abnormal values indicate airflow limitation, constituting the obstructive component of COPD. Many patients have clinical symptoms of COPD (e.g., cough and sputum production) before lung function decreases. These patients are at risk of progressing to more severe disease. Visit www.goldcopd.com for more information. Accessed online 10/4/08. CLUBBING, DIGITAL CLUBBING, OR HYPERTROPIC PULMONARY OSTEOROARTHROPATHY (HPO) D Chronic inflammation and bulbous enlargement of the fingers and toes. Most commonly associated with chronic hypoxemia, chronic bronchitis, emphysema, pulmonary infections, and congenital 28

heart defects. The angle of the skin-nail is greater than 160 degrees. COCCIDIOIDOSIS (SAN JOAQUIN FEVER, VALLEY FEVER) D A fungal infection that can cause respiratory symptoms. E Coccidioides immitis fungal yeast found in soil of Southwest region of North America. Acquired by inhalation, usually during dust storm. S Often asymptomatic, but can lead to serious pneumonia-type infection or meningitis. Chest pain, cough, hemoptysis, dyspnea. X-ray: infiltrates, bronchopneumonia, possible cavitation. Tx Antifungal medication. Pulmonary hygiene. Treat complications. COR PULMONALE (RIGHT HEART FAILURE) D Hypertrophy and thickening of the right heart ventricle. E Caused by pulmonary hypertension. Associated with lung disease. S Usually asymptomatic until cor pulmonale is quite advanced. Lightheadedness, fatigue, chest pain, dyspnea, venous distention, peripheral edema, hypoxemia, cyanosis. Characteristic heart sounds. EKG changes specific to right heart. Heart function can be evaluated with echocardiography, radionuclide studies, and cardiac catheterization (increased PAP and PVR). X-ray: enlarged right ventricle. Risk of pulmonary embolism is increased. Tx Treat underlying lung disease, resolve pulmonary hypertension, and relieve rightsided heart failure. Oxygen. Diuretics. Anticoagulant to prevent pulmonary embolism. 29

CRYPTOCOCCOSIS D Fungal systemic and respiratory tract infection. Occurs mainly in meninges (brain and spinal cord), lungs, and skin. E Cryptococcus neoformans is a fungal yeast that grows in pigeon droppings, soil, fruits, and vegetables. Found throughout the world. Infection acquired by inhalation. Increased risk with immunosuppression, AIDS, sarcoidosis, or Hodgkin’s disease. S Usually asymptomatic, or mild illness, but meningitis can develop. Fever, cough, hemoptysis, dyspnea, and headache. Diagnostic tests: analysis of blood and spinal fluid for antibodies to Cryptococcus. X-ray: infiltrates, possible lesion, and cavitation. Tx Varies by severity of illness. Treat symptoms and complications. Antifungal medication. CYSTIC FIBROSIS (MUCOVISCIDOSIS, PANCREATIC ENZYME DEFICIENCY) D Hereditary disease of the autonomic nervous system that causes exocrine glands to produce excess abnormal secretions, resulting in tissue and organ damage, especially in the lungs and digestive tract. E Cystic fibrosis (CF) caused by inheriting two defective mutations of the CF gene. Control of the production of a protein that regulates transport of chloride and sodium across cell membranes is disrupted, resulting in dehydration and increased viscosity of secretions. CF affects multiple organs and the exocrine glands. Adverse effects especially noted in the lungs, pancreas, liver, and sweat glands. S Cough with copious amounts of viscous mucopurulent mucus, chest congestion, 30

digital clubbing, dyspnea, hypoxemia, cyanosis. Increased sweat chloride. Enlarged lymph nodes, blocked bile ducts in the liver, gallbladder obstruction, pancreatic obstruction, intestinal obstruction (meconium ileus), digestive problems, nutritional deficiencies, infertility. Delayed growth in adolescents. Frequent pulmonary infections, with increased incidence of bronchitis, pneumonia, bronchiectasis, atelectasis. Breath sounds: rhonchi, wheezes. PFT: obstructive disease pattern. Tx Aggressive bronchial hygiene, secretion control, and clearance. CPT, vibratory PEP, or vibratory vest. Bronchodilators, dornase alfa, acetylcysteine, corticosteroids, oxygen. Infection control and antibiotics. Identify and treat nutritional deficiencies. Pancreatic enzyme replacements. Gene therapy (experimental). Liver and/or lung transplant when other therapies fail. Life expectancy is improving over the decades; half of CF patients now live 33 years or longer. Most CF patients eventually die of respiratory failure; a smaller number die of heart failure or liver disease. DROWNING, NEAR-DROWNING D Submersion in liquid with suffocation due to aspiration of liquid or laryngospasm. E Liquid submersion with rapid absorption of water into alveoli and bloodstream. Can be freshwater (hypotonic), or salt water (hypertonic). Dry-drowning is asphyxia due to laryngospasm with complete airway obstruction. S Cough expelling mucoid water, unconsciousness, convulsions, pulmonary 31

edema, hypervolemia, hypoxemia, acidosis, atelectasis, cardiac arrhythmias, cardiopulmonary arrest. Tx Secure patent airway. Prevent aspiration. Correct acidosis, and administer NaHCO3 and steroids. Restore fluid and electrolyte balance. High-concentration oxygen. Cardiopulmonary resuscitation and mechanical ventilation if indicated. EMPHYSEMA D Dilation, enlargement, and destruction of air spaces beyond terminal bronchioles. Emphysema (pink puffer) is classified as COPD. Three pathologic types include: centrilobar (centriacinar), panlobular (panacinar), and bullous (subcutaneous). Note: Subcutaneous emphysema is differentiated from other types by presence of large air-filled spaces in the soft tissues, usually in apical and anterior subpleural areas; air “bubbles” can be seen and crepitus can be felt. E Smoking, air pollutants, occupational exposure to inhaled irritants, aging, chronic bronchitis, and infection. Increased airway resistance, with air trapping. Panlobular emphysema associated with heredity factors and alpha, antitrypsin deficiency (A1AD), also called A1AT deficiency. S Cough, variable mucous production, dyspnea, cyanosis, orthopnea, increased use of accessory muscles, labored breathing, pursed-lip breathing, barrel chest, possible digital clubbing, weight loss, and engorged neck veins. Cor pulmonale can develop. ABG: hypoxemia, hypercapnia, compensated respiratory acidosis, and 32

chronic respiratory failure. Breath sounds: diminished, rhonchi, wheezes. PFT: obstructive disease and decreased DLCO (decreased diffusing capacity). X-ray: hyperinflation, increased A-P diameter, depressed diaphragm, bullae, and blebs. Tx Stop smoking. Avoid pollutants. Low-concentration oxygen (with consideration for hypoxic drive breathing), bronchial hygiene, expectorants, bronchodilators, and steroids. Antibiotics for infection. Diuretics and digitalis as indicated. Maintain good nutrition. Pulmonary rehabilitation. When other treatments fail, surgical resection, lung volume reduction, or lung transplantation is considered. For A1AD, treatment involves alpha1 proteinase inhibitor augmentation. EMPYEMA D Presence of purulent fluid in the pleural space. Also see Pleural Effusion. E Infection and complications of other diseases, including: pneumonia, pulmonary abscess, tuberculosis, or bronchiectasis. S Varies by severity of effusion. Dyspnea, tachypnea, chest pain, cough, hemoptysis, hypoxemia. Breath sounds: diminished, or crackles over affected area. X-ray: radiopacity in area of fluid accumulation, pleural thickening. Tx Chest tube drainage. Oxygen. Treat symptoms and complications. FIBROSIS, PULMONARY D Fibrosis is the replacement of the normal components of a structure with fiber-containing tissue. Process can occur in lungs, organs, and other structures. 33

E Pulmonary fibrosis can result because of age, disease, or complications of other medical conditions. Any dysfunction that promotes prolonged or repetitious lung injury can begin an inflammatory process and release of mediators, followed by fibrosis. Some causes include ARDS, aspiration, infection, bronchiectasis, pneumonitis, sarcoidosis, oxygen toxicity, necrosis, and inhalation of noxious gases. S Dyspnea, increased work of breathing, hypoxemia, and decreased compliance. Breath sounds: rales over affected area. Decreased compliance. X-ray: fibrotic changes, atelectasis, and mediastinal shift toward fibrotic area. Tx No known effective therapy. Supportive treatment of symptoms and complications. Oxygen. Avoid exposure to pulmonary irritants. FLAIL CHEST D Fracture of two or more ribs in more than one location, resulting in unstable area of the chest wall. Unstable portion of chest wall moves in opposite direction of the rest of thorax. E Chest trauma, impact injuries. S Paradoxical respirations with chest wall moving in on inspiration and out on expiration. Pain in affected area, dyspnea, increased work of breathing, hypoxemia. X-ray: rib fractures, atelectasis. Tx Stabilize chest wall. Pain management. Oxygen for hypoxemia. Mechanical ventilation for respiratory failure. 34

GUILLAIN-BARRÉ SYNDROME (INFLAMMATORY DEMYELINATING POLYNEUROPATHY) D Polyneuropathy is ascending (from feet upward) muscle paralysis due to simultaneous malfunction of many nerves throughout the body, including nerves of the autonomic nervous system. Can be acute or chronic. Can be a short-term illness or permanent. Note: Rare variant form is a descending paralysis. E Idiopathic. Presumed cause is an autoimmune reaction. The body’s immune system attacks the myelin sheath, which surrounds the axon of many nerves. Most often occurs after an infection, a flulike illness, surgery, or an immunization. (Symptoms usually begin within 1 to 8 weeks.) Occurs frequently in diabetics. Other possible causes include heredity, alcoholism, anemia, malnutrition, hypothyroidism, liver failure, kidney failure, excess amounts of vitamin B6, and certain cancers. Additionally, causes of acute polyneuropathy include infection; toxic substances; and certain drugs, like anticonvulsants, antibiotics, sedatives, sulfonamides, and chemotherapy drugs. S Ascending muscle weakness beginning at the feet/legs, and progressively upward. Can rapidly progress to become medical emergency, although some mild cases resolve spontaneously over several months. Pins-and-needles sensation, numbness, burning pain, and loss of sensation. Possible dysphagia and aspiration. Eventually can lead to muscle paralysis, including 35

paralysis of the diaphragm and muscles of ventilation, causing respiratory failure. Diagnostic procedures: electromyography, nerve conduction studies, and analysis of cerebrospinal fluid via lumbar puncture (high protein level). Also certain blood and urine lab tests (i.e., to rule out or detect diabetes, kidney failure, or thyroid disorder). Tx Monitor pulmonary mechanics, especially VC and NIF. Treat symptoms and complications. Ventilatory support as indicated. Nutritional support. Physical therapy. Plasmapheresis; infusion of immune globulin, corticosteroids, and immunosuppressants as indicated. Early treatment generally leads to quicker improvement, although residual weakness can last 3 years. HEMOTHORAX D Presence of blood in the intrapleural space. E Chest trauma, injury, puncture, or surgery. S Varies from asymptomatic to severely compromised ventilation. Dyspnea, tachycardia, tachypnea. Percussion is dull over affected area. Breath sounds decreased or absent over affected area. Tracheal shift away from affected side. Tx Chest tube drainage. Treat cause of bleeding. Treat complications. Ensure adequate ventilation. HISTOPLASMOSIS D Systemic fungal infection and respiratory tract infection. E Histoplasma capsulatum fungal yeast found in soil and bird excreta. Found mainly in Ohio and Mississippi river valleys. Acquired by inhalation. 36

S Varies from asymptomatic to fatal. Flulike symptoms, dyspnea, chest pain, and cough. Pneumonia can develop. X-ray: miliary calcification. Tx Treat symptoms and complications. Antifungal medication. INFLUENZA D Contagious viral respiratory tract infection commonly know as the flu. Types of influenza virus are A, B, and C. E Influenza viral organism infecting the respiratory tract. Usually acquired by airborne droplet inhalation. Can also be acquired by touching contaminated surface, then touching mouth or nose. S Flu symptoms, cough, chest congestion, headache, extreme tiredness. Can also cause sinusitis, laryngitis, bronchitis, and pneumonia. Complications can be fatal. Tx Prevention with flu vaccine. Treat symptoms and complications. Antibiotics if secondary bacterial infection develops. INTERSTITIAL LUNG DISEASE D A disease in the interspace area of lung tissue. Many causes, including complications of other diseases. Also see ARDS, Bronchiolitis, Fibrosis, Pulmonary Edema, and Pneumonia. KETOACIDOSIS (DIABETIC KETOACIDOSIS) D Metabolic acidosis associated with diabetes mellitus. E Diabetes mellitus. Insufficient insulin. Production of keto acids and acetone that decreases the blood pH. Stress. S Severe hyperventilation (Kussmaul breathing) with specific acetone odor. Metabolic acidosis. Vomiting, dehydration, headache. 37

Tx Correct metabolic acidosis. Regulate glucose and insulin level. IV fluids, electrolyte replacement, including HCO3, K, and Na. KYPHOSCOLIOSIS INCLUDING KYPHOSIS AND SCOLIOSIS D Kyphoscoliosis is a combination of kyphosis and scoliosis and is the most severe form. Kyphosis is abnormal anterior-posterior curvature of the spine. Scoliosis is abnormal lateral curvature of the spine. These spinal/ thoracic deformities can result in restricted ventilation and increased work of breathing. E Congenital defect, neuromuscular disorder, TB of the bone, or idiopathic. S Visible spinal/thoracic deformity, dyspnea on exertion, increased work of breathing, hypercarbia, hypoxemia, atelectasis. Tx Monitor for sufficient ventilation. Treat hypercarbia, increase ventilation with BiPAP, or full ventilatory support if indicated. Oxygen for hypoxemia. Pulmonary hygiene. Prevent pulmonary infections and atelectasis. LEGIONNAIRE’S DISEASE D Diffuse pneumonia caused by bacterial organism, Legionella pneumophila. E Ingestion of Legionella pneumophila. Found in contaminated water. S Malaise, muscle aches, headache, fever, chills, cough. Breath sounds: crackles, rhonchi, wheezes. Serologic testing can confirm presence of organism. X-ray: bilateral patchy infiltrates with possible consolidation. Disease can resolve spontaneously or cause respiratory failure. Tx Treat symptoms and complications. Antibiotics, pulmonary hygiene, oxygen. 38

LOU GEHRIG’S DISEASE See Amyotrophic Lateral Sclerosis (ALS). LUNG CANCER/ADENOMA/NEOPLASM See Bronchogenic Carcinoma MYASTHENIA GRAVIS D Neuromuscular disorder causing weakness and easy fatigability of the muscles, characterized by the descending trend. Most frequently involves the face, throat, and muscles of ventilation. E Idiopathic. Autoimmune disorder suspected. Reduced transmission of nerve impulses at the neuromuscular junction. Possible link to excess acetylcholinesterase, or lack of acetylcholine. S Weakness and fatigue with exertion. Early signs include facial muscle weakness, and ocular muscle weakness, especially droopy eyelids and double vision. Dysphagia, dysphasia. Can lead to respiratory failure. Diagnostic: Tensilon test; Tensilon is a short-acting anticholinesterase drug. If Tensilon improves the patient’s condition temporarily, it is a myasthenic crisis. If Tensilon worsens the patient’s condition, it is a cholinergic crisis. Tx Monitor VC and NIF for pulmonary deterioration, and treat as necessary. Ventilatory support if indicated. Rest, plasmaphereisis, immunosuppressants, corticosteroids, anticholinesterase therapy (pyridostigmine or neostigmine). Atropine for cholinergic crisis (due to excessive anticholinesterase therapy). Removal of thymus gland (thymectomy) if a thymoma is present. NEUROMUSCULAR DISEASE See Amyotrophic Lateral Sclerosis (ALS), Guillain-Barré Syndrome, Myasthenia Gravis 39

OBSTRUCTIVE PULMONARY DISEASES: See Chronic Obstructive Pulmonary Disease OXYGEN TOXICITY D Medical complications resulting from exposure to high-concentration oxygen over extended period of time. E Toxicity based on reactivity of free radicals. Usually associated with 40% FiO2 or higher. (In premature neonates, RLF associated with PaO2 over 100 torr.) S Substernal pain, cough, nausea/vomiting, and tachypnea. Can cause atelectasis, decreased lung compliance, pulmonary edema, pulmonary hemorrhage, fibrosis, refractory hypoxemia, hyaline membrane formation, and respiratory distress syndrome. In premature neonates, retrolental fibroplasia (RLF), also called retinopathy of prematurity (ROP). Tx Avoid use of excessive oxygen. Utilize CPAP/PEEP therapy to reduce oxygen while maintaining adequate PaO2. Also see Acute Respiratory Distress Syndrome symptoms and treatment. PECTUS CARINATUM (PIGEON BREAST) D Chest abnormality with excessive protrusion of the sternum and increased A-P diameter of the chest. Can be caused by other illnesses. Usually asymptomatic. PECTUS EXCAVATUM (FUNNEL CHEST) D Chest abnormality with excessive concavity of the sternum. Congenital defect. Usually asymptomatic. PICKWICKIAN SYNDROME (OBESITY HYPOVENTILATION) D Hypoventilation associated with obesity. Also see Sleep Apnea. 40

E Obesity, upper airway obstruction during sleep, or CNS abnormality. S Hypersomnolence, hypoventilation, hypoxemia, cyanosis, hypercapnia. Can lead to cor pulmonale. Tx Weight reduction. Treat complications and improve ventilation. CPAP or BiPAP. Oxygen. PLEURAL EFFUSION D Presence of fluid in the pleural space. E Multiple causes. Transudates due to plasma filtering from blood vessels as in heart failure or hypoproteinemia. Exudates are an inflammatory effusion due to pulmonary emboli, empyema, pneumonia, or other pulmonary infection. S Varies by severity of effusion. Dyspnea, tachypnea, chest pain, cough, hemoptysis, hypoxemia. Breath sounds: decreased, or crackles over affected area. X-ray: reveals location of effusion with radiopaque homogeneous mass, obliteration of costophrenic angle, mediastinal shift away from affected area, and possible atelectasis. Tx May need thoracentesis, chest tube drainage. Oxygen. Treat underlying cause, symptoms, and complications. PLEURITIS (PLEURISY) D A disease causing inflammation of the pleura. E Infection, irritation, and inflammation of the pleura caused by bacteria, virus, neoplasm, or autoimmune diseases like lupus. S Dyspnea and localized chest pain (pleuritic) that can begin suddenly. Pain worse on inspiration or with cough. Auscultation: pleural friction rub. X-ray: pleural thickening and pleural effusion and possible atelectasis. Can result in pneumonia. 41

Tx Treat underlying cause. Pulmonary hygiene, encourage deep breathing and cough while splinting. Nonsteroidal antiinflammatory drugs. Antibiotics for bacterial infection. PNEUMOCONIOSIS D Group of occupational diseases causing chronic inflammation of the lungs and interstitial fibrosis due to inhalation of dust or chemical fumes. E Prolonged exposure with inhalation of certain dusts or chemical fumes. Occupational diseases in this group have names referring to type of exposure: asbestosis, beryliosis, silicosis, and coal worker’s disease. Seen most often among miners. S Variable by exposure time period, and concentration of dust/fumes inhaled. Can be asymptomatic. Cough, hemoptysis, dyspnea, hypoxemia, chest pain. Can result in pneumonia. X-ray: infiltrates, haziness, possible nodules. Tx No known cure. Prevention as prescribed by OSHA: wear dust mask, limit exposure to causative agent. Treat symptoms and complications. Pulmonary hygiene. Bronchodilators. Oxygen. PNEUMONIA D Inflammation and infection of the lungs. E Infection caused by many types of microscopic organisms, bacteria, virus, or fungus. Infection can occur by inhalation or carried to lungs via bloodstream. Higher risk in people very young, very old, immunocompromised, postoperative, debilitated, bedridden, paralyzed, unconscious, malnourished, or receiving mechanical ventilation. Some of the many types of pneumonia are bacterial, viral, 42

aspiration, interstitial, bronchopneumonia, Pneumocystis jirovecii (previously known as carinii), TB, dust/chemical fume pneumoconiosis, and hypersensitivity allergic pneumonitis. One idiopathic pneumonia is cryptogenic organizing pneumonitis (also called idiopathic bronchiolitis obliterans with organizing pneumonia, or BOOP). S Variable by type and severity of pneumonia. Cough with sputum production, dyspnea, chest pain, chills, fever, hypoxemia. Breath sounds: rhonchi, crackles, wheezes. X-ray: reveals location and extent of infection; radiopacity, infiltrates, cavitation, and consolidation. Sputum culture can reveal type of pulmonary infection. Tx Variable by type and severity of pneumonia. Prevention via vaccine. Pulmonary hygiene, deep-breathing exercises, secretion clearance. Oxygen. Bronchodilators. Medication for fever reduction. Antiinflammatory agents, corticosteroids, steroids. Antibiotics for bacterial infection. For allergic pneumonitis and pneumoconiosis, avoid causative agents. PNEUMONITIS D Inflammation of the lungs. See Pneumonia. PNEUMOTHORAX D Presence of air in the intrapleural space or within other areas of the thorax. Can be spontaneous or traumatic. E Trauma, penetrating injury, lung puncture, rib fracture, rupture of a lung bleb, rupture of the chest wall. Tension pneumothorax is an acute medical emergency in which air leaks into pleural space but cannot escape. Also can be spontaneous pneumothorax (idiopathic, and not resulting from injury). 43

S Immediate onset of pain, dyspnea, tachypnea, and tachycardia. Hypoxemia. Increased work of breathing can result in respiratory failure. Breath sounds: diminished or absent over affected area. X-ray: hyperlucency and absent vascular markings at location of pneumothorax, atelectasis, and trachea deviated away from affected side. Small spontaneous pneumothorax can be asymptomatic. Tx Small spontaneous pneumothorax can resolve without treatment. Otherwise: thoracentesis, chest tube, oxygen. Mechanical ventilation for respiratory failure. PSITTACOSIS (CHLAMYDIA PSITTACI INFECTION, PARROT FEVER, ORNITHOSIS) D Intracellular parasite infection. E Inhalation of Chlamydia psittaci, a gramnegative bacterium found in bird droppings. Can be asymptomatic or cause systemic infection and severe pneumonia. Cough with possible sputum production, hemoptysis, fever, chills, dyspnea, hypoxemia, tachypnea. Can result in respiratory failure. Confirmed by blood culture positive for Chlamydia. Tx Avoid exposure to suspect cause. Treat symptoms and complications. Antiinfective drugs. Also see Pneumonia treatment. PULMONARY ABSCESS D Localized collection of purulent material in the lung that causes inflammation and necrosis. Usually caused by aspiration of infectious organism. Treat with antibiotics and pulmonary hygiene. PULMONARY EDEMA D Accumulation of excessive fluid in the alveoli and interstitium. 44

E Caused by cardiogenic and noncardiogenic disorders. Any dysfunction that increases capillary permeability or decreases colloidal osmotic pressure can cause fluid accumulation in the pulmonary system. Examples are hypervolemia, congestive heart failure, heart disease, myocardial infarction, sepsis, renal failure, hypertension, ARDS, near-drowning, pneumonia, embolism, oxygen toxicity, smoke inhalation, and severe hypoxemia. Dyspnea, hypoxemia, cyanosis, cough with pink, frothy secretions, hyperventilation, tachycardia, orthopnea, and anxiety. Breath sounds: rales. X-ray: prominent vascular markings, diffuse fluffy infiltrates with butterfly pattern, possible cardiomegaly. Tx Diuretic, digitalis, morphine, highconcentration oxygen. Mechanical ventilation with PEEP therapy as indicated. PULMONARY EMBOLISM (PE), THROMBOEMBOLISM D Sudden partial or complete blockage of pulmonary artery blood flow. E Most often, blockage is a blood clot (thrombus). Usually formed in leg or pelvic vein (deep vein thrombosis or DVT), but can form in arm vein or in right side of heart. Predisposing factors include blood stasis, prolonged bed rest, blood clotting disorder, surgery, obesity, paralysis, fracture in leg, hip or pelvis, stroke, myocardial infarction, and cancer. Other types of emboli are fat, amniotic fluid, cancerous tumor fragments, foreign materials, and air emboli from IV infusion. S Depends on degree of obstruction. Dyspnea, chest pain, anxiety, hyperventilation, tachycardia, arrhythmias, hypoxemia, cyanosis, 45

cough, hemoptysis, atelectasis. Breath sounds: rales, rhonchi, wheezes. Can cause pulmonary necrosis, cor pulmonale, heart failure, or respiratory failure. Diagnostic tests include ventilation/perfusion scan (V/Q scan), pulmonary angiography, CT scan, ultrasound, and D-dimer blood test. Tx Prevention of blood stasis. Compression elastic stockings, leg exercises, increase activity, anticoagulant drugs, thrombolytic therapy, and clot filter placed in vein. Oxygen. Mechanical ventilation if respiratory failure develops. PULMONARY HYPERTENSION D A condition in which blood pressure in the pulmonary arteries is abnormally high. Normal PAP systolic pressure is 1525 mm Hg. Normal PAP diastolic pressure is 5-15 mm Hg. E Two types include primary and secondary. Primary hypertension is idiopathic but likely due to spasms of muscle layer in pulmonary arteries. Secondary hypertension (much more common) can occur as a result of any disease or disorder that affects the lungs, heart, or pulmonary blood flow. (Pulmonary emboli, cardiogenic shock, hypervolemia, heart failure, COPD, ARDS, or pulmonary fibrosis.) Dyspnea on exertion, lightheadedness, chest pain, weakness, and peripheral edema. Can lead to pulmonary embolism or cor pulmonale. Definitive diagnosis via pulmonary artery catheter. Tx Treat underlying disease. Treat complications. Oxygen. Vasodilators, nitric oxide, diuretics. Anticoagulant to prevent pulmonary embolism. 46

RESPIRATORY FAILURE D Pulmonary system failure classified as: hypoxemic respiratory failure (inability to maintain adequate oxygen delivery to tissues) or hypercapnic respiratory failure (inability to maintain normalized removal of carbon dioxide from tissues). Can be acute medical emergency, or chronic condition. E Can be caused by medical complications and any disorder that affects the lungs. S Depends on degree of hypoxemia and degree of hypercapnia. Clinical analysis and ABG to determine severity. Symptoms range from dyspnea, anxiety, and respiratory distress to unconsciousness. Tx Oxygen for hypoxemia. BiPAP or full ventilatory support for hypercapnia. RESTRICTIVE DISEASE See specific listings. SARCOIDOSIS D Disease characterized by granulomas and inflammation in the lymph nodes, lungs, liver, eyes, skin, and/or other tissues. Usually occurs in age group 30 to 50 years old. E Idiopathic. Possible causes include a hypersensitive response to environmental factors, a genetic predisposition, or extreme immune response to infection. S Sometimes asymptomatic. Can cause malaise, fever, cough, dyspnea, hypoxemia, skin rash, skin lesions, enlarged liver, spleen, or lymph glands. Spontaneous pneumothorax, pulmonary fibrosis, pulmonary hypertension, cor pulmonale, or organ failure can develop. Tx Treat symptoms and complications. Pulmonary hygiene. Steroids helpful for some. Transplant if organ failure develops. 47

SILICOSIS D Respiratory disease caused by silica dust exposure, which leads to inflammation, interstitial fibrosis, and scarring of lung tissue. E Inhalation of silica dust. Silica is a naturally occurring crystal found in rock beds and sand. Pulmonary symptoms can be caused by acute exposure to large amount of silica or long-term exposure to small amounts. Occupational workers at higher risk are: miners, metal workers, stone cutters, sand-blasters, road and building construction workers, and glass workers. S Variable, depending on exposure time and amount. Dyspnea, chronic cough, pulmonary edema, progressive massive pulmonary fibrosis, and obliteration of normal lung structures. Tx No known cure. Prevention as prescribed by OSHA: wear dust mask, limit exposure to silica. Treat symptoms and complications. SLEEP APNEA, OBSTRUCTIVE SLEEP APNEA (OSA), CENTRAL SLEEP APNEA D Sleep apnea syndromes comprise a group of sleep disorders including obstructive sleep apnea (OSA), central sleep apnea, and mixed sleep apnea. These sleep disorders characterized by repeated episodes of cessation of breathing during sleep. Apneic episodes cause severe hypersomnia during the day, and other symptoms as listed below. Apneic periods range from a few seconds to 2 minutes or longer. Apnea considered significant if there are at least 5 episodes per hour of apnea lasting longer than 10 seconds. The condition 48

is severe if more than 15 apneic episodes occur per hour. Note: There are many other sleep disorders including: insomnia, narcolepsy (isolated sleep paralysis), nocturnal myoclonus (restless leg syndrome [RLS]), night terrors, sleepwalking, nocturnal asthma, nocturnal COPD disturbances, neuromuscular-related sleep disorders, and pickwickian syndrome. E OSA (most common type) is caused by obstruction of the upper airway during sleep. Causes of obstruction include obesity, anatomical anomaly resulting in narrowed airway, enlarged tonsils, or enlarged adenoids. Central sleep apnea (less common) is a neurologic disorder caused by dysfunction in the brainstem, brain tumor, Ondine’s curse, or idiopathic central hypoventilation. The brain fails to signal the body to breathe. Mixed sleep apnea (rare) is a combination of obstructive and central sleep disorders. S Symptoms that can occur in all three sleep disorders are: daytime hypersomnolence, fatigue, irritability, difficulty concentrating, slowed thought processes, confusion, headaches, and hallucinations. Also, arrhythmias and hypertension can occur with moderate to severe hypoxemia. Prolonged severe sleep apnea can result in myocardial infarction, heart failure, and respiratory failure. Diagnosis and type of sleep disorder is best confirmed using polysomnography in a sleep laboratory, including: EEG, EKG, electromyogram (EMG), pulse oximetry, chest and abdomen motion detectors, airflow measurement sensor, and electrooculogram (EOG). 49

In OSA, a distinctive sign is snoring, which does not usually occur in central sleep apnea. Sleep partner or parent can also give history of noticeable episodes of irregular breathing, apnea, and snoring. Tx OSA therapy includes weight reduction; various devices to reduce snoring and splint the airway open; avoiding alcohol, cigarettes, and sedatives at bedtime; CPAP; oxygen. Surgery to remove excess airway tissue, remove tonsils, or correct airway abnormalities. Central sleep apnea therapy includes antidepressant drugs and oxygen. CPAP is beneficial in some patients, not in others. Mixed sleep apnea includes a combination of therapies. SMOKE INHALATION D Inhalation of smoke into the lungs. Fire, smoke, fumes causing pulmonary damage. S Depends on amount of smoke inhalation. Burns over face and/or body, dyspnea, hypoxemia. Can lead to respiratory failure. Carboxyhemoglobin (HbCO) greater than 5% causes symptoms. Tx Hyperbaric oxygen (HBO) therapy if available or 100% oxygen. Mechanical ventilation for respiratory failure. Steroids. THRUSH D Fungal infection that can occur in the oral cavity. Caused by Candida albicans. Prevent by rinsing mouth after using inhaled steroids. TUBERCULOSIS (TB, MYCOBACTERIUM TUBERCULOSIS) D Serious bacterial infection usually affecting the pulmonary system but can also 50

affect other parts of the body (extrapulmonary TB). Pulmonary tuberculosis results in inflammatory reaction, tubercles, and necrotizing lesion with caseating granuloma in the center. Fibrotic tissue eventually replaces much of the granulomatous lesion. Miliary TB is disseminated form of TB in which the infection spreads through the lymphatics and bloodstream to other organs. Caused by infection with Mycobacterium tuberculosis (MTB). Inhalation of airborne droplet nuclei. MTB is a gram-positive bacteria known by acid-fast characteristic. S Can be asymptomatic to death in the latent phase. Signs/symptoms of TB include: positive PPD skin test; sputum sample with positive acid-fast stain; cough with mucopurulent sputum, hemoptysis, dull chest pain, dyspnea, tachycardia, fatigue, weight loss, night sweats, fever, and enlarged lymph nodes. High-risk groups include: impoverished, debilitated, diabetic, immunocompromised, and malnourished. X-ray: infiltrates, consolidation, and cavitation; often in apical segment. Tx Treatment consists of long-term drug therapy with antibiotics/antitubuculotics for 6-9 months. Drugs include isoniazid (INH), rifampin, ethambutol, pyrazinamide, and streptomycin. Treat complications and relieve symptoms. Pulmonary hygiene. Ensure respiratory isolation to protect others. If left untreated, active TB can seriously damage lungs or other organs and can be fatal.

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LNOTESL

MICROBES, WMD, EQPT DISINFECTION See references 3, 14, 19, and 24 MICROBIAL ORGANISMS Viral Organisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fungal Organisms . . . . . . . . . . . . . . . . . . . . . . . . . . Protozoan Organisms . . . . . . . . . . . . . . . . . . . . . . . Bacterial Organisms Associated with Disease . . . . BIOTERRORISM AGENTS Dangerous Biologic Warfare Agents . . . . . . . . . . . Personal Protective Equipment . . . . . . . . . . . . . . . EQUIPMENT DISINFECTION Cleaning. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Disinfection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sterilization. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

54 54 54 55 58 58 59 59 60

SEE ALSO

Microbes, WMD, Eqpt Disinfection

Pulmonary Diseases

53

MICROBES, WMD, EQPT DISINFECTION

Microbes, WMD, Eqpt Disinfection

LMICROBIAL ORGANISMSL VIRAL ORGANISMS Associated with the following diseases: • Common cold and common flu (influenza) • AIDS (human immunodeficiency virus or HIV) • Bronchiolitis (respiratory syncytial virus or RSV) • Chickenpox (varicella virus) • Croup/LTB (RSV, adenovirus, or parainfluenza virus) • Cytomegalovirus (CMV) • Hepatitis • Measles/German measles/rubella • Mononucleosis (Epstein-Barr virus) • Mumps • Poliomyelitis (RNA virus) • Rabies • Roseola infantum • Smallpox (variola virus) • Viral encephalitis FUNGAL ORGANISMS Associated with the following diseases: • Actinomycosis • Aspergillosis • Blastomycosis • Coccidioidosis • Cryptococcosis • Histoplasmosis • Thrush (Candida albicans) PROTOZOAN ORGANISMS • Pneumocystis jirovecii (previously known as carinii)

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BACTERIAL ORGANISMS ASSOCIATED WITH DISEASE BACTERIAL ORGANSMS

DISEASE/DISORDER

Bacillus anthracis Bordetella pertussis, G Chlamdia psittaci, G Clostridium botulinum, G

Anthrax infection—cutaneous, injested, or inhaled Whooping cough, nasopharyngeal infection Psittacosis, parrot fever, ornithosis, pneumonia Botulism—foodborne, wound infection, or infantile, causing paralysis Habitat: soil and feces Gas gangrene; Habitat: soil and feces Tetanus or lockjaw, rigid muscle paralysis, respiratory failure Cause: bloodstream infection from infected wound, rusty nail, splinter, animal or insect bite Habitat: dirt, soil, and feces Diphtheria, pharynx and larynx mucosal necrosis, airway obstruction, skin infection Q-fever, Rocky Mountain fever, pneumonia, Rickettsia disease Habitat: ticks, mites, lice

Clostridium perfringens, G Clostridium tetani, G

Corynebacterium diptheriae, G Coxiella burnetii (parasitic, bacteria-like organism)

55

Continued

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BACTERIAL ORGANISMS ASSOCIATED WITH DISEASE—cont’d BACTERIAL ORGANSMS

DISEASE/DISORDER

Diplococcus pneumoniae Escherichia coli, G

See Streptococcus Pneumonia, cystitis Habitat: intestinal tract VRE blood infection, pneumonia, very serious nosocomial infection

Enterococcus faeciun, or VRE (vancomycin-resistant enterococcus) Haemophilis influenzae, G (different than viral influenza) Klebsiella pneumoniae, G(or Friedlander’s bacillus) Legionella pneumophila, G MRSA Mycobacterium tuberculosis, G Mycoplasma pneumoniae, G (different type bacteria than MTB)

Epiglottitis, laryngitis, sinusitis, nasopharyngitis, meningitis, respiratory infection, pneumonia, bronchitis Necrotizing pneumonia, lung abscess, respiratory infection, UTI, septicemia, endocarditis Legionnaire’s disease, diffuse pneumonia, pneumonitis Habitat: contaminated water See Staphylococcus Tuberculosis (TB or MTB), infection of lungs and other organs Atypical pneumonia Habitat: sputum, blood, GI tract

Neisseria meningitidis (or meningococcal Meningitis, serious infection, and inflammation of the brain and spinal meningitis) cord meninges; spread by respiratory droplets; meningitis also caused by other bacteria Pneumococcus pneumoniae See Streptococcus Proteus vulgaris, G UTI, pneumonia, gastroenteritis, bacteremia Pseudomonas aeruginosa, G− Nosocomial respiratory infection, pneumonia Habitat: colon, skin, water, soil, equipment Salmonella enteritidis and Salmonella Salmonellosis, food poisoning due to ingestion of contaminated food, typhimurium contact with infected animal feces, or reptiles Serratia marcescens, G Serious pneumonia, empyema, septicemia, wound infections Staphylococcus aureus and MRSA Nosocomial infection, pneumonia, empyema, septicemia, meningitis, (methicillin-resistant S. aureus), G cystitis, pimples. Habitat: respiratory tract, GI tract skin Streptococcus pneumoniae, G Pneumonia, empyema, meningitis, sinusitis, otitis, strep species also Pneumococcus pneumoniae associated w/strep throat, endocarditis, skin lesions, and UTI Diplococcus pneumoniae (same bacteria known by 3 names) VRE See Enterococcus

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LBIOTERRORISM AGENTSL The following have been identified by the U.S. government as the biologic agents that are most dangerous to the population if used as weapons of terrorism. For comprehensive information about bioterror agents, visit the CDC website at

http://www.cdc.gov/. DANGEROUS BIOLOGIC WARFARE AGENTS • Bacillus anthracis (anthrax) • Clostridium botulinum toxin (botulism) • Yersinia pestis (plague) • Variola virus (smallpox) • Staphylococcal enterotoxin B (SEB) • Francisella tularensis (tularemia) • Brucella melitensis (brucellosis, Mediterranean or Malta fever) • Venezuelan equine encephalitis virus (VEE) • Nerve agents: sarin, cyanide, and skinblistering compounds PERSONAL PROTECTIVE EQUIPMENT Health care personnel treating suspect cases must use impermeable gloves, isolation gowns, and high-filtration masks. Frequent and thorough handwashing using proper technique is always important. Many microbial agents and toxins can be dispersed in aerosols of a particle size that can penetrate the lungs (1 to 10 microns). Particles can remain suspended for hours and penetrate distal bronchioles and terminal alveoli. The aerosol is colorless, odorless, and completely invisible. Other potential routes of exposure are ingestion, via contamination of food or water, and percutaneous, via contact with exposed skin. The oral and percutaneous routes are less severe in terms of casualties and fatalities than the 58

respiratory route. Adverse effects range from minor skin irritations to complete incapacitation and death.

LEQUIPMENT DISINFECTIONL CLEANING Removing all foreign material, soil, and particles. Equipment is best cleaned by soaking and washing in mild, fragrance-free detergent, using lint-free towels. Equipment must be disassembled, cleaned, and sometimes dried before disinfection or sterilization. DISINFECTION Process used to destroy most pathogenic microorganisms (except spores). However, spores can be destroyed by certain highlevel disinfectants with adequate exposure time, making some disinfectants true sterilization agents. Disinfection prevents infection and cross contamination, and is a good process for most respiratory equipment. High-level disinfection or sterilization is needed for invasive equipment. Equipment must sometimes be rinsed and air-dried after disinfection. COMMON LOW- AND MEDIUM-LEVEL DISINFECTANTS • Alcohols • Phenolics • Quaternary ammoniums • Iodophors (iodine mix; also an antiseptic) • Acetic acid (vinegar). Good disinfectant for home or health care use. Articles are washed, rinsed, and then soaked for 30 to 60 minutes in vinegar diluted with water to make a 1:3 solution; rinsed again and air dried. 59

COMMON HIGH-LEVEI DISINFECTANTS Exposure times soaking in solution to reach disinfection and sterilization vary by product and can change. • Glutaraldehyde (Cidex) 2% solution ◆ Disinfection: 10 minutes ◆ Sterile/sporicidal: 3 hours • Bleach (sodium hypochlorite) ◆ Disinfection: dilute with water 1:10 for quick surface cleaning, blood spills, or home use ◆ Sterile/sporicidal: soak in 1:50 solution (about 1000 ppm) for 10 minutes • Hydrogen peroxide (also an antiseptic 6% solution ◆ Disinfection: 10 minutes ◆ Sterile/sporicidal: 6 hours at 20º C • Peracetic acid 0.35% specially formulated anticorrosive solution is sporicidal STERILIZATION Process used to completely destroy and/or remove all forms of microbial life, including spores. Sterilization methods include: • High-level disinfectants (as listed above) • Autoclaving • Boiling • Dry heat • Ethylene oxide (important to clean and dry completely first) • Ionizing radiation (gamma rays) • Incineration (for disposable articles) Note: Always refer to manufacturer’s instructions and employer’s policy regarding proper use of products on each type of equipment. Also, follow guidelines on dilution, duration of use, testing of solution, cautions, and hazardous material information. 60

MEDICATIONS

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Medications

See references 11, 14, 19, and 24 GENERAL INFORMATION . . . . . . . . . . . . . . . . . . . . . 63 Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 Routes of Administration for Pulmonary Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63 Ensure the Five Rs for Drug Administration. . . . . 64 Calculating Drug Dosages . . . . . . . . . . . . . . . . . . . . 64 Calculating Pediatric Safe Dosages . . . . . . . . . . . . 64 BRONCHODILATORS . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Adverse Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Adrenergic Bronchodilators . . . . . . . . . . . . . . . . . . 66 Anticholinergic Bronchodilators . . . . . . . . . . . . . . 67 Table 1: Adrenergic Bronchodilators (Beta2 Specific). . . . . . . . . . . . . . . . . . . . . . . . . . . . 68 Table 2: Other Sympathomimetic Bronchodilators (Non–Beta2 Specific) . . . . . . . . 70 Table 3: Bronchodilator Combination Drugs . . . . . . 72 Table 4: Anticholinergic Bronchodilators . . . . . . . 73 XANTHINE DRUGS . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Adverse Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Table 5: Xanthine Drugs. . . . . . . . . . . . . . . . . . . . . . 75 LEUKOTRIENE INHIBITORS . . . . . . . . . . . . . . . . . . . . 76 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Adverse Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Table 6: Leukotriene Inhibitors . . . . . . . . . . . . . . . . 77 CROMOLYN AND NEDOCROMIL . . . . . . . . . . . . . . . . 78 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Adverse Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Table 7: Cromolyn and Nedocromil . . . . . . . . . . . . 79 CORTICOSTEROIDS. . . . . . . . . . . . . . . . . . . . . . . . . . . 80 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 Adverse Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . 81 Table 8: Corticosteroid Antiinflammatory Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 Table 9: Mucolytics and Wetting Agents . . . . . . . . 85

Table 10: Aerosolized Antiinfective Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 NEUROMUSCULAR BLOCKERS . . . . . . . . . . . . . . . . 88 Table 11: Neuromuscular Blocking Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88 ADJUNCT MEDICATIONS . . . . . . . . . . . . . . . . . . . . . 89 Surfactant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 Nitric Oxide (NO) (Pulmonary Vasodilator) . . . . . 89 Adverse Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . 90 Vasodilators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 Vasopressors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 Diuretics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Cardiac Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Sedatives and Analgesics . . . . . . . . . . . . . . . . . . . . 92

SEE ALSO PULMONARY DISEASES Stepwise Approach for Managing Asthma in Adults and Youths 12 Years of Age . . . . . . . . 19

SEE ALSO THERAPEUTIC MODALITIES Medications

Medical Gases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94 Medication Delivery Devices . . . . . . . . . . . . . . . . . 99 Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101

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MEDICATIONS New drugs are continuously being added. Also, indications, contraindications, and safe dosage amount can change. Children and older adults generally require reduced dosages. Always verify drug information with the most current drug reference. One contraindication for any drug is hypersensitivity or an allergy to the drug. For the most current information on any drug, including those pending approval, visit the U.S. Food and Drug Administration Web site at http//www.fda.gov.

LGENERAL INFORMATIONL DEFINITIONS Drug—Any chemical that alters an organism’s functions or processes Pharmacokinetics—Study of absorption, metabolism, and excretion of drugs in the body Metabolism—Chemical process carried on within the body to maintain life Drugs are absorbed most rapidly from large surface areas, such as the lungs, or by IV. The liver is the major site of metabolism. After being metabolized, the drug is eliminated from the body primarily by the kidneys. TachyphyIaxis—Rapid development of drug tolerance, requiring higher doses to achieve the same results ROUTES OF ADMINISTRATION FOR PULMONARY MEDICATIONS • Inhalation • Intratracheal • Oral • SQ • IV • IM 63

Inhalation via nebulizer, MDI, or DPI. Advantages include direct delivery to lungs, rapid onset of action, and reduced systemic side effects. Oral respiratory medications (tablet, capsule, or pill). Have a slower onset of action than the inhalation route, although the duration of action may be longer. Intravenous and intratracheal administration of respiratory medications. Provides a very rapid onset of action; both are often used during emergencies. ENSURE THE FIVE Rs FOR DRUG ADMINISTRATION • Right patient • Right medication • Right dose • Right route • Right time CALCULATING DRUG DOSAGES 1 mL  1 cc  20 drops Calculate active ingredient of drug from percent strength solutions. Remember that percent solution represents grams of drug/100 mL of solution. For simple calculations, use 1 mL and multiply the percent strength by 10. Remember: 1 mL of 1%  10 mg 1 mL of 5%  50 mg Calculate percent strengths of solutions given as ratios. Divide the ratio. For example: 1:100  1% solution (1  100  0.01  1%) 1:20  5% solution (1  20  0.05  5%) CALCULATING PEDIATRIC SAFE DOSAGES Refer to manufacturer’s literature and an approved drug reference book first. Clark’s 64

rule is one method to calculate estimated safe dosage (ESD) for children. This rule is based on the estimation of 150 pounds for the average weight of an adult in the general population. CLARK’S RULE ESD  (child’s weight in pounds  average adult dose)  150 For example: ESD 2 mg 

75 pounds  4 mg adult dose 150

LBRONCHODILATORSL Bronchodilators affect the autonomic nervous system. The autonomic nervous system is divided into the sympathetic branch and the parasympathetic branch. INDICATIONS Prevention and treatment of reversible airflow obstruction or bronchospasms. Clinical benefits include decreased dyspnea, decreased WOB, improved breath sounds, improved air movement, improved flow rates, and improved exercise tolerance. CONTRAINDICATIONS Not indicated for those with significant tachycardia or arrhythmias. Use caution in those with hypertension, coronary artery disease, hyperthyroidism, and diabetes. Note: propranolol or other beta-blocker drugs can block bronchodilating action of adrenergic drugs. ADVERSE REACTIONS Adverse reactions to adrenergic bronchodilators are more common in drugs that are 65

less specific for beta2 receptors. Side effects include the following: • Tachycardia • Diaphoresis • Heart palpitation • Nausea • Hypokalemia • Tremors • Tachyphylaxis • Nervousness • Paradoxical bronchospasm with excessive use • Headache • Vertigo ADRENERGIC BRONCHODILATORS Sympathetic branch drugs are called adrenergic or sympathomimetic. The sympathetic branch produces the “fight or flight” response and directly innervates the smooth muscles. The drugs work by stimulating one or more receptors in the sympathetic branch known as alpha, beta1 and beta2 receptors. Both B1 and B2 drugs are called beta agonists (see Tables 1-3). • Alpha response results in vasoconstriction of arteriolar smooth muscles and increased blood pressure (vasoconstriction). • Beta1 (B1) response results in increased heart rate and increased strength of cardiac contractions. • Beta2 (B2) response results in direct bronchodilation of the lungs, stimulates mucociliary acivity, and has a weak vasodilating effect. B2 is the preferred response when direct bronchodilation is desired without the adverse effect of increased heart rate. However, slight B1 stimulation is sometimes a side effect of B2 drugs. 66

ANTICHOLINERGIC BRONCHODILATORS Parasympathetic branch drugs are called anticholinergic, antimuscarinic, or parasympatholytic. They affect the smooth muscle with the opposite effect of sympathetic stimulation. Parasympathetic stimulation results in bronchoconstriction and decreased heart rate. The goal of bronchodilation via this branch is to block parasympathetic stimulation, thereby blocking the mechanisms that cause bronchoconstriction and indirectly resulting in bronchodilation (thus the term back door bronchodilators). The mechanism of action is to inhibit vagaIly induced bronchospasm and bradycardia by antagonizing acetylcholine at muscarinic receptors in the lungs. Anticholinergics have a slower onset of action than B2 bronchodilators, but generally a longer duration of action. They are not used in emergencies, but are used as maintenance therapy. They can be mixed with B2 bronchodilators to achieve bronchodilation by two different methods. INDICATIONS Maintenance treatment of bronchospasms associated with COPD and some cases of asthma. Only effective if bronchoconstriction is due to cholinergic activity. CONTRAINDICATIONS Hypersensitivity to atropine, soy products, and peanuts. Not indicated for acute bronchospasms where rapid response is required. ADVERSE REACTIONS • Nervousness • Tachycardia • Vertigo • Palpitations • Headache • Cough • Blurred vision • Dry mouth • Nausea • Thick secretions (See Table 4)

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TABLE 1: ADRENERGIC BRONCHODILATORS (BETA2 SPECIFIC) Generic Names Brand Names

Routes of Administration

Normal Adult Dosages

Onset of Action

Duration of Action

Nebulizer MDI (90 mcg/puff) DPI (200 mcg/cap) Tablets (2 or 4 mg) Syrup (2 mg/5 mL)

2.5-5 mg/NS every 4-6 hr 1-3 puffs every 4-6 hr 200 mcg every 4-6 hr 2-4 mg every 6-12 hr 2-4 mg every 6 hr

5 min 5 min 5 min 30 min 30 min

4-6 hr 4-8 hr 4-6 hr 6-12 hr 6 hr

Nebulizer 0.63 mg or 1.25 mg in NS 3 mL vial

Pediatric dose age 2-12 yr; one vial TID or QID

5 min

4-6 hr

*arformaterol Brovana

15 mcg

1 dose BID

7-12 min

12 hr

bitolterol Tornalate

Nebulizer MDI (0.37 mg/puff)

2.5 mg every 6-8 hr 2 puffs every 6-8 hr

4 min

6-8 hr

albuterol Aerolin Proventil Respolin Salbutamol Ventolin Volmax AccuNeb (pediatric dose)

*formoterol Foradil

MDI (12 mcg/puff)

1 puff BID

levalbuterol Xopenex

MDI (45 mcg/puff) Nebulizer

1-2 puffs every 4-6 hr 0.63-1.25 mg/NS every 4-8 hr 5-10 min

4-8 hr

pirbuterol Maxair

MDI (0.2 mg/puff)

2 puffs every 4-6 hr

5 min

5-6 hr

terbutaline Brethaire Brethine Bricanyl

MDI (0.2 mg/puff) Tablets Subcutaneous

2 puffs every 4-6 hr 2.5 to 5 mg TID 0.25 mg every 4-8 hr

5 min 30 min 10 min

4-8 hr 6-8 hr 4-8 hr

*salmeterol Serevent

MDI (25 mcg/puff) DPI (50 mcg/puff)

2 puffs BID 1 puff BID

10-20 min

12 hr

5-15 min

12 hr

Notes: The medications in this table are direct bronchodilators with B2-receptor specificity. They are differentiated by the time for onset of action and the duration of action. Also see Table 3, including Combivent, Duoneb, and Advair. *Not for acute bronchospams.

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TABLE 2: OTHER SYMPATHOMIMETIC BRONCHODILATORS (NON–BETA 2 SPECIFIC) Generic Names Brand Names

Routes of Administration

Normal Adult Dosages

Onset of Action

Duration of Action

epinephrine Adrenalin IV or intratracheal 0.5 to 1.0 mg  repeat PRN 1-3 hr 1-2 min Bronkaid Nebulizer (1%) 2.5 to 5 mg PRN *(A, B1, B2) Epinephrine is used primarily in emergency situations, such as status asthmaticus and cardiopulmonary arrest. (Increases heart rate, blood pressure, and bronchodilation.) isoetharine Bronkosol Bronkometer *(B1, B2)

Nebulizer MDI (340 mcg/puff)

2.5 to 5 mg every 4-6 hr 2 puffs QID

isoproterenol Isuprel *(B1, B2)

Nebulizer (0.5%)

0.25 to 0.5 mL NS QID Maximum: 5 doses daily

5 min

4 hr

1-5 min

1-2 hr

metaproterenol Metaprel Alupent *(B1, B2)

Nebulizer MDI (0.65 mg/puff) Tablets

15 mg every 4 hr 2-3 puffs every 4 hr 10-20 mg every 6-8 hr

5 min 5 min 30 min

3-4 hr 3-4 hr 6-8 hr

racemic epinephrine Vaponefrin Nebulizer (2.25%) 0.25 to 0.5 mL  NS PRN 10 min 1-4 hr MicoNephrin *(A, B1, B2) Racemic epinephrine is used primarily for the alpha effects of reducing edema in the upper airway, reducing stridor, and treating croup. Notes: The medications in Table 2 are less specific for B2 and more specific for alpha or B1 receptors. These drugs are sometimes indicated primarily for purposes other than or in addition to bronchodilation to increase heart rate or blood pressure. *Receptors describes the specificity of the drug for certain receptors: A, Alpha—increases blood pressure , Strong stimulation of receptor , Moderate stimulation of receptor B1, Beta1—increases heart rate B2 , Beta2—direct bronchodilation

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TABLE 3: BRONCHODILATOR COMBINATION DRUGS Brand Names Generic Names (Common Names) Duoneb albuterol ipratropium bromide (albuterol and Atrovent) Combivent albuterol ipratropium bromide (albuterol and Atrovent) Advair* salmeterol fluticasone (Serevent and Flovent)

Normal Adult Dosage

Onset of Action

Duration of Action

Nebulizer 1 vial every 6 hr or QID 3 mL vial contains 3 mg albuterol and 0.5 mg Atrovent in NS

albuterol, 5 min Atrovent, 20 min

albuterol, 4-8 hr Atrovent, 5-8 hr

MDI 2 puffs every 6 hr or QID Maximum 12 puffs daily; 1 puff contains 90 mcg albuterol and 18 mcg ipratropium DPI diskus 1 puff BID 1 puff contains 100, 250, or 500 mcg Flovent, pIus 50 mcg Serevent; labeled as 100/50, 250/50, or 500/50

albuterol, 5 min Atrovent, 20 min

albuterol, 4-6 hr Atrovent, 5-8 hr

Serevent, 10-20 min Serevent, 12 hr Flovent, varies Flovent, varies

*Advair is not fast-acting and is not recommended for relief of acute bronchospasms. Rinse mouth after use to avoid thrush.

TABLE 4: ANTICHOLINERGIC BRONCHODILATORS Generic Names Brand Names ipratropium bromide Atrovent tiotropium bromide Spiriva HandiHaler atropine sulfate (Strong B1 used mainly to increase heart rate.)

Routes of Administration

Normal Adult Dosages

Onset of Action

Duration of Action

Nebulizer (0.02% sol) MDI 18 mcg/puff

0.5 mg/NS every 6 hr or QID 2.5 to 5 mg every 4-6 hr

20 min 20 min

5-8 hr 5-8 hr

DPI 18 mcg/capsule IV or intratracheal Nebulizer

1 DPI capsule QID 0.5-2 mg PRN 1 mg QID

20 min 5 min 5-20 min

24 hr 1-4 hr 1-4 hr

See also Table 3: Combination Drugs.

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LXANTHINE DRUGSL INDICATIONS Symptomatic relief of bronchoconstriction. Xanthine (methylxanthine) drugs inhibit phosphodiesterase, the enzyme that degrades cyclic adenosine monophosphate (cAMP). This results in relaxation of bronchial airways and pulmonary vasodilation. Xanthine drugs are used in emergency treatment of bronchoconstriction and for maintenance therapy. (Refer to Asthma Stepwise Approach in the “Pulmonary Diseases” section.) CONTRAINDICATIONS Hypersensitivity to xanthine compounds (including caffeine). Those with active peptic ulcer or seizure disorder (unless treated with anticonvulsants). Use cautiously in those with cardiac arrhythmias and tachycardia. ADVERSE REACTIONS • CNS stimulation • Irritability • Seizures • Nausea • Diarrhea • Stomach pain • Tachycardia • Hypotension

• • • • • • •

Nervousness Dizziness Insomnia Vomiting Diuresis Palpitations Arrhythmias

To minimize side effects and maximize effectiveness, monitor blood theophylline levels to maintain therapeutic level of 10 to 20 mcg/mL. Toxic level 20 mcg/mL. (See Table 5)

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TABLE 5: XANTHINE DRUGS Generic Names Brand Names

Routes of Administration

Normal Adult Dosages

Onset of Action

Duration of Action

aminophylline Phyllocontin Truphyhine

IV Emergency Maintenance

4.7 to 7 mg/kg followed by maintenance 0.5 to 0.9 mg/kg/hr

5-15 min

Varies

theophylline Thea-Dur, Theolair, Theovent SloBid, Aerolate, Bronkodyl, Elixophyllin, Uniphyl, Quibron-T

PO tablet or liquid

Maximum daily dose is the lesser of 13 mg/kg or 900 mg; average is 400 mg/day, divided into even doses every 6-8 hr (extended release tablets every 8, 12, or 24 hr)

15-60 min Varies

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LLEUKOTRIENE INHIBITORSL INDICATIONS Prophylaxis and long-term maintenance treatment of asthma. These medications work by blocking leukotrienes that cause inflammation and bronchoconstriction. Some patients are able to reduce dependence on steroidal medications when using leukotriene inhibitors. (Refer to the Asthma Stepwise Approach in the “Pulmonary Diseases” section.) CONTRAINDICATIONS Not for acute bronchospasms. Not for acute asthmatic episodes. ADVERSE REACTIONS • Headache • Muscle aches • Weakness • Nausea • Vomiting • Diarrhea • Liver inflammation • Low white blood cell count • Infection • Fever (See Table 6)

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TABLE 6: LEUKOTRIENE INHIBITORS Generic Names Brand Names

Routes of Administration

Normal Adult Dosages

Onset of Action

Duration of Action

montelukast sodium Singulair

Tablet PO

4-10 mg nightly

1-4 hr

24 hr

zafirlukast Accolate

Tablet PO

20 mg BID

1-3 hr

12 hr

zileuton Zyflo

Tablet PO

600 mg QID

1-2 hr

6-8 hr

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LCROMOLYN AND NEDOCROMILL INDICATIONS Prophylaxis and maintenance treatment of mild to moderate asthma. These medications are nonsteroidal antiinflammatory drugs (NSAIDs). These drugs work by inhibiting mast cell degranulation during antigenantibody reaction. This prevents the release of chemical mediators, including histamine, serotonin, and slow-reacting substance of anaphylaxis (SRS-A). The mediators cause inflammation and bronchospasm. Cromolyn and nedocromil sodium are more beneficial in children with asthma than in adults. (Refer to the Asthma Stepwise Approach in the “Pulmonary Diseases” section.) CONTRAINDINDICATIONS Not for acute bronchospasms. Not for acute asthmatic episodes. ADVERSE REACTIONS • Headache • Dizziness • Nausea • Rash • Pharyngitis • Cough • Bronchospasm • Dyspnea (See Table 7)

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TABLE 7: CROMOLYN AND NEDOCROMIL Generic Names Brand Names cromalyn sodium Intal

nedocromal sodium Tilade

Onset of Action

Duration of Action

(Age 4 and older) 20 mg QID 2 puffs QID 20 mg QID

20-30 min

2-6 hr

(Age 12 and older) 2 puffs QID

20-30 min

3.5 hr

Routes of Administration

Normal Adult Dosages

Nebulizer 20 mg/2 mL NS MDI 800 mcg/puff Spinhaler 20 mg/capsule MDI 1.75 mcg/puff

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LCORTICOSTEROIDSL INDICATIONS Prophylaxis and long-term maintenance therapy of inflammatory lung diseases. Intranasal steroids are used to control seasonal allergic and nonallergic rhinitis. Corticosteroids (glucocorticoids) are used to treat inflammatory pulmonary disease, including asthma and COPD. Corticosteroids reduce inflammation by stabilizing leukocyte lysosomal membranes and may enhance the effectiveness of B2 bronchodilators. Corticosteroids also suppress immune responses, including response of pulmonary mucosa to allergens. Natural corticosteroids are endogenous hormones produced in the adrenal cortex. Corticosteroids are used in emergency long-term maintenance treatment of bronchoconstriction. (Refer to Asthma Stepwise Approach in the “Pulmonary Diseases” section; see also Advair in Table 3: “Bronchodilator Combination Drugs” [Flovent and Serevent]). Inhaled corticosteroids have distinct advantages over systemic corticosteroids, including delivery of medication directly to the lungs using a smaller dose and fewer adverse effects, because only a small portion of the drug is absorbed into the bloodstream. Systemic corticosteroids are used when inhaled drugs are insufficient in relieving inflammation and bronchospasms. Systemic corticosteroids have a much higher incidence and severity of side effects. Abrupt withdrawal can cause serious to fatal effects. Systemic

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corticosteroids are also indicated for shock (different dosage guidelines) and other nonpulmonary indications. CONTRAINDICATIONS Not for acute episode of bronchospasms (give fast-acting bronchodilator first). Not for those with systemic fungal infections. ADVERSE REACTIONS • Headache • Cushingoid state • Dizziness • Muscle wasting • Seizures • Arrhythmias • Insomnia • Bronchospasm • Nausea • Cough, hoarseness • Weight gain • Sore mouth • Water retention • Candidiasis or thrush (See Table 8)

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TABLE 8: CORTICOSTEROID ANTIINFLAMMATORY DRUGS Generic Names Brand Names

Routes of Administrationa

beclomethasone Beclovent Rotocaps, MDI/DPI 42-50 mcg/puff Beclodisk, Vanceril QVAR HFA budesonide Pulmicort ciclesonide Alvesco dexamethasone Decadron

Normal Adult Dosagesb

Onset of Actionc

Duration of Action

Varies

Varies

Varies

Varies

DPI 40-80 mcg/puff

2 puffs TID or QID, or 2-4 puffs BID (max 20 puffs/day) 1-2 puffs BID

DPI 200 mcg/puff Nebulizer

1-3 puffs BID 0.5 mg/NS BID

Within 24 hr Varies

MDI 80 or 160 mcg/puff

160 mcg QID

Varies

Varies

MDI 84 mcg/puff

2-3 puffs BID or QID

1 hour

2-3 days

flunisolide Aerospan Aerobid

MDI 80 mcg/puff MDI 250 mcg/puff

2 puffs BID 2 puffs BID (max 8 puffs/day)

Varies

MDI 44, 110, or 220 mcg/puff DPI 50, 100, or 250 mcg/puff

2 puffs BID (max 1000 mcg/day)

Within 24 hr 2-3 days

hydrocortisone Solu-Cortef

Tablet, PO IV

5-30 mg BID-QID 4 mg/kg every 4-6 hr

Varies

Varies

methylprednisolone Medrol Solu-Medrol

Tablet, PO IV

4-48 mg daily 1-2 mg/kg every 4-6 hr

1-3 hr Rapid

1-2 days 7 days

Tablet or liquid, PO

5-60 mg daily

Varies

Varies

fluticasone Flovent (Rotadisk)

prednisone Prednisone, Deltasone, Meticorten, Orasone, Sterapred

Varies

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Continued

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TABLE 8: CORTICOSTEROID ANTIINFLAMMATORY DRUGS—cont’d

a

Generic Names Brand Names

Routes of Administrationa

Normal Adult Dosagesb

triamcinolone Azmacort

MDI 100 mcg/puff

2-4 puffs BID-QID Varies (maximum 16 puffs/day)

Other routes exist (e.g., nasal, intramuscular) but are not covered here. Maximum dosage for those previously on other corticosteroids is higher. c Corticosteroids can take 1-4 weeks to reach full effectiveness. Always rinse mouth after use of corticosteroid to prevent thrush. Roflumilast (Daxas) is a new antiinflammatory drug being evaluated and pending FDA approval. b

Onset of Actionc

Duration of Action Varies

TABLE 9: MUCOLYTICS AND WETTING AGENTS Generic Names Brand Names

Normal Adult Dosages

Notes

acetylcysteine Mucomyst

2 to 4 mL of 10% or 20% solution TID or QID; PRN by nebulizer

Action: mucolytic—breaks disulfide bonds in mucus and decreases viscosity. Give with bronchodilator to prevent bronchospasm. After opening, store in refrigerator; use within 4 days. (Also an acetaminophen OD antidote.)

dornase alfa PulmoZyme

2.5 mL of 1 mg/mL solution daily PRN Use approved nebulizer such as Hudson Updraft or Marquest Acorn II

Action: mucolytic—hydrolyzes sputum DNA and decreases mucosal viscosity and elasticity. Used to treat CF or other infection or disease with purulent mucus. Can cause pharyngitis and cough. Do not mix with other drugs in nebulizer.

saline 0.9% NS Isotonic NaCL

2-5 mL by nebulizer or instill intratracheal PRN

Action: humidifies and thins secretions. Often given with bronchodilator to prevent bronchospasm. (Is also a drug diluent.) Continued

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TABLE 9: MUCOLYTICS AND WETTING AGENTS—cont’d Generic Names Brand Names

Normal Adult Dosages

Notes

saline 3% 2-5 mL by nebulizer PRN Hypertonic NaCL

Action: lung irritant to induce sputum. Can cause bronchospasms; may need bronchodilator. Use caution in those with edema or salt restrictions.

saline 0.45% Hypotonic NaCL

Action: humidify and thin secretions, deposits more distally. Less irritating to mucosa than 0.9% normal saline.

2-5 mL usually by ultrasonic nebulizer PRN

sodium bicarbonate 2 to 5 mL of 2% to 7.5% NaHCO3 solution by nebulizer or instill intratracheal PRN

Action: mucolytic—breaks saccharide chains in mucus, lowers surface tension, and decreases adhesiveness. Give bronchodilator first to prevent bronchospasm. Caution in edema, salt restrictions, or metabolic alkalosis.

Notes: Mucolytics are used to thin and liquefy thick, tenacious secretions. Mucolytics increase the production of respiratory tract fluids and reduce viscosity of secretions. Secretions can then be more easily expectorated or suctioned. Many mucolytics can cause bronchospasms, which can be minimized or avoided by giving a bronchodilator just before or with mucolytic, depending on compatibility.

TABLE 10: AEROSOLIZED ANTIINFECTIVE MEDICATIONS Generic Name Brand Names (Type of antiinfective) tobramycin Nebcin, TDBI (Antibiotic used to treat CF and many bacterial pulmonary infections) pentamidine isethionate NebuPent, Pentam 300 (Antiprotozoal agents used to treat and prevent PCP) ribavirin Virazole (Antiviral used to treat RSV and prophylactic for patients at risk for severe infection)

Normal Adult Dosage Nebulizer 80 mg BID for 28 days

Nebulizer 300 mg in 6 mL sterile water every 4 weeks 6 g in 300 mL sterile water via continuous nebulizer for 12-18 hr daily for 3 to 7 days

Notes Give B2 bronchodiIator first to prevent bronchospasms. May need to increase flow rate to 8-12 L/m, depending on solution viscosity. Give B2 bronchodilator first to prevent bronchospasms. Clinician should use protective barrier mask; patient should use Respirgard II nebulizer. Administer using large-volume small particle aerosol generator (SPAG).

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Pending FDA approval: colistimethate (Coly-Mycin, Colistin) inhaled nebulizer, to treat Pseudomonas aeruginosa. Must mix and use immediately to avoid extreme adverse reactions.

LNEUROMUSCULAR BLOCKERSL Neuromuscular blocking agents are used to induce skeletal muscle relaxation/paralysis to facilitate intubation and to assist mechanical ventilation (see Table 11).

TABLE 11: NEUROMUSCULAR BLOCKING AGENTS Generic Name Brand Names

Normal Adult Dosage

Onset of Action

Duration of Action

Succinylcholine IV 0.6 to chloride 1 mg/kg Anectine Depolarizing*

1 min 4-10 min

Pancuronium IV 0.4 to Pavulon 0.1 mg/kg Nondepolarizing†

1 min

40-60 min

Tubocurarine IV 0.165 mg/kg 1 min chloride Tubarine Nondepolarizing†

30-90 min

Vecuronium IV 0.09 mg/kg 1 min bromide bolus 0.01Norcuron† 0.015 mg/kg Nonmaintenance depolarizing†

15-25 min

*Depolarizing agents have no antidote. † Nondepolarizing agent antidote is Neostigmine or Tensilon.

88

LADJUNCT MEDICATIONSL SURFACTANT Surfactant is used to prevent and treat IRDS in premature infants. Dose varies by manufacturer and is based on body weight at birth. Surfactant is given intratracheally to each lung zone. The newest surfactant drugs undergoing clinical trials that are also used to treat adults with pneumonia, ARDS, and other diseases include the following: • beractant (Survanta) • calfactant (Infasurf) • poractant (Curosurf) • In addition, pending FDA approval for neonates and for adults with pneumonia or ARDS, are the following drugs: ◆ lucinactant (Surfaxin) ◆ lusupultide (Venticute) NITRIC OXIDE (NO) (PULMONARY VASODILATOR) • Nitrous oxide (NO) gas is a pulmonary vasodilator that increases oxygenation, reduces pulmonary artery pressure (PAP), and reduces pulmonary vascular resistance (PVR). • Used to treat pulmonary hypertension, pulmonary artery hypertension (PAH), persistent pulmonary hypertension of the newborn (PPHNB), and hypoxic respiratory failure. • NO has proven effective at increasing oxygenation in cases of severe hypoxemia, including ARDS, COPD, lung transplantation (and other organ transplants), and neonatal applications. • Current therapeutic range for delivery of NO is 2 to 30 ppm; higher levels (up to 80 ppm) are undergoing clinical trials and are proving effective in many cases. However, close 89

monitoring is necessary with higher levels because of the much higher incidence of adverse effects. ADVERSE REACTIONS • Increased methemoglobin (MetHb); the goal is to maintain MetHb well below 3%. • Increased nitrogen dioxide (NO2), a toxic by-product of NO therapy; the goal is to maintain NO2 below 1 ppm. • Other adverse reactions include pulmonary edema, platelet inhibition, cellular damage, and rebound problems. • NOTE: Higher levels of NO are parallel with higher risk of adverse effects. VASODILATORS INHALED PULMONARY VASODILATORS ◆ Nitric oxide, as described previously. ◆ iloprost (Ventavis); to treat severe adult PAH. ◆ tolazoline (Vasodil); to reduce PVR in PPHN; also to reduce PAP. OTHER VASODILATORS ◆ atenolol (Tenormin) ◆ captopril (Capoten) ◆ clonidine (Catapres) ◆ epoprostenol (Flolan) ◆ nitroglycerin (Nitrostat, Transderm-Nitro) ◆ nitroprusside (Nipride) ◆ prazosin (Minipress) ◆ treprostinil (Remodulin) VASOPRESSORS To treat hypotension; these drugs increase blood pressure: • dobutamine (Dobutrex) • dopamine (Intropin) • epinephrine • norepinephrine (Levophed) 90

DIURETICS Used to treat hypervolemia, hypertension, pulmonary edema, and general edema: • acetazolamide (Diamox) • bumetanide (Bumex) • chlorothiazide (Diuril) • furosemide (Lasix) • torsemide (Demadex) CARDIAC DRUGS Many of these drugs have multiple effects and uses. BRADYCARDIA To treat bradycardia, these drugs increase the heart rate: ◆ atropine ◆ epinephrine (Adrenalin) TACHYCARDIA To treat tachycardia, these drugs decrease the heart rate: ◆ adenosine (Adenocard) ◆ propranolol (lnderal) ◆ verapamil (Calan) CONGESTIVE HEART FAILURE, ATRIAL FIBRILLATION/ FLUTTER, SUPRAVENTRICULAR TACHYCARDIA (SVT), AND PAROXYSMAL ATRIAL TACHYCARDIA To treat congestive heart failure, atrial fibrillation/flutter, SVT, and paroxysmal atrial tachycardia, digoxin slows heart rate and strengthens heart contractions. ◆ digoxin (Lanoxin) ANGINA The following drugs are used to treat angina: ◆ isosorbide dinitrate (lsordil) ◆ nitroglycerine ◆ propranolol (lnderal) 91

SEDATIVES AND ANALGESICS Are used to produce sedation, anesthesia, muscle relaxation, anxiety relief, pain relief, and/or sleep. Most sedatives are CNS depressants and can cause respiratory depression; as a result, vital signs and respiratory rate should be monitored. SEDATIVES/TRANQUILIZERS—BENZODIAZEPINES The following drugs are used for antianxiety and sedation: ◆ diazepam (Valium) ◆ lorazepam (Ativan) ◆ chlordiazepoxide (Librium) ◆ propofol (Diprivan) NARCOTIC ANALGESICS—OPIATES The following drugs are used for pain relief and sedation: ◆ codeine ◆ fentanyl (Sublimaze) ◆ meperidine (Demerol) ◆ propoxyphene (Darvon) ◆ morphine (Duramorph, MS Contin) (Morphine is also used to improve exercise tolerance in COPD.)

92

THERAPEUTIC MODALITIES See references 6, 10, 24, and 25 94 94 97 97 98 99 101 103 105 106 106 106 106 106 106 106 110 107 107 108 108 109 109 109 110 110 110 110 111 114

115 118

Continued

93

Therapeutic Modalities

MEDICAL GASES. . . . . . . . . . . . . . . . . . . . . . . . . . . . Oxygen Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . Helium Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . Hyperbaric Oxygen Therapy (HBO or BHOT) . . . Nitric Oxide (NO) . . . . . . . . . . . . . . . . . . . . . . . . . . MEDICATION DELIVERY DEVICES . . . . . . . . . . . . . THERAPIES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CPT/PD POSITIONS . . . . . . . . . . . . . . . . . . . . . . . . . ARTIFICIAL AIRWAYS AND SUCTIONING . . . . . . . TUBE CUFF PRESSURE . . . . . . . . . . . . . . . . . . . . . . Combitube . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ORAL PHARYNGEAL AIRWAY . . . . . . . . . . . . . . . . . NASAL PHARYNGEAL AIRWAY/NASAL TRUMPET . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . SUCTIONING . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Appropriate Vacuum Pressures . . . . . . . . . . . . . . Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hazards and Complications . . . . . . . . . . . . . . . . . INTUBATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EXTUBATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ESOPHAGEAL OBTURATOR AIRWAY (EOA) . . . . . LARYNGEAL MASK AIRWAY (LMA) . . . . . . . . . . . . PASSY-MUIR SPEAKING VALVE (PMV) . . . . . . . . . Key Points . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . DIAGNOSTIC TOOLS . . . . . . . . . . . . . . . . . . . . . . . . . Pulse Oximetry . . . . . . . . . . . . . . . . . . . . . . . . . . . . AARC Clinical Practice Guideline: Pulse Oximetry . . . . . . . . . . . . . . . . . . . . . . . . . . Transcutaneous Oxygen Monitoring (TcPO2) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . AARC Clinical Practice Guideline: Transcutaneous Blood Gas Monitoring of Oxygen (PtcO2) and Carbon Dioxide (PtcCO2) for Neonatal and Pediatric Patients . . . . . . . . . . . . . . . . . . . . Capnography (ETCO2) . . . . . . . . . . . . . . . . . . . . . .

AARC Clinical Practice Guideline: Capnography/Capnometry During Mechanical Ventilation (MV) . . . . . . . . . . . . . . . BREATHING RETRAINING EXERCISES . . . . . . . . . Diaphragmatic Breathing . . . . . . . . . . . . . . . . . . . Pursed-Lip Breathing . . . . . . . . . . . . . . . . . . . . . . .

118 123 124 124

SEE ALSO MEDICATIONS

LMEDICAL GASESL OXYGEN THERAPY Oxygen Tank Factors (L/psi) E cylinder  0.28 (or round to 0.3) G cylinder  2.4 H cylinder  3.1 (or round to 3) Oxygen Tank Duration of Flow Calculations (in minutes) Gauge pressure in psi  tank factor liter flow (L/m) Example: How long will an E cylinder with 2200 psi last running at 6 L/m? 2200  0.3 110 minutes, or  1 hour, 50 minutes 6 Oxygen and Air Entrainment Ratios Therapeutic Modalities

FiO2

Oxygen:Air

24% . . . . . . . . . . 1:25 28% . . . . . . . . . . 1:10 35% . . . . . . . . . . 1:4.3 40% . . . . . . . . . . 1:3 60% . . . . . . . . . . 1:1 70% . . . . . . . . . . 1:0.6 100% . . . . . . . . . . 1:0 94

OXYGEN THERAPY OXYGEN DELIVERY DEVICE

OXYGEN FLOW RATE (LPM)

FiO2

NOTES

Nasal cannula (NC) 1-6

24%-44%

Simple mask Venturi mask

5-8 Variesa

40%-60% 24%-50%

Aerosol mask with Venturi

Variesa

21%-100%

Partial rebreather mask (PRB) Nonrebreather mask (NRB)

8-15

60%-80%

8-15

80%-100%

Oxymizer

1-6

28%-46%

1 L/m 24%, 2 L/m 28%, 3 L/m 32%. 4 L/m 36%, 5 L/m 40%, 6 L/m 44%. Minimum flow is 5 L/m to flush carbon dioxide (CO2) from mask. Oxygen (O2) flow rate is set per manufacturer instructions to achieve exact FiO2. O2 flow rate is set per manufacturer instructions to achieve exact FiO2. Face mask, face tent, or tracheostomy collar (either cool or heated) can be used. PRB is a nonrebreather with flaps removed. Reservoir bag is kept at least two-thirds full with O2 flow ⬎7 L/m to flush out CO2. Highest FiO2 is achieved by using three flaps. Reservoir bag is kept at least two-thirds full with O2 flow ⬎7 L/m to flush out CO2. Delivered FiO2 is slightly higher than NC because of the reservoir.

95

Continued

96

OXYGEN THERAPY—cont’d

a

OXYGEN DELIVERY DEVICE

OXYGEN FLOW RATE (LPM)

FiO2

NOTES

Oxygen conserving

1-6

24%-44%

Oxygen concentratorb

1-6

—

OxyMask

1-⬎15

24%-90%

Resuscitation bag (Ambu bag) High-flow heated cannula (Vapotherm)

15-flush

100%

Adult: 5-40 Neonate: 1-8

21%-100%

O2 is delivered on inspiration only. FiO2 and SpO2 may be less than on NC. Device (OCD) is used only while patient is awake. Uses a molecular sieve to produce O2 from room air. Is used in home care or alternate care when wall O2 is not available. Delivers FiO2 slightly less than NC previously listed. Open design mask allows oral care. Is good for nose and mouth breathers. Actual FiO2 varies. Increase flow rate to increase FiO2. Refer to manufacturer’s literature. Delivers tidal volume and oxygen to patient, usually for emergency and transport. Specially designed nasal cannula or transtracheaI cannula used to provide heated humidity. For adults, can use at flow rates up to 40 L/m nasal and 20 L/m tracheal. Vapotherm is one type of heated cannula.

Different manufacturers of Venturi masks require different flow rates to achieve exact FiO2. Follow the manufacturer’s guidelines. Concentrator FiO2 output usually ranges between 93% and 99%, whereas high-pressure wall outlet oxygen source delivers FiO2 at 100%. Concentrator can also be used with mask oxygen, but may need to connect two concentrators to deliver adequate flow rate. Note: High-flow devices meet total patient demand for minute volume.

b

HELIUM THERAPY Helium is a low-density gas used to decrease WOB in cases of large airway obstruction (asthma, COPD, croup, stridor). Is usually given via nonrebreather or simple mask. Voice distortion is a short-term side effect. Two mixtures available are 80/20 and 70/30 (helium/oxygen percentage). With an oxygen flowmeter, flow rate must be adjusted for helium as follows: 80/20 Divide desired flow rate by 1.8 to get set flow rate. Example: A flow rate of 10 L/m using 80/20 helium/oxygen gas is wanted. Where is the oxygen flowmeter set? 10  1.8  5.5 L/m 70/30 Divide desired flow rate by 1.6 to get set flow rate. Example: A flow rate of 8 L/m using 70/30 helium/oxygen gas is wanted. Where is the oxygen flowmeter set? 8  1.6  5.0 L/m HYPERBARIC OXYGEN THERAPY (HBO OR HBOT) • HBO is oxygen therapy at pressures greater than one atmosphere, also known as ATA (atmospheric pressure absolute). 1 ATA 760  mm Hg • HBO is usually given at 2 to 3 ATA, but can be higher. Duration and frequency vary greatly, based on condition. • HBO using 100% oxygen increases oxygenation (PaO2) much more than 100% oxygen alone. Tissue oxygenation is also greatly increased. • The patient breathes 100% oxygen during HBO therapy. Pressurization is achieved 97

using the HBO chamber, either monoplace or multiplace. • In addition, refer to atmospheric pressure in the Formulas and Facts section. INDICATIONS • Air or gas embolism • Decompression sickness • Carbon monoxide (CO) or cyanide poisoning. HBO is the fastest method of removing CO from blood (about 22 min at 3 ATA) • Gangrene, necrotizing soft tissue infection, ischemic skin grafts, and radiation necrosis • Exceptional blood loss • To speed wound healing and promote neovascularization (via HBO hyperoxia effects) • To treat cerebral edema, crush injuries, and burns (via HBO hyperoxia and vasoconstriction effects that decrease edema while increasing tissue oxygenation) HAZARDS AND COMPLICATIONS • Ear or sinus trauma/tympanic membrane rupture (important to properly “clear ears” to prevent this) • Pneumothorax, air embolism, oxygen toxicity, and CNS toxicity • Claustrophobia, sudden decompression, and temporary visual changes • Fire (chamber fire prevention includes no alcohol or petroleum products, no sprays, no makeup, no deodorant, clothing 100% cotton to avoid static electricity) NITRIC OXIDE (NO) See the Medications section.

98

MEDICATION DELIVERY DEVICES MEDICATION DELIVERY DEVICE

NebuIizer, small reservoir Nebulizer, continuous Nebulizer, large reservoir Heart MiniHeart AeroEclipse (Breathactivated nebulizer)

OXYGEN FLOW RATE (L/m)a

DURATION OF TREATMENT (AVERAGE)

6-8

10 min

10 2 8

7-8 hr 3-4 hr 5 min

NOTES

Typical nebulizer treatment, hand-held or mask. Can also give in-line with ventilator, BiPAP, CPAP, or continuous aerosol therapy. Continuous nebulizer treatment. Medication and saline amounts are variable, based on physician’s order for mg/hr of medication and manufacturer’s instructions for amount of saline and flow rate. Can give MiniHeart in line with ventilator, CPAP, BiPAP, or aerosol therapy. Inspiration is breath activated. Can also provide continuous flow. Can give concentrated medication solution.

Continued

99

100

MEDICATION DELIVERY DEVICES—cont’d MEDICATION DELIVERY DEVICE

a

OXYGEN FLOW RATE (L/m)a

DURATION OF TREATMENT (AVERAGE)

IPPBb

10-15 min

Metered-dose inhaler (MDI)

5 min

Dry powder inhaler (DPI) Spacer

5 min

NOTES

Lung expansion therapy to treat or prevent atelectasis and improve lung function. Can give with medications or saline. Use 50 psi source gas, oxygen, or air. Adjust flow rate and PIP (best range is 18-24 cm H2O), based on patient’s needs and tolerance. Medication delivery uses propellants. Medication must be shaken, then inhaled, one puff at a time with 5-10 sec breath hold. Wait 1 min between puffs. Medication is delivered with dry powder. Is inhaled one puff at a time with 5-10 sec breath hold. Wait 1 min between puffs. Is used with MDIs and some DPIs. Check manufacturer’s instructions for compatibility. Improves medication deposition in the lungs and lessens deposition in the mouth.

Alternatively use air compressor with preset flow rate of 6-8 L/m when applicable. IPPB contraindicated in untreated pneumothorax; also see Precautions after next table.

b

THERAPIES THERAPEUTlC MODALITYa

DURATION OF TREATMENT (AVERAGE)

Acapella PEP or Flutter

5-20 min sessions QID to every 2 hr while patient is awake

EZ PAP

10 min sessions QID

Incentive spirometry

10 breaths every 1-2 hr while patient is awake

NOTES Description: Good alternative for chest physical therapy (CPT) vibratory/ oscillatory positive expiratory pressure therapy. Is used to treat or prevent atelectasis, mobilize and remove secretions, reduce air trapping in COPD, and improve lung function. Operation: Patient blows into device. Oscillation rate is adjustable (on Flutter by angle of tilt; on Acapella by rotating knob). Can give nebulizer in-line with Acapella. Encourage cough after treatment. Description: Lung expansion therapy to treat or prevent atelectasis and improve lung function. Operation: Use mask or mouthpiece. Oxygen or air flow starts at 5 L/m and adjusts up to max 15 L/m, based on patient needs and tolerance. Manometer is in-line to measure pressure (average 10-20). Can give alone with source gas, or add nebulizer in line. Encourage cough after treatment. Description: Lung expansion therapy prevents and treats alelectasis. Normal is 50 mL/kg.

101

Continued

102

THERAPIES—cont’d

a

THERAPEUTlC MODALITYa

DURATION OF TREATMENT (AVERAGE)

Vibratory vest

30 min sessions QID

Description: Good alternate for CPT. Provides chest wall oscillations. Is used to improve airway clearance in diseases with impaired secretion clearance including CF, asthma, and COPD. Operation: Select appropriate vest size. Set pressure to 4-6. Set frequency to 10, 12, or 14 Hz, starting at low frequency, and adjusting upward every 10 minutes, based on patient tolerance. Encourage cough after treatment.

CPT/PD

10-15 min sessions

Description: CPT is percussion and vibration to target areas of the lung. Postural drainage (PD) is gravity drainage of target areas of the lung. CPT/PD is used to present and reverse atelectasis, improve mobilization, remove secretions, and improve lung function. Encourage cough after treatment (see CPT/PD positions).

NOTES

Therapy Precautions and Possible Contraindications: Clinically unstable, unstable hemodynamic or cardiac status, increased ICP, recent neurosurgery, pulmonary emboli, empyema, rib fracture, pneumothorax, recent postoperative or injury with severe pain, hemoptysis, and conditions prone to hemorrhage. Contraindications for vest and CPT: rib fracture, pulmonary empyema, and untreated pneumothorax. See also Medications for indications and contraindications of specific medications.

LCPT/PD POSITIONS20L

UPPER LOBES, APICAL SEGMENTS Patient sits and leans back on a pillow at a 30-degree angle. Percuss between the clavicle and top of the scapula on both sides. UPPER LOBES, POSTERIOR SEGMENTS Patient leans forward on a pillow at a 30-degree angle. Percuss over the upper back on both sides.

UPPER LOBES, ANTERIOR SEGMENTS Bed is flat. Patient lies flat on the back. Percuss between the clavicle and nipple on both sides. RIGHT MIDDLE LOBE, LATERAL/ MEDIAL SEGMENTS Foot of the bed is elevated 15 degrees. Patient lies head down on the left side, rotated onequarter turn backward. Percuss under the breast on the right side.

103

LINGULAR SEGMENT OF THE LEFT UPPER LOBE Foot of the bed is elevated 15 degrees. Patient lies head down on the right side, rotated one-quarter turn backward. Percuss between the nipple and armpit on the left side.

LOWER LOBES, SUPERIOR SEGMENTS Bed is flat. Patient lies on the stomach with two pillows under the hips. Percuss over the middle of the back at the tip of the scapula on both sides of the spine. LOWER LOBES, ANTERIOR BASAL SEGMENTS Foot of the bed is elevated 30 degrees. Patient lies head down on the right side and then on the left. Percuss over the lower ribs just below the axilla on both sides. LOWER LOBES, LATERAL BASAL SEGMENTS Foot of the bed is elevated 30 degrees. Patient lies head down on the right side and then on the left, rotated one-quarter turn inward toward the bed. Percuss over the lower ribs on both sides.

104

LOWER LOBES, POSTERIOR BASAL SEGMENTS Foot of the bed is elevated 30 degrees. Patient lies head down on the stomach with a pillow under the hips. Percuss over the lower ribs, close to the spine on both sides.

ARTIFICIAL AIRWAYS AND SUCTIONING

AGE

ET TUBE INTERNAL DIAMETER (MM)

LARYNGOSCOPE BLADE SIZE

SUCTION CATHETER (FRENCH SIZE)

Newborn 1000 g 1000-2000 g 2000-3000 g 3000 g

25 3 2.5 3.5-4.0

0 0 1 1

5 6 6-8 6-8

6 months

3.5-4.0

1-2

6-8

4

1-2

8

2-3 years

4.5-5.0

2

8

4-7 years

5.0-6.0

2

8-10

8-10 years

1 year

6.0-6.5

2-3

10

12 years

7

2-3

10

15 years

7.0-7.5

3

10-12

Adult female

7.5-8.5

3-4

12

Adult male

8.0-9.5

3-4

14

Calculation: (ID [mm] of ET tube 2)  3  French catheter size.

105

LTUBE CUFF PRESSUREL Cuff pressure should always remain below 20 mm Hg (26 cm H2O) to prevent edema and necrosis. COMBITUBE • Can be used as an alternate for ET tube. • One must ensure proper placement.

LORAL PHARYNGEAL AIRWAYL Is used to maintain a patent oral airway in the unconscious patient. Is not well tolerated by the conscious patient. Is also used as a bite block and to facilitate oral suctioning. Proper size for the patient is from tip of chin to the angle of jaw. Insert upside down until the tip is at the end of the tongue, then rotate 180 degrees into the proper position.

NASAL PHARYNGEAL AIRWAY/NASAL TRUMPET Is used to maintain a patent nasal airway in the conscious or unconscious patient and to facilitate deep tracheal suctioning. The diameter should be slightly less than the patient’s naris. Lubricate for easy placement. Needs to be periodically changed with a clean nasal trumpet and relubricated.

LSUCTIONINGL INDICATIONS • Inability to cough effectively • Inability to clear problematic secretions without assistance and breath sounds with coarse rhonchi APPROPRIATE VACUUM PRESSURES Adults: 80 to 120 mm Hg Children: 80 to 100 mm Hg Infants: 40 to 80 mm Hg 106

(See appropriate suction catheter size for specific ET tubes on the previous page.) PROCEDURE Hyperoxygenate, hyperventilate, instill saline, and insert suction catheter proper distance. Apply intermittent vacuum to aspirate secretions, keeping suction time less than 15 seconds. Oxygenate and ventilate patient as necessary. Assess patient for problems, including bradycardia, skin color changes, decreased pulse ox saturation, and changes in respiratory rate. Observe for complications and hazards as mentioned below. HAZARDS AND COMPLICATIONS • Changes in vital signs • Bradycardia, arrhythmias, blood pressure changes, hypoxemia, laryngospasm, bronchospasm, uncontrolled coughing, gagging, vomiting, atelectasis, increased ICP, and cardiopulmonary arrest • Most common: airway trauma and bleeding • Late complications: trachea necrosis and respiratory infection

LINTUBATIONL • Prepare all equipment: several tubes, tape or other tube-securing device, syringe, stylet, laryngoscope blades, oral airways, bite block, lubricant, and suction equipment. Check cuff. Nurses should be prepared with medications. • Hyperoxygenate and ventilate the patient before intubation. • Limit intubation attempt to a maximum of 30 seconds. • Watch for hazards and complications as listed previously in Suctioning. • After intubation, inflate cuff and secure tube. 107

• Assess for successful intubation: ◆ ETCO detector if available 2 ◆ Equal bilateral breath sounds and lung expansion ◆ Warm air and moisture condensate appearing in tube ◆ No increase in abdominal distention • Verify placement of tube with chest x-ray.

LEXTUBATIONL • Ensure the patient meets extubation criteria (see the table on page 197). • Explain the procedure to the patient. • Preoxygenate and ventilate the patient. • Suction the trachea and oropharynx. • Remove the tape or tube connectors. • Deflate the cuff. • Remove the cuff at end inspiration while the patient coughs. • Suction the oropharynx. • Place the patient on oxygen. • Assess for dyspnea, hypoxemia, or stridor; treat as indicated. • Monitor patient’s vital signs.

ESOPHAGEAL OBTURATOR AIRWAY (EOA) • EOA can be used when intubation is not possible. • Is designed for short-term use only (1 to 2 hours). • Provides better ventilation than bag-mask because it blocks air from entering the stomach. • End is plugged because it is inserted into the esophagus, not into the trachea.

108

• Mask clips onto the end of the tube; 16 holes at the level of the oropharynx allows air to be delivered to the lungs by a resuscitation bag. • Cuff is inflated to block air from entering the stomach and to prevent aspiration of gastric contents. • Before removing the EOA, the trachea must be intubated to protect the lungs from aspiration. The patient will usually vomit when the EOA is removed; therefore suction equipment should be ready. The EOA should not be used on patients under 16 years of age.

LLARYNGEAL MASK AIRWAY (LMA)L • Can be used as an alternative to the ET tube. • Is acceptable for short-term use and surgical procedures. • Patient must be sedated to depress the gag reflex.

PASSY-MUIR SPEAKING VALVE (PMV) KEY POINTS • Allows the patient to verbally communicate, improves secretion management swallowing, reduces aspiration, and can expedite weaning. • Helps restore a more normalized physiologic and breathing pattern, and restores airflow through the oral and nasal cavities during exhalation. • Is designed to be attached to the end of a tracheostomy tube, whether on or off a ventilator. • Manufacturer’s instructions should be reviewed for the proper PMV to be used for each patient.

109

• Cuff should always be deflated when the PMV is on; otherwise, the patient will be unable to breathe. • Patient’s vital signs are monitored while the PMV is on; it should be used only when the patient is awake. • Following manufacturer’s cleaning instructions, the PMV is cleaned daily by swishing in mild soap and warm water, rinsing in water, and air drying. Other products or methods of cleaning should not be used. • Speech therapists work in conjunction with respiratory therapists to ensure the best patient assessment and use of PMVs. INDICATIONS The PMV can be used with patients from infant to adult who have a tracheostomy tube. Patient should be alert, responsive, and medically stable. Patient must be able to generate sufficient air during exhalation around the tube and through the upper airway (may need many attempts). CONTRAINDICATIONS Contraindications include unconsciousness, extremely thick and copious secretions, severe tracheal or laryngeal stenosis, severe respiratory infection, laryngectomy. In addition, the PMV is not used with a foam cuff tube or an ET tube.

LDIAGNOSTIC TOOLSL PULSE OXIMETRY Pulse oximetry (PO) is a good noninvasive technique for continuous or quick measurement of oxygen saturation (SpO2), which closely parallels ABG SaO2. The normal SpO2 is 95%. It uses a spectrophotometer 110

to measure the percent of oxyhemoglobin and shows heart rate. An accurate reading is indicated by good waveform and heart rate correlating with palpable pulse. Ear and finger pulse oximeters are most accurate in patients with good perfusion who have actual saturation of 70% or higher. Factors that can cause erroneous saturation reading include: • Poor perfusion • Motion artifact • Hypothermia • Artificial fingernails or nail polish • Abnormal hemoglobin (e.g., methemoglobin or carboxyhemoglobin) AARC CLINICAL PRACTICE GUIDELINE: PULSE OXIMETRY* PO 1.0 Procedure Pulse oximetry (SpO2) PO 2.0 Procedure and Definition PO provides estimates of arterial oxyhemoglobin saturation (SaO2) by using selected wavelengths of light to noninvasively determine the saturation of oxyhemoglobin (SpO2). PO 3.0 Setting PO may be performed by trained personnel in a variety of settings that include but are not limited to hospitals, clinics, and home. PO 4.0 Indications ◆ To monitor the adequacy of arterial oxyhemoglobin saturation ◆ To quantitate the response of arterial oxyhemoglobin saturation to therapeutic *Guidelines from Respiratory Care and The American Association for Respiratory Care.

111

intervention or to a diagnostic procedure (e.g., bronchoscopy) ◆ To comply with mandated regulations or recommendations PO 5.0 Contraindications The presence of an ongoing need for measurement of pH, PaCO2, total hemoglobin, and abnormal hemoglobins may be a relative contraindication to PO. PO 6.0 Hazards and Complications • Is considered a safe, noninvasive procedure, but device limitations, false-negative results for hypoxemia, and/or false-positive results for normoxemia or hyperoxemia may lead to inappropriate treatment of the patient. • Tissue injury may occur at the measuring site as a result of probe misuse (e.g., pressure sores from prolonged application or electrical shock and burns from substitution of incompatible probes). PO 7.0 Device Limitations and Validation of Results Factors, agents, or situations that may affect readings or limit the precision, performance, or application of PO include: • Motion artifact • Abnormal hemoglobins (primarily carboxyhemoglobin [COHb] and methemoglobin [metHb]) • Intravascular dyes and exposure of measuring probe to ambient light during measurement • Low perfusion states • Skin pigmentation • Nail polish or nail coverings with finger probe • Inability to detect saturations 83% with the same degree of accuracy and precision seen at higher saturations 112

• Inability to quantitate the degree of hyperoxemia present • For continuous, prolonged monitoring to ensure that high/low alarms are appropriately set SpO2 results should be documented in the patient’s medical record and should detail the conditions under which the readings are obtained (e.g., date, time of measurement, and PO reading, patient’s position, activity level, location). During monitoring, patient’s activity should be according to the physician’s order, including inspired oxygen concentration or supplemental oxygen flow, type of oxygen delivery device, probe placement site and probe type, clinical appearance of patient—subjective assessment of perfusion at measuring site (e.g., cyanosis, skin temperature), and agreement between patient’s heart rate as determined by PO and by palpation and oscilloscope. When disparity exists between SpO2 and SaO2 readings and the patient’s clinical presentation, possible causes should be explored before results are reported. Discrepancies may be reduced by monitoring at alternate sites or appropriate substitution of instruments or probes. If such steps do not remedy the disparity, results of PO should not be reported; rather, a statement describing the corrective action should be included in the patient’s medical record, and direct measurement of arterial blood gas (ABG) values should be requested. The absolute limits that constitute unacceptable disparity vary with patient condition and specific device. Clinical judgment must be exercised. 113

PO 8.0 Assessment of Need When direct measurement of SaO2 is not available or accessible in a timely fashion, a SpO2 measurement may suffice temporarily if the limitations of the data are appreciated. SpO2 is appropriate for continuous and prolonged monitoring (e.g., during sleep, exercise, bronchoscopy). SpO2 may be adequate when assessment of acid-base status and/or PaO2 is not required. PO 9.0 Assessment of Outcome The following should be used to evaluate the benefit of PO: ◆ SaO results should reflect the patient’s 2 clinical condition (i.e., validate the basis for ordering the test). ◆ Documentation of results, therapeutic intervention, and/or clinical decisions based on the SaO2 measurement should be noted in the medical record. Note: Brief synopsis of AARC Guidelines for Pulse Oximetry. Reference: AARC Clinical Practice Guidelines. Accessed September 2008 at RCJournal.com.

TRANSCUTANEOUS OXYGEN MONITORING (TcPO2) TcPO2 reads the partial pressure of oxygen on the skin. The normal value is the same normal value as PaO2 age-appropriate value. The device uses a heated anode that improves local vasodilation. The site chosen should have good capillary circulation and no large vessels in the area. The electrode should be moved periodically to prevent burns. TcPO2 has proven most beneficial in neonates, because in others, thicker skin and skin texture affect accuracy of readings. TcPO2 has also proven beneficial in HBO therapy because in 114

HBO, TcPO2 can be used to trend large variances in PO2 (e.g., a change from 80 to 500). AARC CLINICAL PRACTICE GUIDELINE: TRANSCUTANEOUS BLOOD GAS MONITORING OF OXYGEN (PtcO2) AND CARBON DIOXIDE (PtcCO2) FOR NEONATAL AND PEDIATRIC PATIENTS* TCM 1.0 Procedure Transcutaneous monitoring (TCM) of oxygen (PtcO2) and carbon dioxide (PtcCO2) in neonates, infants, and small children. TCM 2.0 Description and Definition TCM measures skin surface PO2 and PCO2 to provide estimates of arterial partial pressure of oxygen and carbon dioxide (PaO2 and PaCO2). The devices induce hyperperfusion by local heating of the skin and measure the partial pressure of oxygen and carbon dioxide (CO2) electrochemically. TCM 3.0 Setting TCM may be performed by trained personnel in a variety of settings including, but not limited to, hospitals, extended care facilities, and patient transport. TCM 4.0 Indications Monitoring the adequacy of arterial oxygenation and/or ventilation is needed. Quantitating the response to diagnostic and therapeutic interventions as evidenced by PtcO2 and/or PtcCO2 values is also needed. TCM 5.0 Contraindications In patients with poor skin integrity and/or adhesive allergy, TCM may be relatively contraindicated. *Guidelines from Respiratory Care and The American Association for Respiratory Care.

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TCM 6.0 Hazards and Complications PtcO2 and/or PtcCO2 monitoring is considered a safe procedure, but because of device limitations, false-negative and false-positive results may lead to inappropriate treatment of the patient. In addition, tissue injury may occur at the measuring site (e.g., erythema, blisters, burns, skin tears). TCM 7.0 Device Limitations and Validation of Results PtCO2 is an indirect measurement of PaO2 and, similar to PaO2, does not reflect oxygen delivery or oxygen content. Complete assessment of oxygen delivery requires knowledge of hemoglobin, saturation, and cardiac output. In a similar way, PtcCO2 is an indirect measurement of PaCO2, but knowledge of delivery and content is not necessary to use PtcCO2 as an indicator of adequacy of ventilation. Factors, agents, or situations that may affect readings or limit the precision, performance, or application of TCM include: • Prolonged stabilization time is required after electrode placement. • Improper calibration, trapped air bubbles, and damaged membranes are possible and may be difficult to detect. • Hyperoxemia (PaO2 100 torr) • Hypoperfused state (e.g., shock, acidosis) • Improper electrode placement or application • Vasoactive drugs • Nature of the patient’s skin and subcutaneous tissue (e.g., skinfold thickness, edema) Validation. ABGs should be compared with transcutaneous readings taken at the time of arterial sampling to validate the transcutaneous values. This validation should be performed initially and periodically as dictated 116

by the patient’s clinical state. During validation studies in patients with functional shunts, the electrode site and arterial sampling site should be on the same side of the shunt. When disparity exists between transcutaneous and arterial values and the clinical presentation of the patient, possible causes should be explored before results are reported. Monitoring at alternate sites, recalibration, or appropriate substitution of instruments may reduce discrepancies. If such steps do not remedy the disparity, transcutaneous results should not be reported; instead, a statement describing the corrective action should be included in the patient’s chart, and some other mode of monitoring should be established (e.g., PO and/or arterial blood analysis). The absolute limits that constitute unacceptable disparity vary with the patient’s condition and specific device. Clinical judgment must be exercised. To help ensure consistency of care-based transcutaneous blood gas readings, the operator should verify that high- and low-limit alarms are set appropriately; appropriate electrode temperature is set; electrode placement is appropriate; systematic electrode site change occurs; and specific manufacturer’s recommendations for maintenance, operation, and safety are followed. TCM 8.0 Assessment of Need When direct measurement of arterial blood is not available or accessible in a timely fashion, PtcO2 and/or PtcCO2 measurements may suffice temporarily if the limitations of the data are appreciated. TCM is appropriate for continuous and prolonged monitoring (e.g., during mechanical ventilation, CPAP, and 117

supplemental oxygen administration). PtcO2 values can be used for diagnostic purposes, as in the assessment of functional shunts (e.g., persistent pulmonary hypertension of the newborn [PPHN], persistent fetal circulation, or to determine the response to oxygen challenge in the assessment of congenital heart disease). TCM 9.0 Assessment of Outcome Results should reflect the patient’s clinical condition (i.e., validate the basis for ordering the monitoring). Documentation of results, therapeutic intervention (or lack of it), and/or clinical decisions based on the transcutaneous measurements should be noted in the medical record. Note: Brief synopsis of AARC Guidelines for Transcutaneous Blood Gas Monitoring of Oxygen (PtcO2) and carbon dioxide (PtcCO2) for Neonatal and Pediatric Patients. Reference: AARC Clinical Practice Guidelines. Accessed September 2008 at RCJournal.com.

CAPNOGRAPHY (ETCO2) Capnography is the measurement of CO2 and the resulting waveforms using infrared analyzers. The readings represent end-tidal CO2 (ETCO2). The normal value is 5.3% or 40 mm Hg. Capnography can give an estimation of PaCO2 and trend the changes in PaCO2. Most often used in-line with mechanical ventilation. AARC CLINICAL PRACTICE GUIDELINE: CAPNOGRAPHY/CAPNOMETRY DURING MECHANICAL VENTILATION (MV)* CO2 MV 1.0 Procedure Capnography is the continuous analysis and recording of CO2 concentrations in respiratory *Guidelines from Respiratory Care and The American Association for Respiratory Care.

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gases. Although the terms capnography and capnometry are sometimes considered synonymous, capnometry suggests measurement (i.e., analysis alone) without a continuous written record or waveform. Capnographic waveforms may be time based or volume based. CO2 MV 2.0 Description and Definition For the purposes of this guideline, capnography refers to the evaluation of CO2 in the respiratory gases of mechanically ventilated patients. A capnographic device incorporates one of two types of analyzers: mainstream or sidestream. Mainstream analyzers insert a sampling window into the ventilator circuit for measurement of CO2, whereas a sidestream analyzer aspirates gas from the ventilator circuit, and the analysis occurs away from the ventilator circuit. Analyzers use infrared, mass, or Raman spectra, or a photoacoustic spectra technology. Flow measuring devices are used in volume-based capnographs. CO2 MV 3.0 Setting Procedure may be performed by trained health care personnel in any setting in which mechanically ventilated patients are found (e.g., hospital, extended care facility, during transport). CO2 MV 4.0 Indications On the basis of available evidence, capnography should not be mandated for all patients receiving MV support, but it may be indicated for the following: ◆ 4.1. Evaluation of the exhaled CO , es2 pecially end-tidal CO2, is the maximum partial pressure of CO2 exhaled during a tidal breath (just before the beginning of inspiration) and is designated PetCO2. 119

4.2. Monitoring the severity of pulmonary disease and evaluating the response to therapy are indicated, especially therapy intended to improve the ratio of dead space to tidal volume (VD/VT), the matching of ventilation to perfusion (V/Q), and possibly to increase coronary blood flow. ◆ 4.3. Is used as an adjunct to determine whether tracheal rather than esophageal intubation has taken place (low or absent cardiac output may negate its use for this indication). Colorimetric CO2 detectors are adequate devices for this purpose. ◆ 4.4. Continued monitoring of the integrity of the ventilatory circuit, including the artificial airway, is indicated. ◆ 4.5. Evaluation of the efficiency of mechanical ventilatory support by determining the difference between the arterial partial pressure for CO2 (PaCO2) and for PetCO2. ◆ 4.6. Adequacy of pulmonary, systemic, and coronary blood flow is monitored. Effective (nonshunted) pulmonary capillary blood flow is estimated by a partial rebreathing method. An adjunctive tool is used to screen for pulmonary embolism (evidence inclusive). Monitoring the matching of ventilation to perfusion during independent lung ventilation for unilateral pulmonary contusion is indicated. ◆ 4.7. Inspired CO is monitored when CO 2 2 gas is administered therapeutically. ◆ 4.8. Graphic evaluation of the ventilatorpatient interface and evaluation of the shape of the capnogram may be useful in detecting rebreathing of CO2, obstructive pulmonary disease, waning neuromuscular ◆

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blockade (curare cleft), cardiogenic oscillations, esophageal intubation, cardiac arrest, and contamination of the monitor or sampling line with secretions or mucus. ◆ 4.9. Volume of CO elimination is measured 2 to assess metabolic rate and/or alveolar ventilation. CO2 MV 5.0 Contraindications No absolute contraindications to capnography in MV patients exist, provided the data obtained are evaluated with consideration given to the patient’s clinical condition. CO2 MV 6.0 Hazards and Complications Capnography with a clinically approved device is a safe, noninvasive test associated with few hazards. With mainstream analyzers, the use of too large a sampling window may introduce an excessive amount of dead space into the ventilator circuit. Care must be taken to minimize the amount of additional weight placed on the artificial airway by the addition of the sampling window or, in the case of a sidestream analyzer, the sampling line. CO2 MV 7.0 Limitations of Procedure or Device Capnography, when performed using a device calibrated and operated as recommended by the manufacturer, has few limitations. It is important to note that although the capnograph provides valuable information about the efficiency of ventilation, it is not a replacement or substitute for assessment of the PaCO2. • The difference between PetCO2 and PaCO2 increases as dead space volume increases, and the difference between the PaCO2 and 121

PetCO2 has been shown to vary in the same patient over time. • Alterations in breathing pattern and tidal volume may introduce error into measurements designed to be made during stable, steady-state conditions. • Interpretation of results must take into account the stability of physiologic parameters such as minute ventilation, tidal volume, cardiac output, ventilation/perfusion ratios, and CO2 body stores. • Certain situations may affect the reliability of the capnogram, including the following: ◆ Type of device ◆ Contamination of the monitor or sampling system by secretions or condensate ◆ Sample tube of excessive length ◆ Sampling rate that is too high ◆ Obstruction of the sampling chamber ◆ Use of filters between the patient airway and the sampling line of the capnograph, which may lead to lowered PetCO2 readings ◆ Low cardiac output, which may cause a false-negative result when attempting to verify ET tube position in the trachea ◆ Reported false-positive results with ET tube position in the pharynx and when antacids and/or carbonated beverages are present in the stomach ◆ Possible decreased tidal volume delivery during volume modes, some dual control modes, and time-cycled, pressure-limited ventilation with low continuous flow rates if the sampling flow rate of a sidestream analyzer is too high, especially in neonates and pediatric patients 122

◆

Inaccurate measurement of expired CO2 that may be caused by leaks of gas from the patient-ventilator system, preventing collection of expired gases, including leaks in the ventilator circuit and leaks around tracheal tube cuffs or uncuffed tubes

CO2 MV 8.0 Assessment of Need Capnography is considered a standard of care during anesthesia and is recommended to be available for patients with acute ventilatory failure on MV support. Capnography is recommended as an adjunctive method to ensure proper ET tube position. Assessment of the need to use capnography with a specific patient should be guided by the clinical situation. The patient’s primary cause of respiratory failure and the acuteness of the condition should be considered. CO2 MV 9.0 Assessment of Outcome Results should reflect the patient’s condition and should validate the basis for ordering the monitoring. Documentation of results (along with all ventilatory and hemodynamic variables available), therapeutic interventions, and/or clinical decisions made based on the capnogram should be included in the patient’s chart. Note: Brief synopsis of AARC Guidelines for Capnography/ Capnometry during Mechanical Ventilation. Reference: AARC Clinical Practice Guidelines. Accessed September 2008 at RCJournal.com.

BREATHING RETRAINING EXERCISES • Are useful for COPD patients. • Breathing retraining exercises, such as diaphragmatic and pursed-lip breathing, can 123

assist the patient in taking deeper and more efficient breaths. (Many COPD patients take small, quick, shallow breaths.) • Can also help reduce dyspnea, reduce the severity and frequency of dyspneic episodes, and improve exercise tolerance. DIAPHRAGMATIC BREATHING • Helps the lungs expand and take in more air. • Patient should lie as supine as possible, with one hand on the abdomen and the other hand on the chest. • When inhaling, the patient should press on the abdomen and extend it outward as far as possible. The hand over the abdomen should move outward; the hand on the chest should not move. • After mastering the technique while supine, the patient should practice the exercise while sitting or standing. • Effective exercise program lasts 20 to 30 minutes BID or TID. PURSED-LIP BREATHING Patient should breathe in through the nose (4 to 5 sec) and out through the mouth (6 sec) while pressing the lips together. • Helps the patient move air out slower and breathe deeper. • Prevents the small airways from collapsing during exhalation. • Reduces dyspnea and improves ventilation and improves the ability to exercise.

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ABGs, LABS, AND HEMODYNAMICS* See references 6, 11, 14, 23, and 24 NORMAL LABORATORY VALUES IN INTERNATIONAL SYSTEM OF UNITS . . . . . . BLOOD GAS SAMPLING SITES . . . . . . . . . . . . . . . BLOOD GAS SAMPLING ERRORS . . . . . . . . . . . . . BLOOD GAS MACHINE ELECTRODES . . . . . . . . . . ARTERIAL BLOOD GASES—ADULT NORMAL VALUES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . MIXED VENOUS BLOOD GASES—ADULT NORMAL VALUES . . . . . . . . . . . . . . . . . . . . . . . . . BLOOD GASES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Causes of Abnormal Blood Gases . . . . . . . . . . . . RELATIONSHIP OF PH, PACO2, AND HCO3 IN ACUTE CONDITIONS . . . . . . . . . . . . . . . . . . . . INTERPRETATION OF BLOOD GASES . . . . . . . . . . BICARBONATE ADMINISTRATION TO CORRECT PH LEVELS . . . . . . . . . . . . . . . . . . . . . . COPD PATIENT NORMAL VALUES . . . . . . . . . . . . . FORMULA FOR ESTIMATING NORMAL PAO2 (USEFUL FOR AGES 10 TO 80 YEARS) . . . . . . . . FORMULA FOR ESTIMATING SATURATION . . . . 4-5-6-7-8-9 RULE . . . . . . . . . . . . . . . . . . . . . . . . . . . . OXYHEMOGLOBIN DISSOCIATION CURVE . . . . . BLOOD GAS FORMULAS . . . . . . . . . . . . . . . . . . . . . HEMODYNAMIC PARAMETERS . . . . . . . . . . . . . . . MEDICAL CONDITIONS AND HEMODYNAMIC CHANGES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . MISCELLANEOUS VITAL SIGNS . . . . . . . . . . . . . . . URINE LABORATORY TESTING . . . . . . . . . . . . . . . . ADULT LABORATORY VALUES . . . . . . . . . . . . . . . . SPUTUM ANALYSIS . . . . . . . . . . . . . . . . . . . . . . . . . CEREBROSPINAL FLUID (CSF) LABORATORY TESTING . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

126 127 127 128 128 129 129 129 129 130 130 130 131 131 131 131 132 134 136 137 137 138 142 142

SEE ALSO VENTILATORS, CPAP, AND BIPAP

*Note: All parameters in this section are adult values.

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ABGs, Labs, and Hemodynamics

Mechanical Ventilation Formulas . . . . . . . . . . . . 194

NORMAL LABORATORY VALUES IN INTERNATIONAL SYSTEM OF UNITS Laboratory Test Albumin Amylase (serum) AST Basophils Bilirubin, total Calcium, serum Calcium, urine CO2 (bicarbonate) Chloride Cholesterol, total Cholesterol, LDL Cholesterol, HDL Creatinine (urine) Eosinophils Glucose, urine Glucose, plasma Hematocrit

ABGs, Labs, and Hemodynamics

Hemoglobin LDH Lactic acid Leukocytes (WBC) Lymphocytes Monocytes Neutrophils Phosphorus Platelets (thrombocytes) Potassium Red blood cell count (RBC) Sodium Triglycerides, fasting Normal Urea, plasma (BUN) Urinalysis: pH Specific gravity WBC (leukocytes)

126

Normal Range in SI Units 35-50 g/L 0.88-2.05 nkat/L 0.11-0.66 μkat/L 0.0-0.3 fraction of WBCs 0-17 μmol/L 2.1-2.6 mmol/L 0.0-7.5 mmol/24 hr 22-30 mmol/L 98-106 mmol/L 5.17 mmol/L 2.59 mmol/L 1.55 mmol/L F 5.3-15.9 mmol/day M 7.1-21.2 mmol/day 0.0-0.8 fraction of WBCs 0.003 mmol/L 3.9-6.1 mmol/L F 0.36-0.46 fraction of RBCs M 0.37-0.49 fraction of RBCs F 7.4-9.9 mmol/L M 8.1-11.2 mmol/L 4.5 μkat/L 0.5-2.2 mmol/L 4.5-11.0  109/L 0.16-0.46 fraction of WBCs 0.04-0.11 fraction of WBCs 0.45-0.75 fraction of WBCs 0.81-1.45 mmol/L 150-420  109/L 3.5-5.0 mmol/L F 4.2-5.5  l012/L M 4.6-6.2  1012/L 135-145 mmol/L 0.45-1.69 mmol/L 2.8-8.9 mmol/L 5.0-9.0 1.001-1.035 4.5-15.0  109/L

Conversion Factor (U.S. to SI Units)

 10  0.01667  0.01667  0.01  17.1  0.25  0.025 N/A N/A  0.02586  0.02586  0.02586  88.4  0.01  0.05551  0.05551  0.01  0.6206  0.016667 N/A N/A  0.01  0.01  0.01  0.323 N/A N/A N/A  0.01129  0.357 N/A NA

LBLOOD GAS SAMPLING SITESL Three most common sites for obtaining blood gases are radial, brachial, and femoral. Best site is radial artery, because of collateral blood flow. The Allen test or modified Allen test is positive if collateral blood flow is present. The Allen test should be performed before any radial puncture. The procedure for ABGs includes: • Verify patient identification. • Use aseptic technique. • Wear gloves. • Wipe site with alcohol or other prep solution. • Palpate pulse. • Puncture at an angle. • Apply pressure to site for 5 to 10 minutes after puncture.

BLOOD GAS SAMPLING ERRORS Potential Error Erroneous Result Air bubbles

• pH increases • PO2 increases or decreases toward 150 mm Hg (room air value) • PCO2 decreases toward 0 mm Hg (room air value)

Too much heparin

• pH decreases • PO2 increases or decreases toward 150 mm Hg (room air value) • PCO2 decreases toward 0 mm Hg (room air value)

Sample not iced or improper cooling

• pH decreases • PO2 increases • PCO2 decreases

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If temperature correction not done or is incorrect: ◆ Patient with increased temperature: pH decreased, PO2 and PCO2 increased ◆ Patient with decreased temperature: pH increased, PO2 and PCO2 decreased

BLOOD GAS MACHINE ELECTRODES pH Sanz electrode PCO2 Severinghouse electrode PO2 Clark electrode Other values can be calculated from these results. The co-oximeter gives values for hemoglobin, oxyhemoglobin, carboxyhemoglobin, and methemoglobin. Blood gas machine calibration and maintenance on a regular schedule is mandatory for accurate and valid results.

ARTERIAL BLOOD GASES ADULT NORMAL VALUES

128

PARAMETER

NORMAL VALUE

NORMAL RANGE

pH PaCO2 PaO2 HCO3 BE Hb O2 content SaO2 COHb MetHb

7.4 40 mm Hg 100 mm Hg 24 mEq/L 0 14 g/dL 20 vol% 98% 0 0

7.35-7.40 35-45 mm Hg 80-100 mm Hg 22-26 mEq/L 2 to 2 12-18 g/dL 15-20 vol% 95% 2% 2%

MIXED VENOUS BLOOD GASES ADULT NORMAL VALUES PARAMETER

NORMAL VALUE

NORMAL RANGE

pH PvCO2 PvO2 HCO3 SvO2

7.37 45 mm Hg 40 mm Hg 24 mEq/L 73%

7.32-7.42 40-50 mm Hg 38-42 mm Hg 22-26 mEq/L 70-75%

LBLOOD GASESL CAUSES OF ABNORMAL BLOOD GASES Respiratory • Insufficient alveolar ventilation acidosis • Pulmonary disease, CNS depression, drugs causing respiratory depression Respiratory • Alveolar hyperventilation alkalosis • Stress, emotional upset, hypoxia, fever, CNS trauma Metabolic acidosis

• Lactic acidosis, ketoacidosis (diabetes), renal failure, diarrhea

Metabolic alkalosis

• Hypokalemia (most common cause), low chloride, diuretics, corticosteroids, vomiting, nasogastric tube

RELATIONSHIP OF pH, PaCO2, AND HCO3 IN ACUTE CONDITIONS pH

PaCO2 (mm Hg)

HCO3 (mEq/L)

& 0.10

 10

2

 0.05

& 10

&1 129

INTERPRETATION OF BLOOD GASES INTERPRETATION pH PaCO2 HCO3 Respiratory Acidosis/Ventilatory Failure  & Acute N & & Chronic/compensated N Acute superimposed  & & on chronic Respiratory Alkalosis/Hyperventilation &  Acute N   Chronic/compensated N Metabolic Acidosis   Acute N   Compensated N Metabolic Alkalosis & & Acute N & & Compensated N N, Normal.

BICARBONATE ADMINISTRATION TO CORRECT pH LEVELS One ampule of bicarbonate (44 mEq/L) will result in approximate pH & of 0.10.

LCOPD PATIENT NORMAL VALUESL The COPD patient with CO2 retention breathing on hypoxic drive has different “normal” blood gases than other patients. The “normal” values are a state of compensated respiratory acidosis, with decreased PaO2. Accurate interpretation of these blood gases can be more difficult, especially when the patient has acute respiratory acidosis superimposed on chronic ventilatory failure. The following formula can be used to estimate the “normal” PaCO2 for a patient with chronic respiratory acidosis: (Current HCO3  25)  2  40 “normal” PaCO2 130

Example: Blood gases pH, 7.33; PaCO2, 78; HCO3, 40; PaO2, 84 What is the patient’s normal PaCO2? How do you correct this problem? Patient’s normal PaCO2 is approximately 70. The patient probably needs the supplemental oxygen turned down. Further assessment is necessary.

FORMULA FOR ESTIMATING NORMAL PaO2 (USEFUL FOR AGES 10 TO 80 YEARS) 110  ½ age  Normal PaO2

FORMULA FOR ESTIMATING SATURATION 4-5-6-7-8-9 RULE PO2 (mm Hg)

Saturation (%)

40 50 60

70 80 90

OXYHEMOGLOBIN DISSOCIATION CURVE • Shift to left. Increased oxygen affinity with higher oxygen content for a given PO2 level. Less oxygen is available to the tissues. The P50 is 27. Causes of shift to left:& pH,  PCO2,  temperature,  2,3-diphosphoglycerate (2,3-DPG), CO poisoning, fetal Hb. • Shift to right. Decreased oxygen affinity with lower oxygen content for a given PO2 level. P50 is 27. Causes of shift to right:  pH, & PCO2,& temperature,& 2,3-DPG. • The normal P50 is 27, which means PO2 27 mm Hg  50% saturation. 131

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BLOOD GAS FORMULAS CaO2 CvO2 C(a-v)O2 Pa-vDO2 PAO2 P(A-a)O2 or A-aDO2

PaO2

PARAMETER

NORMAL VALUE

CALCULATIONS AND SIGNIFICANCE OF VALUES

Oxygen content of arterial blood Oxygen content of mixed venous blood Arterial to venous oxygen content difference Partial pressure of arterialto-venous difference Alveolar PO2 or alveolar air equation A-a gradient or alveolarto-arterial oxygen difference

15-20 vol%

(Hb  1.34  SaO2)  (PaO2  0.003) Content of oxygen in arterial blood. (Hb  1.34  SvO2)  (PvO2  0.003) Content of oxygen in mixed venous blood. CaO2  CvO2 Index of tissue oxygenation. PaO2  PvO2 Index of tissue oxygenation. (PB−PH2O)  FiO2 − (PaCO2  0.8) Sample: (760 47)  0.21  (40  0.8)  100 PAO2 − PaO2 Evaluate for presence of diffusion defect, percent pulmonary shunt, and effectiveness of oxygen therapy.

Arterial partial pressure of oxygen

12-15 vol% 3.5-5.0 vol% 50 mm Hg 100 mm Hg on room air 20 mm Hg on room air 25-65 mm Hg on FiO2 100% 80-100 mm Hg

Assess arterial oxygenation.

PvO2 PECO2 QS/QT

RQ SaO2 SvO2 VD/VT

VCO2 VO2

133

—

Mixed venous partial pressure of oxygen Exhaled carbon dioxide

40 mm Hg 30 mm Hg

Assess cardiac output, tissue perfusion, and oxygen utilization.

Measurement of CO2 in expired gas. Done by analyzing gas sample. % Shunt Normal 5% (A-aDO2) ⫻ 0.003 ⫼ (CaO2 − CvO2) ⫹ (A-aDO2 ⫻ 0.003) Moderate defect Cardiac output that is shunted or perfusion without ventila10-20% tion. Refractory hypoxemia. lncreased in atelectasis, pneuSevere defect ⬎20% monia, pulmonary edema, and anatomical or heart defects. Respiratory quotient 0.7-1.0 VCO2 ⫼ VO2. Ratio of CO2 production to oxygen consumption. Arterial oxygen saturation 98% Hemoglobin saturation of oxygen in arterial blood. Venous oxygen saturation 73% Hemoglobin saturation of oxygen in venous blood. Deadspace to tidal volume 20-40% (PaCO2 − PECO2) ⫼ PaCO2 ratio Measures deadspace ventilation or ventilation without perVD anatomical ⫽ mL/lb 40-55% for patient fusion. Increase in pulmonary embolism, pulmonary tumor, VD mechanical ⫽ 10 mL/in on ventilator pulmonary hypertension, and rapid shallow breathing. Carbon dioxide production 200 mL/min Measurement of CO2 production. Influenced by many bodily factors such as metabolism, substrate, and buffering. Oxygen consumption 250 mL/min VO2 ⫽ CO ⫻ C(a-v)O2 Metabolic rate or amount of oxygen used by body. Oxygen transport 1000 mL/min lndicates amount of oxygen delivered to tissues.

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HEMODYNAMIC PARAMETERS PARAMETER

NORMAL VALUE

CALCULATIONS AND SIGNIFICANCE OF VALUES

—

Pulse pressure

40 mm Hg

Systolic BP ⫺ diastolic BP. Measures force of pulse.

BP

Blood pressure

Systolic 90-130 mm Hg Diastolic 60-90 mm Hg

Hypertension if high, hypotension if low.

CI

Cardiac index

3.0-4.5 L/min/m2

CO ⫼ BSA. Cardiac function is relative to body size.

CO or QT

Cardiac output (and Fick equation)

4-8 L/min

HR ⫻ SV ⫼ 1000. Alternately use the Fick equation: VO2 ⫼ (CaO2 ⫺ CvO2 ⫻ 10) Note: VO2 is 250 mL/min.

CVP

Central venous pressure

1-6 mm Hg

Mean right atrial pressure. Estimates right ventricle preload. Is also used to give fluid and drugs.

EF

Ejection fraction

65-75%

SV ⫼ end diastolic volume. Cardiac function is relative to contractility.

HR

Heart rate

60-100 bpm

Bradycardia ⬍60 bpm; tachycardia ⬎100 bpm

ICP

Intracranial pressure

0-15 mm Hg

Assess intracranial pressure via ICP monitor.

LVP

Left ventricle pressure

Systolic 90-130 mm Hg Diastolic 1-12 mm Hg

Determines left ventricle pressure.

135

MAP

Mean arterial pressure

85-100 mm Hg

Systolic BP ⫹ (2x diastolic BP) ⫼ 3. Is also used to calculate SVR.

PAP

Pulmonary artery pressure

Systolic 18-30 mm Hg Diastolic 6-15 mm Hg

To determine PAP and calculate PVR.

PAP

Mean pulmonary artery pressure

10-20 mm Hg

PAP systolic ⫹ (2 ⫻ PAP diastolic) ⫼ 3. Is also used to calculate PVR.

PCWP PWP

Pulmonary capillary Wedge pressure

4-12 mm Hg

Estimates left ventricle filling and preload. Is equal to left atrial pressure. Is elevated in left heart failure.

PVR

Pulmonary vascular resistance

1.5-3.0 mm Hg/L/min or 120-240 dynes

(Mean PAP ⫺ PWP) ⫼ CO. Multiply result by 80 for dynes. Measures resistance in pulmonary vasculature.

RVP

Right ventricle pressure

Systolic 20-30 mm Hg Diastolic 1-6 mm Hg

Determines right ventricle pressure.

SI

Stroke index

40-60 mL/beat/m2

SV ⫼ BSA. Cardiac function is relative to body size.

SV

Stroke volume

60-130 mL/beat

(CO in L/m ⫼ HR) ⫻ 1000 Sample 7 ⫼ 80 ⫻ 1000 ⫽ 87 mL/beat. Cardiac function.

SVR

Systemic vascular resistance

15-20 mm Hg/L/min or 1000-1600 dynes

(MAP ⫺ CVP) ⫼ CO. Multiply result by 80 for dynes. Measures resistance in systemic circulation, and gives indication of vascular problems.

136

MEDICAL CONDITIONS AND HEMODYNAMIC CHANGES MEDICAL CONDITION

CVP

PAP

PCWP

CO

PVR

N or &

N or &

N

N

N or &

N

&

&

&&



N or &

&

N or &

N or &

N

N or 

N or &

N



&

&



&

N or &

Hypervolemia

&

N or &

&

&

N



Hypovolemia

N or 

N or 





N

&

Left heart failure (CHF)

N or &

&

&&



N or &

&

&

&&

N

N or 

&&

N

Right heart failure (cor pulmonale)

N or &

N or &

N

N or 

N or &

N

Septicemia

N or 





&

N



ARDS Cardiogenic shock COPD High PEEP (BP andvenous return)

Pulmonary embolism

SVR

N, Normal. Note: All changes are specific to single-disease conditions. Those with more than one disease or multiple medical problems can have different hemodynamic changes.

MISCELLANEOUS VITAL SIGNS RR Temperature

PARAMETER Respiratory rate Temperature

NORMAL VALUE 8-20/min Oral: 97.6-99.6º F

SIGNIFICANCE OF VALUES Indication of bradypnea or tachypnea Indication of hypothermia or hyperthermia Axillary: 96.6-98.6 º F Tympanic: 98.6-100.6 º F Rectal: 98.6-100.6 º F

URINE LABORATORY TESTING TEST

NORMAL VALUE

SIGNIFICANCE OF VALUES

Urine output

1200-2000 mL/day

Urine pH

4.5-8.0

Urine glucose

Negative

Is dependent on fluid intake; normally nearly equal. HI: High fluid intake LO: Low fluid intake, dehydration, kidney failure HI: Metabolic alkalosis, infection, low-protein diet LO: Metabolic acidosis, high-protein diet Presence may indicate diabetes.

Urine protein Urine specific gravity

Negative; trace 1.005-1.030

137

Presence may indicate kidney disease. HI: Concentrated urine LO: Renal insufficiency

138

ADULT LABORATORY VALUES LABORATORY TEST

NORMAL VALUES

POSSIBLE SIGNIFICANCE OF VALUES

Albumin

3.5-5 g/dL

Alkaline phosphatase Ammonia Amylase AST (aspartate aminotransferase) or SGOT (serum glutamic-oxaloacetic transaminase) (enzyme) Bicarbonate (see CO2) Bilirubin, total BUN (blood urea nitrogen) Adult Child Calcium (Ca)

25-125 U/L 12-55 mcg mol/L 4-25 U/mL

Protein component important in nutritional assessment; LO: malnutrition, proteinuria, leukemia HI: liver disease, obstructive jaundice HI: liver dysfunction, intestinal problem HI: pancreatitis HI: myocardial infarction, liver disease, trauma, surgery

Chloride (Cl) (electrolyte)

6-40 U/L 0.3-1 mg/dL

HI: liver disease, hepatitis, jaundice, biliary obstruction

8-25 mg/dL 5-18 mg/dL 8-11 mg/dL

HI: kidney failure

98-186 mEq/L

HI: hyperparathyroidism, cancer; LO: hypoparathyroidism, renal failure, trauma, pancreatitis HI: metabolic acidosis, dehydration; LO: metabolic alkalosis, diuretics, vomiting, nasogastric suction

Cholesterol, total LDL (low-density lipoprotein) HDL (high-density lipoprotein) CO2 (carbon dioxide) content, or HCO3 (bicarbonate) (electrolyte)

200 mg/dL 150 mg/dL 40 mg/dL 22-30 mEq/L

CPK (enzyme) (creatine phosphokinase) CPK-MB Creatinine Digoxin

Ketones

30-150 U/L 4% 0.5-1.3 mg/dL Therapeutic: 0.8-2 ng/mL 70-110 mg/dL M: 42-52% F: 37-47% M: 14-18 g/dL F: 12-16 g/dL 3 mg/dL

Lactic acid

0.5-2 mEq/L

Glucose (fasting blood sugar) Hematocrit Hemoglobin

139

HI, High value; LO, low value.

HI: increased lipids, conducive to premature arteriosclerosis (except HDL, known as “good cholesterol”) (Not arterial blood gas [ABG] PaCO2; is a bicarbonate); HI: metabolic alkalosis, compensated respiratory failure, CO2 retention; LO: metabolic acidosis HI: myocardial infarction, CVA, trauma, surgery HI: kidney failure Toxic meditation level is 2.4 HI: hyperglycemia is due to lack of insulin, diabetes mellitus HI: polycythemia, COPD, dehydration; LO: anemia, hemorrhage HI: polycythemia, COPD, dehydration; LO: anemia, hemorrhage HI: diabetic ketoacidosis Anaerobic metabolism by-product; HI: hypoxia, hemorrhage, shock, CHF, high-protein diet Continued

140

ADULT LABORATORY VALUES—cont’d LABORATORY TEST

NORMAL VALUES

LDH (lactic dehydrogenase) (enzyme) 60-160 U/L 1.4-2.0 mEq/L Magnesium (Mg⫹⫹) Phosphorus

2.6-4.5 mg/dL

Platelets (Thrombocytes)

150,000-420,000/mm3

Potassium (K⫹) electrolyte

3.5-5 mEq/L

Protein, total

6-8.4 g/dL

PT (prothrombin Time) PTT (partial thromboplastin time) RBC (red blood cells)

10.0-12.5 sec 25-45 sec M: 4.6-6.2 million/mm3 F: 4.2-5.5 million/mm3

POSSIBLE SIGNIFICANCE OF VALUES HI: myocardial infarction, pulmonary embolism, hepatitis HI: renal insufficiency, tissue trauma; LO: pancreatitis, alcoholism, impaired absorption HI: renal failure, endocrine disorder; LO: hyperthyroidism, malabsorption HI: thrombocytosis, polycythemia vera, granulocytic leukemia, certain cancers, iron deficiency, splenectomy, infection HI: metabolic acidosis, excess K⫹ intake, kidney failure, burns, surgery, cardiac arrhythmias, MI, ECG-spiked T wave; LO: metabolic alkalosis, diuretics, diarrhea, vomiting, nasogastric suction, steroids, malnutrition, ECG flat or inverted T wave Important in nutritional assessment; LO: malnutrition, proteinuria, leukemia HI: abnormal blood clotting factor HI: abnormal blood clotting factor HI: poIycythemia, COPD, dehydration; LO: anemia, hemorrhage, blood loss

Sodium (Na⫹) (electrolyte)

135-145 mEq/L

Theophyline

Therapeutic: 10-20 mcg/mL 35-150 mg/dL ⬍0.2 ng/mL 0.4-5.2 mcg U/mL 4,600-10,000/mm3

Triglycerides Troponin-T (enzyme) TSH (thyroid-stimulating hormone) WBC (white blood cells) (leukocytes) WBC differential neutrophils (segments/bands)

50-75%

Lymphocytes

20-40%

Monocytes

1-9%

Eosinophils Basophils

1-5% 0.3-2.0%

HI: high sodium intake, dehydration; LO: diuretics, diarrhea, renal failure, CHF Toxic medication level: ⬎20 mcg/mL HI: increased lipids, conducive to early arteriosclerosis HI: myocardial infarction HI: hypothyroidism; LO: hyperthyroidism HI: leukocytosis, bacterial infection, leukemia, kidney failure, MI, injury, surgery LO: leukopenia, viral infection, aplastic anemia, chemotherapy; HI: infection, neoplasm, trauma; LO: HIV infection, autoimmune disease, bone marrow disease HI: viral infection, lymphocytic leukemia: LO: immunodeficiency, AIDS, steroids HI: viral or fungal infection, monocytic leukemia, mononucleosis, tuberculosis HI: asthma, allergies, parasitic infection HI: leukemia, CA, poor thyroid function; LO: stress, hyperparathyroidism

141

SPUTUM ANALYSIS CHARACTERISTIC

POSSIBLE SIGNIFICANCE OF RESULTS

Mucoid—clear, thin Normal. Can be normal if under 100 mL/day. Mucoid—white or Otherwise, can indicate pulmonary white/clear, thin infection and bronchitis. Pulmonary infection or disease. Yellow, viscous, possibly purulent Pulmonary infection or disease. Green, viscous, Stagnant sputum. Possible grampurulent, bad odor negative bacteria. Hemoptysis. Pulmonary trauma, Red, bloody, infection, or disease. Possible blood-tinged bleeding tumor, CF, or TB. Dark brown or rusty Old retained secretions, pulmonary infection, or trauma. Possible healred (old, dried ing at source of bleeding, although blood) disease may still be present. Pulmonary edema. Pink, frothy Notes: Sputum culture: Identifies type of bacteria present. Sputum gram stain: Identifies gram-positive or gram-negative infection. Sputum sensitivity: Identifies the drug that will kill the bacteria.

CEREBROSPINAL FLUID (CSF) LABORATORY TESTING CHARACTERISTIC

NORMAL VALUES

POSSIBLE SIGNIFICANCE OF RESULTS

CSF color

Clear, odorless

White cells

0-4 per mm3

CSF pressure (not same as ICP)*

80-200 mm

Cloudy may indicate infection, meningitis. Yellow may indicate brain hemorrhage or tumor in brain or spinal cord. Blood may indicate brain hemorrhage, stroke, or skull fracture. HI: infection, meningitis, TB, syphilis. HI: may indicate edema, hemorrhage, stroke, infection, brain tumor, cyst, meningitis.

*ICP (intracranial pressure) normal value is 0 to 15 mm Hg.

142

See references 6, 24, and 25 PULMONARY FUNCTION TESTING . . . . . . . . . . . . Indications for PFTS . . . . . . . . . . . . . . . . . . . . . . . ATPS AND BTPS . . . . . . . . . . . . . . . . . . . . . . . . . . . . ATS STANDARDS . . . . . . . . . . . . . . . . . . . . . . . . . . . SPIROMETRY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . INTERPRETING PFTS RESULTS BASED ON PERCENT OF PREDICTED VALUE . . . . . . . . . ASSESSING PERCENT IMPROVEMENT AFTER BRONCHODILATOR . . . . . . . . . . . . . . . . . PFT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lung Volumes and Capacities . . . . . . . . . . . . . . . Obstructive versus Restrictive Disease Patterns . . . . . . . . . . . . . . . . . . . . . . . . . Normal PFT Values and Calculations for Adults . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . PFT Abbreviations and Descriptions . . . . . . . . . . PFT Special Tests . . . . . . . . . . . . . . . . . . . . . . . . . . CHEST X-RAYS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Low- and High-Density Structures on X-Rays . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . X-Ray Projections. . . . . . . . . . . . . . . . . . . . . . . . . . Normal Anatomic Structures in the Chest X-Ray . . . . . . . . . . . . . . . . . . . . . . . Abnormalities in the Chest X-Ray and Terminology . . . . . . . . . . . . . . . . . . . . . . . . . Normal Structures . . . . . . . . . . . . . . . . . . . . . . . . . Abnormal Structures . . . . . . . . . . . . . . . . . . . . . . .

144 144 144 144 144 145 145 145 145 146 147 149 152 155 155 155 156 158 161 163

SEE ALSO PULMONARY DISEASES ABGs, LABS, AND HEMODYNAMICS VENTILATORS, CPAP, AND BiPAP Mechanical Ventilation Formulas . . . . . . . . . . . . 194

FORMULAS AND FACTS 143

PFTs and X-Rays

PFTs AND X-RAYS

PFTs and X-Rays

LPULMONARY FUNCTION TESTINGL INDICATIONS FOR PFTS • Assess the respiratory system. • Test for presence of lung disease. Identity the type of lung disorder: obstructive versus restrictive. • Evaluate extent of pulmonary dysfunction. • Assess progression of lung disease. Aid in establishing a course of therapy for the dysfunction.

LATPS AND BTPSL • Volumes measured by spirometry are at ambient temperature, pressure, and saturated (ATPS) conditions. • These measurements are then adjusted for temperature difference between spirometer and patient’s body temperature, pressure, and saturated (BTPS) conditions.

LATS STANDARDSL • Guidelines safeguard against procedural errors and ensure accurate results. • Equipment must be calibrated, maintained, and cleaned on schedule. • Patient must be thoroughly instructed and given three attempts when appropriate. • Many PFTs are very effort-dependent; consequently, the patient must be motivated to put forth the best possible effort.

LSPIROMETRYL • Spirometry can measure VC/FVC, IC, IRV, VT, ERV, and flow rates. • Spirometry cannot measure RV, FRC, and TLC. These require special testing, discussed at the end of this chapter. 144

INTERPRETING PFT RESULTS BASED ON PERCENT OF PREDICTED VALUE Normal: 80% to 120% of prediction Mild disorder: 65% to 79% of prediction Moderate disorder: 50% to 64% of prediction Severe disorder: Less than 50% of prediction Note: Also refer to Gold Expert Panel COPD Classification Stages on page 27.

ASSESSING PERCENT IMPROVEMENT AFTER BRONCHODILATOR Nonsignificant improvement is less than 15%; significant improvement is 15% or greater, and the greatest improvements may be indicative of asthma.

LPFTL LUNG VOLUMES AND CAPACITIES

IC

TLC

IRV

VC/ FVC VT

FRC RV

ERV RV 145

OBSTRUCTIVE VERSUS RESTRICTIVE DISEASE PATTERNS VOLUMES AND CAPACITIES

OBSTRUCTIVE DISEASE

RESTRICTIVE DISEASE

TLC

&



VC or FVC

N or



IC

N or

N or

FRC

&

N or

VT

Varies

N or

IRV

N or



ERV

N or

N or

RV

&

N or

FEV 0.5 second



N or

FEV 1.0 second



N or

FEV 2.0 seconds



N or

FEV 3.0 seconds



N or

FEF 200-1200



N or

FEF 25%-75%



N or

MVV or MBC



N or

Peak flow



N or

See “PFT Abbreviations and Descriptions” on pages 149 and 150 for a description of each abbreviation used in this table.

Obstructive disease pattern: Decreased flow rates, increased RV, increased TLC. Restrictive disease pattern: Decreased volumes, decreased TLC. Obstructive pulmonary diseases include asthma, bronchitis, bronchiectasis, emphysema, cystic fibrosis, and bronchopulmonary dysplasia. Most other lung dysfunctions are restrictive pulmonary diseases or disorders. 146

NORMAL PFT VALUES AND CALCULATIONS FOR ADULTS* CALCULATION FOR NORMAL VALUES VOLUMES AND CAPACITIES TLC 80 mL/kg VC or FVC 65 mL/kg IC 50 mL/kg FRC 30 mL/kg VT 7 mL/kg IRV 40 mL/kg ERC 17 mL/kg RV 16 mL/kg RV/TLC ratio 20% of TLC

NORMAL VALUES FOR 60-KG FEMALE

NORMAL VALUES FOR 70-KG MALE

4800 mL 3900 mL 3000 mL 1800 mL 420 mL 2400 mL 1020 mL 960 mL 20% of TLC

5600 mL 4550 mL 3500 rnL 2100 mL 490 mL 2800 mL 1190 mL 1120 mL 20% of TLC

*Normal values are based on normal adults with ideal body weight (IBW). Normal value calculation factors also include age, height, gender, and race. Normal values decrease with age. See “PFT Abbreviations and Descriptions” on pages 149 and 150 for a description of each abbreviation used in this table. Continued

147

148

NORMAL PFT VALUES AND CALCULATIONS FOR ADULTS*—cont’d CALCULATION FOR NORMAL VALUES FLOW RATES AND TIME PERCENTAGE FEV 0.5 second 60% of FVC FEV 1.0 second 80% of FVC FEV 2.0 seconds 94% of FVC FEV 3.0 seconds 97% of FVC FEF 200-1200 or MEFR 6 L/sec FEF 25-75% or MEFR 4.7 L/sec MISCELLANEOUS PULMONARY MECHANICS MVV or MBC 150-170 L/min PF Peak flow or PEFR 400-600 L/min MEP   80 cm H2O MIP or NIF 80 to 100 cm H2O IS 50 mL/kg

NORMAL VALUES FOR 60-KG FEMALE

NORMAL VALUES FOR 70-KG MALE

2340 mL 3120 mL 3670 mL 3780 mL 360 L/min 280 L/min

2730 mL 3640 mL 4280 mL 4410 mL 360 L/min 280 L/min

150 L/min 400 L/min   80 cm H2O 80 to 100 cm H2O 3000 mL

170 L/min 600 L/min   80 cm H2O 80 to 100 cm H2O 3500 mL

*Normal values are based on normal adults with ideal body weight (IBW). Normal value calculation factors also include age, height, gender, and race. Normal values decrease with age. See “PFT Abbreviations and Descriptions” on pages 149 and 150 for a description of each abbreviation used in this table.

PFT ABBREVIATIONS AND DESCRIPTIONS Abbreviations

Descriptions

Lung Volume VT or TV

Tidal volume. Volume of air that is inhaled and exhaled during normal quiet breathing.

IRV

Inspiratory reserve volume. Maximum volume of air that can be inhaled after a normal VT inspiration.

ERV

Expiratory reserve volume. Maximum volume of air that can be exhaled after a normal VT inspiration.

RV

Residual volume. Volume of air remaining in the lungs after a maximal exhalation. Includes air-trapping, which cannot be measured by simple spirometry; it requires special testing. Increased FRC or increased RV/TLC ratio (20%) indicates an obstructive disorder.

RV/TLC ratio

Decreased FRC and TLC indicate a restrictive disorder.

Lung Capacity (contains two or more volumes) TLC

Total lung capacity. Total volume of air contained in the lungs. TLC  IC  FRC. In addition, TLC  VC  RV, and TLC  VT  IRV  ERV  RV.

VC or FVC

Vital capacity or forced vital capacity. Maximum volume of air that can be exhaled after a maximal inhalation. VC  VT  IRV  ERV. FVC is equal in volume to VC, but the patient must exhale as quickly and forcefully as possible to assess flow rates.

IC

Inspiratory capacity. Maximum amount of air that can be inspired after a normal VT exhalation. IC  VT  IRV.

149

PFT ABBREVIATIONS AND DESCRIPTIONS—cont’d Abbreviations

Descriptions

PFT Flow Rates and Time Percentage FRC

Functional residual capacity. Volume of air remaining in the lungs after a normal VT exhalation. FRC  ERV  RV. Includes RV air-trapping, which cannot be measured by simple spirometry; it requires special testing. Increased FRC or increased RV/TLC ratio (20%) indicates an obstructive disorder. Decreased FRC and TLC indicates a restrictive disorder.

FEV 0.5 FEV 0.5/%FVC

Forced expiratory volume in first 0.5 second of FVC. 0.5 Time% is normally 60% of FVC.

FEV 1.0 FEV 1/%FVC

Forced expiratory volume in first 1.0 second of FVC. 1.0 Time% is normally 80% of FVC.

FEV 2.0 FEV 2/%FVC

Forced expiratory volume in first 2.0 seconds of FVC. 2.0 Time% is normally 94% of FVC.

FEV 3.0 FEV 3/%FVC

Forced expiratory volume in first 3.0 seconds of FVC. 3.0 Time% is normally 97% of FVC.

FEF 200-1200 or MEFR

Forced expiratory flow after first 200 mL exhaled, until next 1200 mL exhaled during FVC. Is also called maximum expiratory flow rate. Measures function of large airways.

FEF 25-75% or MMFR

Forced expiratory flow over middle 50% of FVC. Is also called maximal midexpiratory flow rate. Measures function of small and medium airways.

150

PFT ABBREVIATIONS AND DESCRIPTIONS—cont’d Abbreviations

Descriptions

Miscellaneous Pulmonary Mechanics MVV or MBC

Maximum voluntary ventilation or maximum breathing capacity. Measures status of respiratory muscles, compliance, and resistance. Patient breathes as fast and deep as possible for 12-15 seconds into spirometer with accumulator recording. Exaggerates air trapping. Is very sensitive and can give an indication of an obstructive disease in the early stages. Is very dependent on effort.

PF or PEFR

Peak flow or peak expiratory flow rate. Patient inhales deeply and blows all air into device at maximal speed.

MEP

Maximal expiratory pressure. Assesses respiratory muscle strength. Patient inhales deeply and expires all air into the device to measure peak expiratory pressure.

MIP

Maximal inspiratory pressure. Assesses respiratory muscle strength. Patient inhales maximally, and peak inspiratory pressure is measured. Is the same as NIF.

NIF

Negative inspiratory force. Assesses respiratory muscle strength. Patient inhales maximally, and peak inspiratory pressure is measured. Is the same as MIP.

IS

Incentive spirometry. Measures inspiratory respiratory muscle strength, improves lung aeration, and prevents atelectasis.

151

152

PFT SPECIAL TESTS TEST

NORMAL VALUE

DESCRIPTION

DLCO Lung diffusion for carbon monoxide or gas diffusion testing

Single-beam DLCO 25 mL/min/mm Hg

Measures factors that affect diffusion of air across A-C membrane; detects if surface area for diffusion is reduced. Patient inhales a small concentration of carbon monoxide, helium, and air. Patient exhales into device that analyzes gas concentrations and recalculates DLCO. DLCO reduced in emphysema, pulmonary fibrosis, embolism, and sarcoidosis.

Steady-state DLCO 17 mL/min/mm Hg Body plethysmograph, Normal predicted values for TGV, body box, or TLC, and FRC thoracic gas volume (TGV) Helium dilution (closed circuit)

Equilibrium at 7 min Normal FRC

Is the most accurate method for measuring FRC, RV, and TLC. Measures total TGV, including air trapped in smallest airways. Patient pants at FRC against closed shutter, at approximately two breaths per second while pressures and volumes are measured. TGV increases in obstructive diseases and decreases in restrictive disorders. Method measures the FRC and then calculates RV and TLC; is not as accurate as plethysmograph for detecting trapped air. Patient breathes mixture of air with 10% helium until equilibrium takes place at approximately 5 minutes. If equilibrium takes longer (up to 20 min), an obstructive disease is indicated. FRC increases in obstructive diseases and decreases in restrictive disorders.

Nitrogen washout (open circuit)

Less than 8 minutes to reach less than 2.5% nitrogen in lungs

Normal FRC

SBN2 Single-breath nitrogen elimination (includes closing volume [CV] and closing capacity [CC])

Phase III N2 rise should be ⬍1.5%

Method calculates the FRC and RV; is not as accurate as plethysmograph for detecting trapped air. Also measures evenness of distribution of ventilation, with breath-by-breath curve. Patient breathes 100% oxygen for 2-7 minutes, exhaling all gas into an analyzer until nitrogen remaining in the lungs is less than 2.5%. Then patient exhales completely. Fractional concentration of alveolar nitrogen (FAN2) is noted and FRC is computed. Greater than 7 minutes to reach 2.5% nitrogen remaining in lungs indicates poor distribution of ventilation, obstructive disorder, or possible pulmonary embolism. Calculated FRC increases in obstructive diseases and decreases in restrictive disorders.

153

Measures the evenness of distribution of inspired gases. Patient exhales maximally, inspires 100% oxygen maximally, then slowly exhales the gas until lungs feel empty. The exhaled gas passes through N2 analyzer that measures the change in concentration of nitrogen. The first 750 mL of air exhaled is mostly dead space, and is discarded (phases I and II). The next 500 mL of exhaled air (phase III) is used to measure distribution. The rise of N2 percentage in phase Ill should be less than 1.5%. A phase Ill N2 rise ⬎1.5% indicates uneven distribution of ventilation or uneven flow rates, with possible pulmonary embolism. CV is phase IV and should ⫽ 10%20% of VC. CC is phase V and should ⫽ 30-40% of TLC. CV% increased in small airway obstruction. Is very sensitive for detecting early airway closure. Continued

154

PFT SPECIAL TESTS—cont’d TEST

NORMAL VALUE

DESCRIPTION

Flow-volume loop

Normal volumes and flow rates as predicted

Volume of isoflow VisoV and Vmax50

10-20% of VC

Measures the volumes and flow rates of the vital capacity. Expiratory flow above baseline, inspiratory flow below baseline. Patient inspires to TLC, exhales forcefully for FVC, then inhales maximally to TLC again. Graphic loop results. Can detect obstructive and restrictive patterns, decreased volumes, decreased decreased flow rates, airway resistance and small airway disease. Consists of two maximal expiratory flow curves. First FVC uses air, second FVC uses oxygen 20% ⫹ helium 80%. Volume remaining in lungs after second FVC is the volume of isoflow, normally 10-20% of VC. VisoV increased in small airway disease. Vmax50 measures flow at 50% of the VC, similar to FEF 25-75%. Vmax50 measures changes in airway resistance in small and medium airways. Measures blood flow distribution. Radiographic study of the arteries after injecting radiopaque dye. Motion and still pictures are obtained with observation of blood flow through blood vessels. Can detect unperfused blood vessels and pulmonary embolism. Measures gas and blood flow distribution (ventilation and perfusion). Involves inhalation of radiolabeled gas (zenon), and injection of radioisotope, followed by study of mismatches between ventilation and perfusion. Can detect poorly ventilated areas, unperfused blood vessels, and pulmonary embolism.

Pulmonary angiogram or arteriogram

V/Q scan or ventilation/perfusion scan

LCHEST X-RAYSL LOW- AND HIGH-DENSITY STRUCTURES ON X-RAYS The x-ray consists of low-density and highdensity structures. LOW-DENSITY STRUCTURES Low-density structures appear dark (radiolucent) on x-ray because less of the x-ray is absorbed and more of the x-ray reaches the film. Normal lungs appear radiolucent because they contain air, which has the least density of all. HIGH-DENSITY STRUCTURES High-density structures appear white (radiopaque or radiodense) on an x-ray because more of the x-ray is absorbed and less of the x-ray reaches the film. The higher the density, the whiter it appears. The bones are the densest naturaloccurring density, followed by fat and then water. X-RAY PROJECTIONS POSTERIOR-ANTERIOR (P-A) PROJECTION X-rays pass through the patient from back to front, with the chest on the film. The P-A projection offers a better view and is preferable to the A-P projection. ANTERIOR-POSTERIOR (A-P) PROJECTION X-rays pass through the patient from front to back, with the back on the film. This typical portable x-ray is used for the patient who is bedridden, critically ill, or difficult to move. APICAL LORDOTIC VIEW This projection visualizes the lung apices. LATERAL VIEW This projection provides a side-to-side view. Lateral decubitus can be used to diagnose a pleural effusion, because the fluid can be visualized as “layering out.” The lateral neck x-ray is used for diagnosing epiglotittis, croup, or foreign bodies. 155

OBLIQUE POSITION Slanting diagonal view helps localize lesions. NORMAL ANATOMIC STRUCTURES IN THE CHEST X-RAY MEDIASTINUM Area between the lungs. It includes the heart, blood vessels, trachea, main bronchi, lymphatic vessels, nerves, and connective tissue. HILUM The hilar regions on both sides of the sternum include the pulmonary arteries, veins, and some segmental bronchi. The left hilum is normally slightly higher than the right. Some small, round, radiopaque densities are normal in the hilar area, because these represent blood vessels seen on end. HEART The heart is predominantly on the left side of the sternum. The right heart border creates a slight bulge on the right side of the spine. The cardiothoracic (C/T) ratio should be less than 50%. The ratio describes the total size of the heart in relation to the total size of the thorax. The aortic arch and ascending aorta are located at the level of the second rib at the junction of the manubrium and the body of the sternum. The left pulmonary artery can be viewed below the aortic arch. LUNG PARENCHYMA Vascular markings are normal in the lungs and should be visualized throughout both lung fields. Vascular markings are the lung tissue, blood vessels, and lymphatics. The carina can be visualized at the point of bifurcation of the right and left mainstem bronchi at the level where the second rib joins the sternum. The trachea is easily located, and the tip of the tube should be positioned at 2 to 156

3 centimeters above the carina on the patient who is intubated or has had a tracheostomy. PLEURAL SURFACE Surrounding the perimeter of the lungs are the visceral pleura and parietal pleura, with a potential space between them. The visceral pleura covers both lungs and lines the interlobar fissures. The parietal pleura lines the inside of the chest wall and covers the sides of the pericardium and the hemidiaphragms. The two pleurae fuse together in the area of the hue. The pleural space normally cannot be viewed on an x-ray, but if fluid or air enters it, the pleural space can be visualized. Both costophrenic angles should come to a sharp point, indicating that fluid is not in the pleural space. DIAPHRAGM The right hemidiaphragm is dome shaped and higher than the left because of the presence of the liver under the right and the heart pushing down on the left. The anterior portion of the liver is near the fifth rib. The upper domes of the diaphragm should be smooth and rounded. SOFT TISSUES Soft tissues, which include tissues, muscle, and fat in the chest and neck areas, are checked for subcutaneous emphysema. BONES The clavicles, ribs, and sternum are easily located, and they make good landmarks for locating other structures. The inferior angle of the scapula is located at the eighth rib posteriorly. If the patient is inhaling maximally, the tenth or eleventh ribs should be visible. The ribs should be visualized for any fractures. The contour of the spine should be examined for any abnormal curvature. 157

158

ABNORMALITIES IN THE CHEST X-RAY AND TERMINOLOGY TERM AND DESCRIPTION

POSSIBLE PATHOLOGIES

Infiltrates White appearance or radiodensities Air bronchograms Dilated, bulbous, and outlined bronchi

Any ill-defined radiodensity that can indicate many different pathologic conditions as listed in this table. lnfiltrates can be patchy, solid, localized, or diffuse. Includes bronchiectasis, idiopathic respiratory distress syndrome (IRDS) stage 3, pulmonary edema, pulmonary hemorrhage, or pneumonia. Bronchography with the injection of a contrast medium aids in diagnosis. Indicates pulmonary edema. Typically indicates pneumonia but can also indicate pleural effusion, tumor, or other solid abnormality. Indicates pleural effusion. Lateral decubitus x-ray helps diagnosis.

Butterfly pattern Consolidation Solid white appearance Castophrenic blunting Obliterated or rounded angle or meniscus with basilar infiltrates Increased C/F ratio or C/T greater than 50%

Diaphragm with flattened domes Diffuse Fluffy infiltrates—diffuse

Describes the total size of the heart in relation to the total size of the thorax. C/T ratio greater than 50% indicates cardiomegaly, heart disease, congestive heart failure (CHF), or chronic obstructive pulmonary disease (COPD). Indicative of hyperinflation and COPD. Is spread bilaterally throughout the lungs. Indicates pulmonary edema.

Ground-glass pattern Heart abnormalities, failure (CHF). See also CIT ratio Hemidiaphragms One significantly higher than the other Hilar region—enlarged Honeycomb pattern Hyperinflation or increased anteriorposterior diameter Dark appearance Hyperlucent or increased radiolucency Dark appearance Kerley B lines Perpendicular lines Mediastinal shift Miliary pattern Peripheral wedge-shaped density

Indicates acute respiratory distress syndrome (ARDS) or IRDS. X-ray can help diagnose right heart failure (cor pulmonale) or left heart failure (CHF). Indicates possible unilateral phrenic nerve paralysis. Can be indicative of lymphoma, sarcoidosis, or engorged pulmonary vessels. Indicates ARDS, IRDS, interstitial fibrosis, or edema. Indicates excessive air, which is indicative of COPD and emphysema.

Increased air is indicative of bullae, pneumothorax, COPD, or emphysema. Indicates interstitial edema or edema as a result of left heart failure. Shift away from affected side in pneumothorax. Shift toward affected side in atelectasis. Alveoli is filled with fluid. Indicates pulmonary embolus.

159

Continued

160

ABNORMALITIES IN THE CHEST X-RAY AND TERMINOLOGY—cont’d TERM AND DESCRIPTION

POSSIBLE PATHOLOGIES

Platelike or patchy infiltrates Pulmonary arteries—dilated Radiopaque or radiodense White appearance Radiolucent Dark appearance, air Reticular pattern White streaks Reticulogranular Pattern of diffuse infiltrates Soft tissue with radiolucent streaks Spinal curvature

Indicates atelectasis. Indicates pulmonary hypertension. Is normal for bones and organs. Otherwise, appearance indicates infiltrates, atelectasis, pneumonia, edema, pleural effusion, or other pathologic condition. Is normal for lungs.

Vascular markings

Indicates interstitial infiltrates or fibrosis. Indicates ARDS or lRDS. Indicates subcutaneous emphysema. Is best viewed on lateral projection. Abnormal curvature indicates kyphosis, scoliosis, kyphoscoliosis, humpback, bone deformities related to aging, or other spinal defects. Is normal for lymphatics, lung tissues, and blood vessels. Increased vascular markings include pulmonary edema, fibrosis, or other pathologic conditions. Absent peripheral vascular markings include pneumothorax.

NORMAL STRUCTURES 15

10 8

1

14 11 12 2 13 7

3

6

5

16

4

17 9

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

Aortic knob Main pulmonary artery Left atrium Left ventricle Descending aorta Right atrium Ascending aorta Superior vena cava Gastric bubble

10. 11. 12. 13. 14. 15. 16. 17.

Trachea Right main bronchus Left main bronchus Left pulmonary artery Right pulmonary artery Pleural line Right hemidiaphragm Left hemidiaphragm

Schematic diagram of normal structures seen on a chest x-ray. Posterior-anterior view.24

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Right ventricle Pulmonary outflow tract Main pulmonary artery Right pulmonary artery Left pulmonary artery Pulmonary veins Left atrium Left ventricle Right hemidiaphragm Left hemidiaphragm Aortic arch Trachea Right upper lobe bronchus Left upper lobe bronchus Scapulae Manubrium Sternum

16 12 17

11 15

13 5 14 4 6 7 8

3 2 1 9

10

Schematic diagram of normal structures seen on a chest x-ray. Lateral view.24

161

Normal frontal chest film. Note medial ends of clavicles (small arrows) with spinous process (large arrow) framed between them.24

Normal lateral chest film.24

162

ABNORMAL STRUCTURES

Bilateral pleural effusions with obliteration of costophrenic angles.24

Pneumothorax. Complete atelectasis of left lung (arrows), resulting from large left pneumothorax.24

163

Plate atelectasis. Posterior-anterior chest film shows linear areas of plate atelectasis in both lower lobes.24

ARDS is associated with diffuse reticulogranular infiltrates or ground-glass appearance.24

164

EKGs

SEE ALSO MEDICATIONS

165

EKGs

See references 6, 24, and 25 EVALUATION OF EKG RHYTHMS . . . . . . . . . . . . . . 166 QRS Complex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167 Einthoven Triangle . . . . . . . . . . . . . . . . . . . . . . . . . 167 12-Lead EKG Placement . . . . . . . . . . . . . . . . . . . . 168 3-Lead EKG in Lead II . . . . . . . . . . . . . . . . . . . . . . . 168 EKG Paper . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169 INTERPRETATION OF RHYTHMS . . . . . . . . . . . . . . 169 Torsades de Pointes . . . . . . . . . . . . . . . . . . . . . . . . 178 EKGs and Corresponding Lead Changes . . . . . . 178 MYOCARDIAL INFARCTION . . . . . . . . . . . . . . . . . . . 178 Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178 Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179 Acute Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . 179 Old Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179 Reciprocal ST Depression . . . . . . . . . . . . . . . . . . . 180 Non–Q-Wave Infarction . . . . . . . . . . . . . . . . . . . . . 180 BUNDLE BRANCH BLOCKS . . . . . . . . . . . . . . . . . . . 180 Left BBB . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 180 Right BBB . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 ELECTROLYTE OR DRUG EFFECTS . . . . . . . . . . . . 181

EKGs

LEVALUATION OF EKG RHYTHMS13L Rate (Adult) • Bradycardia: 60/min • Normal: 60 to 100/min • Tachycardia: 100/min Rhythm • Is rhythm regular or irregular? P Waves • Are P waves present? • Does one P wave appear before each QRS? PR Interval • How much time does it take for the impulse to spread from the SA node through the atrial muscle and AV node? • Measures from the beginning of the P wave to the ventricular (QRS) complex. • Normal is 0.12 to 0.20 second. • Is the interval prolonged? Shortened? QRS Complex • How much time does it take for the impulse to spread through the right and left ventricles? • Measures from the beginning of the QRS to the end of the QRS. • Normal is 0.06 to 0.12 second. • Are the QRS complexes normal shape and configuration? QT Interval • How much time does it take for the impulse to spread through the ventricles and for repolarization to occur? • Measures from the beginning of the QRS to the end of the T wave. • Normal is 0.32 to 0.44 second. ST Interval • Is there deviation in the ST segment? • ST elevation suggests infarction; ST depression suggests ischemia. 166

QRS COMPLEX

Refractory Period

PR Segment R

Relative Refractory Period

Atrial Depole

P T

S QRS

PRI

A t r i a l

V e n t

Q

Vent Depole

R e p o l e

R e p o l e

EINTHOVEN TRIANGLE

I

Right Arm

– –

Left Arm

+ –

ACL

II

III + + Left Leg

167

12-LEAD EKG PLACEMENT4

1

RA

LA

2 3 4 5

V3 V1 V2

RL

V5 V4

V6

LL

(ground)

3-LEAD EKG IN LEAD II1



Ground


168

EKG PAPER2

0.20 sec

One large square is 0.20 seconds

0.04 sec

One small square is 0.04 seconds

Horizontal lines measure time. Vertical lines measure amplitude or voltage.

QUICK HEART RATE ESTIMATE Count each large square between R waves as follows: 300, 150, 100, 75, 60, 50.

LINTERPRETATION OF RHYTHMS2L NORMAL SINUS RHYTHM Rate Rhythm P waves PR QRS

60-100 bpm Regular Similar; 1:1 with QRS 0.12-0.20 second; constant 0.1 second

169

SINUS BRADYCARDIA Rate Rhythm P waves PR QRS

60 bpm Regular Similar; 1:1 with QRS 0.12-0.20 second; constant 0.1 second

SINUS TACHYCARDIA Rate Rhythm P waves PR QRS

170

101-180 bpm Regular Similar; 1:1 with QRS; at very fast rates, P wave looks like T wave 0.12-0.20 second; constant 0.1 second

SINUS ARRHYTHMIA Rate Rhythm P waves PR QRS

60-100 bpm Irregular; is often associated with breathing Similar; 1:1 with QRS 0.12-0.20 second; constant 0.1 second

PREMATURE ATRIAL CONTRACTION Rate Rhythm P waves PR QRS

Variable Regular with premature beats Premature; 1:1 with QRS Is dependent on prematurity of the beat Is usually 0.1 second, but may be wide From the left, beats 2 and 7 are PACs

171

SUPRAVENTRICULAR TACHYCARDIA Rate Rhythm P waves PR QRS

150-250 bpm Regular Is usually obscure but 1:1 with QRS 0.12-0.20 second when present Is usually 0.1 second

ATRIAL TACHYCARDIA Rate Rhythm P waves PR QRS

172

150-250 bpm Regular P waves appear different; may be difficult to distinguish P waves from T waves May be shorter or longer than normal; may be hard to measure Is usually 0.1 second

ATRIAL FLUTTER Rate Rhythm P waves PR QRS

Atrial 250-450 bpm; ventricular rate is variable Atrial regular; ventricular may be regular or irregular No P waves. Flutter (sawtooth shaped) waves are observed Is not measurable Is usually 0.1 second

ATRIAL FIBRILLATION Rate Rhythm P waves PR QRS

Atrial 400-600 bpm; ventricular variable Ventricular irregular No P wave; fibrillatory waves may be present; erratic, wavy baseline Is not measurable Is usually 0.1 second

173

PREMATURE VENTRICULAR CONTRACTION Rate Rhythm P waves PR QRS

60-100 bpm Regular with PVCs Absent; may appear after QRS complex None 0.12 second; wide and bizarre

VENTRICULAR TACHYCARDIA Rate Rhythm P waves PR QRS

174

150-300 bpm, typically 200-250 bpm May be regular or irregular None None 0.12 second

ASYSTOLE Rate Rhythm P waves PR QRS

None None None (“P-wave” asystole) None Absent

VENTRICULAR FIBRILLATION Rate Rhythm P waves PR QRS

Cannot be determined—no discernible waves or complexes to measure Rapid and chaotic—no pattern None None Is not discernible

Fine ventricular fibrillation

Coarse ventricular fibrillation

175

FIRST-DEGREE AV BLOCK Rate Rhythm P waves PR QRS

Is usually normal 60-100 bpm Regular Similar, 1:1 with QRS Prolonged (0.20 second) but constant Is usually 0.10 second

SECOND-DEGREE AV BLOCK, TYPE I (MOBITZ 1–WENCKEBACH) Rate Rhythm P waves PR QRS

176

Atrial ventricular Atrial regular; ventricular irregular Similar, more P waves than QRS Lengthens with each cycle until a P wave appears without a QRS Is usually 0.10 second; QRS cycle is periodically dropped

SECOND-DEGREE AV BLOCK, TYPE II (MOBITZ 2) Rate Rhythm P waves PR QRS

Atrial ventricular Atrial regular; irregular ventricular rhythm Similar; more P waves than QRS May be normal or prolonged; remains constant Is usually 0.10 second; QRS cycle may be absent after P waves

THIRD-DEGREE AV BLOCK Rate Rhythm P waves PR QRS

Atrial ventricular; usually slow ventricular rate between 30-60 bpm Atrial and ventricular; no relationship between the two Similar; more P waves than QRS None; atria and ventricles beat independently of each other May be narrow or wide, depending on level of the block

Complete AV block with a junctional escape pacemaker (QRS  0.08 to 0.10 second)

177

TORSADES DE POINTES

This type of ventricular tachycardia is defined as a polymorphous ventricular tachycardia. The morphology of QRSs varies beat to beat with axis changes. Ventricular rate changes from 150 to 250 bpm. EKGs AND CORRESPONDING LEAD CHANGES For locating ischemia, injury, or infarction: Inferior wall II, III, AVF Lateral wall I, AVL, V5, V6 Septal wall V1, V2 Anterior wall V3, V4

LMYOCARDIAL INFARCTIONL EKG changes may not show immediately. INJURY ST segments elevate within minutes of the onset of chest pain.

178

ISCHEMIA T waves invert fully within 24 hours.

ACUTE INFARCTION Pathologic Q waves 0.03 second or onethird height of QRS start after 1 hour of infarction.

OLD INFARCTION ST segments are normal and Q waves are apparent forever.

179

RECIPROCAL ST DEPRESSION Shows in leads distal from the infarction.

NON–Q-WAVE INFARCTION Flat, depressed ST segments in two or more contiguous leads or may display inverted T waves.

LBUNDLE BRANCH BLOCKSL LEFT BBB Typical sign is “rabbit ears.” QRS 0.12 second V1, V5, V6

180

V1, MCL1 Tachycardic LBBB can appear similar to ventricular tachycardia.

RIGHT BBB Typical sign is RSR or “rabbit ears.” V1, V2, MCL1 Large S also seen in 1, V5, V6.

LELECTROLYTE OR DRUG EFFECTSL Hyperkalemia. Tall, peaked T waves, wide QRS, possible loss of P waves. Patient is at risk for asystole and ventricular fibrillation. Digitalis effect. Depressed ST segment and inverted T waves. Hypokalemia. Flat T waves, large U waves in all leads. Can progress into torsades, ventricular fibrillation, ventricular tachycardia, and can exacerbate digitalis toxicity. 181

LNOTESL

CHEST TUBES AND BRONCHOSCOPY

183

Chest Tubes and Bronchoscopy

See references 6, 11, 15, 24, and 25 STANDARD THREE-BOTTLE SYSTEM . . . . . . . . . 184 CHEST TUBES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185 Removal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185 Troubleshooting and Maintenance . . . . . . . . . . 185 BRONCHOSCOPY . . . . . . . . . . . . . . . . . . . . . . . . . . . 187 Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187 Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . 187 Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188 Vital Supplies . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188 Important Preprocedure Instructions . . . . . . . . 189 Bronchoscopy Physician Assistant Duties . . . . . 189 Flexible Fiberoptic Bronchoscopy . . . . . . . . . . . 189 Rigid Tube Bronchoscopy . . . . . . . . . . . . . . . . . . 190

Chest Tubes & Bronchoscopy

184

LSTANDARD THREE-BOTTLE SYSTEM24L To pleural space

cm H2O

To wall suction –60 cm H2O

–20 cm H2O

Chest tube –20 cm H2O

–20 cm H2O

20 – 10 –

A

B

C

CHEST TUBES AND BRONCHOSCOPY LCHEST TUBESL Chest tubes are sized from small-bore 7 French to large-bore 40 French with radiopaque stripes; they are placed into the pleural space to remove air or fluids. • Bottle A in the illustration controls suction via the level of water within the chamber. • Bottle B isolates room air from the chest tube by creating a water seal (this bottle could be replaced with a Heimlich valve in small-bore tubes). • Bottle C is the collection chamber. INDICATIONS The most common indications include pneumothorax, empyema, hemothorax, hydrothorax, pleural effusion, and to install sealant. Chest tubes are usually secured with sutures and the insertion distance recorded to check for migration. Chest x-rays are also used to verify placement. REMOVAL If removed 48 hours after leaks are no longer present, a 0% incidence of recurrence exists. The most common practice to check for leaks is a 4-hour clamp test. If the condition requiring the chest tube returns, unclamp immediately and assess the cause of the leak. TROUBLESHOOTING AND MAINTENANCE • Malposition is indicated by persistent bubbling or no bubbling at all in the water-seal bottle (B). Chest tubes can end up in the major fissure, where their function is not optimal. 185

• The collection bottle (C) should not be allowed to fill completely. • The water-seal bottle (B) must maintain a water level above the bottom of the tube connecting the collection bottle. • The water level in the suction control bottle (A) controls the suction for the system and must be maintained at the specified level. • Small-bore tubes using a Heimlich valve can be tested for leaks by submerging the valve into water to check for leaks. Bubbles after complete lung expansion indicate a leak. • If the water-seal bottle (B) bubbles persistently, a leak exists. If the skin sutured around the chest tube pulls away from the tube, often a sucking sound can be heard, which can be corrected by occluding the hole with petroleum gauze. Additionally, if the chest tube were to penetrate the lung, the water-seal bottle (B) would bubble persistently. • Tube occlusions, clots, or migration into the walls of the tissue will not allow the chest tube to evacuate fluid. No bubbling at all in the water-seal bottle (B) will indicate this. The absence of bubbling in the water-seal bottle (B) may also be the result of no free air in the pleural space to be evacuated. An inspection of the chest x-ray with findings of a pneumothorax or pleural effusion with the chest tube in place indicates an occlusion of the tube. In addition, no oscillation of fluid in the chest tube during coughing or deep breathing is consistent with an occlusion. • Always check tubing for air leaks. 186

LBRONCHOSCOPYL Definition: Bronchoscopy is the direct visual examination of the airways via insertion of a bronchoscope. TYPES • Flexible fiberoptic bronchoscopy • Rigid-tube bronchoscopy INDICATIONS—DIAGNOSTIC AND THERAPEUTIC • To assess airway patency and examine airways for infiltrates, atelectasis, infection, disease, cancer, abnormal tissue, foreign material, or burn and smoke injuries • To investigate the cause of hemoptysis, unexplained cough, wheeze, or stridor • To aid in difficult intubations or evaluate problems with the endotracheal or tracheal tube • To obtain samples of abnormal tissue, secretions, cell washings, or biopsies for evaluation • To improve airway patency by removing a foreign body, excessive viscous secretions, or mucous plugs • To deliver laser treatment or radiation treatment, cauterize an area, or destroy airway growths CONTRAINDICATIONS • Insufficient personnel and facilities to perform procedure safely or to manage emergency situations (Procedure mandates the presence of bronchoscopy physician, and experienced, competent clinical assistants.) • Refractory hypoxemia with an inability to oxygenate a patient adequately during procedure • Uncorrected bleeding disorder 187

• Unstable hemodynamic or cardiac status • Pregnancy (cautionary; recognize increased risk) MEDICATIONS • Tranquilizer is adminstered for anxiety. Valium and Versed are commonly used benzodiazepines. • Narcotic analgesic similar to morphine or fentanyl can be used to reduce pain and to decrease laryngeal reflexes. • Atropine is administered to dry the airway and to aid visibility; it also reduces the risk of bradycardia and hypotension. • Bronchodilator is administered to prevent bronchospasm. • Anesthetic is applied to throat and nasal passages to numb the area and to reduce the gag reflex. • Airway anesthesia is provided with topical anesthetics (more common) or nerve block. Lidocaine can be given by nebulizer and/or direct instillation into the airways. • Syringes are prefilled with lavage solutions, saline, mucolytics, additional anesthetics, and vasoconstrictors. • Additional emergency medications include resuscitative drugs, antiarrhythmics, narcotic antagonists such as naloxone (Narcan). Intravenous fluids must be immediately available. VITAL SUPPLIES • Biopsy forceps, biopsy needles, brushes, suction supplies, specimen containers, bite blocks, and other supplies as per institutional policy • Oxygen to maintain adequate saturation • Ventilation supplies and equipment 188

• Fluoroscopy machine, if requested by bronchoscopy physician IMPORTANT PREPROCEDURE INSTRUCTIONS • Patient is instructed about the procedure, and informed consent is obtained, unless an emergency exists or the patient is not competent. • Patient should not eat or drink for 4 to 12 hours before the procedure, according to policy. • Dentures should be removed. • Determine whether patient has any allergies, bleeding disorders, or is taking anticoagulants. • Ensure that the patient is clinically stable and that procedure is not contraindicated as previously listed. • Ensure that all equipment and supplies are prepared and machines are operating properly. BRONCHOSCOPY PHYSICIAN ASSISTANT DUTIES • Aid in performing diagnostic and therapeutic procedures as previously listed • Continuously monitor patient’s clinical status • Deliver medications, and instill lavage solutions • Suction to keep airway clearly viewable FLEXIBLE FIBEROPTIC BRONCHOSCOPY DESCRIPTION A long, thin, flexible tube containing fiberoptics that transmits light images as it is advanced into the airways. Three channels include the light transmission channel, 189

visualizing channel, and a multipurpose open channel. The procedure is commonly performed by the physician with respiratory therapy and nursing assistance. ADVANTAGES Procedure is more comfortable to the patient, can be performed under a local anesthetic, and is versatile, offering better access to small airways. DISADVANTAGE Compared to the rigid tube, flexible tube may not have diameter large enough to clear the airway of large foreign bodies or large mucous plugs, or to obtain large biopsies. RIGID TUBE BRONCHOSCOPY DESCRIPTION A rigid open metal tube with a distal light and port for attaching oxygen or ventilation equipment. The tube is inserted into the mouth, through the trachea, and as far as the larger bronchi. To view segmental bronchi, a telescopic tube is used with mirrors. ADVANTAGES The large internal diameter of the tube allows aspiration of larger mucous plugs, and thicker inspissated secretions than the flexible fiberoptic tube. Grasping forceps can be passed through the tube to remove larger foreign bodies and tumor biopsies. DISADVANTAGES The large rigid tube is extremely uncomfortable for a conscious patient. The smaller airways cannot be accessed. Most often performed under general anesthesia in the operating room by a surgeon or otorhinolaryngologist with the assistance of an anesthesiologist. 190

VENTILATORS, CPAP, AND BIPAP

191

Ventilators, CPAP, and BiPAP

See references 6, 24, and 25 MECHANICAL VENTILATION . . . . . . . . . . . . . . . . . . 193 Indications for Mechanical Ventilation . . . . . . . . 193 Mechanical Ventilation Miscellaneous Notes . . . . 193 Miscellaneous Formulas . . . . . . . . . . . . . . . . . . . . 193 Mechanical Ventilation Formulas (by Alphabetical Abbreviations) . . . . . . . . . . . . 194 Initial Setup Parameters for Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196 Continuous Patient Assessment and Weaning Parameters for Mechanical Ventilation. . . . . . . . . . . . . . . . . . . . 197 MODES OF VENTILATION . . . . . . . . . . . . . . . . . . . . . 198 Airway Pressure Release Ventilation (APRV) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198 Automode . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198 Chest Cuirass—Extrathoracic Negative Pressure Ventilators (Including the Iron Lung) . . . . . . . . . . . . . . . . . . . . . . . . . . . 199 Continuous Positive Airway Pressure or Positive End-Expiratory Pressure (CPAP or PEEP) . . . . . . . . . . . . . . . . . . . . . . . . . . 199 Extracorporeal Membrane Oxygenation (ECMO) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 200 High-Frequency Ventilation and Oscillation (HFV and HFO) (Adults) . . . . . . . . . . . . . . . . . . . 200 General Guidelines for Initial Setup of HFO Ventilator for an Adult . . . . . . . . . . . . . 201 Inverse Ratio Ventilation (IRV) . . . . . . . . . . . . . . . 201 Intravascular Membrane Oxygenation and Carbon Dioxide Removal (IVOX) . . . . . . . . 202 Liquid Perfluorocarbon Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202 Negative Pressure Ventilators . . . . . . . . . . . . . . . 202 Pressure Control (PC) . . . . . . . . . . . . . . . . . . . . . . . 202 PEEP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203 Pressure-Regulated Volume Control (PRVC) . . . . . . . . . . . . . . . . . . . . . . . . . . . 203 Pressure Support Ventilation (PSV or PS) . . . . . . 204 Synchronous Intermittent Mandatory Ventilation (SIMV or IMV) . . . . . . . . . . . . . . . . . 204 SIMV Pressure Control plus Pressure Support (SIMV PC  PS) . . . . . . . . . . . . . . . . . . 205

Ventilators, CPAP, and BiPAP

Volume Control or Assist Control (VC or AC) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205 Volume Support (VS) . . . . . . . . . . . . . . . . . . . . . . . 206 OTHER VENTILATOR CONTROLS . . . . . . . . . . . . . . 207 Expiratory Retard . . . . . . . . . . . . . . . . . . . . . . . . . . 207 Flowrate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .207 I:E Ratio. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208 Inspiratory Pause or Plateau . . . . . . . . . . . . . . . . . 208 Inspiratory Time . . . . . . . . . . . . . . . . . . . . . . . . . . . 208 Pressure Limit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208 Pressure Rise Time or Slope . . . . . . . . . . . . . . . . . 208 Sensitivity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209 Sigh . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209 Waveforms or Flow Patterns . . . . . . . . . . . . . . . . 209 CPAP AND BIPAP THERAPY . . . . . . . . . . . . . . . . . . . 212 CPAP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212 BIPAP. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213 VENTILATOR ALARMS . . . . . . . . . . . . . . . . . . . . . . . 214 COMPLICATIONS OF VENTILATION . . . . . . . . . . . . 214 TROUBLESHOOTING . . . . . . . . . . . . . . . . . . . . . . . . . 215 Problem: Abnormal ABGS . . . . . . . . . . . . . . . . . . . 215 Problem: Increased Intracranial Pressure (ICP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216 Problem: Spontaneous Respiratory Rate . . . . . . 216 Problem: Inadvertent or Auto-PEEP . . . . . . . . . . .216 Problem: High-Peak Pressures . . . . . . . . . . . . . . . 216 Problem: Low Pressures or Low-Exhaled Volumes . . . . . . . . . . . . . . . . . . 217 Problem: Inspiratory Time Too Long and I:E Ratio Too High . . . . . . . . . . . . . . . . 217 Problem: Patient Fighting Ventilator . . . . . . . . . . 217 Problem: Ventilator Malfunction or Failure to Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217

SEE ALSO THERAPEUTIC MODALITIES Artificial Airways and Suctioning . . . . . . . . . . . . 105

ABGS, LABS, AND HEMODYNAMICS Blood Gas Formulas . . . . . . . . . . . . . . . . . . . . . . . . 132

PFTS AND X-RAYS

192

VENTILATORS, CPAP, AND BIPAP NOTE: The values in this chapter are adult values provided as a reference only. Clinicians must also refer to the policies and protocols set forth by the employer.

LMECHANICAL VENTILATIONL INDICATIONS FOR MECHANICAL VENTILATION • Apnea • Acute respiratory failure—hypercapnic or hypoxemic • Impending respiratory failure MECHANICAL VENTILATION MISCELLANEOUS NOTES • Always keep a resuscitation bag and all emergency equipment on hand. • Humidity must be provided with either a heat and moisture exchanger (HME) or a heated humidification system. • Ventilator circuits, in-line suction catheters, and filters should be changed regularly. • Equipment calibration, cleaning, and maintenance must be performed on a regular basis. MISCELLANEOUS FORMULAS 1 mL  1 cc Elastance  1/compliance Resistance  $ Pressure/Flow Compliance  $ Volume or $Pressure Compliance lung and thorax: normal CLT  0.1 L/cm H2O 193

194

MECHANICAL VENTILATION FORMULAS (BY ALPHABETICAL ABBREVIATIONS) Abbreviation

Parameter

CD

CD  (VT  tubing expansion volume)  Varies based on CS and RAW (PIP – PEEP) Static (lung) compliance CS  (VT  tubing expansion volume)  0.1 to 0.2 L/cm H 2O or 100-200 mL/cm H2O (Plateau pressure  PEEP) 8-20 breaths/min Rate or frequency f  60  TC or f  VE  VT Set above patient demand; usually Flowrate Flowrate  VE  (I  E) or flowrate  VE  30-50, but can exceed 80 L/min %TI decimal or flowrate  VT  (TI  60) 1:2, 1:3, or 1:4 lnspiratory-to-expiratory ratio I:E  TI :TE See PMean Negative inspiratory force Measured with manometer; also called MIP or 80 cm H2O maximal inspiratory pressure Peak inspiratory pressure PPeak  PPlateau  RAW or PIP can be 40 cm H2O; keep as low as possible viewed on manometer Plateau pressure PPlateau  PPeak  RAW or view on manometer 32 cm H2O with inspiratory hold Mean airway pressure Most ventilating factors affect PMean Keep as low as possible (i.e., each 1 PEEP  1 mean)

CS f Flowrate I:E Ratio Mean Psr NIF PPeak or PIP PPlateau PMean

Dynamic compliance

Formula

Normal Values

QS/QT  (AaDO2)  0.003  (CaO2  CvO2)  (AaDO2)  0.003

Normal 5%; moderate defect 10-20%; severe defect 20%

RAW  PPeak  PPlateau  flowrate L/sec RAW trend  PPeak  PPlateau

0.5 to 2.5 cm H2O/L/sec 10 cm H2O on ventilator; keep as low as possible Varies based on inspiratory time and rate Varies based on insp time and rate 0.8 to 1.2 second 20% to 33%

QS/QT

% Shunt

Rate RAW RAW Trend

See “f” Airway resistance Airway resistance trend

TC TE TI TI% Tubing Exp Vol

Cycle time Expiratory time Inspiratory time % Inspiratory time Tubing expansion volume

VA VD Mech VD/VT

Alveolar ventilation Mechanical deadspace Deadspace to tidal volume

VE

Minute ventilation

TC  (TI  TE) or TC  (60  f) TE  (60  f)  TI or TE  TC  TI TI  (60  f)  TE or TI  TC  TE TI%  (TI  TC) Adult circuit: 3 mL/cm H2O; neonate circuit 1 mL/cm H2O VA  (VT  VD)  f 10 mL/inch VD/VT (PaCO2  PECO2)  PaCO2; anatomical VD  1 mL/lb VE  VT  f

VT

Tidal Volume

VT  VE  f

195

Varies; is nearly the same as VE Near zero unless clinically indicated 20-40% off ventilator 40-55% on ventilator 4-8 L/min off ventilator 5-10 L/min on ventilator 7 mL/kg spontaneous breaths 6-10 mL/kg ventilator breaths

INITIAL SETUP PARAMETERS FOR MECHANICAL VENTILATION Rate VT VE O2 PEEP PS Flowrate I:E Ratio Inspiratory time Sensitivity

10-15/min 6-10 mL/kg 5-10 L/m 40-60%* 5 cm H2O† 5 to 10 cm H2O 30-50 L/m‡ 1:2, 1:3, or l:4 0.8-1.2 sec or 20-33% 0.5 to 2.0 cm or flow trigger 1-3 L/m below baseline or bias fIow

*lnitial oxygen up to 100% depending on pulse oxygen saturation and situation (i.e., respiratory arrest). † PEEP may be set to zero in cases of low blood pressure. ‡ Must meet or exceed patient demand, which can exceed 80 L/min. Notes: These initial setup values are generic settings for adults and may be appropriate when little or no information is known about the patient. As clinical data become available, these settings must be adjusted, based on data as listed in this section. Alarms must also be set appropriately. See detailed information about each of these parameters in the tables in this section.

The following parameters are important to assess frequently for stability and changes: • Patient and equipment • Overall medical condition, vital signs, skin color, and nutritional status • EKG, hemodynamics, laboratory tests, and x-rays • Breath sounds, secretions, and work of breathing • Need for suction or bronchodilator • Proper function of ventilator; all parameters, pressures, volumes, and alarms • Need for parameter changes 196

• Clean and problem-free equipment from endotracheal or tracheostomy tube to ventilator • Circuit clear of excess condensate • Secure endotracheal or tracheostomy tube with proper cuff pressure • Adequate humidity and properly elevated head of bed (See Troubleshooting in this section.)

CONTINUOUS PATIENT ASSESSMENT AND WEANING PARAMETERS FOR MECHANICAL VENTILATION

PARAMETER ABGs pH PaCO2 PaO2 Pulse oximetry SpO2 Respiratory rate (spontaneous) Tidal volume (spontaneous) Minute ventilation Vital capacity NIF

NORMAL VALUES

ACCEPTABLE RANGE ON VENTILATOR (and acceptable range for weaning)

7.40 40 mm Hg 100 mm Hg 95%

7.35-7.45 35-45 mm Hg 70 mm Hg 95%

8-20/min

8-20/min

7 mL/kg

5 mL/kg

5-10 L/m

5-10 L/m

65 mL/kg 80 cm H2O

10 mL/kg 20 cm H2O or better

A-a Gradient

25-65 mm Hg on 100% 10-15 mm Hg on 21% 300 mm Hg on 100% QS/QT 5% 20% VD/VT 40-55% on ventilator 20-40% off ventilator 60% Note: Descriptions and formulas for the values in this table are listed in the Mechanical Ventilation Formulas table earlier in this chapter, and in the ABG, Labs, and Hemodynamics chapter.

197

LMODES OF VENTILATIONL AIRWAY PRESSURE RELEASE VENTILATION (APRV) • Is designed to recruit collapsed alveoli and optimize ventilation while minimizing barotrauma. • Is useful in treating ARDS and ALI. • Can be described as a high-tech CPAP pressure with regular, brief, intermittent releases of airway pressure. Release phase facilitates CO2 removal. APRV maintains patency of alveoli by maintaining a constant pressure with fixed inspiratory time. • Tidal volumes are delivered during transient decreases in intrathoracic pressure. • Uses long inspiratory time to improve oxygenation. • Breaths can be triggered by the patient. • In clinical trials, APRV is better tolerated than IRV, with lower PIPs and similar improvements in oxygenation. AUTOMODE • Combination of modes that automatically facilitates weaning at the earliest possible opportunity; switches to a partial support mode as soon as the patient triggers two spontaneous breaths. • Ventilation mode changes back to full support mode if an apneic period occurs. • May not be appropriate for the patient who needs VT, VE, and a rate closely monitored and controlled. • Setting all applicable parameters and alarms for both applicable modes is important. • Combination modes available are PC and PS, PRVC and VS, and VC and VS (see individual presentations in this section). 198

CHEST CUIRASS—EXTRATHORACIC NEGATIVE PRESSURE VENTILATORS (INCLUDING THE IRON LUNG) • Negative pressure is applied via suction to the outside of the chest. • Negative pressure produces inspiration by making the chest rise and expand. • Ventilation is controlled by adjusting the level of negative pressure and the inspiratory time. • Is no longer commonly used, because modern ventilators use positive pressure. However, these ventilators are still used for certain cases (e.g., long-term management of some patients with chronic respiratory failure). CONTINUOUS POSITIVE AIRWAY PRESSURE OR POSITIVE END-EXPIRATORY PRESSURE (CPAP OR PEEP) • See CPAP and BiPAP Stand-Alone Devices later in this section. • PEEP/CPAP describes breathing at pressures greater than zero baseline pressure. • Optimally, improves oxygenation, increases compliance, increases FRC, and decreases atelectasis. • Is generally recommended to add or increase CPAP/PEEP with PaO2 60 or FiO2 40%. • Common range of PEEP used is 3 to 12 cm H2O or higher, if indicated. PEEP of 3 to 5 cm H2O basically restores physiologic PEEP lost as a result of the presence of an artificial airway. • Use cautiously in the patient with low blood pressure or increased FRC. • PEEP/CPAP often is combined with other modes when used in conventional ventilation (e.g., SIMV, VC). 199

• Technically, PEEP involves a mechanical rate; in CPAP, all breaths are spontaneous. • Refer to Complications and Auto-PEEP in the Troubleshooting section. • Optimal PEEP is the least amount of PEEP necessary to provide adequate oxygenation without adverse effects. Parameters defining optimal PEEP are the following: ◆ Increasing PaO 2 ◆ Increasing static compliance ◆ Blood pressure not decreasing to unacceptable level ◆ Cardiac output not decreasing to unacceptable level ◆ Stable hemodynamic pressures ◆ PAP and PWP stable and not increasing to unacceptable level EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO) • Is used to treat newborns with acute respiratory failure and to treat severe acute hypoxemic respiratory failure, including ARDS. • Involves an arteriovenous circuit for diverting most cardiac output through an artificial lung that facilitates exchange of CO2 and O2. HIGH-FREQUENCY VENTILATION AND OSCILLATION (HFV AND HFO) (ADULTS) • Mode of ventilation uses rates over 60. Terms used are high-frequency ventilation (HFV), high-frequency jet ventilation (HFJV), high-frequency positive-pressure ventilation (HFPPV), and high-frequency oscillation or high-frequency oscillatory ventilation (HFO). • Hertz (Hz) describes cycles per second; 1 Hz  rate of 60. Rate  Hz  60 (e.g., 3 Hz is a rate of 180). 200

• In HFV, the rates are high (61 to 2000). Tidal volumes are very low (~2-5 mL/kg). HFO technically means the rate is 300 (5 Hz or higher). • Tidal volumes can be slightly above, equal to, or even lower than dead space ventilation. • HFV is designed to provide adequate ventilation while minimizing alveolar collapse via high-expiratory lung volumes. HFV has proved effective over decades of use for neonates. It currently is used for adults with conditions such as ARDS to improve oxygenation while minimizing barotrauma when other modes of ventilation fail. The patient must be sedated for HFV and HFO.

GENERAL GUIDELINES FOR INITIAL SETUP OF HFO VENTILATOR FOR AN ADULT Hz (rate)

6 Hz (remember to decrease rate to decrease CO2)

MAP (cm H2O)

4-8 above MAP on conventional ventilator

P

Adjust for adequate chest wiggle

Flowrate

Adjust to obtain desired MAP (approximately 20-40 L/min)

FiO2 (%)

100% (assuming failure to oxygenate with conventional ventilation)

TI (sec)

33

Note: Setting can vary greatly based on patient needs and type of ventilator. The facility’s protocols should always be followed.

INVERSE RATIO VENTILATION (IRV) • Is used to recruit alveoli and improve oxygenation via prolonged inspiratory time. • Used to treat ARDS and other cases when other methods of improving oxygenation fail. • I:E ratio usually ranges from 1.5:1 to 4:1. 201

• Patient must be sedated and sometimes paralyzed because IRV is very uncomfortable. • Case studies report IRV can improve oxygenation in the patient with ARDS. INTRAVASCULAR MEMBRANE OXYGENATION AND CARBON DIOXIDE REMOVAL (IVOX) • Devices are currently undergoing clinical studies for use in lung-protective ventilatory strategies and for cases including severe respiratory failure. • IVOX can remove up to 30% of CO2 in certain patients with almost normal CO2 levels, allowing reduction of IPPV. LIQUID PERFLUOROCARBON MECHANICAL VENTILATION • Liquid ventilation involves perfluorocarbonassociated gas exchange. • Perfluorocarbons dissolve O2 and CO2, facilitating pulmonary gas exchange. The lungs are partially filled with the fluid, and mechanical ventilation is provided with conventional ventilators. • This mode currently is being studied to treat ARDS. NEGATIVE PRESSURE VENTILATORS See Chest Cuirass—Extrathoracic Negative Pressure Ventilators (Including the Iron Lung). PRESSURE CONTROL (PC) • Provides full ventilatory support. A minimum guaranteed rate is dialed in, with preset pressures. Tidal volumes vary. • Breaths are time cycled and can be patient triggered. • Inspiratory phase is pressure limited and delivered at preset PC above PEEP level. 202

• Flowrate is high initially to meet patient demand and then decelerates. • PC is a good choice for the patient with unacceptably high pressures in other modes (e.g., SIMV, VC). PC can help prevent barotrauma in conditions such as ARDS. PC can be used with IRV when indicated. • Clinicians must be alert for significant changes in VT and VE, because these vary and can change to unacceptable levels. PEEP See CPAP and PEEP. PRESSURE-REGULATED VOLUME CONTROL (PRVC) • Full ventilatory support should be provided. • Guaranteed minimum rate is dialed in. Ventilated breaths and spontaneous breaths are delivered at preset VT. • PRVC is a pressure limited mode with preset inspiratory time. • Flowrate is initially high to meet patient demand and then decelerates. • Main difference between VC and PRVC is the following: the ventilator automatically adjusts the inspiratory pressure level in PRVC, based on changes in lung mechanics on each breath. Changes occur in increments of 1 to 3 cm H2O. PRVC always uses the lowest pressure needed to deliver the desired VT and VE. PRVC is a good choice for the patient with little or no spontaneous breathing capacity and with unacceptably high pressure in other modes. • Appropriately setting the upper pressure limit is important because it serves two purposes: (1) it becomes an alarm and automatically switches to exhalation when reached so that 203

full VT is not delivered; and (2) it should be set as low as possible while ensuring adequate tidal volume. Whenever the PIP reaches 5 cm H2O below the upper pressure limit, a “Limited Pressure” alarm is activated and the delivered VT may be less than the preset VT. • Because VT varies, clinicians must be alert to any significant changes in VT and VE. PRESSURE SUPPORT VENTILATION (PSV OR PS) • Is designed for patients with spontaneous breathing capacity who still need partial ventilatory support. • Is not for patients with no or only minimal respiratory drive. • Assists each spontaneous breath with inspiratory pressure at the level dialed in. • Helps increase spontaneous tidal volume, improving ventilation and oxygenation; also helps reduce WOB. • Can be used alone with PEEP/CPAP or in combination with certain modes. • Inspiratory flowrate is initially high to meet patient demand and then decelerates. • PS 5 cm H2O is considered a minimal assist to help overcome the resistance of breathing through the circuit. A commonly used range is 5 to 15; however, 20 or more is used as needed. PS often is set to achieve a target VT of 6-10 mL/kg. SYNCHRONOUS INTERMITTENT MANDATORY VENTILATION (SIMV OR IMV) • Can provide full or partial ventilatory support. • SIMV plus PS is a good choice for many patients. SIMV has a number of uses, ranging from apnea, to some spontaneous breathing, to weaning and extubation. 204

• SIMV is not a good choice for patients with consistently high and unmanageable PIP. • Ventilator provides a guaranteed minimum tidal volume, rate, and minute volume. The dialed-in rate is provided at the preset VT. Additional spontaneous breaths can be purely spontaneous or, more commonly, supported with PS. SIMV PRESSURE CONTROL PLUS PRESSURE SUPPORT (SIMV PC  PS) • Can provide full or partial ventilatory support. • Combines PC and PS with a synchronized rate (see individual sections on PC and PS for full information). • Delivers the set rate of mandatory breaths using the PC mode and assists with spontontaneous breaths using the PS mode. • Because tidal volume varies, clinicians must be alert to significant changes in VT and VE. • Inspiratory flowrate is initially high to meet patient demand and then decelerates. • Is indicated for the patient with unacceptably high PIP in other modes and those needing high flowrates who have some spontaneous breathing. • Patients can have some purely spontaneous breaths between cycles with no PS. A mismatch between PC and PS breaths is a common problem causing respiratory distress in this mode. Therefore beginning with PC and PS breaths at or near the same pressure (i.e., set both at 20) is often best. VOLUME CONTROL OR ASSIST CONTROL (VC OR AC) • VC or AC is designed to provide full ventilatory support. 205

• Every breath is delivered at a constant preset tidal volume (time-cycled and patienttriggered breaths are given with the same tidal volume). • Guaranteed minimum VT, and rate and minute volume, are provided. • Patients can trigger spontaneous breaths as long as sensitivity is set appropriately, but these breaths are delivered at the same tidal volume as ventilator breaths. • PS is not an option in this mode. • Is a good choice for the patient with decreased sensorium who needs full support, as long as lung mechanics are normal and peak pressures do not rise to unacceptable levels. However, SIMV as an alternative should be considered, because SIMV is better tolerated, and VC or AC can cause higher mean pressure, as well as hyperventilation if spontaneous rate rises. VOLUME SUPPORT (VS) • Is designed for the patient who spontaneously breathes but still requires partial ventilatory support. VS is also used as a weaning mode with preset backup in the case of apnea. • Is not indicated for the patient with insufficient respiratory drive. • Helps reduce WOB, increases ventilation, and improves oxygenation in the patient who spontaneously breathes. • Differs from PS in that VS provides automatic weaning of PS as long as the patient’s tidal volume matches the minimum tidal volume required. • Inspiratory flow is decelerating, giving high initial flowrate to meet patient demand. • Each breath is patient triggered, and the ventilatory uses the lowest PS necessary to 206

achieve preset minimum expected VT and VE. Ventilator automatically adjusts inspiratory PS in increments of 1-3 cm H2O. Desired rate is dialed in and is part of automatic ventilatory calculations, but the actual rate and inspiratory time are patient-dependent unless the patient has an apneic period. PRVC is an automatic backup, with the same set VT and backup rate. • Ventilator should be set to achieve target VT of 6-10 mL/kg. • Because VT varies, the clinician must be alert to significant changes in VT and VE. • All applicable parameters and alarms must be set appropriately. Appropriately setting the upper pressure limit is important because the upper pressure limit serves two purposes: (1) it is an alarm and automatically switches to exhalation when reached so that full VT is not delivered; and (2) it should be set as low as possible while ensuring adequate tidal volume. Whenever the PIP reaches 5 cm H2O below the upper pressure limit, a “Limited Pressure” alarm is activated and delivered VT may be less than preset VT. (VT can also increase; ventilator will deliver up to 150% of set minimum VT.)

LOTHER VENTILATOR CONTROLSL EXPIRATORY RETARD Prolongs exhalation and decreases the FRC, which is the opposite effect of PEEP. It mimics pursed-lip breathing and is useful with patients with COPD. FLOWRATE Peak inspiratory flow of gas. Must adjust it to meet or exceed patient demand. Usual range 207

is 30-50 L/m, but can exceed 80 L/m. If set too high, can increase RAW and PIP. If set too low, can cause increased WOB, and make TI too long. I:E RATIO Best ratio is 1:2, 1:3, or 1:4. Patients with COPD need more time to exhale; therefore a longer I:E ratio (1:3 or 1:4) is recommended. INSPIRATORY PAUSE OR PLATEAU Inflation hold maneuver during which the patient is made to hold the tidal volume at the end of inspiration for a short time. If used, it is usually set at 0.5 to 1 second. Improves distribution of ventilation and can increase PaO2. Increases inspiratory time and decreases expiratory time, thereby decreasing the I:E ratio. If the I:E ratio needs to be maintained and the inspiratory pause added, the flowrate can be increased to decrease the inspiratory time. INSPIRATORY TIME Important time parameter where inspiratory time is set by clinician, then the ventilator calculates the remaining time as expiratory time, as calculated by the preset rate. This also sets the I:E ratio. Usual range for TI time is 0.8 to 1.2 seconds, or 20% to 33%. Too short TI along with a low flowrate can result in decreased VT. Too long TI can cause too short TE and patient discomfort. PRESSURE LIMIT A peak pressure alarm and also a parameter to set in certain modes (as described in applicable modes). The upper pressure alarm is usually set at 5 to 10 above actual or desired PIP. 208

PRESSURE RISE TIME OR SLOPE Is used to slow the rate at which peak inspiratory pressure is reached. If used, inspiratory gas flow should meet or exceed patient demand. If too slow, WOB will increase. SENSITIVITY Is used to allow the patient to trigger breaths. The usual range is 0.5 to 2.0 cm H2O, or flow trigger 1-3 L/m below baseline or bias flow. Must be sensitive enough for the patient to easily trigger breaths without increasing WOB but not so sensitive that the ventilator automatically cycles. SIGH Can be used to simulate normal breathing sighs. Helps prevent atelectasis. If used, set at 6-10 per hour at 1½ times the set tidal volume. Monitor PIP to ensure it is not too high during sighs. WAVEFORMS OR FLOW PATTERNS Square wave-flow pattern: Produces a constant flow throughout inspiration. Is useful for noncompliant lung conditions such as ARDS or pneumonia. Sine wave flow pattern: Flow begins slowly and increases to a peak, then decreased at the end of inspiration. Simulates normal breathing and gives good distribution of ventilation. Accelerating flow pattern: Flow begins slowly and rises to a peak, then it ends at the end of inspiration. Can reduce turbulent flow and decrease mean airway pressure in those with increased RAW. Decelerating flow pattern: Flow is very fast during the beginning of inspiration and peaks, then gradually decreases. Is useful for patients who need high flow rates. 209

Pressure (cm H2 O) Flow (L/min) Volume (mL)

40 30 20 10 0 -10 -20 -30 -40 -50

2

4

6

8

10

12

14

0

2

4

6

8

10

12

14

0

2

4

10

12

14

24 20 16 12 8 4 0

600 500 400 300 200 100 0

6 8 Time (seconds)

Spontaneous breathing at an elevated baseline pressure (CPAP). The flow, pressure, and volume curves show spontaneous breathing with a CPAP of approximately 5 cm H2O. The flow curve is sinusoidal, the pressure curve fluctuates approximately 1-3 cm H2O around the baseline pressure, and the volume delivered varies. These observations are typical during spontaneous breathing.24

Volume (mL)

Pressure (cm H2 O) Flow (L/min)

60 40 20 0

2

-20

4

6

8

10

12

14

-40 -60

Patient-triggered breath

Ventilator-triggered breath

24 20 16 12 8 4 0

0

2

4

0

2

4

6

8

10

12

14

10

12

14

600 500 400 300 200 100 0

6 8 Time (seconds)

Volume ventilation in the assist-control mode. Some breaths are time triggered and others are patient triggered. A square wave flow pattern is shown, and volume is consistent, breath to breath.24

210

Volume (mL)

Pressure (cm H2 O) Flow (L/min)

60 40 20 0

2

4

0

2

4

0

2

4

-20

6

8

10

12

14

6

8

10

12

14

10

12

14

-40 -60

24 20 16 12 8 4

Trigger

0

600 500 400 300 200 100 0

6 8 Time (seconds)

Pressure support breaths (PSV). The patient trigger for each breath is evident. Flow is decelerating, and the pressure waveform approaches a square wave.24

Volume (mL)

Pressure (cm H2 O) Flow (L/min)

60 40 20 0

2

-20

4

6

8

10

12

14

-40 -60

24

Mandantory breath

20

Pressure-support breath

16 12 8 4 0

0

2

4

0

2

4

6

8

10

12

14

10

12

14

800 600 400 200 0

6 8 Time (seconds)

Synchronized intermittent mandatory ventilation with pressure support. Mandatory breaths have a square flow waveform with a constant volume of 600 mL. The pressure support breaths have a decelerating flow waveform and a pressure pattern approaching a square wave. In this example, an elevated baseline of approximately 5 cm H2O (PEEP) is also seen.24

211

LCPAP AND BIPAP THERAPYL This section pertains mainly to stand-alone CPAP and BiPAP machines and the controls found on these machines. Precautions and hazards of CPAP and BiPAP are the same as those for PEEP and PS. Excessive airway pressures are avoided, and blood pressure (especially if using high pressures) and vital signs are both monitored. Alarms are set appropriately. The incidence of patient discomfort and noncompliance can be reduced by two steps: (1) mask and nasal devices are properly fitted to maintain desired pressure and improve patient comfort, and (2) patient education is provided before beginning therapy. CPAP DESCRIPTION Continuous positive airway pressure (CPAP) is the same therapy as PEEP, but the term CPAP is used when the patient is spontaneously breathing with no mechanical ventilation rate. CPAP is spontaneous breathing at pressure greater than zero. Is usually set at 3 to 12 cm H2O; or higher, if needed. CPAP increases FRC, increases compliance, decreases atelectasis, and increases oxygenation. Is also used for obstructive sleep apnea (OSA) to overcome upper airway obstruction by splinting the airway open. RAMP The ramp button, when pressed, causes a decrease in CPAP pressure that slowly builds back up to the set pressure. Many patients find it easier to start with the low pressure and slowly get used to the higher pressure, or fall asleep before the machine reaches set pressure. 212

C-FLEX C-Flex is a very brief drop in pressure at the beginning of exhalation, after which pressure quickly returns to set pressure. Designed to increase patient comfort, C-Flex makes it easier to exhale. The pressure drop is variable based on patient need and tracked by the machine on a breath-by-breath basis. C-Flex can be set between 1 and 3, with 1 being the least pressure relief and 3 being the most. AUTO-CPAP AND SMART CPAP Both automatically adjust pressure to meet patient needs, and they always use the lowest pressure necessary. The clinician programs the minimum and maximum CPAP levels into the machine. They are used mainly for OSA patients when further study of best pressure is needed or for those with challenging breathing patterns during sleep. A “smart card” type of computer disk can be inserted in equipped machines to record sleep events and pressures. BIPAP Biphasic (or bilevel) positive airway pressure (BiPAP) is similar to a combination of CPAP and pressure support. PIPAP is also called NPPV or noninvasive positive pressure ventilation. BiPAP is useful in providing ventilatory support for patients with respiratory insufficiency. Most machines come equipped with alarms and may have option of adding a mechanical backup rate. Newer machines provide display screens with multiple options, and can also be used with trach patients. IPAP lnspiratory positive airway pressure (IPAP) is similar to pressure support. Increases 213

ventilation by increasing VT, decreases work of breathing, and improves oxygenation. Set IPAP above EPAP level, usually between 5 and 20 cm H2O. EPAP Expiratory positive airway pressure (EPAP) is similar to PEEP/CPAR. EPAP is spontaneous breathing at a pressure greater than zero. Is usually set at 3 to 12 cm H2O or higher, if needed. Increases FRC, increases compliance, decreases atelectasis, and increases oxygenation. Is also used for OSA to overcome upper airway obstruction by splinting the airway open.

LVENTILATOR ALARMSL Alarms available on most ventilators include high and low pressures, high and low rates, and high and low minute volumes. These alarms should be set near the patient’s current actual parameters; alarms will then activate with any significant changes. In addition, alarm volume is adjusted so that it is clearly audible. Apnea alarm should be set with minimal delay time for onset of alarm. If backup ventilation is available, all ventilating parameters are set for both modes appropriate for the patient.

LCOMPLICATIONS OF VENTILATIONL The most common complications associated with mechanical ventilation are due to the positive airway pressure. Higher pressures have the potential to cause more complications. Intermittent positive pressure ventilation (IPPV) and PEEP/CPAP complications include barotrauma, pneumothorax, pneumomediastinum, subcutaneous emphysema, 214

increased PVR, increased PAP reduced venous return, decreased cardiac output, decreased blood pressure, edema as a result of increased antidiuretic hormone (ADH), and decreased urine output. Mechanical ventilation with inappropriate settings can also result in hyperventilation or hypoventilation. In addition, the potential hazard of ventilator/CPAP machine malfunction exists.* (See hazards of artificial airways, intubation, and suctioning in Modalities.)

LTROUBLESHOOTINGL PROBLEM: ABNORMAL ABGS Solutions: Most common parameter changes to correct abnormal ABGs are the following: Adjusting PaO2

Adjusting PaCO2

To increase PaO2: &FiO2, &PEEP, &Rate,&VT

To decrease PaCO2: &Rate, &VT

To decrease PaO2: FiO2, PEEP, Rate

To increase PaCO2: Rate, VT

MECHANICAL VENTILATION PARAMETER CHANGE FORMULAS Parameter

Formula

Adjusting PaO2 FiO2 needed  level by adjusting (desired PaO2  current FiO2)  FiO2 current PaO2

Notes If 60% FiO2 is needed, consider increasing PEEP

Adjusting PaCO2 Desired VE  current level by adjusting VE  (current PaCO2 minute volume  desired PaCO2) *More information about ventilating patients with ARDS can be found online at the ARDSnet Protocol web site: http//www.ardsnet.org/lowvtrefcard.pdf.

215

PROBLEM: INCREASED INTRACRANIAL PRESSURE (ICP) Solution: Use Hyperventilation is used to decrease ICP. Hyperventilation can be used to decreae ICP if the ICP rises above 10. Patients with head trauma, intracranial swelling, or other conditions that raise ICP can benefit from deliberate hyperventilation to a mild state of respiratory alkalosis. Normally, this is done by increaseing the rate above normal and maintaining normal tidal volume. Hyperventilation causes cerebral vasoconstriction, resulting in decreased cerebral blood flow and decreased lCP. This is a temporary measure, because the kidneys will compensate after several days. PROBLEM: INCREASED SPONTANEOUS RESPIRATORY RATE Solution: The cause, most commonly hypoxemia, acidosis, pain, or anxiety, is treated. PROBLEM: INADVERTENT OR AUTO-PEEP Can be calculated by performing brief expiratory pause and viewing the increase in pressure on the manometer. Solution: Ways to decrease auto-PEEP include decreasing air-flow obstruction by providing adequate bronchodilator therapy and suctioning the airway. In addition, VT and TI are decreased, TE and flowrate are increased, and the square wave flow pattern is used. PROBLEM: HIGH PEAK PRESSURES Solutions: If the problem is due to increased RAW: Secretions are suctioned, bronchodilator is given, flowrate is decreased, condensate is drained, no tubing kinks are determined, and no malposition of the ET tube is confirmed. If the patient is biting the tube, a bite block 216

is added if necessary. In addition, waveform is changed and any inspiratory pause or hold is removed. Decreasing VT and increasing the rate to maintain VE can be considered. If the problem is due to decreased lung compliance: The cause is treated—for pneumothorax, chest tube; for pneumonia, antibiotics, CPT, etc.; and for ARDS, increasing PEEP and TI, and changing mode to PC. PROBLEM: LOW PRESSURES OR LOW EXHALED VOLUMES Solution: The leak, most likely in the circuit, attachments, or cuff, is found and corrected. PROBLEM: INSPIRATORY TIME TOO LONG AND I:E RATIO TOO HIGH Solutions: Decreasing inspiratory time, increasing flowrate, decreasing VT, and removing any inspiratory hold or plateau. PROBLEM: PATIENT FIGHTING VENTILATOR Solutions: All parameters are set appropriately for the patient and readjusted as necessary. Patient may need higher flowrate or adjusted sensitivity. If PIP increases, high pressure problem is considered. Vital signs are checked. Whether patient needs sedation or is ready for weaning is determined. PROBLEM: VENTILATOR MALFUNCTION OR FAILURE TO CYCLE Solution: Appropriate sensitivity setting is checked. If that is not the problem, the patient is removed from the ventilator. One therapist provides manual ventilation and oxygen with resuscitation bag, and another therapist checks ventilator functions and also checks for inadvertent changes made to the ventilator settings. The problem is corrected or the ventilator is replaced. 217

LNOTESL

NEONATAL AND PEDIATRIC RESPIRATORY CARE See references 6, 24, and 25 CARDIOPULMONARY EVENTS AT BIRTH . . . . . . . 221 Fetal Growth and Development of the Pulmonary System . . . . . . . . . . . . . . . . . 221 Neonatal/Newborn Data . . . . . . . . . . . . . . . . . . . . 222 High-Risk Neonatal Deliveries . . . . . . . . . . . . . . . 223 ASSESSMENT OF THE NEONATAL PATIENT. . . . . 224 Apgar Scores . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224 Apgar Score at 1 Minute . . . . . . . . . . . . . . . . . . . . 224 Infant and Pediatric Vital Signs . . . . . . . . . . . . . . 225 Normal Values for Respiratory Rate, Heart Rate, and Blood Pressure . . . . . . . . . . . . 225 Therapeutics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225 Neonatal and Pediatric Artificial Airways and Suction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226 Neonatal and Pediatric Oxygen and Ventilation. . . . . . . . . . . . . . . . . . . . . . . . . . . 226 Oxygen Delivery Devices . . . . . . . . . . . . . . . . . . . 227 Other Oxygen Delivery Devices and Therapeutic Modalities

219

Neonatal and Pediatric Respiratory Care

(see Therapeutic Modalities)

General Guidelines for Initial Setup of Pressure Ventilation for the Infant or Young Child . . . . . . . . . . . . . . . . . . . . . . . . . . . 229 General Guidelines for Initial Setup of HFO Ventilator for the Neonate . . . . . . . . . . 230 NEONATAL CARDIAC AND PULMONARY DISORDERS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230 Legend . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230 Abdominal Wall Abnormalities. . . . . . . . . . . . . . . 230 Airway Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 Apnea of Prematurity. . . . . . . . . . . . . . . . . . . . . . . 231 Asthma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 Bronchiectasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 Bronchiolitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 Bronchopulmonary Dysplasia (BPD) . . . . . . . . . . 232 Choanal Atresia. . . . . . . . . . . . . . . . . . . . . . . . . . . . 232 Congenital Diaphragmatic Hernia . . . . . . . . . . . . 233 Congenital Heart Disease . . . . . . . . . . . . . . . . . . . 233 Croup, Laryngotracheobronchitis . . . . . . . . . . . . 234 Cystic Fibrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234 Epiglottitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234

Gastroesophageal Reflux Disease (GERD) . . . . . . 235 Heart Defects (Congenital) . . . . . . . . . . . . . . . . . . 235 Infant Respiratory Distress Syndrome (IRDS/RDS), Hyaline Membrane Disease (HMD) . . . . . . . . . . . . . . . . . . . . . . . . . . . 236 Lung Malformations . . . . . . . . . . . . . . . . . . . . . . . 236 Meconium Aspiration Syndrome (MAS) . . . . . . 236 Persistent Pulmonary Hypertension of the Newborn (PPHN) . . . . . . . . . . . . . . . . . . . 237 Respiratory Syncytial Virus (RSV) . . . . . . . . . . . . 238 Sudden Infant Death Syndrome (SIDS) . . . . . . . 238 Tracheoesophageal Fistula (T-E Fistula) . . . . . . . 239 Transient Tachypnea of the Neonate (Type II RDS or TTN) . . . . . . . . . . . . . . . . . . . . . . 239

SEE ALSO PULMONARY ASSESSMENT PULMONARY DISEASES MEDICATIONS THERAPEUTIC MODALITIES

Neonatal and Pediatric Respiratory Care

VENTILATORS, CPAP, AND BIPAP

220

NEONATAL AND PEDIATRIC RESPIRATORY CARE CARDIOPULMONARY EVENTS AT BIRTH Initiation at Birth Lung Expansion Closure of Ductus Arterious

Increased PO2

Umbilical Flow Closes

Decreased PO2

Decreased Pulmonary Vascular Resistance

Increased Pulmonary Blood Flow

Decreased Pulmonary Artery Pressure

Lung Fluid Reabsorbed

Foramen Ovale Closes

Decreased Right Heart Pressure

Physiologic differences include rounder jaw, larger tongue, and trachea cartilage soft (2-6 cm long). The epiglottis is longer and less flexible; it lies higher and is more horizontal. Metabolic and ventilator requirements include basal metabolic rate is 1 kcal/kg/hr (twice that of adults), which means oxygen consumption and CO2 production are also two times higher.

FETAL GROWTH AND DEVELOPMENT OF THE PULMONARY SYSTEM Fetal Period Embryonic Pseudoglandular

Weeks’ Gestation 0-5 1-6

Canalicular

17-24

Terminal sac

24-40

221

• Changes at 24 weeks’ gestation: Respiratory bronchioles, alveolar ducts, alveoli, and type II cells develop. • Changes at 30-32 weeks’ gestation: Alveoli, alveolar ducts, respiratory bronchioles, and capillaries continue to develop. Surface area grows considerably. Before 32 weeks, more sphingomyelin than lecithin is present, making the lecithin/sphingomyelin (L/S) ratio 1. At approximately 32 weeks, lecithin production rapidly increases, sphingomyelin production decreases, and the L/S ratio increases to 1. • Changes at approximately 35 weeks’ gestation: L/S ratio reaches 2. Phosphocholine transferase system (a key pathway for lecithin production) develops. If the L/S ratio is 2, this means lungs are not yet well developed and hyaline membrane disease is a possibility (incidence is much higher than with L/S ratio 2). • Changes at 40 weeks’ gestation (full term): L/S ratio  4-6. Fetal Blood Gases: Normal Values Umbilical vein:

pO2: ~30 torr and ~80% saturation pCO2: ~40 torr Bicarb: ~18 mEq/L

• Deoxygenated blood exits the fetus and returns to the placenta through two umbilical arteries. • During this period, oxygen diffuses into the fetal blood. • Oxygenated blood returns to the fetus through the umbilical vein. NEONATAL/NEWBORN DATA • Approximately 33% of fetal lung fluid exits the lungs before labor begins. During labor, vaginal squeezing helps expel about 20%. 222

•

•

•

•

The remainder of fetal lung fluid is expelled within 24 hours after birth. At birth, the fetal lungs still contain considerable fluid. The infant must overcome surface tension, forces of tissue resistance, and viscosity of fluid in airways. This requires about 40 to 80 cm H2O on first inspiration. Airways must be cleared, which may require bulb suctioning of the mouth and nares or deep suctioning. Towel is used to dry and stimulate infant (more vigorous stimulation may be appropriate, depending on the Apgar score). Thermoregulation is important. The infant must be kept warm with blankets, cap, radiant warmer, or incubator. Newborn Arterial Blood Gases: Normal Values Just after Birth pH & from ~7.20 to 7.30 during first 3-4 hours, then to 7.40 over next 2 days. pO2 & from 30 to 60 torr and about 90% saturation. pCO2  from ~55 to 35 torr over the first 3 hours. Bicarb  from ~23 to 20 mEq/L, remains for several days and slowly rises to normal.

HIGH-RISK NEONATAL DELIVERIES Many factors can contribute to high-risk neonatal deliveries, including the following: • Mother with preeclampsia, eclampsia, hypertension or hypotension, diabetes, age 16 or 35, prior or current C-section, premature rupture of membranes, and drug or alcohol abuse • Premature or postterm delivery • Abnormal fetal position • Trauma • Anesthesia, and other drugs administered during labor and delivery 223

ASSESSMENT OF THE NEONATAL PATIENT APGAR SCORES 0

1

2

Heart rate

Absent

100/min

100/min

Respiratory effort

Absent

Slow, irregular

Active effort, crying

Slight flexion of extremities

Active

Muscle tone Limp Reflex irritability

No response Grimace

Coughing or sneezing

Color

Blue or pale Blue extremities Pink and pink body throughout

Note: Apgar score range is 0-10.

APGAR SCORE AT 1 MINUTE • 7-10  normal score Monitor patient; maintain thermal environment. • 4-6  moderately depressed neonate Provide tactile stimulation by slapping the feet or drying with a towel. Provide oxygen via bag and mask using 5 L/min. Provide manual ventilation as needed. Watch for improvement; if no improvement, treat as score of 0-3. • 0-3  severely depressed neonate requiring emergency care Suction airway, insert ET tube, and ventilate and perform chest compressions at 100120/min. In addition, administer medications, including epinephrine, sodium bicarbinate, and others (see Neonatal Resuscitation and Medications). 224

INFANT AND PEDIATRIC VITAL SIGNS

NORMAL VALUES FOR RESPIRATORY RATE, HEART RATE, AND BLOOD PRESSURE Age (yr) Newborn 1 2 3 4 7 14

Respiratory Rate Heart Rate 30-40 25-35 25-35 20-35 20-35 15-25 15-20

125 120 110 105 100 90 80

Blood Pressure 72/48 90/60 90/60 95/60 100/60 110/60 120/70

Note: Low–birth-weight preterm neonates have a lower blood pressure (e.g., at ~2000 g, blood pressure is about 50/30 mm Hg).

Breathing Patterns in Neonates • Normal respiratory rate is 30 to 60 minutes for the full-term infant. • Normal spontaneous tidal volume averages 6 to 8 mL/kg. • Normal heart rate is 120 to 130 beats per minute. • Periodic breathing is common in premature infants with apneic episodes of 5 to 10 seconds. • Apneic periods 20 seconds can lead to respiratory acidosis, decreased oxygen saturation, and bradycardia. Monitor apneic periods and treat as necessary, including supplemental oxygen and CPAP. THERAPEUTICS See Therapeutic Modalities section for complete information on the following: • Artificial airways and suctioning • Intubation and extubation • Medication delivery devices • Therapies 225

NEONATAL AND PEDIATRIC ARTIFICIAL AIRWAYS AND SUCTION

Age Newborn 1000 g 1000-2000 g 2000-3000 g 3000 g 6 mo 1 yr 2-3 yr 4-7 yr 8-10 yr 12 yr 15 yr

ET Tube Internal Diameter (mm)

Laryngoscope Blade Size

Suction Catheter (French size)

2.5 3.0 3.5 3.5-4.0 3.5-4.0 4.0 4.5-5.0 5.0-6.0 6.0-6.5 7.0 7.0-7.5

0 0 1 1 1-2 1-2 2 2 2-3 2-3 3

5 6 6-8 6-8 6-8 8 8 8-10 10 10 10-12

CUFF PRESSURES Many neonatal size tubes are cuffless. If a cuff is present, the tube cuff pressure should always remain below 20 mm Hg (26 cm H2O) to prevent edema and necrosis. VACUUM PRESSURE—ACCEPTABLE RANGES Children: 80 to 100 mm Hg Infants: 40 to 80 mm Hg NEONATAL AND PEDIATRIC OXYGEN AND VENTILATION Excessive oxygen utilization and high PaO2 (80) should be avoided whenever possible in infants, especially if premature. Problems include retinopathy of prematurity (ROP), retrolental fibroplasia (RLF), and bronchopulmonary dysplasia (BPD). In addition, thermoregulation for newborns is very important. 226

OXYGEN DELIVERY DEVICES Device

Oxygen Flow Rate (L/min)

FiO2 (approx %)

Notes

Nasal cannula (neonatal)

¼-2

22-45 (or higher as needed)

Nasal cannula (pediatric)

1-6

24-44

Oxygen hood

7-12

21-100

Source gas for neonatal nasal cannula is usually not at 100%; instead, FiO2 is reduced by air entrainment via blender to achieve desired FiO2. Approximate values with 100% oxygen source gas: 1 L/min  24% 2 L/min  28% 3 L/min  32% 4 L/min  36% 5 L/min  40% 6 L/min  44% Keep flow 7 L/min to flush out CO2. Maintain thermal environment at 32°-34° C. Provides easy access to the patient and precise FiO2. Is useful for the pediatric patient who needs supplemental oxygen but is unwilling to use the mask or nasal cannula. Disadvantages: FiO2 is not precise. Fire hazards exist; alcohol or oils should not be used on patients, and toys that may spark inside the tent are not allowed.

Oxygen tents (croup 10-12 tent, mist tent, aerosol tent)

21-40

227

OTHER OXYGEN DELIVERY DEVICES AND THERAPEUTIC MODALITIES See Therapeutic Modalities Section CPAP FOR INFANTS • Indications: For infants with PaO2 50 on FiO2 50%, with acceptable PaCO2. Is useful for newborns with increased WOB, tachypnea, grunting, nasal flaring, apnea of prematurity, and other disorders as listed in this section. • Initial CPAP: 4-5 cm H2O; increase in 1 to 2 increments to  10 as needed. Patient is monitored for increased oxygenation, increased SpO2, and decreased WOB, with problems resolved before weaning. Wean oxygen to 40%, then wean CPAP off and place on another oxygen delivery device with slightly higher FiO2. • If CPAP fails: Mechanical ventilation may be indicated. Failure is indicated by an inability to improve PaO2, an inability to reduce WOB, and & PaCO2. • See Ventilation section for more information on CPAP, hazards, and complications. MECHANICAL VENTILATION See Therapeutics section for more information on intubation, extubation, suctioning, and artificial airways. See Ventilation section for more information on many modes of ventilation, along with indications, setup, parameters, monitoring, hazards, complications, and weaning. PRESSURE VENTILATION For infants and young children, positive pressure ventilation is normally used rather than volume ventilation. For initial ventilator setup, parameters vary greatly based on patient needs. The clinician must assess the patient and monitor saturation, ABGs, and patient response to ventilation. 228

GENERAL GUIDELINES FOR INITIAL SETUP OF PRESSURE VENTILATION FOR THE INFANT OR YOUNG CHILD Infant

Young Child

Rate (breaths/min)

20-40

12-25

PIP (cm H2O)

15-20

20-25

PEEP (cm H2O)

2-6

2-10

FiO2 (%)

40-60 or higher as needed*

40-60 or higher as needed

VT (mL/kg)

5-7

5-8

TI (sec)

0.4-0.6 or up to 1.0 if indicated

0.5-1.0

TE (sec)

0.5-1.5

0.5-1.5

I:E ratio

1:1-1:1.5

1:2

*Newborn: Titrate oxygen to keep SpO2 at 88%-93% to help prevent RLF and ROP. 1 mo (if not at risk for BPD): use standard protocol, generally titrating oxygen to maintain SpO2 92%.

HFV AND HFO—HIGH-FREQUENCY VENTILATION AND OSCILLATION HFV is a mode of ventilation that uses rates 60. Terms used are HFV, HFJV, HFPPV, and HFO; all are referred to as HFV, as in HF ventilation, HF jet ventilation, HF positive pressure ventilation, and HF oscillation or HF oscillatory ventilation. Hertz (Hz) means cycles per second. 1 Hz  rate of 60. The rate is found by multiplying the Hertz by 60 (e.g., 4 Hz  4  60  a rate of 240). HFO or HFOV is a term that technically means the rate is 300 (5 Hz). In HFV-HFO, rates are very high (61-2000). Tidal volumes are very low (~2-5 mL/kg). Tidal volumes can be slightly above, equal to, or even lower than dead space ventilation. HFV is designed to provide adequate ventilation 229

while minimizing alveolar collapse via high expiratory lung volumes. HFV has proved effective over decades of use in neonates. It can improve oxygenation while minimizing barotrauma when other modes of ventilation fail. The patient is sedated for HFV and HFO.

GENERAL GUIDELINES FOR INITIAL SETUP OF HFO VENTILATOR FOR THE NEONATE Hz (rate)

10 Hz (remember to decrease rate to decrease CO2)

MAP (cm H2O) 2-4 greater than MAP on conventional ventilator P

Adjust for adequate chest wiggle

FiO2 (%)

5%-10% greater than previous FiO2

TI (%)

33%

Settings can vary greatly based on patient needs and type of HFO ventilator used. Facility’s protocols should always be followed.

NEONATAL CARDIAC AND PULMONARY DISORDERS LEGEND D Definition E Etiology S Signs, symptoms, diagnostic tests Tx Treatment ABDOMINAL WALL ABNORMALITIES D Congenital abnormalities. E Omphalocele and gastroschisis. S Severe difficulty in breathing. Tx Mechanical ventilation. 230

AIRWAY DISEASES D Congenital abnormalities. E External and internal obstructions (five types of tracheoesophageal fistulas). S Difficulty breathing. Tx Supportive care, HFV, and/or surgery. APNEA OF PREMATURITY D Is a common disorder, easily controlled, and usually resolves over time. E Is caused by prematurity. S Apneic episodes of 5-10 seconds are followed by 10-15 seconds of rapid breathing. Apneic spells are abnormal if 20 seconds or if associated with cyanosis, pallor, hypotonia, or bradycardia. Tx Continuous SpO2 monitoring, mechanical stimulation, managing the cause, CPAP, theophylline or caffeine, doxapram, transfusion, and/or mechanical ventilation. ASTHMA See Pulmonary Diseases. BRONCHIECTASIS See Pulmonary Diseases. BRONCHIOLITIS D Acute infection of the lower respiratory tract. E Is usually caused by RSV and is often follows an upper airway viral infection. S Inspiratory wheezing and increased airway resistance progresses to possible apnea. Chest x-ray shows hyperinflation and areas of consolidation. Clinical testing uses immunofluorescent assay. Tx Mild cases may be resolved by using humidification and oral decongestants at 231

home. More serious cases require bronchodilators, croup tent, NC, and antibiotics to control secondary bacterial infections. Severe cases may require ribavirin. BRONCHOPULMONARY DYSPLASIA (BPD) D During the first few weeks, immaturity, malnutrition, oxygen toxicity, and mechanical ventilation have been implicated as causes. The process is related to trauma to the lungs (lung collapse), volutrauma requiring increased FiO2, leading to inflammation, diffuse alveolar damage, pulmonary dysfunction, and death. E Is caused by pulmonary damage or dysfunction (e.g., progressive vascular leakage, atelectasis, emphysema). S May start with little or no oxygen or ventilation support and progress into distress within 2 to 3 weeks. Others may begin with pneumonia or sepsis and need very high levels of support. ABGs reveal hypoxemia and hypercapnia secondary to airway obstructions or air trapping, pulmonary fibrosis, or atelectasis. Resistance is increased and compliance is decreased. Tx The best management is to prevent its onset. Therapy is short term and includes supportive, oxygen, CPT, bronchodilators, and steroids (dexamethasone). Supplemental oxygen and/or mechanical ventilation may be required for months or even years. CHOANAL ATRESIA D Congenital condition involves narrowing or blockage of the nasal airway by membranous or bony tissue. The cause is unknown but is thought to be persistence 232

E S

Tx

of the membrane between the nasal (one or both sides) and oral spaces during fetal development. Because infants are obligate nose breathers, an acute breathing problem is created. Is a congenital abnormality. Physical examination may show obstruction of the nose. Suction catheter may not pass through one or both nares. The neonate is unable to feed and breathe simultaneously. Contrast-enhanced x-ray film or CT scan may show occlusions. With bilateral choanal atresia, the newborn may need resuscitation at delivery. Airway may be required to support breathing if the infant cannot tolerate mouth breathing. Rarely, intubation or tracheotomy may be required. If necessary, surgery is performed to correct disorder.

CONGENITAL DIAPHRAGMATIC HERNIA D Congenital abnormality affects the lungs and organ placement. E Lung hypoplasia decreases alveolar count; decreased pulmonary vasculature, pulmonary hypotension, and unusual anatomy of the inferior vena cava; Bochdalek’s hernia (left lateral and posterior), and Morgagni’s hernia (medial and anterior). S Severe respiratory distress, scaphoid abdomen, decreased breath sounds, displaced organs, and severe cyanosis. Tx ET tube, paralysis, HFV, ECMO, and surgery. CONGENITAL HEART DISEASE D Congenital abnormalities. E Presentation is categorized as either cyanotic or acyanotic. 233

S

Tx

Cyanotic heart disease exhibits rightto-left shunt; acyanotic heart disease exhibits a left-to-right shunt. Supportive.

CROUP, LARYNGOTRACHEOBRONCHITIS (LTB) D Upper airway viral disorder results in subglottic swelling and obstruction. E Is caused by parainfluenza virus or RSV or influenza virus. Is the most common cause of airway pathologic obstruction in children. Bacterial superinfection with Staphylococcus aureus, group A Streptococcus pyogenes, or Haemophilus influenzae may worsen croup. S Symptomatic after 2 to 3 days of nasal congestion, fever, cough, inspiratory stridor, and barking cough. Dyspnea, cyanosis, exhaustion, and agitation occur. X-ray studies rule out epiglottitis and confirm subglottic narrowing of trachea (Steep sign). Tx Depending on severity (e.g., breath sounds, cough, suprasternal retractions, cyanosis), home-to-hospital care is indicated. Care starts with cool mist, racemic epinephrine, dexamethasone, or budesonide-tomechanical ventilation as indicated. CYSTIC FIBROSIS See Pulmonary Diseases. EPIGLOTTITIS D Acute, often life-threatening infections of the upper airway cause obstruction secondary to supraglottic swelling. E Is caused by H. influenza, type B, infection. S High fever, sore throat, stridor, and labored breathing. Includes muffled voice and difficulty swallowing, or drooling. 234

Tx

X-ray studies show significantly thickened epiglottis, flattened (thumb sign), and swollen aryepiglottic folds. Sedation, intubation or tracheostomy, bacterial culture, and antibiotic therapy as indicated. Extubation should not be attempted until swelling has decreased enough to yield an airway leak around the ET tube when the balloon is deflated.

GASROESOPHAGEAL REFLUX DISEASE (GERD) D Regurgitation of stomach contents. E Caused by physiologic effects. Results in respiratory reactive airway disease, aspiration pneumonia, laryngospasm, stridor, chronic cough, choking spells, and apnea. S A sudden life-threatening event, chronic head and neck problems. Tx Management through medications or surgical intervention. HEART DEFECTS (CONGENITAL) D Congenital abnormalities of two types: acyanotic and cyanotic. Acyanotic disease exhibits a left-to-right shunt. Cyanotic disease exhibits a right-to-left shunt. Acyanotic heart lesions include patent ductus arteriosus, ventricular septal defect (VSD), atrial septal defect (ASD), and coarctation of the aorta. Cyanotic heart lesions include tetralogy of Fallot and transposition of great vessels. E Are congenital defects. S Is defect specific—signs, symptoms, test, and x-ray findings. Tx Is defect specific with supportive therapy. Can require full range of therapies and medications, oxygen, ventilation, and possibly surgery. 235

INFANT RESPIRATORY DISTRESS SYNDROME (IRDS/RDS), HYALINE MEMBRANE DISEASE (HMD) D RDS or hyaline membrane diseases are diseases of prematurity, qualitative surfactant deficiency, decreased alveolar surface area, increased smaIl airway compliance, and presence of ductus arterious. E Is a lung parenchymal disorder or disease. S Tachypnea, retractions, nasal flaring, apnea, paradoxical breathing, audible grunting, possible cyanosis, systemic hypotension, hypothermia, and poor perfusion are symptoms. Auscultation reveals inspiratory crackles. Diagnosis is based on chest x-ray studies, which show diffuse, hazy, reticulogranular densities, and low lung volumes. Tx CPAP (titration by 1 to 2 cm H2O), HFV with PEEP, and PIP 30 cm H2O, and surfactant treatment  3. LUNG MALFORMATIONS D Are congenital abnormalities. E Lobar cysts, pulmonary sequestration, cystic adenomatoid lung malformation, and lobar emphysema are causes. S Difficulty breathing is primary symptom. Tx Supportive care and surgery. MECONIUM ASPIRATION SYNDROME (MAS) D Amniotic fluid consists of fetal lung fluid, transudate, fetal urine, and meconium. E Is caused by meconium in the amniotic fluid and aspirating meconium. S Fetal tachycardia and absent fetal cardiac accelerations during labor. At birth, low umbilical artery pH, APGAR 5 and meconium aspirated from trachea. Observation for MAS is warranted. 236

Tx

Gasping respirations, tachypnea, grunting, and retractions. Chest x-ray shows irregular pulmonary densities, atelectasis, and hyperlucent areas (air trapping). ABG decreased PO2 with mixed acidosis. Possible right-to-left shunting in persistent pulmonary hypertension. Oropharynx is suctioned at delivery, blow-by humidified oxygen is delivered, and an ET tube is inserted for suctioning. The ET tube is removed and inspected for meconium. If the tube is stained with meconium (two to four times), the procedure is repeated. If patient’s condition worsens, CPAP or, if indicated, intubation and mechanical ventilation are started.

PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN) D Complex syndrome with many causes that increase PVR, resulting in right-toleft shunting, severe hypoxemia, and mixed acidosis. E Vascular spasms, increased muscle wall thickness, and decreased cross-sectional area of the pulmonary vessels. S Rapid changes in SpO2 occur without changes in FiO2, or hypoxemia develops unproportional to lung disease detected with chest x-ray or PaCO2 measurements. Infants with significant shunt through the ductus arterious 5% can be found by comparing two SpO2 monitors, one on the right arm and the other on either leg. Tx Oxygen (hypoxemia) and surfactant (RDS), glucose (hypoglycemia), and inotropic agents (cardiac output or systemic hypotension). If not corrected, HFV via 237

mechanical ventilator with sedation or paralysis to reduce pain and anxiety, which contributes to PPHN. Persistent cases may require the use of nitric oxide and screening for using ECMO. RESPIRATORY SYNCYTIAL VIRUS (RSV) D Causes an illness that is usually similar to a moderate-to-severe cold and is very contagious. RSV most often resolves on its own (10 to 14 days) and does not cause major health concerns but can become a problem when it is severe or leads to complications. Premature babies and patients with immune system problems or heart and lung problems may be at risk. E Is highly contagious, spreading via secretions (saliva or mucus) when the patient coughs, sneezes, or talks. Two main types of RSV exist, and patients cannot develop full immunity to the virus. The infection affects the nose, throat, and upper respiratory system, often exhibiting symptoms similar to pneumonia, croup, laryngotracheobronchitis, or bronchiolitis. Symptoms include mild sore throat, cough, stuffy or runny nose, earache, and fever; possibly difficulty breathing. Tx Although no treatment for RSV is available, secondary bacterial infections may be treated with antibiotics, and fluids will prevent dehydration. SUDDEN INFANT DEATH SYNDROME (SIDS) D Is the leading cause of death of patients 1 year old (40%). E Unexpected death while sleeping is believed to be from hypoxia or ischemia. S Is identified through history. 238

Tx

Apnea monitoring and family training for emergencies.

TRACHEOESOPHAGEAL FISTULA (T-E FISTULA) D Fistula extending from near the carina to the lower esophagus. Five types include: (1) atresia (esophageal separation); (2) fistula only (trachea and esophagus connected to both stomach and lungs); (3) atresia plus upper fistula (trachea and esophagus connected above carina); (4) atresia plus lower fistula (trachea and esophagus connected below carina); and (5) atresia plus double fistula (trachea and esophagus connected above and below carina). E None definite. Risk factors include first pregnancy, advanced maternal age, hormone use during pregnancy, twin birth, chromosomal abnormalities, and hereditary factors. S Excessive secretions, coughing, and cyanosis. Depending on fistula type, air can be forced into stomach and/or aspiration pneumonia reflux. Chest x-ray, CT, and/or MRI are used to identify and diagnose condition. Tx Oxygen, ventilatory support, and surgery. TRANSIENT TACHYPNEA OF THE NEONATE (TYPE II RDS OR TTN) D Cause is unclear but most likely fetal lung liquid, which increases airway resistance and decreases lung compliance, resulting in hyperinflation and/or air trapping. E Lung parenchymal disorder or disease. S In the first few hours, respiratory rate increases, pH and CO2 are normal. Chest 239

Tx

240

x-ray studies suggest pneumonia; perihilar streaking is a result of lymphatic engorgement, possible pleural effusions in the costophrenic angles, and interlobular fissures. Low FiO2 oxyhood, or NC; CPAP if increased FiO2 is required; patient’s position is frequently changed (to increase fluid clearance); IV antibiotics (for 3 days), and mechanical ventilation (rare). Clearing of fluids should occur within 24 to 48 hours.

BLS AND ACLS See references 7 and 15 SYNCHRONIZED CARDIOVERSION . . . . . . . . . . . . 242 Synchronize with the R Wave . . . . . . . . . . . . . . . . . 242 Pad Placement . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242 BASIC LIFE SUPPORT (BLS). . . . . . . . . . . . . . . . . . . 243 Important Differences in Newborn CPR . . . . . . . 243 BLS Airway, Breathing Maneuvers for Adults, Children, and Infants . . . . . . . . . . . . . . . . . . . . . . 244 ADVANCED CARDIAC LIFE SUPPORT (ACLS) . . . . . . . . . . . . . . . . . . . . . . . . . . 246 Pulseless Arrest Algorithm . . . . . . . . . . . . . . . . . . 246 TREATABLE CAUSES IN PULSELESS ARREST . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250 POST-CARDIAC ARREST CARE . . . . . . . . . . . . . . . . 251 ACUTE CORONARY SYNDROMES . . . . . . . . . . . . . 252 BRADYCARDIA (ADULT WITH A PULSE) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253 UNSTABLE ADULT TACHYCARDIA WITH A PULSE . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254 WIDE-COMPLEX STABLE ADULT TACHYCARDIA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255 NARROW-COMPLEX STABLE ADULT TACHYCARDIA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 256 SHOCK. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 PEDIATRIC ADVANCED LIFE SUPPORT (PALS) . . . . . . . . . . . . . . . . . . . . . . . . . . 258 PALS Pulseless Arrest Algorithm . . . . . . . . . . . . . 258 NEONATAL RESUSCITATION GUIDELINES . . . . . . 262 Anticipation of Need for Resuscitation . . . . . . . 262 NEONATAL FLOW ALGORITHM . . . . . . . . . . . . . . . 263

BLS and ACLS

SEE ALSO MEDICATIONS EKGs

241

BLS AND ACLS LSYNCHRONIZED CARDIOVERSIONL SYNCHRONIZE WITH THE R WAVE TO REDUCE RISK OF PRODUCING VF. Use synchronize mode for: 1. Supraventricular tachycardia due to reentry 2. Atrial fibrillation 3. Atrial flutter 4. Atrial tachycardia 5. Monomorphic ventricular tachycardia with a pulse PAD PLACEMENT Alternate pad placement 2. Anterior – Posterior 3. Anterior – Left infrascapular 4. Anterior – Right infrascapular

BLS and ACLS

1. Default pad placement

See Unstable Adult Tachycardia with a pulse algorithm on page 254. 242

LBASIC LIFE SUPPORT (BLS)L 1. Tap the victim’s shoulder and shout, “Are you OK?” 2. If victim cannot speak or breathe, activate EMS. Call 911. If alone, yell for help! 3. Check for pulse for up to 10 seconds. 4. Begin CPR starting with chest compressions. • If victim is a child or infant and unresponsive and you did not witness event and are alone, perform resuscitation for 1 minute; then call 911. • If pulse is present, ventilate at a rate of one breath every 5-6 seconds for adult; one breath every 3-5 seconds for infant/child. • See the chart on p. 244 for BLS maneuvers. IMPORTANT DIFFERENCES IN NEWBORN CPR • Rescue breathing rate for newborn with a pulse is 40 to 60 breaths per minute. • The compression depth is one third of the chest. • To resuscitate, 90 compressions and 30 ventilations are delivered per minute (approximately 120 events, 3 compressions to one ventilation). • Avoid simultaneous compressions and ventilations.

243

244

BLS AIRWAY, BREATHING MANEUVERS FOR ADULTS, CHILDREN, AND INFANTS MANEUVER

ADULT Lay rescuer: ⬎7 yr old HCP: Adolescent and older

C

Carotid

Circulation—HCP: Check pulse. (ⱕ10 second) Compression landmarks

CHILD Lay rescuer: 1-8 yr old HCP: 1 yr to adolescent

INFANT ⬍1 yr old Brachial or femoral

Compression rate Compression-ventilation ratio

Just below nipple line (lower half of sternum) Heel of only one hand, Two or three fingers. Heel of one hand over sternum, the other hand or same as for adults. HCP (2 rescuers): two on top. thumb-encircling hands At least 2.0 inches Approximately 1/ 3 depth of chest (approximately 2 inches for a child and 1.5 inches for an infant.) Perform at least 100 compressions per minute. 30:2 (1 or 2 rescuers) 30:2 (1 rescuer); 15:2 (2 rescuers)

A

Airway

Head tilt–chin lift. If trauma or spinal injury is suspected, use jaw thrust.

B

Breathing—initial: Look for absent breathing or gasping.

Deliver each breath over 1 Deliver each breath over 1 second until visible second until visible chest rise. chest rise.

Compression method: Push hard and fast and allow complete recoil. Compression depth

Lower half of sternum, between nipples

D

Breathing—HCP: Rescue breathing without chest compressions for those with a pulse. Breathing—HCP: Rescue breaths for CPR with advanced airway. Breathing—FBO: Repeat thrusts until successful. If person is unconscious, perform CPR.

Approximately 10-12 breaths Approximately 12-20 breaths per minute. per minute.

Defibrillation (AED): Automated external defibrillator

Use adult pads (Do not use infant pads on adults.)

* Pads should not touch each other.

Approximately 8-10 breaths per minute. (1 breath every 6-8 second.) If unconscious, perform CPR. Perform finger sweep if FBO is visible. Perform abdominal thrusts. If the person is obese or pregnant, perform chest thrusts instead.

Perform five back slaps and five chest thrusts.

Use AED after five cycles of Infants ⬍1 yr CPR (out of hospital). Use Manual defibrillator pediatric system for child preferred. Can use AED 1-8 yr, if available. HCP: with pediatric pads.* For sudden collapse (out Use adult AED if no of hospital) or in-hospital other defibrillator arrest, use AED as soon available. Use infant as available. pads if available.

245

246

LADVANCED CARDIAC LIFE SUPPORT (ACLS)L PULSELESS ARREST ALGORITHM Step 1 • • • •

BLS algorithm. Call for help; give CPR. Give oxygen when available. Attach monitor and defibrillator when available.

Step 2 Check rhythm. Is it a shockable rhythm? Yes Step 3–YES: Shockable Rhythm—VF/VT • Give 1 shock:  Manual biphasic: Is device specific (usually 120-200 J).  AED: Is device specific.  Monophasic: 360 J. • Resume CPR immediately after the shock; perform five cycles of CPR. • Establish IV/IO access

No Step 3–NO: Nonshockable Rhythm—Asystole/PEA Resume CPR for five cycles. • When IV/IO is available, give vasopressor:  Administer epinephrine (1 mg IV/IO) and repeat every 3 to 5 minutes or  May administer 1 dose of vasopressin (40 U IV/IO) to replace first or second dose of epinephrine. • Give five cycles of CPR.

Step 4 Check rhythm. Is it a shockable rhythm?

Step 4 Check rhythm. Is it a shockable rhythm? Yes Step 5–YES: Shockable Rhythm—VF/VT Continue CPR while defibrillator is charging. • Give 1 shock:  Manual biphasic: Is device specific (usually 120-200 J; if unknown, use maximum).  AED: Is device specific.  Monophasic: 360 J. • Resume CPR immediately after the shock. • When IV/IO is available, give vasopressor during CPR (preshock or postshock):  Administer epinephrine (1 mg IV/IO) and repeat every 3 to 5 minutes or  May administer 1 dose of vasopressin (40 U IV/IO) to replace first or second dose of epinephrine.  Consider advanced airway and capnography.  Give five cycles of CPR.

No Go To Asystole/ PEA Step 5

Yes Step 5–YES: Shockable Rhythm—VF/VT Go to Step 7–YES: Shockable Rhythm—VF/VT.

No

Step 5–NO: Nonshockable Rhythm—Asystole/PEA If asystole or PEA is present, resume CPR for five cycles. • Treat reversible cause • Give five cycles of CPR. If pulse is present, begin postresuscitation care.

Step 6

247

Check rhythm. Is it a shockable rhythm?

Continued

248

LADVANCED CARDIAC LIFE SUPPORT (ACLS)—cont’dL Yes Step 7–YES: Shockable Rhythm—VF/VT

No Go To Asystole/ PEA Step 5

Continue CPR while defibrillator is charging. • Give 1 shock:  Manual biphasic: Is device specific (usually 120-200 J; if unknown, use maximum).  AED: Is device specific.  Monophasic: 360 J. • Resume CPR immediately after the shock.  Amiodarone (300 mg IV/IO) once, then consider additional 150 mg IV/IO once later. • After five cycles of CPR, repeat step 4 and continue from there.

J, Joules; PEA, pulseless electrical activity.

Notes: • For CPR cycles, refer to the BLS chart in this section. • During CPR, secure an advanced airway and confirm placement. • Push hard and fast (at least 100/min). • Ensure full chest recoil. • Minimize interruptions in chest compressions. • One cycle of CPR = 30 compressions, and then 2 breaths. Five cycles ⫽ approximately 2 minutes • After an advanced airway is in place, continuous chest compressions should be given without pauses for breaths.  Give 8 to 10 breaths per minute. • Check rhythm every 2 minutes. • Find and treat any potential contributing factors such as hypothermia, hypokalemia, hyperkalemia, hypovolemia, hypoxia, hydrogen ion (acidosis), tamponade (cardiac), thrombosis (coronary or pulmonary), tension pneumothorax, or toxins.

249

250

TREATABLE CAUSES IN PULSELESS ARREST Reversible Cause

Possible Management Strategies

Hypovolemia

Replace fluid volume with crystalloids or colloids.

Hypoxia Acidosis

Assure patent airway and adequate ventilation; administer oxygen.

Hypokalemia Hyperkalemia Hypothermia

Respiratory: Improve minute volume by increasing rate and/or depth of ventilation. Metabolic: Identify and treat underlying cause. May include sodium bicarbonate IV. Rapid potassium infusion not advised. Calcium chloride (10%); sodium bicarbonate IV; glucose plus insulin; nebulized albuterol; furosemide; kayexalate; dialysis Initiate rewarming; begin standard ACLS care; follow temperature-specific guidelines

Tension pneumothorax Pericardial tamponade Toxins

Chest decompression

Pulmonary thrombosis

Fibrinolytics; percutaneous mechanical thromboembolectomy; surgical embolectomy Prepare for 12-lead ECG and percutaneous coronary intervention if return of spontaneous circulation.

Coronary thrombosis

Pericardiocentesis Administer antidote if indicated.

LPOST-CARDIAC ARREST CAREL Spontaneous circulation resumes (ROSC)

Ensure appropriate oxygenation and ventilation • Maintain SaO2 ≥ 94% • If persistent apnea  Consider advanced airway  Maintain etCO 35 to 40 mmHg 2

If blood pressure