The Textbook of Emergency Cardiovascular Care and CPR [1st ed.] 0781788994, 9780781788991, 9781451103588, 9781469801629

Table of contents :
Contributors
Foreword
Preface

Part One: Acute Coronary Syndromes
1 Pathophysiology and Initial Triage of Acute Coronary Syndromes
John M. Field
2 Sudden Cardiac Death: Epidemiology, Pathophysiology, and Future Directions
Steven H. Mitchell and Graham Nichol
3 Evaluation, Differential Diagnosis, and Approach to the Patient with Possible Acute Coronary Syndrome
Judd E. Hollander
4 Community and Prehospital Strategies for Managing Patients with Acute Coronary Syndromes
Joseph P. Ornato
5 Emergency Department Management of Acute Coronary Syndromes
Charles V. Pollack Jr. and Richard L. Summers
6 Heart Failure and Acute Pulmonary Edema in the Emergency Department
W. Frank Peacock
7 Cardiogenic Shock Complicating Acute Coronary Syndromes
John M. Field
8 Ultrasonography in Emergency Cardiovascular Care
Anthony J. Dean and Sarah A. Stahmer

Part Two: Basic Life Support
9 Pathophysiology of Cardiac Arrest
Karl B. Kern
10 Circulatory Adjuncts to Improve Coronary Perfusion Pressure
Karl B. Kern
11 Basic Life Support: Science to Survival
Michael R. Sayre and Diana M. Cave

Part Three: Defibrillation
12 Restoring Life: The Story of Human Defibrillation and Modern CPR
Mark E. Silverman
13 Defibrillation: Practice
Vincent N. Mosesso Jr. and Cheryl Rickens
14 Ventricular Fibrillation and Defibrillation: Experimental and Clinical Experience with Waveforms and Energy
Roger D. White and Richard E. Kerber

Part Four: Airway Management in Basic and Advanced Life Support
15 Respiratory Physiology in ECC: Principles of Oxygenation and Ventilation
Elizabeth H. Sinz and Kane High
16 Monitoring and Maintaining a Patent Airway
Elizabeth H. Sinz and Kane High
17 Oxygen Administration and Supraglottic Airways
Michael Shuster
18 Endotracheal Intubation and Management of the Difficult Airway
Kane High

Part Five: Arrhythmias
19 Life-Threatening Arrhythmias: Evaluation, Identification, and Assessment
Peter J. Kudenchuk
20 The Electrophysiology of Arrhythmias
Peter J. Kudenchuk
21 Pulseless Cardiac Arrest
Peter J. Kudenchuk
22 Tachycardia with Pulses: Narrow and Wide
Peter J. Kudenchuk
23 Bradycardia
Peter J. Kudenchuk
24 Electrical Therapies
Peter J. Kudenchuk

Part Six: Pharmacology in Emergency Cardiovascular Care
25 Drugs for Control of Rhythm
Peter J. Kudenchuk
26 Cardiovascular Function and Vascular Tone: Physiology for ECC
Raúl J. Gazmuri and Beatrice M. Correa
27 Nonadrenergic Vasopressors in ECC
Helmut Raab, Martin Dünser, and Volker Wenzel

Part Seven: Post–Cardiac Arrest Syndrome and Management
28 Post–Cardiac Arrest Syndrome and Management
Robert W. Neumar and Jerry Nolan

Part Eight: Special Resuscitation Situations
29 Toxicology in Emergency Cardiovascular Care
Allan R. Mottram and Timothy B. Erickson
30 Drowning
David Szpilman, Anthony J. Handley, Joost Bierens, Linda Quan, and Rafáel Vasconcellos
31 Hypothermia
Eric A. Weiss
32 Electrical Current and Lightning Injury
Mary Ann Cooper, Christopher J. Andrews, and Ronald L. Holle
33 Severe, Life–Threatening Asthma
Jill M. Baren
34 Anaphylaxis
Michael E. Winters
35 Cardiopulmonary Resuscitation in Pregnancy
Carolyn M. Zelop and Edward P. Grimes

Part Nine: Stroke
36 Stroke
Edward C. Jauch and Todd J. Crocco

Part Ten: Ethics
37 Ethics in Emergency Cardiovascular Care
Kenneth V. Iserson

Part Eleven: Education and Research
38 Careers in Resuscitation Medicine
Benjamin S. Abella and Lance B. Becker

Index

Citation preview

The Textbook of

Emergency Cardiovascular Care and CPR

AHA Editors

Peter J. Kudenchuk, MD, FAHA, FACC, FACP, F HRS

Professor of Medicine

ACEP Editors

Michael J. Bresler, MD, FACEP

Clinical Professor

University of Washington School of Medicine

Division of Emergency Medicine

Division of Cardiology, Arrhythmia Services

Stanford University School of Medicine

University of Washington Medical Center

Palo Alto, California

Seattle, Washington

Robert E. O'Connor, MD, MP H, FACEP, FAAEM,

FAHA

Professor and Chair

Amal Mattu, MD, FACEP, FAAEM Associate Professor

Department of Emergency Medicine University of Maryland School of Medicine

Department of Emergency Medicine

Program Director

University of Virginia Health System

Emergency Medicine Residency

Charlottesville, Virginia

University of Maryland Medical System

Terry l. Vanden Hoek, MD, FACEP Associate Professor of Medicine Section of Emergency Medicine

Baltimore, Maryland

Scott M. Silvers, MD, FACEP

Assistant Professor and Vice Chair

University of Chicago Medical Center

Department of Emergency Medicine

Chicago, Illinois

Mayo Clinic Jacksonville, Florida

Acquisitions Editor: Frances R. DeStefano Managing Editors: Chris Potash and Julia Seto Project Manager: Rosanne Hallowell Manufacturing Manager: Kathleen Brown Marketing Manager: Kimberly Schonberger Creative Director: Doug Smock Cover Designer: Joseph DePinho Production Services: Aptara, Inc. © 2009 by Lippincott Williams & Wilkins, a Wolters Kluwer business

530 Walnut Street

Philadelphia, PA 19106 LWW.com All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilizing by any information storage and retrieval system without written per­ mission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Printed in China

Library of Congress Cataloging-in-Publication Data The textbook of emergency cardiovascular care and CPR I editor-in-chief, John M. Field; ACEP associate editors, Michael]. Bresler, Amal Mattu, Scott M. Silvers ; AHA associate editors, Peter]. Kudenchuk, Robert O'Connor,

Terry VandenHoek. p.; em.

Includes bibliographical references and index. ISBN-13: 978-0-7817-8899-1 (alk. paper) ISBN-10: 0-7817-8899-4 (alk. paper) 1. Cardiovascular emergencies. 2. CPR (First aid) I. Field, John M. [DNLM: 1. Cardiovascular Diseases-therapy. 2. Cardiopulmonary Resuscitation-methods. 3. Emergency Medical Services-methods. WG 166 T3545 2009] RC675.T49 2009 616.1'025-dc22 2008028088 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for any conse­ quences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of this information in a particu­ lar situation remains the professional responsibility of the practitioner. The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug. Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA) clear­ ance for limited use in restricted research settings. It is tl1e responsibility of health care providers to ascertain the FDA status of each drug or device planned for use in their clinical practice. The publishers have made every effort to trace copyright holders for borrowed material. If they have inadver­ tently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity. To purchase additional copies of this book, call our customer service department at (800) 638-3030 or fax orders to (301) 223-2320. International customers should call (301) 223-2300. Visit Lippincott Williams & Wilkins on the Internet: at LWW.com. Lippincott Williams & Wilkins customer

service representatives are available from 8:30 am to 6 pm, EST.

10 9 8 7 6 5 4 3 2 1

To LaDora and Julie

Contents

Contributors xi Foreword xv Preface xvii

Part One: Acute Coronary Syndromes 1

Pathophysiology and Initial Triage of Acute Coronary Syndromes 1

John M. Field 2

Sudden Cardiac Death: Epidemiology, Pathophysiology, and

Future Directions 11

Steven H. Mitchell and Graham Nichol 3

Evaluation, Differential Diagnosis, and Approach to the Patient with Possible

Acute Coronary Syndrome 25

Judd E. Hollander 4

Community and Prehospital Strategies for Managing Patients with Acute Coronary Syndromes 43

Joseph P. Ornata 5

Emergency Department Management of Acute Coronary Syndromes 63

Charles 6 7

V

Pollack Jr. and Richard L. Summers

Heart Failure and Acute Pulmonary Edema in the Emergency Department 96 W

Frank Peacock

Cardiogenic Shock Complicating Acute Coronary Syndromes 115

John M. Field 8

Ultrasonography in Emergency Cardiovascular Care 129

Anthony J. Dean and Sarah A. Stahmer

Part Two: Basic Life Support 9

Pathophysiology of Cardiac Arrest 149

Karl B. Kern vii

viii

CONTENTS

1 0 Circulatory Adjuncts to Improve Coronary Perfusion Pressure 161

Karl B. Kern 11 Basic Life Support: Science to Survival 169

Michael R. Sayre and Diana M. Cave

Part Three: Defibrillation

.....-----.-- ··································································································································································

12 Restoring Life: The Story of Human Defibrillation and Modern CPR 193

Mark E. Silverman 13 Defibrillation: Practice 201

Vincent N Mosesso Jr. and Cheryl Rickens

14 Ventricular Fibrillation and Defibrillation: Experimental and Clinical Experience with Waveforms and Energy 222

Roger D. White and Richard E. Kerber

Part Four: Airway Management in Basic and Advanced Life Support

----

---------··································································································································································

15 Respiratory Physiology in ECC: Principles of Oxygenation and Ventilation 233

Elizabeth H. Sinz and Kane High 16 Monitoring and Maintaining a Patent Airway 242

Elizabeth H. Sinz and Kane High 17 Oxygen Administration and Supraglottic Airways 253

Michael Shuster 18 Endotracheal Intubation and Management of the Difficult Airway 273

Kane High

Part Five: Arrhythmias 1 9 Life-Threatening Arrhythmias: Evaluation, Identification, and Assessment 295

Peter J. Kudenchuk 2 0 The Electrophysiology of Arrhythmias 300

Peter J. Kudenchuk 21 Pulseless Cardiac Arrest 309

Peter J. Kudenchuk

CONTENTS

22 Tachycardia with Pulses: Narrow and Wide 313

Peter J. Kudenchuk 23 Bradycardia 341

Peter J. Kudenchuk 2 4 Electrical Therapies 3 62

Peter J. Kudenchuk

Part Six: Pharmacology in Emergency Cardiovascular Care 25 Drugs for Control of Rhythm 3 79

Peter J. Kudenchuk 26 Cardiovascular Function and Vascular Tone: Physiology for ECC 395

Raul J. Gazmuri and Beatrice M. Correa 27 Nonadrenergic Vasopressors in ECC 410

Helmut Raab, Martin Diinser, and Volker Wenzel

Part Seven: Post-Cardiac Arrest Syndrome and Management 28 Post-Cardiac Arrest Syndrome and Management 427

Robert

W Neumar

and Jerry Nolan

Part Eight: Special Resuscitation Situations 2 9 Toxicology in Emergency Cardiovascular Care 443

Allan R. Mottram and Timothy B. Erickson 3 0 Drowning 477

David Szpilman, Anthony J. Handley, Joost Bierens, Linda Quan, and Rafael Vasconcellos 31 Hypothermia 490

Eric A. Weiss 3 2 Electrical Current and Lightning Injury 498

Mary Ann Cooper, Christopher J. Andrews, and Ronald L. Holle 3 3 Severe, Life-Threatening Asthma 512

Jill M. Baren 3 4 Anaphylaxis 530

Michael E. Winters

ix

x

CONTENTS

3 5 Cardiopulmonary Resuscitation in Pregnancy 53 8

Carolyn M. Zelop and Edward P Grimes

Part Nine: Stroke

�----- ··································································································································································

36 Stroke 544

Edward

C.

Jauch and Todd J. Crocco

Part Ten: Ethics

r----- ··································································································································································

3 7 Ethics in Emergency Cardiovascular Care 5 67

Kenneth

V Iserson

Part Eleven: Education and Research

------ ··································································································································································

38 Careers i n Resuscitation Medicine 587

Benjamin S. Abella and Lance B. Becker Index

593

Contributors Benjamin S. Abella, MD, MPhil Assistant Professor Department of Emergency Medicine Clinical Research Director Center for Resuscitation Science University of Pennsylvania Philadelphia, Pennsylvania Christopher]. Andrews, BE, MBBS, MEngSc, PhD, DipCSc, EDIC, FACLM General Practitioner and Consultant in Electrical and Lightning Injuries Indooroopilly Medical Center Queensland, Australia Jill M. Baren, MD, FACEP, FAAP, MBE Associate Professor of Emergency Medicine and Pediatrics University of Pennsylvania School of Medicine Attending Physician Emergency Medicine Hospital of the University of Pennsylvania Philadelphia, Pe1msylvania Lance B. Becker, MD, FAllA Professor of Emergency Medicine University of Pennsylvania School of Medicine Center for Resuscitation Science and Department of Emergency Medicine Translational Research Laboratory University of Pennsylvania Philadelphia, Pennsylvania Joost Bierens, MD, PhD Professor of Emergency Medicine Director, Department of Anesthesiology VU University Medical Center Amsterdam, The Netherlands Michael]. Bresler, MD, FACEP Clinical Professor Division of Emergency Medicine Stanford University School of Medicine Palo Alto, California

Anthony J. Busti, PharmD, BCPS Associate Professor Department of Internal Medicine Diplomate, Accreditation Council for Clinical Lipidology Texas Tech University Health Sciences Center School of Pharmacy Dallas/Ft. Worth Regional Campus Dallas, Texas Diana M. Cave, RN, MSN Emergency Services Legacy Health System Legacy Emanuel Hospital & Health Center Portland, Oregon Mary Ann Cooper, MD Professor Departments of Bioengineering and Emergency Medicine University of illinois at Chicago University of illinois Hospital Chicago, illinois Beatrice M. Correa, MD Department of Internal Medicine Rosalind Franklin University of Medicine and Science/ The Chicago Medical School North Chicago, illinois Todd J. Crocco, MD Associate Professor and Chair Department of Emergency Medicine West Virginia University Hospital Morgantown, West Virginia Anthony J. Dean, MD Assistant Professor of Emergency Medicine University of Pennsylvania School of Medicine Director of Emergency Ultrasound Department of Emergency Medicine University of Pennsylvania Medical Center Philadelphia, Pennsylvania

xi

xii

CONTRIBUTORS

Martin Diinser, MD Department of Anesthesiology and Critical Medicine Innsbruck Medical University lnnsbruck, Austria 7 0 ye a r s M a l e sex D i a betes m e l l itus

P r o b a b l e i s c h e m i c sym p t o m s i n a b s e n c e o f a ny o f t h e intermedi ate l i k e l i h o o d chara cteristics Recent cocaine use

Examination

T r a n s i e n t M R m u r m u r , hyp o t e n s i o n , d i a p h o r e s i s , p u l m o n a ry e d e m a , or roles

E x tr a c a r d i a c vas c u l a r d i s e a s e

C h e s t d i s c o m fo r t r e p r o d u c e d by palpation

ECG

N ew o r p r e s u m a b ly n ew t r a n s i e n t S T - s e g m e n t d evi a t i o n (� 1 m m) o r T -wave i nve r s i o n i n m u l ti p l e precordial leads

F i x e d Q wave s ST- s e g m e n t d e p r e s s i o n 0 . 5-1 m m o r T -wave i nver s i o n � 1 m m

T -wave fl a tte n i n g o r i nversi o n < 1 m m i n l e a d s with d o m i n a n t R wave s N o r m a l E CG

Ca r d i a c m a r k e rs

E l eva ted c a r d i a c Tn l , TnT, o r CK - M B

Normal

Normal

RCS , a c u te c o r o n a ry syn d r o m e ; CA D , c o r o n a ry artery d 1 s e a s e ; CK - M B , M B f r a c t 1 o n o f c r e a t m e k m a s e , ECG , e l e c tr o c o r d 1 o g r a m ; Ml, myo c a r d 1 0 l m f a r c t1 o n ; M R , m 1 t r a l r e g u r g 1tat1 o n ; T n l , tro p o n 1 n l ; T n T , tro p o n m T S o u r c e : M o d 1 f 1 e d w1th p e r m i S S i o n from B r a u nwa l d E , M a r k D B , J o n e s R H , et a l . Unsta b l e a n g 1 n a : d 1 a g n os1s a n d m a n a g e m ent. RHCPR p u b l 1 c a t 1 o n n o . 9 4 - 0 6 0 2 (1 24) R o c kvi l l e , M D · A g e n cy f o r H e a l t h C a re P o l i cy a n d R e s e a r c h a n d t h e N a t 1 o n a l H e a rt , Lu n g , a n d B l o o d I n s t 1 t u t e , U S P u b l i c H e a l t h Semc e , U . S . D e p a r t m e n t of H e a l t h a n d H u m a n S e rv1 c e , 1 9 9 4 .

CHAPTER 1

from long-term epidemiologic studiesY However, tradi­ tional risk factors are weak predictors of an ACS , and prog­ nostic scores have been developed from clinical trials to help physicians assess the risk of adverse cardiovascular events in patients likely to have symptoms due to CAD . 2 8-30 Although typical chest discomfort increases the probability of CAD , atypical features do not exclude AC S . In the Multicenter Chest Pain Study focusing on the subgroup of patients with chest discomfort presenting to an emergency department (ED), 1 5 % of patients with pleuritic chest pain and 2 2 % of those with stabbing pain were "ruled in" for AMJ.29 TA B LE 1 - 3

•

•

P AT H O P H Y S I O L O G Y A N D I N I T I A L T R I A G E

Assessment of the Risk of CAD Using Initial History, Physical Examination, Electrocardiogram, and Cardiac Markers In this context, two key questions are asked when patients are evaluated for possible ischemic discomfort: • •

What is the likelihood that symptoms are due to obstructive coronary artery disease (Table 1 -2)? If the answer to this question is yes (intermediate or high likelihood), what is the risk of an adverse major cardiac event (Table 1 -3)?

S h o r t - T e r m R i s k o f D e a t h o r N o n fa t a l M I i n P a t i e n ts With U A / N STE M I "

Low R i s k

Feature

7

High Risk

I ntermedi ate Risk

A t least 1 o f th e following fe a tures m ust b e presen t:

No h igh -risk fe a ture, b u t must h ave 1 o f th e following:

No h igh - or in term e diate -risk fe a ture b u t m ay h ave any o f th e following fe a tures:

H i s t o ry

A c c e l e r a t i n g t e m p o of i s c h e m i c sym p t o m s i n p r e c e d i n g 4 8 h

P r i o r M I , p e r i p h e r a l or c e r e b rovas c u l a r d i s e a s e , or CA B G ; p r i o r a s p i r i n use

Ch a r a c t e r o f p a i n

P r o l o n g e d o n g o i n g (> 2 0 m i n) rest p a i n

P r o l o n g e d (> 2 0 m i n) r e s t a n g i n a , n ow r e s o lve d , with m o d e r a t e o r high likelihood of CAD R e s t a n g i n a (> 2 0 m i n) o r r e l i eved with r e s t o r s u b l i n g u a l NTG N o c tu r n a l a n g i n a N ew- o n s e t o r p r o g r e ssive CCS c l a s s I I I or IV a n g i n a in t h e p r e c e d i n g 2 we e k s with o u t p r o l o n g e d (> 2 0 m i n) r e s t p a i n b u t with i n t e r m e d i a t e o r h i g h likelihood of CAD

Cl i n i c a l fi n d i n g s

P u l m o n a ry e d e m a , m o s t l i k e ly d u e t o isc h e m i a N ew o r wo rs e n i n g M R m u r m u r 53 o r n ew/wo rs e n i n g r o l e s Hyp o t e n s i o n , b r a dyca r d i a , t a c hyc a r d i a A g e > 7 5 ye a r s

A g e > 7 0 ye a r s

ECG

A n g i n a a t r e s t w i t h tra n s i e n t ST- s e g m e n t c h a n g e s > 0 . 5 m m B u n d l e - b r a n c h b l o c k , n ew o r p r e s u m e d n ew S u s ta i n e d ve n t r i c u l a r t a c hyc a r d i a

T -wove c h a n g e s P a th o l o g i c Q wave s o r r e sti n g ST- s e g m e n t d e p r e s s i o n < 1 m m i n m u l ti p l e l e a d g r o u p s (a n t e r i o r , i n f e r i o r , l a t e r a l)

Normal or unchanged ECG

Ca r d i a c m a r k e rs

E l eva t e d c a r d i a c T n T , Tn i , o r CK - M B (e . g . , T n T o r T n l > 0 . 1 n m L)

S l i g h t ly e l eva t e d c a r d i a c T n T , Tn l , o r CK - M B (e. g . , TnT > 0 . 0 1 but 20 mm Hg between the right and left arms), and the chest radiogra­ phy shows mediastinal or aortic widening. 34·35

Pulmonary Embolism The incidence of pulmonary embolism (PE) is estimated at over 1 in 1 ,000 patients, but the diagnosis is often missed and

•

A P P R O A C H T O T H E P AT I E N T

27

the incidence may be higher.36 Risk stratification depends on the pretest probability for PE. Several scoring systems exist to characterize patient risk for PE, including the Canadian (Wells) score, the Charlotte rule, the Geneva score, and oth­ ers.37-40 Patients with symptoms suggestive of PE and right ventricular dysfunction or hemodynamic instability are at high risk for PE and major comorbidity and death.

Pneumothorax Pneumothorax can occur spontaneously or following trauma or pulmonary procedures . Patients with primary sponta­ neous pneumothorax tend to be younger males who are tall and thin. Secondary spontaneous pneumothorax occurs with greatest frequency in patients with chronic obstructive pul­ monary disease, cystic fibrosis, or asthma.41 Tension pneu­ mothorax is diagnosed clinically by the presence of unilat­ eral decreased breath sounds, hypotension, and shifting of the trachea in the opposite direction.

Mediastinitis Mediastinitis is less frequent and occurs following odonto­ genic infections, esophageal perforation, and iatrogenic complications of cardiac surgery or upper gastrointestinal and airway procedures. "Hamman's crunch," heard over the anterior chest, is strongly suggestive. Mortality for patients with mediastinitis remains high ( 1 4%-42 %), even when it is treated with operative debridement and antibiotics.42 -45

Pericardia! Tamponade Pericardia! tamponade results in a direct compromise in car­ diac filling, producing a picture resembling cardiogenic shock that requires emergent reduction in pericardia! pressure by pericardiocentesis. Tamponade may occur with aortic dissec­ tion, after thoracic trauma, or as a consequence of acute peri­ carditis from infection, malignancy, uremia, or other causes.

Other Conditions Other conditions are more common but less serious . Gastroesophageal reflux disease, esophageal spasm, hiatal hernias, as well as upper abdominal processes can cause chest pain. Gastrointestinal causes account for the symptoms of a sizable number of patients who complain of chest pain and do not have an ACS . Respiratory infections such as pneu­ monia and bronchitis are frequently accompanied by chest discomfort but can usually be identified on the basis of cough and fever. Chest tightness is a common complaint in patients with acute exacerbations of asthma, which can often be distinguished by wheezing on examination. Acute decompensated heart failure can result in chest discomfort that may or may not represent an ACS because heart failure is the result of chronic CAD and other

28

H 0 L L A N DE R

cardiovascular conditions in some patients.46 •47 Valvular heart disease, such as aortic stenosis, can result in chest pain that often signifies severe disease, while mitral valve prolapse is associated with chest pain that may have few if any long-term consequences. Infectious or inflammatory causes of chest dis­ comfort include pericarditis, myocarditis, and endocarditis. Chest heaviness or discomfort may be noted with pleu­ ral effusions. Pulmonary malignancy can cause chest pain if there is pleural involvement. Musculoskeletal causes of chest pain include muscle strains and costochondritis as well as overuse syndromes. Herpes zoster can usually be identified as the cause of chest pain, but in rare instances the pain may be evident prior to the exanthem.

�lectrocardiograna The standard 1 2 -lead electrocardiogram (ECG) is the single best test to identify patients with STEMI immediately upon ED presentation/ despite the fact that it has relatively low sensitivity for the detection of ACS . The sensitivity of ST­ segment deviation for the detection of AMI is 3 5 % to 5 0 % , leaving more than half o f all AMI patients unidentified.7 ·48

TA B LE 3 - 2

•

However, even among patients with ST-segment-elevation MI (STEMI), ECG variables can further risk-stratify the likelihood of 3 0-day mortality (Table 3 -2).49 ECG criteria that increase the risk of AMI in ED patients with chest pain are shown in Tables 3 - 2 and 3 -3 . 2 0 Patients with normal or nonspecific ECGs have a 1 %-5 % incidence of AMI and a 4% to 2 3 % incidence of unstable angina.7•48•50• 5 1 Patients with nondiagnostic ECGs or with ischemia that is not known to be old have a 4% to 7% incidence of AMI and a 2 1 % to 48 % incidence of unstable angina. Demonstration of new ischemia increases the risk of AMI to 2 5 % to 7 3 % , and the unstable angina risk to 1 4% to 4 3 % .7 A normal diagnos­ tic 1 2 -lead ECG cannot conclusively exclude ACS . 7 • 5 2 The ECG should be used in conjunction with clinical history and cardiac markers to determine admission location and treat­ ment for patients with ACS .

Continuous ECG Monitoring Because of the relatively poor sensitivity of the standard 1 2 -lead ECG to detect patients with ACS , additional elec­ trocardiographic strategies have been proposed. A contin­ uous 1 2 -lead ECG monitors and records new ECGs every

M u l tiva r i a te S i g n i f i c a n c e of t h e E l e c tr o c a r d i o g r a m i n P a t i e n ts With STE M ! E n r o l l e d i n G U ST0 - 1

E l e ctroca r d i o g r a p h i c Feature

O d d s R a t i o (9 5% Cl)

Sum o f ST - s e g m e n t d evi a t i o n (1 9 vs . 8 m m)

1 . 5 3 (1 . 3 8-1 . 6 9)

S u m o f ST - s e g m e n t d e c r e a s e (-1 vs. -7 m m)

0 . 7 7 (0 . 7 2-0 . 8 3 )

H e a r t r a t e (84 vs . 6 0 b p m)

1 . 4 9 (1 . 4 1 - 1 . 5 9)

S u m ST - s e g m e n t i n c r e a s e i n I I , I I I , a n d aVF (6 vs . 0 m m)

0 . 7 9 (0 . 7 1 -0 . 8 9)

QRS d u r a t i o n 1 0 0 vs . 8 0 m s e c •

A n t e r i o r i n fa r c t

1 . 5 5 (1 . 4 3-1 . 6 8)

•

O th e r l o c a ti o n

1 . 0 8 (1 . 0 3-1 . 1 3)

A n t e r i o r i n fa r c t i o n •

QRS duration 100 msec

1 . 0 8 (1 . 0 3-1 . 1 3)

•

QRS duration 50 msec

0 . 6 1 (0 . 4 3-0 . 8 6)

0 . 6 7 (0 . 5 0-0 . 9 0) 1 . 4 1 (0 . 9 8-2 . 0 2)

2 . 4 7 (2 . 0 2-3 . 0 0) •

O th e r l o c a ti o n

1 . 1 7 (0 . 9 8-1 . 4 1 )

S o u r c e : H a t h away W R , P e t e r s o n E D , Wa g n e r G S , et a l . P r o g n os t i c s 1 g n 1 f 1 c o n c e of t h e 1 n 1 t 1 a l e l e c tr o c a r d i o g r a m 1n p a t 1 e n ts w1th a c u t e myo c a r d 1 a l 1 nf a r c t 1 o n JAMA 1 9 9 8 ; 2 7 9 . 3 8 7-3 9 1 .

CHAPTER 3

TA B LE 3 - 3

•

•

A P P R O A C H T O T H E P AT I E N T

29

E l e c t r o c a r d i o g r a p h i c F e a t u r e s P r e d i ctive o f A M I in P a t i e n ts With A c u te C h e s t P a i n

E l e ctroca r d i o g r a p h i c Feature

li k e l i h o o d R a t i o (9 5 % CI)

N ew ST - s e g m e n t e l evati o n 2:1 m m

5. 7-5 3 . 9 "

N ew Q wave

5 . 3-2 4 . 8"

A ny ST - s e g m e n t e l eva t i o n

1 1 . 2 (7 . 1 -1 7 . 8)

N ew c o n d u c t i o n d e f e c t

6 . 3 (2 . 5-1 5 . 7)

N ew S T - s e g m e n t d e p r es s i o n

3 . 0-5 . 2 °

A ny Q wave

3 . 9 (2 . 7-5 . 7)

A ny ST - s e g m e n t d e p r e ss i o n

3 . 2 (2 . 5-4 . 1 )

T wave p e a k i n g a n d / o r i nve r s i o n 2: 1 m m N ew T -wave i nver s i o n A ny c o n d u c t i o n d e f e c t

3 . 1b 2 . 4-2 . 8 " 2 . 7 (1 . 4-5 . 4)

' I n h e t e r o g e n e o u s stu d 1 e s t h e l i k e l i h o o d r o t 1 o s o r e r e p o rt e d a s r a n g e s . b D o t o n o t o v a l i a b l e to c a l c u l a t e c o n f i d e n c e I n t e rva l s . S o u r c e : P o nJ U A A , H e m m e l g o r m B R , G uyott G H , et ol Is th1s p o t 1 e n t h ovmg a myo c o r d l o l mforctl o n ? JAMA 1 9 9 8 , 28 0 : 1 2 5 6-1 2 6 3 , w1th p e r m i SS i o n .

2 0 seconds . When the ST-segment baseline is altered, it sets off an alarm and prints a copy of the new ECG. This technology is most often employed in chest pain-observa­ tion units, where it might be useful for monitoring patients who present with non-AMI AC S for ECG evidence of injury.48 B ecause of costs, concerns regarding labile ST­ segment and T-wave changes from hyperventilation or patient movement, and a lack of ED-based prospective studies demonstrating clinically relevant differences in outcome, continuous 1 2 -lead ECGs have not been recom­ mended for routine use.48

Additional ECG Leads Other ECGs with 1 5 , 1 8 , and 22 leads have been studied.48•53 In one study, addition ofV4R, V8 , and V9 increased the sen­ sitivity to detect ST-segment elevation to 5 9 % without a loss of specificity. 53 The addition of V4R to V6R and V7 to V9 as posterior leads led to an 8 % increase in sensitivity for AMI relative to a standard 1 2 -lead ECG but at the cost of a 7 % decrease in specificity. 54 Twenty-two-lead and body-sur­ face-mapping ECGs have not been sufficiently studied to recommend their use . Right-sided leads (rV4) should be used in the setting of inferior wall infarction to assess possi­ ble RV involvement.48

left-bundle-branch block (LBBB) (Table 3 -4). In the setting of a LBBB, the presence of ST-segment elevation 2: I mm and concordance with the QRS complex or ST-segment depression ::::: I mm in leads VI , V2 , or V3 suggest AMI.55 ST-segment elevation 2: 5 mm that is discordant with the QRS complex increases the likelihood of AMI but has poor specificity. Uncomplicated right ventricular pacing causes sec­ ondary repolarization changes of opposing polarity to that of the predominant QRS complex. Most leads have pre­ dominant negative QRS complexes followed by ST-segment elevation and positive T waves . ST-segment elevation ::::: 5 mm is most indicative of AMI in leads with predominantly negative QRS complexes. Any ST-segment elevation con­ cordant with the QRS complex in a predominantly positive QRS complex is highly specific for AMI. The QRS com­ plex is predominantly negative in leads VI to V3 . ST-seg­ ment depression in these leads had 8 0 % specificity for AMI. s 6

Risk-Stratification Algorithms Although clinical and computer algorithms can successfully risk­ stratify patients, they are not able to reliably identify a group of patients at such low risk of an A CS that they could be safely and immediately released from the Emergency Department.

ECG Confounders There are several clinical conditions where ECG interpre­ tation of ACS is difficult, particularly paced rhythms and

Several risk-stratification algorithms have been studied and validated.

30

HOLLANDER

TA B LE 3 - 4 • S o m e Cl i n i c a l Co n d i t i o n s Wh e r e t h e E l e c t r o c a r d i o g r a m I n te r p r e t a ti o n C a n B e D i ffi c u l t -------

M ay h ave ST Se g m e n t E l eva t i o n i n t h e A b s e n c e o f A M I E a rly r e p o l a r i z a t i o n left ve n tr i c u l a r hyp e r t r o p hy Pericard itis Myo c a r d i t i s l e f t ve n tr i c u l a r a n e u rys m s I d i o p a t h i c hyp e rt r o p h i c s u b a o rt i c ste n o s i s (I H SS) Hyp o t h e r m i a

characteristics (Fig. 3 - 1 ). It does not incorporate cardiac marker results . The Goldman algorithm stratifies patients into groups with risks of AMI that vary from 1 % to 7 7 % . The sensitivity o f the Goldman chest pain protocol for pre­ dicting AMI is 8 8 % to 9 1 % with a specificity of 7 8 % to 92 % . 57 It does not identify any group with < 1 % risk who might be safe for ED release. Even in the group of patients deemed to be low risk, the addition of initially negative car­ diac troponin I was still associated with a 5 % rate of 3 0-day adverse outcomes . 5 8 The Goldman algorithm can be used to predict the need for intensive care unit (ICU) admission, development of cardiovascular complications, and outcome in a clinical decision or short-stay observation unit. 14

P a c e d rhyt h m s left b u n d l e - b r a n c h b l o c k M ay h ave S T- se g m e n t D e p r essi o n s i n t h e A b s e n c e o f I s c h e m i a Hyp o k a l e m i a D i g o x i n effect

The Goldman criteria protocol does not identify any group with < 1 % risk who might be safe for ED release. Even in the group of patients deemed to be low risk, the addition of initially negative cardiac troponin I was still associated with a 5% rate of 30-day adverse outcomes.

C o r p u l m o n a l e a n d r i g h t h e a r t str a i n E a rly r e p o l a r i z a t i o n left ve n tr i c u l a r hyp e r t r o p hy P a c e d rhyt h m s left b u n d l e - b r a n c h b l o c k M ay h ave T-wave I nve r s i o n s i n t h e A b s e n c e o f I s c h e m i a P e rs i s t e n t j uve n i l e p a tt e r n S t o k e s-R d a m s syn c o p e o r s e i z u r e s

ST-segment elevation or Q waves on the ECG, other ECG findings indicating myocardial ischemia, low systolic blood pressure, pulmonary rales above the bases, or an exacerbation of known ischemic heart disease all predicted complications. This algorithm has been independently validated and strict adherence to the protocol would reduce ICU admissions by 1 6 % , resulting in potentially large cost savings . 59

P o stta c hyc a r d i a T -wave i nversi o n P o s t p a c e m a k e r T -wave i nversi o n I n tr a c r a n i a l p a t h o l o gy (CNS b l e e d s) M i t r a l va lve p r o l a p s e Pericard itis P r i m a ry o r s e c o n d a ry myo c a r d i a l d i s e a s e s P u l m o n a ry e m b o l i s m o r c o r p u l m o n a l e f r o m o t h e r c a u s e s S p o n ta n e o u s p n e u m o t h o r a x Myo c a r d i a l c o n t u s i o n left ve n tr i c u l a r hyp e r t r o p hy P a c e d rhyt h m s left b u n d l e - b r a n c h b l o c k S o u r c e : H o l l a n d e r J E A c u t e c o r o n a ry syn d r o m e s : u n s ta b l e a n g m a , myo c a r d i a l 1 s c h e m 1 a a n d m f a r c t 1 o n I n Tmta n e l l 1 J E , K e l e n G D , Sta pczynsk1 J S , e d s . Emerg e n cy Medrcm e . A Co mprehensrve Study Gurde , 6 t h e d . N ew Y o r k · M c G r aw­ H i l l , 2 0 0 3 · 3 4 3-3 5 2 .

Goldman Risk Score The Goldman risk score was derived through analysis of clinical data on a large cohort of patients presenting to the ED with chest pain. It has been prospectively validated and is useful as an initial risk stratification tool.4 The final algo­ rithm is heavily based on ECG findings and chest pain

ACJ,TIPI The ACI-TIPI is a computer-generated method to deter­ mine the likelihood of AC S at the time of initial clinical evaluation. The ACI-TIPI ECG incorporates age, sex, presence of chest or left arm pain, a chief symptom of chest or left arm pain, pathologic Q waves, and the pres­ ence and degree of ST-segment elevation or depression and T-wave elevation or inversion. It reports the percent likelihood of "acute cardiac ischemia" on the electrocar­ diographic record. Four studies including 5 ,496 patients have found that when combined with physician impres­ sion, the ACI-TIPI has a sensitivity of 8 6 % to 9 5 % and a specificity of 7 8 % to 92 % for predicting AC S . 5 7 When house staff without prior emergency medicine training use the ACI-TIPI, it can speed the time to a disposition deci­ sion. 60 In a study of over 1 0 ,000 patients with potential AC S , in the subset of patients ultimately not felt to have cardiac ischemia, use of ACI-TIPI was associated with a non-statistically significant reduction in coronary care unit (CCU) admissions from 1 5 % to 1 2 % and a slight increase in ED discharges to home from 49 % to 5 2 % .61 The ACI-TIPI h as no t b een widely incorporated into clin­ ical practice in EDs . The ACI-TIPI has not been shown to make a clinically relevant difference in diagnostic accu­ racy compared with contemporary emergency physician judgment.

CHAPTER 3

Yes

77%

98% free from myocardial infarction 10 years later. 130 Repeat car­ diac catheterizations an average of 9 years later found that approximately 90% of patients did not develop even single­ vessel CAD . 1 3 1 Thus, a recent cardiac catheterization with normal or minimally diseased vessels almost eliminates the possibility of an ACS, unlike a recent negative stress test, which is still associated with a 5% event rate at 30 days . 1 2 8

En Disposition

Once other life-threatening conditions have been excluded, patients without definite ACS on the ECG should be risk­ stratified based upon the likelihood that they may have an ACS . The single best tool for the initial risk stratification of chest pain patients is the ECG/ despite the fact that it will

•

A P P R O A C H T O T H E P AT I E N T

37

not identify almost half o f the patients with AMI. Validated tools (such as the TIMI score) should be used rather than simply clinical impression.73

Patients with a < 1 % risk of 30-day adverse events could be released home from the ED withoutfurther diagnostic testing or observation.

Patients with stable anginal patterns do not require inpatient evaluation.73 Patients

P rehospital Pharmacologic Management The AHA Acute Coronary Syndromes algorithm forms the basis for the prehospital treatment of patients with suspected STEMI in most EMS systems (Fig. 1 -7). 2 This algorithm recommends empiric treatment of suspected STEMI patients with oxygen, ASA, nitroglycerin, and morphine sul­ fate if chest discomfort is unrelieved by nitrates. 2 EMS providers should also monitor vital signs and cardiac rhythm and be prepared to provide CPR and prompt defibrillation if necessary. 2

Oxygen

·�·-··· ······························································································· S e e W e b s i t e f o r A H A s c i e n ti f i c s t a t e m e n t

V"

o n p r e h o s p i t a l E CG a n d A CE P p o l i cy s t a t e ­ m e n t o n p r e h o s p i t a l 1 2 - l e a d E CG s .

A number of respected national organizations (includ­ ing the AHA American College of Cardiology, National Association of EMS Physicians , and the National Heart Attack Alert Program) and the ACC/AHA STEMI guide­ lines strongly encourage EMS organizations to implement prehospital 1 2 -lead ECG programs with appropriate med­ ical oversight.5 , 7 1 D espite these endorsements, only a minority of EMS systems currently have 1 2 -lead ECG capability. The national paramedic training curriculum considers 1 2 -lead ECG training as an "enhanced" rather than "core" skillJ ' In the National Registry of Myocardial Infarction (NRMI) , a prehospital 1 2 -lead ECG was recorded in fewer than 1 0 % of STEMI patients . 60•7 2 A recent national survey reported that 67 % of EMS systems in the 2 00 largest U. S . cities have some prehospital ECG equipment and capability.73 Acquisition of a high-quality 1 2 -lead ECG is of para­ mount importance for the effective prehospital triage of patients with suspected ACS symptoms . 54•56•74 Most pre­ hospital ECG devices currently in use throughout the United States are optional "add-on" modules that can be incorporated into a cardiac monitor/defibrillator rather than stand-alone machines. Such integrated devices now cost $9,000 to $2 5 ,000, but the price per unit will likely decrease as use of this technology becomes more com­ monplace. ,

The evidence for routine use of oxygen in ACS patients without evidence of hypoxemia is mixed. Maroko et aU5 were able to demonstrate reduction in infarct size with administration of oxygen in an animal model during acute occlusion of the left anterior descending coronary artery. Madias et al.76 demonstrated improvement in ischemic ECG changes in humans during AMI, but Rawles et al.77 failed to show benefit in a controlled trial of oxygen in uncomplicated AMI patients. However, in the absence of significant harm from the use of oxygen, the AHA guidelines on emergency cardiovas­ cular care recommend administration of oxygen by EMS providers to all suspected ACS patients . 78 In addition, providers should titrate therapy based on oxygen saturation monitoring if the patient is hypoxemic (Sa0 2 >90% ).

Aspirin and Heparin The ACC/STEMI guidelines express concern that advising the public to take an ASA in response to possible STEMI symptoms may be associated with patient delay in calling EMS , as was seen in the NIH-sponsored REACT trial.5 , 3 3 Instead, the guidelines suggest that patients should focus on calling 9 1 1 , which activates the EMS system, where they may receive instructions from emergency medical dispatch­ ers to chew non-enteric coated ASA ( 1 62-3 2 5 mg) while emergency personnel are en route, or emergency personnel can give an ASA while transporting the patient to the hospi­ taJ.S Alternatively, patients can be given ASA soon after has­ pital arrival. Does earlier administration of ASA make a difference? Most paramedic protocols in the United States currently include a dose of chewable ASA (unless contraindicated)

CHAPTER 4

•

C O M M U N I T Y A N D P R E H O S P I T A L S T R AT E G I E S

while en route to the hospital even though published data on the time dependency of ASA therapy are inconclusive. ISIS2 was the first large, international, randomized clinical trial to document the mortality reduction with ASA alone or in combination with fibrinolysis (streptokinase), but there was no evidence that the beneficial effects of ASA were time dependent.79 More recently, Friemark et al.80 studied 1 ,20 0 fibrinolytic-treated STEMI patients and found that patients who received ASA early (before fibrinolytic drug adminis­ tration, n = 3 64) versus late (after fibrinolytic drug admin­ istration, n = 8 3 6) had a lower mortality at 7 days (2 . 5 % vs. 6.0 % , P = 0.0 1 ), 3 0 days (3 . 3 % vs. 7 . 3 % , P = 0.008), and 1 year (5 . 0 % vs . 1 0 . 6 % , P = 0 . 002). Median time from symptom onset to initiation of ASA treatment was signifi­ cantly shorter in early versus late users ( 1 .6 vs. 3 . 5 hours; P 2 mm in the anteroseptal leads, as this in­ creases the specificity for anterior infarctions (see "Electro­ cardiography," below). 22 A new or presumably new bundle­ branch block obscuring ST-segment analysis may also be indicative of STEMI (see "Electrocardiography, " below). 2 3•2 4 If ischemic ST-segment depression or dynamic T-wave changes are found on the ECG, the patient may require aggressive anticoagulant (antiplatelet and antithrombotic) therapy. In summary, triage personnel must maintain high vigi­ lance and a low threshold for consideration of the possibil­ ity of ACS . In the absence of an obvious noncardiac cause for chest discomfort, rapid, triage for possible ACS should be initiated. This also requires that the triage nurse be expe­ rienced in recognizing patients with atypical symptoms, especially in women, the elderly, and diabetic patients.

40

� � 0 :00:

:ll

l0 'i'

.s; it

30

25

20

15 10 5 0

0

2

3

4

5

Number of Recommended TMtlplet '

F I G U R E 5 - 2 • D a ta f r o m t h e CR U S A D E R e g i stry d e m o n st r a t i n g t h e r e l a t i o n s h i p o f m o rt a l i ty to d e g r e e o f r i s k (low/ i n te r m e d i ate/h i g h) a n d to n u m b e r of g u i d e l i n e - r e c o m m e n d e d t h e r a p i e s with i n t h e d e g r e e o f r i s k . M o rt a l i ty r a t e s b y n u m b e r o f a c u t e g u i d e l i n e ­ r e c o m m e n d e d t h e r a p i es r e c e ived b y r i s k g r o u p . T h e r a p i e s = a c u te a s p i r i n , a c u t e b eta b l o c k e r s , a c ute h e p a r i n , G P I I b/ I I I a i n h i b i t o r s , c a r d i a c c a t h e t e r i z a t i o n < 4 8 h o u rs ; B a s e d o n CRUSA D E R i s k S c o r e .

For the potential ACS patient, risk stratification occurs at two parallel yet overlapping levels. First, patients can be strati­ fied into diagnostic categories based on defined clinical, elec­ trocardiographic, and laboratory criteria, which profile a provi­ sional diagnosis (Fig. 5-4). In this scheme patients can also be categorized based upon the initial ECG diagnostic category as having STEMI, other ACS, or possible noncardiac disease, with each category having a separate, implicit potential for adverse outcome. Unfortunately, the selection of the appropri­ ate diagnostic category is not always immediately evident upon arrival of the ACS patient to the ED. Hence, the majority of ACS risk stratification involves differentiating and categorizing the remainder of potential ACS patients (UA, NSTEMI, noncardiac). In this instance, integration of additional clinical TI M I UA Risk Score : 1 °EP at 6

Risk Stratification

0

of the ACS Patient

Risk stratification is the process of categorizing patients according to the severity of their illness, potential for an adverse outcome, and the likelihood of incremental benefit from treatment (see also Chapter 1 ) . The CRUSADE Investigators have evaluated mortality risk stratified by patient risk at presentation (low/intermediate/high), and found a con­ vincing association between the number of guideline-recom­ mended therapies used, patient risk, and mortality (Fig. 5-2). Diagnostic and therapeutic strategies are often linked to this categorization of patients and are tested to result in the best possible outcomes based upon the risk cohort. For example, the TIMI risk score evaluated in the Tactics (TACTICS­ TIMI- 1 8) trial identified patients at intermediate and high risk as benefiting disproportionately from an invasive as opposed to a conservative strategy (Fig. 5-3). 2 5

Risl< Gr0\4) ...._ Low ...._ M oderate ...._ H i gh R isk

35

CONS

0

INV

Cl

OR=0.75 C l (0.57, 1 .00) 20 .3

-

1 1 .8

r---

1 2 .8

,..---

Low

0-2

m os

O R=0.55

(0.33, 0.91 )

30.6

-

1 9 .5

r---

1 6 .1

-

lntermed. 3-4

High

5·7

T I M I Risk S core % o f Pts :

25%

60%

15%

F I G U R E 5 - 3 • B e n efit o f an i n i t i a l i nvasive ve r s u s c o n s e rvative r i s k str a t e gy u s i n g t h e TI M ! r i s k s c o r e i n t h e T A CT I CS -TI M ! 1 8 tr i a l . P a t i e n ts c l a ss i fi e d a s i n t e r m e d i a te t o h i g h r i s k b e n efited f r o m a n i n i t i a l i nvasive strategy c o m p a r e d to t h o s e p a t i e n ts a t l ow r i s k . (F r o m S a b a ti n e M S , M o r r ow D R , G i u g l i a n o R P , e t a l . Circulation 2 0 0 4 ; 1 0 9 [ 7 ] : 8 7 4-8 8 0 , with p e r m i ssi o n . )

CHAPTER 5

•

E M E R G E N C Y D E PA RT M E N T M A N A G E M E N T

67

TA B LE 5 - 2 • Th r o m b o lys i s i n Myo c a r d i a l I n fa r c t i o n (TI M !) R i s k - S c o r i n g Sys t e m f o r U A / N STE M I 0

H i s t o r i c a l A t tr i b u te s

Triage, Focused H & P , ECG

P o i n ts

R g e ;:::: 6 5 ye a r s M o r e t h a n 3 typ i c a l C R D r i s k f a c t o r s

I

K n own C R D (ste n o s i s > 5 0 %)

e

A s p i r i n u s e i n t h e p r e c e d i n g 7 d ays

Other ACS

l

Biomarkers Unstable Angina

P r e s e n t a t i o n A t tr i b u t e s

P o i n ts

2 o r m o r e s eve r e a n g i n a eve n t s i n past 24 hours

l

NSTEMI

F I G U R E 5 - 4 • P a t i e n ts c a n b e s t r a t i f i e d i n t o d i a g n o s t i c c a t e ­ gories that are based upon defined clinical, electroca rdiographic, a n d l a b o r a to ry c r i te r i a .

criteria-described by Braunwald and prospectively vali­ dated-may assist in further risk stratification (see Chapter 1). The usefulness of any risk-stratification scheme derives from how well the system links severity to a specific outcome. There have been numerous attempts at describing the poten­ tial risk of an adverse event for ACS patients by means of a scoring system. The most widely recognized of these systems is the TIMI risk score, which was derived from a large data­ base of ACS patients and validated in several subsequent studies.7 • 19• 2 6• 2 7 A combination of historical and presentation attributes are combined to determine the risk score (Table 5-2). Patients with a score of 0 to 2 are considered at lower risk, while those with scores of 3 to 4 are in an intermediate risk category. A score of 5 to 7 indicates those patients expected to have the highest risk. The TIMI risk score was largely developed from a subgroup of patients at higher risk with either ST-segment depression, positive cardiac troponin, or both. A prospective validation of the system in the setting of unselected ED patients with chest pain revealed a more useful graded assessment of 30day risk of mortality, MI, or the need for urgent revasculariza­ tion in patients presenting with chest pain (Fig. 5-5). 2 8 A limi­ tation in the overall TIMI risk scoring scheme is the paradox that a patient can have a positive troponin but a calculated TIMI risk score of only 1 . While this rarely occurs, it does serve as a reminder that such scores are to be used as a supplement to knowledgeable clinical judgment and not a replacement for it.

Initial Clinical Evaluation From the perspective of the emergency assessment of the ACS patient, there are three major tools integral to the initial risk­ stratification process: a focused history and physical examina­ tion, the ECG, and serum cardiac biomarker determinations

S T s e g m e n t e l evati o n o r d e p r e ssi o n >l mm E l eva t e d c a r d i a c b i o m a r k e rs 'Th e o n t h m e t 1 c s u m of p o s 1t1ve f m d 1 n g s r e l at e s to t h e l i k e l i h o o d of d e ath , myo c a r d i a l I n farcti o n , or u r g e n t revosc u l o m ot 1 o n w1th 1 n 14 d ays. S o u r c e : F r o m A n t m o n E M , Co h e n M, B e r n m k PJ , et o l . The TI M ! r1sk s c o r e f o r u n s ta b l e o n g 1 n o/ n o n -ST e l evo t 1 o n M I · A m e t h o d for p r o g n o st1 c o t 1 0 n a n d t h e r a ­ p e u t i c d e c 1 s 1 o n m o k 1 n g . J A M A 2 0 0 0 ; 2 8 4 (7) : 8 3 5-84 2 .

(Fig. 5-4). These tools are the essential determinants for estab­ lishing a provisional diagnosis for patients with possible ACS. However, there are limitations to the sensitivity and specificity of each of these diagnostic elements, and it is important to interpret the results of these tests in the context of a patient considered to possibly be having an acute event. This requires a Bayesian approach to the evaluation of patients with possible ACS, in which tests are obtained and interpreted based upon a pretest probability assessment. In this way the final diagnos­ tic conclusions are built upon a foundation of relevant clinical evidence and not solely the result of a spurious test abnormal­ ity. Indiscriminate testing, as with ECG and troponin order­ ing, can lead to erroneous conclusions as well as unnecessary treatments and advanced testing (i.e., coronary catheteriza­ tion), all of which have inherent complication potentials, espe­ cially when patients with limited anticipation of benefit are subjected to interventions with potential harm. It is important to develop a realistic balance between concerns over missing an ACS event and the potential harm (and burdens on the health-care system) that overzealous testing can generate.

History and Physical Examination The patient with ACS may present with a variety of symp­ toms-including chest discomfort, referred pain, nausea, vomiting, jaw pain, dyspnea, headache, and light-headedness. Typical stable angina is described as pain that is substernal, occurs on exertion, and is relieved with rest. Patients with these complaints have a greater likelihood of having ACS than patients with none of these features. However, in practice, the presentation is uncommonly classic, and the recognition of a

68

I

p0LLAcK

•

suM MERs

1 00% 90% 80% 70% 60% 50% 40% 30% 20% 1 0% 2

0

N o . o f TI M ! r i s k factors

N 3 0 - d ay d e a th / myo c a r d i a l i n f a r c ti o n / reva s c u l a r i z a t i o n 9 5 % CI

4

3

5

6

_T I M I RISK SCO R E

0

7

2

3

4

5

6

7

1 , 388 2 9 ( 1 2 . 1 %)

1 133 ' 5 7 (5%)

507 5 1 (1 0 . 1 %)

447 8 7 ( 1 9 . 5 %)

231 9 1 (2 2 . 1 %)

102 4 0 (3 9 . 2 %)

20 9 (4 5 %)

1 1 (1 0 0 %)

1 . 4 %-2 . 8 %

3 . 8%-5 . 2 %

7 . 8%-1 2 . 4 %

1 5 . 8%-2 3 . 2 % 1 6 . 8%-2 7 . 4 % 2 9 . 7 %-4 8 . 7 % 2 0 . 9%-6 9 . 1 %

NA

Ch i - s q u a r e p < 0 . 0 0 1 , a n d Co c h r a n - A r m i t a g e t r e n d p < 0 . 0 0 1 . F I G U R E 5 - 5 • R a tes o f m o rt a l i ty, myo c a r d i a l i n f a r c ti o n , a n d r eva s c u l a r i z a t i o n w i t h i n 3 0 d ays o f E D p r e s e n ta t i o n i n u n s e l e c t e d p a t i e n ts w i t h c h est p a i n a s r e l a t e d t o t h e T I M ! r i s k s c o r e . (F r o m P o l l a c k CV J r e t a l . A c a d Em erg Med 2 0 0 6 ; 1 3 [ 1 ] : 1 3-1 8 , w i t h p e r m i ssi o n . )

potential ACS patient from a constellation of symptoms can be difficult, requiring skill in the art of medical history taking. It is extremely important to note that atypical symptoms (pleuritic pain, stabbing or sharp pain, etc.) do not necessarily exclude ACS . In the National Registry of Myocardial Infarction, 3 3 % of patients diagnosed as having an MI did not present with chest pain.3° Chest pain or discomfort descrip­ tions may also be influenced by cultural or geographic settings and might differ from one gender or race to another.3 1 A fail­ ure to recognize atypical symptoms could result in significant delays or failure to provide appropriate treatment.3 2 Chest pain symptoms should probably never be used as the major or sole determining factor in the risk-stratification process . However, concerning symptoms may be combined with other

CLINICAL CLASSIFICATION OF CHEST PAIN Typical angina (definite) 1 . Substernal chest discomfort with a characteristic quality and duration 2 . Provoked by exertion or emotional stress 3 . Relieved by rest or NTG

Atypical angina (probable) Meets two of the above characteristics.

Noncardiac chest pain Meets one or none of the typical anginal characteristics. Source: Modified from Diamond GA. A clinically relevant classification of chest discomfort. ] Am Coil Cardiol 1 98 3 ; 1 (2 Pt 1):574-5 7 5 , with permission.

information, such as predisposing risk factors in the context of a Bayesian approach, to further help make the assessment of overall associated risk. A small subset of ACS patients may present with silent ischemia or "painless" MI and can be exceedingly difficult to identify unless there is a high degree of appropriate clinical sus­ picion.ll This presentation has traditionally has been thought to be more likely in patients with diabetes. The "silent MI" hypothesis is based on the relatively high incidence of ischemic changes noted on screening ECGs in patients with diabetes. However, in a prospective observational study of 528 patients with symptoms suggestive of coronary artery disease on pres­ entation to the ED of a cardiac referral center, the symptoms did not differ significantly in patients with or without dia­ betes.34 The increased frequency of ischemic changes noted on screening ECGs in patients with diabetes may simply reflect their greater baseline prevalence of coronary artery disease. The physical examination in patients with ACS is usu­ ally normal. However, clinical signs of lefr ventricular dys­ function (pulmonary rales, jugular venous distention, S3 gal­ lop, hypotension, mitral regurgitation murmur, etc.) portend an increased risk of a poor outcome. Other physical findings-such as hypoxia, diaphoresis, or an appearance of a mottled skin-may indicate impaired circulation or shock arising from a primary cardiac event. An anxious or fright­ ened appearance in an otherwise reasonable patient may also be a reflection of the severity of the condition. A finding of chest wall tenderness that reproduces the patient's symptom reduces the likelihood of an acute coronary event but should not, by itself, be considered indicative of a noncardiac cause.

CHAPTER 5

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S e e W e b s i t e f o r A CE P ' s c l i n i c a l p o l i cy s ta t e m e n t : " Cr i t i c a l Q u e s t i o n s o n P a t i e n ts S u s p e c t e d with M I . "

Electrocardiography The ECG provides information that helps to stratify the patient's risk of having ACS, establish the diagnosis, and determine the treatment strategy. Even with its noted limi­ tations, the ECG remains the best and most facile tool for the early differentiation of patients with possible ACS . Its diagnostic accuracy is generally enhanced when the ECG is obtained in a patient with ongoing symptoms . 3 5 In the risk-stratification process, the ECG is most important in dif­ ferentiating STEM! from the other possibilities. STEM! should be considered if there is ]-point elevation (origin of the ST segment at its junction with the QRS complex) con­ sistent with myocardial injury. ST-segment deviation is measured 0.04 to 0.06 seconds after the J point, and this defines a sensitivity and specificity for ischemia or injury.

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Myocardial Injury ( ST�Segment Elevation ) "\Vhen there is an injury current of > I mm in two anatomi­ cally contiguous leads, consideration for emergent reperfusion is required. Diagnostic criteria of > I mm (O. I mV) in leads VI to V4 may have reduced specificity for patients with early repolarization, and some evidence supports the use of > 2 mm in the anteroseptal leads as a preferable threshold. 2 1•22

New or Presumably New Bundle�Branch Block The development of a bundle-branch block (right or left) with STEM! increases mortality.36 Patients with left bundle­ branch block (LBBB) have a higher in-hospital mortality complicating STEMI,37 and LBBB obscures the initial and terminal portion of the QRS complex, making identification of a typical injury current difficult. The GUSTO- I investi­ gators, however, proposed that patients with a LBBB having typical ischemic symptoms suggestive of MI and one of three ECG criteria be considered for reperfusion therapy. These criteria include ST elevation of ::::: I mm in leads with a pos­ itive QRS, ST-segment depression ::::: I mm in leads VI to V3 , and ST-segment elevation ::::: 5 mm in leads with a

A

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F I G U R E 5 - 6 • A. 1 2 - l e a d ECG with r i g h t b u n d l e - b r a n c h b l o c k ( R B B B) a n d ST-se g m e n t e l ev a ti o n c o n ­ siste n t with a c u t e myo c a r d i a l i n f a r c ti o n . T h e r e i s e l eva t i o n o f t h e S T s e g m e n t i n p r e c o r d i a l l e a d s V1 to V6 a n d l a t e r a l l e a d s 1 a n d aVL. B. For c o m p a r i s o n , l e a d s V1 to V3 f r o m p a t i e n t with R B B B a n d s e c ­ o n d a ry r e p o l a r i z o t i o n c h a n g e s w i t h o u t a c u te myo c a r d i a l i n f a r c ti o n .

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negative QRS . 3 8•39 The determination of "new" left bundle­ branch block is frequently difficult unless there is a readily available old ECG for comparison. When such evidence is lacking and the diagnosis is uncertain, percutaneous inter­ vention (PCI) has been proposed as preferable to fibrinolytic therapy when PCI can be performed in a timely fashion. Right bundle-branch block (RBBB) obscures only the terminal portion of the QRS complex; therefore identifica­ tion of STEMI can be made by physicians experienced in the interpretation of the 1 2 -lead ECG (Fig. 5 -6).

ST�Segment Depression Consistent With High�Risk Unstable Angina/NSTEMI Patients presenting with ischemic ST-segment depression also have an increased risk for major adverse cardiac events. In the TIMI IIIB registry of patients with unstable angina/non-Q wave MI, 60% of patients had no ECG changes and were at lower risk than those with 1 -mm ST-segment depression, who had an 1 1 % 1 -year rate of death or nonfatal MI.40 In this reg­ istry, patients with only 0.5-mm ST-segment depression had a similar prognosis. In this study T-wave inversion was not help­ ful, but other investigators have found that in patients sus­ pected of ACS, T-wave inversion of > 2 mm in leads with pos­ itive R waves or deep symmetric anterior T-wave inversion suggested acute ischemia.41•42

Nondiagnostic or Normal ECG T-wave inversion s2 mm is nonspecific unless changes occur with chest discomfort and are dynamic. The ECG is currently our best but an imprecise tool for the early detection of ischemia, and as many as 1 0 % of ACS patients may present with a normal ECG.43 Therefore, a normal ECG should not be used to reliably exclude the diagnosis of ACS, especially among patients with a higher pretest probability of disease. Finally, when the initial ECG is nondiagnostic or equivo­ cal, ACC/AHA guidelines recommend repeating the ECG at 5- to 1 0-minute intervals (or using a continuous recording) if there is a high clinical index of suspicion for STEMI. In addi­ tion, a repeat ECG should be performed with recurrent chest discomfort and with resolution of symptoms. This may be a diagnostic opportunity for patients suspected of having ACS .

Biomarkers Determinations of serum cardiac biomarkers play a central role in the diagnosis of acute MI (AMI) and in the differen­ tiation of ACS subtypes. It is extremely important to under­ stand the nuances and limitations of these tests if they are to be used effectively44 (Fig. 5 -7).

..... ........ ..... ................... .......... ................... ............................... ...

S e e W e b s i t e f o r A CC/ A H A g u i d e l i n e s f o r u n s ta b l e a n g i n a a n d N STE M I : " Ca r d i a c Biomarkers of Necrosis a n d the Redefinition of AMI. "45

•

• •

Cardiac biomarkers should be measured in all patients who present with chest discomfort consistent with ACS . A cardiac-specific troponin i s the preferred marker. Patients with negative biomarkers within 6 hours of pain onset should have repeat markers 8-1 2 hours later taking into consideration uncertainties present with timing exact onset of pain and the institutional norms for marker assays.

Myoglobin Myoglobin is a low-molecular-weight protein that is present in both cardiac and skeletal muscle and may be detected in elevated levels in the serum as early as 2 hours after myocar­ dial necrosis begins.46 However, because of its poor cardiac specificity,47 myoglobin should be used only in conjunction with other serum markers to confirm a diagnosis of MI. Myoglobin does have a high sensitivity, which makes it most

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F I G U R E 5 - 7 • Ca r d i a c b i o m a r k e r s a n d r e c o m m e n d a t i o n s f o r s e r i a l m e a s u r e m e n t a n d d i a g n o s i s o f myo c a r d i a l i n f a r c ti o n . T h e b i o ­ m a r k e rs a r e p l otted s h o wi n g t h e m u l ti p l es o f t h e c u t o ff f o r a c u t e myo c a r d i a l i n f a r c t i o n (A M I) o v e r ti m e . T h e d a s h e d h o r i z o n ­ t a l l i n e s h ows t h e u p p e r l i m i t o f n o r m a l (ULN ; d e fi n e d a s t h e 9 9 t h p e r c e n t i l e f r o m a n o r m a l r e f e r e n c e p o p u l a t i o n wi t h o u t myo c a r d i a l n e c r o s i s ; t h e c o effi c i e n t o f va r i a t i o n o f t h e a ssay s h o u l d b e :s l O %) . T h e e a r l i est r i si n g b i o m a r k e r s a r e myo g l o b i n a n d CK i s o ­ f o r m s ( l e f t m o s t c u rve) . C K - M B (dash e d curve) r i s e s to a p e a k o f two to five t i m e s t h e U LN a n d typ i c a l ly r e t u r n s to t h e n o r m a l r a n g e with i n 2 t o 3 d ays after A M I . T h e c a r d i a c - s p e c i f i c tr o p o n i n s s h ow s m a l l e l eva t i o n s a b ove t h e U LN i n s m a l l i n f a r cti o n s ( e . g . , a s i s often t h e c a s e with NST E M I) b u t r i s e t o 2 0- 5 0 t i m es t h e U LN i n t h e setti n g o f I o r g e i n f a r c t i o n s (e. g . , a s i s typ i c a l ly t h e c a s e i n STE M I ) . T h e tr o p o n i n l eve l s m ay stay e l ev a t e d a b ove t h e U LN f o r 7 d ays o r m o r e a ft e r A M I . CK , c r e a t i n e k i n a s e ; CK- M B , M B f r a c t i o n o f c r e a ti n e k i n a s e ; CV, c o effi c i e n t o f va r i a ti o n ; M I , myo c a r d i a l i n f a r c ti o n ; NSTE M I , n o n-ST- e l eva t i o n myo c a r d i a l i n f a r c ti o n ; U A / NSTE M I , u n s ta b l e o n g i n o / n o n-ST - e l eva t i o n myo c a r d i a l i n f a r c ­ t i o n . (M o d i f i e d f r o m S h a p i r o B P , J a ffe A S . Ca r d i a c b i o m a r k e r s . I n : M u r p hy J G , Ll oyd M A , e d i t o r s . Mayo Clinic Cardiology: Con cise Textb o o k . 3 r d e d . R o c h este r , M N : M ayo Cl i n i c S c i e n ti f i c P r ess a n d N ew Yo r k : I n fo r m a H e a l t h c o r e U S A , 2 0 0 7 : 7 7 3-8 0 . U s e d with p e r ­ m i ssi o n o f M ayo F o u n d a ti o n f o r M e d i c a l E d u c a t i o n a n d R e se a r c h . )

CHAPTER 5

useful for excluding MI if the level is normal after the first few hours of symptom onset. From the perspective of the risk-stratification process, myoglobin levels should only enter in the decision-making process in low-risk patients who present very early in their symptomatic course, when more specific tests may still be normal.

CK and CK�MB Creatine kinase (CK) is a ubiquitous enzyme that is found in striated muscle and tissues of the brain, kidney, lung, and gas­ trointestinal tract. This biomarker has low sensitivity and speci­ ficity for cardiac damage and may be commonly elevated in noncardiac conditions such as trauma, seizures, and hyperther­ mia. The CK-MB isoenzyme of CK is much more cardiac-spe­ cific than CK alone and may be useful in the early diagnosis of AMI.47 CK-MB typically is detectable in the serum 4 to 6 hours after the onset of infarction, peaks in 1 2 to 24 hours, and nor­ malizes in 2 to 3 days. Since some small percentage of CK-MB exists in non cardiac tissues, the ratio of CK-MB to CK > 5 % is usually used in conjunction with the total elevation of CK to determine tl1e likelihood of a cardiac origin. Since elderly patients typically have less muscle mass, it is possible to see a rise in the ratio of CK-MB to CK even when the total CK is normal. These conditions and other comorbid states that might affect CK measurements have limited the specificity of the test, and its value has recently diminished in importance in the risk­ stratification process. However, since CK and CK-MB values normalize in 2 to 3 days after an infarction and up to 1 week before troponin normalizes, CK and CK-MB can be useful for detecting a new MI in a returning ACS patient whose troponin has not yet normalized from a recent infarct. CK-MB may be further characterized into subforms or isoforms. CK-MB2 is almost exclusively found in myocar­ dial tissue, while CK-MB 1 is more common in the plasma. Measurement of the isoforms of CK-MB greatly improves the specificity of the test. However, the CK-MB subform assay has not found widespread adoption.

Troponin Of all the currently available cardiac biomarkers, the troponins have had the greatest impact on ACS risk stratification, and they are considered the preferred markers for the diagnosis of myocardial injury.48 Troponins (T, I, C) are found in both stri­ ated and cardiac muscle, but the cardiac isoforms of troponin T and I differ structurally from those of skeletal muscle, and hence elevations of serum levels of these isoforms above nor­ mal are very specific for myocardial necrosis. Troponin I has been found to be slightly more specific than troponin T, mainly due to fewer false-positive errors, and therefore has been more commonly used over the past few years. There is a possibility of false-positive (for ACS) troponins (both I and T levels) in patients with renal disease, polymyositis, dermato­ myositis, pulmonary embolism, congestive heart failure, or in those with positive rheumatoid factor or with heterophilic antibodies of a murine nature.44 It is important that the clini­ cian not presuppose that elevated troponins are falsely positive in these conditions, because these patients can also have an ongoing ACS event. Serial measurements should indicate a

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time-dependent increase in the levels of the troponin values if there is truly an acutely evolving cardiac event. Troponin measurements are often used in the ED setting to help identify low-risk patients who may be sent home with close follow-up. The experimental evidence to support this widespread practice is not definitive and is very case-dependent. The cardiac troponins historically were measured upon admission to the ED and repeated every 4 to 6 hours for up to 12 hours or more.49 At 12 hours, the sensitivity of troponin to discern myocardial injury is >90% in most studies, and many clinicians like to use this evidence to risk-stratify patients.44•47•48•49 It is important to remember that troponins may never be elevated with unstable angina or ischemia with­ out infarction by definition. These patients are also at risk of progression to MI or death. Hence, it is always necessary to consider this information only in the context of a sequential risk-stratification process and the complete patient profile. A provocative test such as a nuclear scan or exercise stress test should be considered to further risk-stratify this patient group. Patients with a normal CK-MB level but an elevated tro­ ponin at low levels have traditionally been considered to have sustained minor myocardial damage or "myocardial leak. " These patients have myocyte necrosis and are still at least at intermediate risk, so careful consideration should be given to their management. The cardiac troponins may remain ele­ vated for up to 2 weeks after MI, which makes them useful as late markers of an ACS event. An elevated troponin level is also useful in the early identification of patients at increased risk for death. There is an increasing risk of morbidity and mortality that is directly related to the absolute serum troponin level. In those cases where CK-MB and troponin assay results are dis­ cordant, an elevated troponin portends a poorer prognosis. 5°

Other Biomarkers The ideal biomarker for use in the risk-stratification process would be one that would appear in the serum within minutes of the onset of the cardiac event and stay elevated for at least 6 to 8 hours. This biomarker would also be very specific for the myocardium and be elevated in response to ischemia prior to the occurrence of infarction. No such biomarker currently exists, despite many forthcoming contenders. The only bio­ marker approved by the FDA for ischemia risk stratification is ischemia-modified albumin (IMA), detected by the albumin cobalt binding (ACB) test.5 1 However, this marker lacks tl1e specificity needed to rule-in ischemia and is relevant in ED risk stratification only as a rule-out tool in patients at very low risk. There is concern that a high false-positive rate may result in harmful treatments and the performance of testing in patients who might otl1erwise have been sent home. Most other "ischemia" biomarkers (C-reactive protein [CRP] , fatty acid-binding protein [FABP] levels, etc.) are in actuality indi­ cators only of an increased risk of atherosclerosis or inflam­ matory conditions that may be associated with plaque rupture. However, they do not directly indicate that the patient is pre­ senting because of an acute ACS event. The appearance of a true ischemia biomarker with ready utility in the ED setting would be a revolutionary development in tl1e early risk strat­ ification of the potential ACS patient.

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Adjunctive Tests

Nuclear Imaging

�ile it is most important to identify the ACS patient from the large number of patients who present to the ED with potential cardiac symptoms, it is often left to the ED physi­ cian ultimately to decide which patients can be safely sent home for an outpatient evaluation. The combination of results from the history, physical exam, ECG, and biomarker determinations are sometimes inadequate to allow for a safe and timely disposition. A number of adjunctive tests have been developed to improve the risk-stratification process. �ile these adjunctive studies have definitely improved the overall disposition decisions of these patients, their use is often limited by logistic complexities and time limitations within the ED framework.

A significant number of studies over the past two decades have examined the ability of early myocardial perfusion imaging (MPI) using technetium-99m sestamibi to risk-stratify poten­ tial ACS patients who present to the ED with nondiagnostic ECGs and negative cardiac biomarkers.57 A positive test has been found to accurately identify patients at high risk for adverse cardiac outcomes, whereas a negative MPI identifies a very low-risk patient group.57 Both rest and stress MPI stud­ ies (depending on the timing of the test after the termination of symptoms) are now considered important endpoints in the risk stratification of these patients. 57 Unfortunately, the avail­ ability of this testing is limited and resource-intensive in most hospitals, and the use of this testing has not resulted in more timely ED dispositions in most cases.

Stress Testing Based upon many years of outpatient experience, 1 2 -lead ECG exercise testing has been introduced into the ED as a tool for risk stratification and the evaluation of patients pre­ senting to the ED with possible ACS . Typically the process begins by identifying low-risk ACS patients with repeated negative or nonspecific ECG and serial cardiac biomarkers. If there is still some doubt about the state of these patients, provocative testing using a standardized exercise stress test can be used to determine their potential risk of developing an ischemic event if discharged. The length of time involved in the initial portion of the risk-stratification protocol usu­ ally results in this group of patients being admitted to the hospital telemetry floor or to some rype of "chest pain unit. " Clinical trials that have studied the practical implementation of these protocols have found that they effectively reduce the need for hospitalization of a significant number of patients without an increase in risk of mortality. 5 2 There is also evi­ dence that this testing can be accurately performed and interpreted by physicians other than cardiologists who are trained and experienced in functional testing, making this approach even more resource-efficient if it can be accom­ plished in the ED .53

Computed Tomography Coronary Angiography There has recently been a consideration of incorporating high-resolution coronary CT angiography (64-slice) into the evaluation of low-risk patients (TIMI score > 2) pre­ senting to the ED with chest pain. 54• 55 The advantage of this study over other methodologies lies in its ease and rapidity of use. Early studies suggest that using this technology may safely allow ED physicians to discharge low-risk patients with negative studies in a timely fashion and without an increased risk of mortality. However, there may currently be some limitations to the widespread adoption of this testing due to the cost of the special equipment used, expertise required to interpret the results, high radiation exposure, and clinical application. Newer imaging modalities are undergoing clinical validation and application at this time. Coronary CT angiography may have a particular utility in acute chest pain syndromes with an intermediate probability of disease, normal or nondiagnostic ECG, and negative car­ diac biomarkers.56

S electing a Strategy and

Initiating Treatment

The appropriate triage and risk stratification of patients pre­ senting to the ED with symptoms suggestive of an acute coronary event remains a continuing challenge for the ED physician. A low threshold for admission has been the stan­ dard because of heightened concern for adverse patient out­ comes and the litigation potential associated with the inad­ vertent discharge of a patient having an ischemic event. This trend toward caution has resulted in a system in which fewer than 3 0 % of patients admitted for chest pain are ultimately determined to have ACS.58 The costs and resource demands required by this inefficient practice are of great concern to many in the health care industry and government. In order to reduce unnecessary admissions while preserving patient safety, a number of protocols and strategies have been applied to the risk stratification of ED patients with chest pain syndrome. These strategies have evolved as new tests and methods have been developed. The first charge of the ED physician is the early recogni­ tion of the STEM! patient, using ECG criteria to initiate timely treatment. After this group is identified, the next step is to differentiate the high-risk ACS patient (rypically with NSTEMI or severe UA) from the remainder of the chest pain population. ECG changes indicative of ischemia, with or without a positive biomarker, may help to define this patient, but are not uniformly present. �ile it is presently uncertain what time frame is required to make this determination of high risk, it is intuitively evident that an early management strategy should result in improved outcomes. Identification of patients with variable levels of risk and appropriate application of strategies, resources, and evolving diagnostic modalities will improve both patient outcomes and resource utilization. Despite all of the available diagnostic aids, ultimately the integration of clinical information and medical decision making will be the responsibility of the physician. This requires both experience and a broad-based knowledge of the disease process and the diagnostic tools used to differ­ entiate the patient's condition. A systematic approach to patient evaluation should include a sequential risk prediction

CHAPTER 5

or probability assessment as performed by the clinician using the focused history, initial ECG, and cardiac biomarkers dis­ cussed above. Based upon the results of these tests and the pretest probability of ACS, further treatment or diagnosis is indicated. Patients with definite high-risk features should not undergo functional testing until stabilized. Others will have expeditious testing or appropriate designated follow-up based upon clinical assessment and exclusion of MI.

General Measures and Aspirin Once patients are identified as having, or likely having, ACS, specific pharmacologic management should be initiated in a risk-appropriate fashion. Patients at higher presumed ACS risk should generally receive more intensive therapy. However, with escalation of therapy comes increased risk (e.g., anticoagulant-related bleeding). Therefore, treatment of ACS must be individualized for each patient and each pres­ entation based on the balancing of potential efficacy with risk. All patients without contraindications, even those with suspected ACS, should be given aspirin (ASA) as soon as possible after presentation. ASA acts as an antiplatelet agent and as such is considered in more detail below. Other general measures include routine telemetry monitoring (for rhythm disturbances and identification of ST-segment changes) and application of supplementary oxygen and pulse oximetry. Ischemia and its common clinical manifestation-chest pain-are treated with nitroglycerin, and with morphine if pain is unrelieved by nitrates and oxygen. Based upon data from the CRUSADE registry, a caution with the use of mor­ phine has been introduced with the recent update (2 007) of the ACC/AHA guidelines; its strength of recommendation was reduced to class IIa from class I.59

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S e e W e b s i t e f o r A CC/ A H A g u i d e l i n e s f o r u n s ta b l e a n g i n a a n d N STE M I : " G e n e r a l Ca r e . " 4 5

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Nitrates Nitroglycerin (NTG) reduces myocardial oxygen demand and improves myocardial oxygen delivery through periph­ eral and coronary vascular effects that reduce both preload and afterload. It is thought that NTG promotes not only the dilation of large coronary arteries but also collateral flow that may reach ischemic regions . NTG should be ini­ tially administered by sublingual tablets (0 .4 mg) or spray, with up to three doses every 5 minutes . Absolute con­ traindications to NTG use include hypotension, obvious volume depletion, clinical or electrocardiographic concern for right ventricular ischemia/infarction, myocardial wall ischemia, or recent use of phosphodiesterase inhibitors (e .g. Viagra, Cialis, and Levitra) for erectile dysfunction.45 Nitrates can also be administered topically in patients without ongoing significant symptoms or risk of hemody-

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namic instability. NTG can be given intravenously to normotensive patients at an initial rate of 5 to 1 0 f.Lg/min and then increased by 1 0 f.Lg/min every 3 to 5 minutes until a symptomatic or blood pressure response is evident. However, blood pressure should generally not be reduced to < 1 1 0 mm Hg in patients who were previously nor­ motensive or to > 2 5 % below the starting mean arterial blood pressure if hypertension was present. Side effects of nitrates include headache and hypoten­ sion. Tolerance to the drug may develop. It is thought that NTG alone does not exert a beneficial effect on mortality in ACS , but its salutary effects on ischemic symptoms and ele­ vated blood pressure keep it firmly in the pharmacologic armamentarium for ACS patients with chest pain.35

Morphine Sulfate In patients whose ischemic symptoms are incompletely relieved by nitrates, morphine sulfate ( 1 -5 mg IV) is rea­ sonable. Acting as both an analgesic and an anxiolytic, it also is a venodilator and therefore may lead to symptomatic benefit for patients with pulmonary congestion as well . Potential adverse effects include hypotension, pruritus, nausea and vomiting, and diminished respiratory drive .45 There have been no randomized controlled trials to advise clinicians on the contribution of morphine to ACS out­ comes or on optimal dosing regimens. Data from a con­ temporary registry, however, suggest that the use of mor­ phine in NSTE AC S patients may actually increase short-term mortality, even after adjustment for risk and other medications. 59 This being said, there are no good data regarding alter­ native analgesics for ACS pain either. In the presence of per­ sistent pain despite nitrates, the emergency physician should: 1 . Consider alternative diagnoses if there is no obj ective evidence of ischemia or infarction. 2. Consider administration of beta-blockers if not already given and there are no contraindications. 3 . Initiate cardiology consultation for coronary angiog­ raphy and PCI with pain refractory to initial manage­ ment.

Morphine sulfate ( 1 -5 mg IV) is reasonable for patients whose symptoms are not relieved despite NTG (e.g., after 3 serial sublingual NTG tablets) or whose symptoms recur despite adequate anti­ ischemic therapy. A cautionary note on morphine use has been raised by data from a large observational registry. Patients in this registry receiving morphine (3 0%) had a higher adjusted likelihood of death, which persisted across all subgroups. 59 Although subject to uncontrolled selection biases, these results raise a safety concern and suggest the need for a randomized trial. Meanwhile, the writing commitree has downgraded the recommendation for morphine use for uncontrolled ischemic chest discomfort from a class I to a class Ila (Updated 2 00 7 ACCIAHA Guidelines Recommendations).

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Beta .. Adrenergic Blocking Agents B eta-adrenergic blockers improved both morbidity and mortality in early ACS clinical trials, but an early mortality benefit was questioned in the reperfusion era in STEMI patients (see below) . These drugs inhibit the effect of cate­ cholamines on the myocardium, resulting in reduced cardiac work and oxygen consumption. They also reduce blood pressure and, by increasing the duration of diastole, improve coronary blood flow. Oral beta-blockers should be administered early for ACS of all types unless contraindications are present. Beta­ blockers may also be beneficial for NSTEMI. They should be given irrespective of the need for revascularization ther­ apies (class I).

·�····· ······························································································· S e e W e b s i t e f o r A CC/A H A f o c u s e d g u i d e l i n e s

�

u p d a te f o r ST E M I : " b e t a - b l o c k e r s . " 4 5

UPDATED RECOMMENDATIONS FOR BETA-BLOCKING AGENTS (STEM!)

Recommendation for oral beta-adrenergic blockade early in STEMI (class I recommendation; level of evidence changed from A to B): Oral beta blockade should be initiated within first 24 hours in STEM! to patients not at high risk" without any of the following: Signs of heart failure Evidence of low output state Increased risk for cardiogenic shock Other relative contraindications Patients with early contraindication to beta blockade should be reevaluated for candidacy for secondary prevention before discharge. Patients with moderate to severe heart failure should receive beta blockade as secondary prevention with a gradual titration scheme. • • • •

Recommendation for W beta-adrenergic blockade early in STEMI (class II recommendation; level of evidence changed from A to B): •

Reasonable to administer IV beta blockade to patients who are

hypaunsive and who do not have •

The above recommendations were largely based on studies evaluating IV beta blockade in patients receiving fibrinolytic therapy. In patients who receive fibrinolytic agents, IV beta-blockers decrease postinfarction ischemia and nonfatal AMI . A small but significant decrease in death and nonfatal infarction has been obs erved in patients treate d with beta-blockers very soon after the onset of symtpoms . 6; In-hospital administration of beta blockers may reduce the size of the infarct, and mortality in patients who do not receive fibrinolytic therapy.60 Beta­ blockers also reduce the incidence of ventricular ectopy and fibrillation. 66 These data were largely observed during clinical trials before the "reperfusion era . " But subsequent studies and reviews did not fu1d reductions in mortality.67-69 IV beta-blockers are often administered in the ED using a dose regimen from the Metoprolol in Acute Myocardial Infarction (MIAMI) trial. 70 To assess modern use, the Clopidogrel and Metoprolol in Myocardial Infarction Trial (COMMIT CCS2) trial studied the admini­ stration of the usual dosing-metoprolol 5 mg IV over 1 5 minutes. 7 1 In COMMIT CCS2 there was no benefit of early administration of iV beta-blockers (Fig. 5 -8). An analysis of prespecified subgroups showed that about 1 0 lives per 1 ,000 were saved by a reduction in ventricular fibrillation (VF) and recurrent MI, but this benefit was offset by an increase in patient death from cardiogenic shock. Lives lost from cardiogenic shock increased with increasing Killip class, likely as a result of an increase in death from heart failure, since left ventricular dysfunction (LVD) increases with infarct size. For this reason careful attention should be given to treating patients with congestive heart failure. A tachycardia in these patients may be compensatory, as heart rate compensates for impaired and decreased stroke volume due to infarction.

• • •

Signs of heart failure Evidence of low-output state Increased risk for cardiogenic shock O ther relative contraindications

IV Beta-adrenergic blockade class III (new recommendation)

2007

IV beta blockade should not be administered to patients who have

any of the following: Signs of heart failure Evidence of low-output state Risk factors for cardiogenic shock" Other relative contraindications: PR interval >0.24 second or higher AV block, active asthma, or reactive airway disease •

•

• •

'Risk factors for cardiogeruc shock include • Age > 70 years • SBP < 1 2 0 mm Tlg • Heart rate > 1 1 0/min or 0 . 2 4 seconds, second- or third­ degree heart block, active asthma, or reactive airway dis­ ease). For patients with severe hypertension, metoprolol may be given intravenously in 5 -mg increments repeated every 5 minutes for a total initial dose of 1 5 mg in the absence of contraindications or clinical evidence of heart failure .

CHAPTER 5

11 10 9Placebo 1 797 deaths (7. 8%)

8

� �·

7

Metaprobl : 1 774 deaths (7.7%)

654

1 % (SE3) proportional risk red uction (p=0 . 7)

r

J

:J

•

E M E R G E N C Y D E PA RT M E N T M A N A G E M E N T

action derives primarily from its irreversible inhibition of cyclo-oxygenase (COX- 1 ) within platelets, which in turn prevents the formation of thromboxane A2 and diminishes platelet aggregation; ASA also likely exerts an additional (though less well defined) intravascular anti-inflammatory effect.73 The benefit of ASA therapy is apparent early and persists with regular dosing.74 Although the optimal dose of ASA has not been established in clinical trials, doses from 1 62 to 3 2 5 mg have generally been employed. Acute doses of > 3 2 5 mg may reduce cardiac morbidity and mortality, but only with an increased risk of stroke; the currently recom­ mended ED dose for ACS is 1 62 to 3 2 5 mg.l5 Nonenteric formulations should be used to promote rapid absorption and activity and a rectal suppository is available for patients intol­ erant of oral medications. IV ASA is not available in the U. S .

. . ..

...... .. .

0 --------,--.--,--, 7 14 21 0 28

75

. ... .

........ ..

. .....

..

...........

..

.

....... .....................................

S e e We b s i t e f o r A CC/ A H A fo c u s e d g u i d e l i n e s u p d a t e f o r STE M I a n d U A / N STE M I : " A n t i p l a t e l e t a n d A n t i c o a g u l a n t Th e r a py. " 4 5

.

Ti me since randomisation (days) Days N u mber of events Metoprolol Placebo

0-6

7-1 3

1 4-20

2 1 -28

1 44 1 1 449

220 249

83 75

30 24

F I G U R E 5 - 8 • E ff e c ts o f m e to p r o l o l a l l o c a t i o n on d e a t h b e f o r e f i r s t d i s c h a r g e fr o m h o s p i t a l i n t h e C O M M ITT CCS 2 Tr i a l . (Re p r i n te d w i t h p e r m issi o n f r o m Ch e n Z M e t a l . Lan c e t 2 0 0 5 ; 3 6 6 : 1 6 2 2-1 6 3 2 , w i t h p e r m i ssi o n . )

Other Pharmacologic Measures Angiotensin converting enzyme inhibitor (ACE-I) ther­ apy has been shown to have a significant benefit in the chronic management of patients with coronary artery dis­ ease and left ventricular dysfunction (LVD) .45 In the acute ACS setting, this should be considered in patients with evi­ dence of LVD, especially diabetic patients. ACE-I can also be used to control blood pressure not adequately responsive to nitrates and beta-blockers . However, they are usually administered after the patient has received reperfusion ther­ apy (if STEMI) and is hemodynamically stable . In most instances, the initiation of ACE-I therapy is not a consider­ ation in early ED management. Calcium antagonists have a limited (if any) role in the early management of ACS , being useful primarily when hypertension is unresponsive to nitrates and beta blockers. Verapamil and diltiazem are the best choices in this class because they tend to slow the heart rateY

Antiplatelet Therapy Perhaps the best data for a long-term beneficial effect of drug treatment in ACS exists for aspirin (ASA). Its mechanism of

The 2 007 focused update o f the ACC/AHA 2004 STEMI guidelines recommend the administration of a proton-pump inhibitor if the patient has history of GI bleed or GI intoler­ ance. Patients already anticoagulated with warfarin should receive ASA if suspected of having ACS unless there is concern for serious coagulopathy, because the antiplatelet effect of ASA is considered beneficial over and above anticoagulation.

The selection, use, and patient risk stratification for antiplatelet and anticoagulant therapy is complex. In addition, clinical trials and information continue to evolve. An institutional interdisciplinary guideline provides the best framework for health care providers and ED physicians to approach the initial and continuing care of individual patients.

Clopidogrel Clopidogrel should be given to those patients with hyper­ sensitivity or maj or gastrointestinal intolerance to ASA. This is rare in the ED , where the more typical approach would be to consider administration of clopidogrel in addi­ tion to ASA. Clopidogrel monotherapy was compared to ASA in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial and was found to be at least as effective as the latter. 76 Nonetheless, clopidogrel is even more effective in combination with ASA, as shown in the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial, which randomized 1 2 , 5 62 patients with UA/NSTEMI either to ASA monotherapy or dual antiplatelet therapy with ASA plus clopidogrel (3 00-mg loading dose, followed by 7 5 mg/day for 3 - 1 2 months) and showed a reduction in ischemic and composite endpoints­ including death, nonfatal MI, and stroke-favoring the

76

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combination arm.77 Patients in the combination arm expe­ rienced significantly more maj or bleeding (3 . 7 % vs . 2 . 7 % in the ASA monotherapy group) and more minor bleeding but no excess of life-threatening bleeding. The net effect of adding clopidogrel to ASA was positive, and this has been supported by contemporary ACS registry data.78 However, there are limitations of the CURE data for U. S . practice, in that invasive management was rare in the trial, platelet gly­ coprotein lib/Ilia receptor inhibitors (GPis) were only rarely used, and coronary artery bypass grafting (CABG)­ for which the use of clopidogrel clearly increases bleeding risk-was not often performed. For those ACS patients in whom a noninterventional approach is planned, CURE provides very strong evidence for the addition of clopido­ grel to ASA. D ata on patients enrolled in CURE who underwent percutaneous coronary intervention (PCI) were reported in a secondary observational substudy analysis called PCI­ CURE.79 In this group the addition of clopidogrel led to similar ischemic advantages as in the overall study. Overall there was a statistically significant 3 1 % reduction in cardio­ vascular death or MI. An overall assessment of the strategy of preloading UA/NSTEMI patients with clopidogrel, man­ aging them with PCI, and then continuing dual therapy for 1 year showed it to be both clinically reasonable and cost­ effective.80 The optimal timing for a loading dose of clopidogrel in UA/NSTEMI management has not been determined. Although there is evidence for a benefit from the loading dose alone (there is a significant reduction in the composite of death, MI, and stroke evident within 24 hours),81 loading with clopidogrel appears to also be associated with an increased bleeding risk among those patients going to CABG within 5 days of clopidogrel administration. Given this increased risk of bleeding at CABG and the difficulty in iden­ tifying early which patients will ultimately require CABG, enthusiasm for loading the drug prior to diagnostic angiog­ raphy peiformed expeditiously has been limited. The longer the delay to angiography, the more benefit can be expected from early loading and daily administration. This approach was supported prospectively by the Clopidogrel for the Reduction of Events During Observation (CREDO) trial.8 2 Clopidogrel in STEMI-Updated Recommendations Clopidogrel irreversibly inhibits the platelet adenosine diphosphate receptor (ADP), resulting in a reduction in platelet aggregation through a different mechanism than aspirin. Since the publication of ECC guidelines in 20 0 5, several important clopidogrel studies have been published and reviewed by the ACC/AHA STEM! writing group; these document its efficacy for patients with STEM!. It was recently approved by the FDA for use in patients with STEM!, either with or without fibrinolytic therapy. Approval was based on results of the Clopidogrel as Adjunctive Reperfusion Therapy (CLARITY-TIM! 2 8) and COMMIT CCS-2 trials, which demonstrated increased effi­ cacy of dual therapy with aspirin with no increase in intra­ cerebral hemorrhage.

UPDATED RECOMMENDATIONS FOR CLOPIDOGREL Patients undergoing reperfusion wim fibrinolytic agents and those not receiving repe1fusion should receive combination antiplatelet merapy wim hom aspirin and clopidogrel.

Recommendation for adjunctive use with fibrinolytics •

•

Clopidogrel 7 5 mg oral daily maintenance dose A loading dose of 3 00 mg was administered in CLARITY TIMI-2 8 , but • Efficacy and safety not demonstrated in patients ?: 7 5 years of age • Patients receiving bolus 4,000 IU heparin dose were excluded

Recommendation for adjunctive use without repetfusion •

•

Clopidogrel 7 5 mg oral daily maintenance dose A loading dose of 3 00 mg was administered in CLARITY TIMI-2 8 , but • Efficacy and safety not demonstrated in patients ?:7 5 years of age • Patients receiving bolus 4,000 IU heparin dose were excluded

No recommendation for adjunctive use upstream from PCI No recommendation was made for upstream use prior to PCI, but it was noted mat clopidogrel appears to be beneficial when PCI is subsequently performed in patients receiving prior fibrinolytic merapy.

In patients up to 7 5 years of age with STEM! who are treated with fibrinolysis, aspirin, and heparin (low-molec­ ular-weight heparin [LMWH] or unfractionated heparin [UFH]), a 3 00-mg oral loading dose of clopidogrel given at the time of initial management (followed by a 7 5 -mg daily dose for up to 8 days in hospital) improved coronary artery patency and reduced maj or adverse cardiovascular events (MACE) . 1 55 The COMMIT trial,67 which included more than 45 ,000 patients, found that those receiving clopido­ grel 7 5 mg had a highly significant 9% reduction in death, reinfarction, or stroke, corresponding to 9 fewer events per 1 , 000 patients treated for only about 2 weeks . There was also no increase in intracerebral hemorrhage . Based on these findings, providers should administer a 3 00-mg oral dose of clopidogrel to ED patients up to 7 5 years of age with STEM! who receive aspirin, anticoagulation, and fib­ rinolysis. The 2 007 Focused Update of the ACC/AHA/ S CAI PCI Guidelines85 further recommend the adminis­ tration of 600 mg clopidogrel as soon as possible to patients undergoing primary PCI. Clopidogrel should not be administered to patients in shock or those who may require urgent surgical procedures.

Anticoagulation Anticoagulation is appropriate for patients deemed to be at intermediate or higher ACS ischemic risk. There are many options for anticoagulation in the upstream envi­ ronment (prior to diagnostic angiography) , including both indirect antithrombin agents (UFH, LMWH, and anti-Xa

CHAPTER 5

inhibitors) and direct antithrombins . The choice may be influenced by many issues, including (1) emergency physi­ cian preference, (2) cardiologist preference, (3) perceived level of ischemic risk, (4) concern for hemorrhagic risk, (5) likely duration of therapy prior to angiography and possi­ ble revascularization, and (6) logistic issues such as FDA labeling and institutional formularies. Clinical trials con­ tinue to evaluate therapi es, and strategi es are evolving with these agents . Extrapolation from clinical trials can be difficult, as these trials are often designed or executed in a fashion that makes uncertain ( 1 ) the equivalent potency of drugs being compared, (2 ) the impact of prerandomization anticoagulation therapy (often administered in the ED), (3) the inconsistency and impact of concomitant antiplatelet therapy, and (4) the inclusion and timing of revascularization procedures.

Unfractionated Heparin UFH is an indirect antithrombin; that is, it requires a cofactor, the circulating protein antithrombin III (AT3). The AT3 -UFH complex then can inactivate thrombin (fac­ tor Ila), factor IXa, and factor Xa. It prevents clot propa­ gation but cannot fragment existing thrombi. 86 There are significant pharmacologic limitations to the use of UFH, notably its relatively poor bioavailability and interpatient variability in anticoagulant effect. Nonetheless, UFH has been used clinically in the management of AC S for decades. UFH use is supported by six relatively small placebo-controlled trials and four more trials that com­ pared the combination of ASA and UFH to ASA alone . 3 ; The addition of ASA appears partially protective against "heparin rebound," in which ACS may recur after initial therapy and stabilization. 87•88 When UFH is used in ACS , it is recommended that it be dosed according to patient weight (initial bolus 60 U/kg, max 4,000 U; then 1 2 U/kg/hr infusion, max 1 ,000 U/hr) and monitored by the activated partial thromboplastin time (aPTT) instead of by fixed dosing (e .g., 5 ,000 or 1 0,000 U bolus, then 1 , 000 U/hr). The target aPTT range is 60 to 80 seconds .87 Because of the dual risks of bleeding from anticoagulation and development of heparin-induced antiplatelet antibodies, daily complete blood counts are recommended for patients receiving UFH therapy. The optimal duration of therapy with UFH has not been clearly established, but most of the trials that have evaluated it in UA/NSTEMI have continued treatment for 2 to 5 days . If necessary, the anticoagulant effect of UFH can be largely reversed with the parenteral administration of protamine sulfate.

Low,Molecular,Weight Heparins LMWHs (e.g., enoxaparin and dalteparin) are the product of chemical or enzymatic depolymerization of UFH (e.g., enoxaparin and dalteparin). Enoxaparin and dalteparin are approved by the U. S . FDA for treatment of UA/NSTEMI and enoxaparin is approved for STEMI, but there are sev-

•

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77

era! other LWMHs in use worldwide with varying molecu­ lar weights . These agents , like the parent compound, require the presence of AT3 and therefore are also indirect antithrombins . However, the LMWH-AT3 complex is more effective at inactivating factor Xa than factor Ila. The molecular weight of the agent determines the anti-Xa: anti­ Ila activity ratio, and this in turn seems to correlate to per­ formance in clinical trials . Important advantages of LMWHs over UFH include substantially better bioavail­ ability (owing to less avid binding to other proteins and cells), a longer half-life that allows once- or twice-daily sub­ cutaneous dosing instead of a continuous intravenous infu­ sion, and, in most patients, no need for ongoing monitor­ ing of anticoagulation activity. When monitoring is required (as in patients with renal insufficiency or morbid obesity), the aPTT does not accurately reflect the extent of anticoagulation with LMWHs. However, measures of anti-factor Xa activity (limited laboratory availability at present) do directly correlate to the degree of anticoagula­ tion provided by LMWHs and therefore may be used to assess for adequate dosing. The therapeutic range of anti-factor Xa activity in AC S is felt to be 0 . 3 to 0. 7 U/mL. 87 While anti-Ila activity would seem more pertinent than anti-Xa activity in the ACS scenario, the latter remains an important therapeutic target. In the clotting cascade, fac­ tor Xa is an "amplifier, " and the inhibition of a single mol­ ecule of Xa will suppress the generation of 50 molecules of thrombin (Ila). 3 ; I n the earliest trial of a LMWH agent in UA/NSTEMI, the combination of nadroparin and ASA resulted in better ischemic outcomes than UFH + ASA. 89 In the Fragmin (i. e . , dalteparin) during Instability in coro­ nary artery disease (FRISC) trial,90 dalteparin was found to be essentially equivalent to UFH in patients with UA/NSTEMI. In this study, however, dalteparin was con­ tinued for 1 month or longer after admission; it therefore does not reflect current standard practice. In five of six tri­ als comparing enoxaparin with UFH, the former was favored, with statistical significance driven primarily by a reduction in nonfatal MI. In the 2 002 ACC/AHA UA/NSTEMI guidelines, enoxaparin was preferred over UFH for patients managed initially by a conservative strat­ egy. H (This continues as a class Ila recommendation in the 2 00 7 guidelines.) Enoxaparin and UFH are considered acceptable class I agents for patients initially managed with an early invasive strategy. However, the lack of ready mon­ itoring of the anticoagulant effect of enoxaparin-from one perspective an advantage in that it reduces cost of care-has also limited its use in the interventional management of UA/NSTEMI, during which cardiologists often prefer to closely monitor aPTT (or its counterpart in the catheteri­ zation lab, the activated clotting time [ACT]), before inflat­ ing balloons, deploying stents, or removing sheaths. In at least one study it was shown that PCI can be performed safely, without additional monitoring, following adminis­ tration of enoxaparin.91 This experience would argue in favor of a consistent anti­ coagulation approach from ED through the catheterization

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laboratory. The Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-wave Coronary Events (ESSENCE) and Thrombolysis in Myocardial Infarction (TIMI)- 1 1 B trials showed clear superiority of enoxaparin over UFH in the medical management setting.92 •93 However, there is still a lack of acceptance for LMWHs among some interven­ tional cardiologists, and this may explain the transitioning of patients from LMWH to UFH during interventional procedures. A transition was shown in a posthoc analysis of the Superior Yield of the new Strategy of Enoxaparin, Revascularization and Glycoprotein lib/Ilia inhibitors (SYNERGY) studl4 to be associated with an increased risk of bleeding. Given this increased risk of bleeding associated with switching patients from LMWH to UFH, decisions regarding initial antithrombotic therapy should be made in a thoughtful, prospective , and multidisciplinary fashion. Frequently used approaches such as withholding the morn­ ing dose of LMWH or waiting until 8 hours after the prior LMWH dose to start UFH have some intuitive appeal based on pharmacokinetics, but these strategies have not been prospectively validated. The SYNERGY study compared 1 0,02 7 patients with high-risk UA/NSTEMI who were randomized to receive either enoxaparin or UFH in a setting where nearly all patients underwent angiography and 5 7 % received adjunc­ tive glycoprotein IIb!IIIa receptor inhibitors (GPis) . The two anticoagulants provided similar protection against death and MI at 3 0 days, but there were some signals (higher TIMI major bleeding rates but similar GUSTO severe bleeding and transfusion rates) suggesting an increased risk of bleed­ ing with enoxaparin.94 Based on these results, enoxaparin was felt to be an equivalent agent to UFH using an early invasive strategy. The LMWHs are cleared by renal elimination and the dose should be adjusted according to the estimated creati­ nine clearance. Adjusting the dose according to the serum creatinine level alone is considered an inadequate approach. The creatinine clearance can be estimated in the ED accord­ ing to the following formula:

Estimated creatinine clearance in males

( 1 40 - age in years)

Estimated creatinine clearance in females

( 1 40 - age in years)

72

X

72

X

(weight in kg)

serum creatinine (mg/dl)

X

X

(weight in kg)

X

0.85

serum creatinine (mg/dl)

Although there is a lower incidence of heparin-induced thrombocytopenia with LMWH, both UFH and LMWH should be avoided if a patient has thrombocytopenia or a history of HIT. A direct thrombin inhibitor in this instance is recommended. The typical dose of enoxaparin in UA/NSTEMI is 1 mg/kg subcutaneously every 1 2 hours. The dosing interval is extended to every 24 hours if the patient's creatinine clear-

ance is < 3 0 mL/hr. The dose of dalteparin in UA/NSTEMI is 1 2 0 U/kg (up to a maximum 1 0,000 U) subcutaneously every 1 2 hours. Although dalteparin is also cleared by renal excretion, there is no specific recommendation in its U.S. package insert for dose adjustment in patients with renal insufficiency. The anticoagulant effect of LMWHs can be partially reversed with protamine sulfate, but in the face of frank hemorrhage, fresh frozen plasma and other blood products should also be given.

Direct Thrombin Inhibitors Direct thrombin inhibitors bind to factor Ila and can inhibit both plasma and clot-bound thrombin. They are termed "direct" because their action does not require the interaction of AT3 . The direct antithrombin agent bivalirudin was inves­ tigated in a small population of AC S patients in the Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events (REPLACE)-2 trial95•96 and in a large cohort of moderate and high-risk UA/NSTEMI patients in the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial.97 In each of these trials the combination of an indirect antithrombin agent with a GPI was compared with bivalirudin and either planned or provisional GPis.98-100 In both studies the use of bivalirudin was associated with noninferior ischemic out­ comes and significantly improved rates of bleeding compli­ cations. Interpolation of these results into clinical practice is complicated by the broad range of risk levels of patients enrolled in the study, incomplete data on the use of thienopy­ ridine before randomization, and the relatively short interval (compared with contemporary practice) between initiation of randomized therapy and diagnostic angiography. There was concern that the bivalirudin groups in both studies had higher rates of ischemic endpoints than standard therapy, albeit these were not statistically significant. There was limited practice exp erience with bivalirudin outside the catheterization laboratory at the time this chapter was written. The ACC/AHA 2 00 7 UA/NSTEMI guidelines recommend that UA/NSTEMI patients managed with upstream bivalirudin be also given at least 3 00 mg of clopidogrel at least 6 hours before the procedure. This regimen is an attractive option for anti­ coagulation in UA/NSTEMI patients at higher risk of bleeding complications (especially if they are being transi­ tioned to the cath lab qui ckly) and in those in whom heparin-induced thromb ocytop enia is a concern. The "upstream" dose of bivalirudin used for ACS patients in ACUITY-which at this writing is not FDA-approved­ was an initial intravenous bolus of 0 . 1 mg/kg, followed by an infusion of 0 . 2 5 mg/kg/hr. Prior to PCI, patients received a second bolus of 0 . 5 mg/kg of bivalirudin, after which the infusion rate was increased to 1 . 2 5 mg/kg/hr. Patients with a creatinine clearance of < 3 0 mL/min were excluded from the study. 97 Although the direct thrombin inhibitors appear to be associated with significantly lower bleeding risk than that seen with indirect agents (e.g., heparin), bleeding complica-

CHAPTER 5

tions may still occur. Protamine sulfate does not reverse the effect of bivalirudin. If significant hemorrhage occurs in a patient being treated with bivalirudin, the agent should be immediately discontinued and fresh frozen plasma as well as other blood products considered as indicated.

Anti�Xa Agents Anticoagulation may also be achieved by inhibition of fac­ tor Xa, inhibiting the downstream production of factor Ila (thrombin) . The anti-Xa agent fondaparinux, like UFH and conventional LWMHs, requires AT3 to bind to its tar­ get. Fondaparinux has no activity against thrombin that is already formed or that is produced after it is administered. The most contemporary experience with fondaparinux in the UA/NSTEMI patient was reported in the Organization to Assess Strategies for Ischaemic Syndromes (OASIS) -5 study. 1 0 1 In this large study, the control antico­ agulation strategy was enoxaparin 1 mg/kg subcutaneously twice daily (once daily if creatinine clearance was < 3 0 mL/min), with supplemental UFH at the time o f PCI if intervention was initiated more than 6 hours after the last subcutaneous dose of enoxaparin. The study arm was fon­ daparinux 2 . 5 mg subcutaneously once daily, which was also supplemented with UFH at the time of PCI if more than 6 hours had elapsed since the previous dose. The addi­ tion of UFH for PCI was based on concern for catheter thrombosis with fondaparinux, which occurred infre­ quently but three times more often than with enoxaparin. Although ischemic e fficacy b etween the two arms was equivalent at 9 days, patients in the fondaparinux arm expe­ rienced significantly fewer bleeding complications. Additionally, the fondaparinux cohort showed significantly lower mortality at 3 0 days and at 1 80 days than those on enoxaparin . 1 0 1 The increased risk of bleeding seen i n the enoxaparin arm of OASIS - 5 has been attributed to ( 1 ) the lack of anti­ Ila activity by fondap arinux, (2) the increased risk of bleeding associated with the combination of enoxaparin and UFH in PCI p atients (SYNERGY) , and ( 3 ) the extended duration (6 days) of enoxaparin use when com­ pared with the ES S ENCE and SYNERGY trials. The ACC/AHA 2 00 7 UA/NSTEMI guidelines concluded that there is not enough evidence available from these trials to recommend a preferred regimen when an early, invasive strategy is used for UA/NSTEMI. More experience with these regimens is still needed. However, based on the available evidence from these trials and the large number of patients treated with an initial noninvasive or delayed invasive strategy, the evidence does suggest preference for an anticoagulant for patients treated with a noninvasive strategy in the order of fondaparinux, enoxaparin , and UFH (least preferred), using the specific regimens tested in these trials . Fondaparinux may prove useful in the med­ ical management of UAINSTEMI patients owing to the convenience in dosing and administration as well as its associated lower rate of bleeding complications, and it receive d a I-B recommendation in the 2 0 0 7

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79

ACC/AHA/NSTE AC S guidelines. Still, i n patients in whom there is planned intervention, concern for catheter thrombosis militates against its use, leaving providers with a need to "switch" antithrombotic strategies in the midst of patient management, which involves the concern for increased risk of bleeding.94 As in the case of bivalirudin, the anticoagulant effect of fondaparinux cannot be reversed with protamine sulfate . Anticoagulation therapy is a cornerstone of UAINSTEMI management. As noted previously, the choice of an agent must be individualized to the patient based on ischemic risk, bleed­ ing risk, and expected course of therapy. Anticoagulation with UFH may now have a more limited role in UAINSTEMI management, given the more recent data on other agents such as enoxaparin, fondaparinux, and bivalirudin.

Platelet Glycoprotein lib/lila Receptor Antagonists Intravenous platelet glycoprotein IIb/IIIa receptor inhibitors (GPis) are recommended for upstream (prior to diagnostic angiography) therapy in UAINSTEMI patients who have elevated troponin levels. In patients with UAINSTEMI but normal troponin, GPis are still indicated if there are dynamic ST-segment changes, especially among patients unlikely to undergo angiography within a few hours. The GP IIb!IIIa receptor is ubiquitous on the surface of the activated platelet. Strands of fibrinogen link between GP IIb/IIIa receptors on adjacent platelets, helping to develop the platelet aggregates that ultimately lead to the blockage of coronary blood flow in ACS . Occupancy of at least 80% of these receptors results in potent antithrombotic activ­ ity. 1 02 Once a platelet has been activated, GPis represent the only therapeutic option for blocking platelet aggregation in ACS . There are two types o f GPis: the humanized murine antibody abciximab, which binds noncompetitively to the IIb!IIIa receptor, and the "small molecules" eptifibatide and tirofiban, which competitively inhibit the receptors by mim­ icking fibrinogen. The small-molecule drugs have relatively short half-lives , and platelet activity can be expected to return to normal within 4 to 8 hours after cessation of ther­ apy; the effect of abciximab is much longer-lived, continu­ ing to inhibit platelet aggregation for 24 to 48 hours after the infusion ends. There are only scant directly comparative data among these agents (with the notable exception of the Do Tirofiban and ReoPro Give Similar Efficacy [TARGET] trial103), but generally the data are best for abciximab in the PCI setting. On the other hand, in the Global Use of Strategies To open O ccluded coronary arteri es (GUSTO)-IV AC S trial, 1 04 abciximab was found to afford inferior outcomes compared with placebo in the medical management of UAINSTEMI; therefore, its use is indicated only among those patients receiving planned PCI within 24 hours .

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•

suM MERs

However, there is clinical trial support for the upstream use of both eptifibatide (Platelet lib/Ilia Underpinning the Receptor for Suppression of Unstable Ischemia Trial [PURSUIT] 1 05) and tirofiban (Platelet Receptor inhibi­ tion in Ischaemic Syndrome Management in Pati ents Limited by Unstable Signs and symptoms [PRISM­ PLUS] 1 06) in high-risk UA/NSTEMI. The benefits afforded by eptifibatide or tirofiban appear to be espe­ cially significant among pati ents with an elevated tro ­ ponin prior to catheterization . 3 5 · 84·107 Both drugs should be given with ASA and anticoagulation when not con­ traindicate d . S tudies have shown that LWMH and bivalirudin can b e used in combination with GPi s , although the original studies u s e d UFH. Eptifibatide i s approved for u s e i n UA/NSTEMI patients treated med­ ically alone or with PCI. The recommended dosage of eptifibatide in patients with AC S and normal renal func­ tion is an intravenous bolus of 1 8 0 pg/kg as soon as pos­ sible, followed by a continuous infusion of 2 pg/kg/min until hospital discharge or until CAB G, for a maximum of 72 hours among those receiving medical management alone or 1 8 to 24 hours post-PCI. In patients with an estimated cre atinine clearance of < 5 0 mL/min, the adjusted dose is an intravenous bolus of 1 8 0 pg/kg, immediately followed by a continuous infusion of 1 pg/kg/min. Tirofiban is also approved for use in both the medical management of UA/NSTEMI as well as in those who undergo PCI. The labeled dose is a bolus of 0.4 pg/kg/min for 3 0 minutes, followed by 0. 1 pg/kg/min through angiog­ raphy, for 12 to 24 hours post-PCI, and for a maximum of 48 to 96 hours for those receiving medical management alone. Both doses should be halved in patients with a creati­ nine clearance of < 3 0 mL/min. An important meta-analysis of the benefit of GPis in UAINSTEMI suggested that an elevated troponin is likely the best indication for initiation of therapy.85 This benefit is magnified in those patients who subsequently undergo PCI. Treatment with a GPI increases the risk of bleeding, although this is typically limited to mucocutaneous and vascular access sites. No trials have shown a statistically sig­ nificant increase in the risk of intracranial bleeding. The ongoing Early Glycoprotein lib/Ilia Inhibition in Non-ST­ Segment Elevation Acute Coronary Syndrome (EARLY­ ACS) trial plans to address the contemporary role of pre­ catheterization GPI therapy. 108 Results are expected in 2 008 or 2 009. In summary, the management and risk stratification of patients with UAINSTEMI is complex and requires the integration of several clinical parameters by a thoughtful and knowledgeable physician. A general schematic of the risk-directed therapeutic approach to the early manage­ ment of UAINSTEMI is shown in Figure 5 -9. The thera­ peutic agents used also require careful consideration and dosing regimens, and integration into risk-based strategies continues to evolve. The current recommendations for these agents are summarized in Table 5 - 3 , from the Update AC C AHA 2 00 7 Gui delines for the Management of UAINSTEMI.

Reperfusion Therapy for STEMI

The primary initial obj ective in patients with STEMI is reperfusion of the myocardium subtended by the infarct­ related artery (IRA). Historically, fibrinolytic therapy (called also thrombolytic therapy) was the first treatment modality to meet this goal. Early attempts combining fibrinolytic therapy and interventional management were abandoned when increased mortality was observed. But as methodology and equipment evolved, primary angioplasty became an alternative treatment, and so-called rescue angioplasty was applied in cases of fibrinolytic failure. Recent attempts to combine a pharmacologic approach (fibrinolytic, anticoagu­ lant) with a catheter-based approach have largely been unimpressive, but investigation continues.

Fibrinolytic Therapy Intravenous fibrinolytic therapy is indicated only in patients with ST-segment-elevation ACS or ST-segment depression that is believed representative of a posterior AMI. Use of fibrinolytic therapy in other patients (e .g., those with ST-segment depression or nondiagnostic ECGs) is contraindicated and may be harmful. Patients may benefit from fibrinolytic therapy for up to 1 2 hours after symptom onset, although risk-benefit analysis may identify those patients more likely to benefit as the time from onset of continuous persistent symptoms increases . Patients also should have no absolute contraindications and should be carefully evaluated when a relative contraindica­ tion exists (Table 5 -4). Additionally, fibrinolysis may also be indicated in patients with any type of BBB (right, left, and atypical-new or old) thought to be obscuring ST­ segment analysis in patients with clinical presentation strongly suggestive of AMI. 2 3 · 2 4· 1 J O- J 16 Fibrinolytic therapy is a proven approach to reperfu­ sion therapy in STEMI. 109·1 1 7 All o f the fibrinolytic agents currently available and under investigation are plasmino­ gen activators. They act by exposing, enzymatically, the active center of plasmin. Aspirin, beta-blockers for recur­ rent ischemia/ 1 and nitrates for recurrent ischemic pain or hypertension with STEMI1 1 8· 1 3 0 remain mainstays o f adjunctive pharmacologic therapy. 1 1 9 Recent data from the Clopidogrel and Metoprolol in Myocardial Infarction Tri al/S econd Chines e Cardiac S tudy (C OMMIT/ C C S - 2 ) 1 2 0 suggest that oral beta-blocker management within 24 hours is effective and safer than early IV load­ ing in most STEMI patients (see above) . Intravenous dos­ ing should still b e considered in STEMI p atients with severe hypertension, tachycardia without congestive heart failure or risk factors for cardiogenic shock, and ongoing ischemic pain. Blood pressure should be optimally con­ trolled before administration of a fibrinolytic agent in order to reduce the risk o f hemorrhagic stroke . The

•

CHAPTER 5

E M E R G E N C Y D E PA RT M E N T M A N A G E M E N T

81

I

Diagnosis of UNNSTE M I i s Likely or Defi n ite

•

I

ASA (Class I , LO E : A) * Clopidogrel if ASA i ntolerant (Class I , LO E : A) •

J

I I

Select Management Strategy

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1

I nvasive Strategy

Conservative Strategy I n itiate anticoag u lant therapy (Class I, LOE : A) : Acceptable options: enoxaparin or U FH* (Class I , LO E : A ) or fondapari nux (Class I , LO E : B ) , b u t enoxaparin o r fondapari nux are preferable (Class l la, LO E : B )

I

•

I n itiate clopidogrel therapy (Class I , LO E : A*) Consider add ing I V eptifi batide or ti rofiban (Class l i b , LO E : B)*

•

Any s u bseq uent events necessitating angiography?:j:

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E F 0 . 4 0 or less (Class l la, LOE : B

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D i agnostic Angiography

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Eva l u ate LVEP

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5 0- 6 0 U / k g I V b o l u s o f UFH is recommended b y the O ASIS 5 I nvesti g a to r s '

N o a d d itional treatm ent

U n fracti o n ated heparin

LD of 60 U / k g (m a x 4 , 0 0 0 U) a s I V b o l u s• M D o f IV i n fu s i o n o f 1 2 U / k g / h r (m a x 1 , 0 0 0 U / h r)-m a i n t a i n a PTT a t 1 . 5-2 . 0 t i m e s c o n t r o l (a p p r o x i m a t e ly 5 0-7 0 s)•

IV GP I I b/I I I a p l a n n e d : t a r g e t A CT 200 s No IV GP IIb/IIIa p l a n n e d : t a r g e t A CT 2 5 0-3 0 0 s e c f o r H e m oT e c ; 3 0 0-3 5 0 s for H e m o c h r o n

IV G P I I b /I I I a N o a d d itional treatm ent p l a n n e d : 6 0-7 0 U / k g d N o IV G P I I b /I I I a p l a n n e d : 1 0 0-1 4 0 I U / K g

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Co n t i n u e i n fu s i o n

LD of IV bolus of 1 80 � g / k g f o l l owed 1 0 m i n l a te r by s e c o n d IV bolus of 180 �g/kg M D of 2 . 0 �g/kg/m i n ; reduce infusion b y 50% i n p a ti e n ts w i t h estim a te d c r e a ti n i n e clearance , >-j $:: m

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D o s i n g Ta b l e f o r A n t i p l a t e l e t a n d A n t i c o a g u l a n t T h e r a py i n P a ti e n ts With U A / N ST E M I (Co n tin u e d)

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Co n ti n u e i n fu s i o n

LD o f IV i n f u s i o n of 0 . 4 �g/kg/m i n for 3 0 min M D o f I V i n fu s i o n o f 0 . 1 �g/kg/m i n ; r e d u c e rote o f i n f u ­ s i o n by 5 0 % i n p a t i e n ts with esti­ m a te d c r e a ti n i n e clearance 7 5 years of age, per the manufacturer, NTproBNP requires correction. Despite sharing a common synthetic pathway, no consistent relationship between these molecules has been described, so measures of BNP cannot be con­ verted to NTproBNP or vice versa. NP interpretation requires consideration of the clinical scenario. B esides non-HF conditions known to cause NP elevations into the gray zone, higher levels than clinically predicted are reported in patients with renal failure or insuf-

T A B LE 6 - 7

•

101

ficiency. 2 4• 2 5 Conversely, BNP levels may be lower than clin­ ically anticipated in two scenarios : ( 1 ) despite rapid release, BNP levels may lag by 1 hour or more in the setting of an acute presentation and (2) obesity results in lower BNP con­ centrations than suggested by the clinical presentation 2 6 (Fig. 6-2). Finally, patients with chronic HF may have persistently elevated BNP levels, thus requiring consideration of their baseline dry weight BNP to accurately diagnose new symp­ toms. Although not well studied, in the setting of chronic elevation, changes exceeding 40 % to 5 0 % of baseline are considered clinically relevant. BNP measurement has also demonstrated economic consequence if unavailable in the ED . The Basel trial was a prospective blinded evaluation of BNP in ED patients pre­ senting with dyspnea managed with and without BNP results. BNP testing resulted in a 3 . 1 -day decrease in subse­ quent length of stay ( 1 3 . 7 vs . 1 0 . 6 days) compared with patients in the blinded cohort. 2 7 Beyond diagnosis, several studies describe the prognos­ tic value of ED BNP testing, identifying a population of patients in whom more aggressive therapy or follow-up may be warranted. In the ED , BNP levels >480 pg/mL are asso­ ciated with a 40% rate of death or HF rehospitalization within the next 6 months versus only 3 % if levels were < 2 3 0 pg/mL. 2 8 In another analysis o f hospitalized H F patients, those with an initial BNP > 1 , 740 pg/mL had an acute mor­ tality of 6 % , versus only 1 .9 % if 7 5 ye a r s , c u t p a i n t i s 4 5 0 p g / m L i f a g e < 7 5 ye a r s , c u t p o i n t i s 1 2 5 p g / m L

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Differential Diagnosis Differentiating HF from other causes of dyspnea is chal­ lenging. The differential diagnosis of patients presenting

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with potential H F (Table 6-8) i s confounded by the fact that there are many HF mimics, and these mimics may actually lead to HF or worsen existing HF (Table 6-9). This includes acute myocardial infarction, which must also be considered as a potential cause of a HF exacerbation. A common con­ founder is coexisting obstructive pulmonary disease. Severe hypertension and peripheral vasoconstriction suggest an acute HF syndrome even in the setting of audible wheezing. Pneumonia and pulmonary embolus can also mimic or exac­ erbate HF. History and physical examination can help in dif­ ferentiation, but the CXR and NP assay results may be mis­ leading in the setting of chronic HF. Prior medical records may assist. Edema is seen in HF but is nonspecific, as is noted in hypoproteinemic states, hepatic or renal failure, and vascular diseases.

3.0 2.0 1 .0 0.0 01 1 0 0 p g / m l ' M ust h ave a t l e ast o n e f r o m e a c h c a t e g o ry.

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•

E x c l u s i o n Cri t e r i a f o r H F M a n a g e m e n t i n a S h o r t Stay/ O b s e rvati o n U n i t'

H e m o dyn a m i c i n s ta b i l i ty U n sta b l e vi t a l s i g n s (B P > 2 2 0/ 1 2 0 m m H g , R R > 2 5 , H R > 1 3 0 b p m) U n sta b l e a i rway o r n e e d i n g > 4 L/ m i n n a s a l c a n n u l a 0 2 f o r S a 0 2 > 9 0 % R e q u i r i n g c o n ti n u o u s va s o a ctive m e d i c a t i o n (e . g . , n i t r o g lyce r i n , n i t r o p r u s s i d e , d o b u ta m i n e , o r m i l r i n o n e) e x c e p t n e s i r i t i d e Evi d e n c e o f c a r d i o g e n i c s h o c k (systo l i c B P < 9 0 m m H g , a l te r e d m e n t a l s t a t u s , p e r i p h e r a l vaso c o n s t r i c ti o n) Cl i n i c a l ly s i g n i fi c a n t a r r hyth m i a (e . g . , n o n s u s ta i n e d VT n o t d u e to e l e c tro lyte i m b a l a n c e) S i g n s of a c u te c o r o n a ry syn d r o m e (E CG c h a n g e or c a r d i a c m a r k e r e l eva t i o n) Ch r o n i c r e n a l fa i l u r e r e q u i r i n g d i a lys i s Co m p l e x d e c o m p e n s a t i o n (u n d e r lyi n g p r e c i p i t a n t i s n o t c l e a rly c a r d i a c o r vo l u m e - r e l a te d ) M u l ti p l e c o m o r b i d i t i e s A c u te m e n t a l s t a t u s a b n o r m a l i ty ECG , e l e ct r o c a r d i o g r a m ; H R , h e a rt r a t e ; R R , r e s p i r a tory r a t e ; Sa o 2 , a r t e n a l oxyg e n s a t u r a t i o n ; VT , ventr i c u l a r t a c hyc a r d 1 0 . ' A ny o n e p o s 1 t1ve r e s u l t e x c l u d e s t h e p a t 1 e n t f r o m t h e h e a rt fa i l u r e p r o t o c o l a n d s u g g ests 1 n p o t 1 e n t m a n a g e m e n t .

for disposition from the observation/acute-care unit are listed in Table 6- 1 5 .

Discharge Home Patients treated for heart failure who are ultimately dis­ charged from the ED or observation unit require outpatient

TA B LE 6 - 1 5

•

follow-up by a physician knowledgeable in the management of HE Social service evaluation may be needed to ensure medication compliance, dietary education, and reenforce­ ment of smoking cessation instructions. Patient education is important, as patients with knowledge of the components of a sodium-restricted diet have 3 0 % fewer rehospitalizations, and smoking cessation has the same mortality effect as the best medication therapies. 5°

D i s c h a r g e G u i d e l i n e s f r o m O b s e rva ti o n / A c u t e C a r e / S h o rt-Stay U n i ts

P a t i e n ts n o t m e e t i n g a l l of t h e fo l l owi n g c r i t e r i a s h o u l d b e c o n s i d e r e d f o r i n p a t i e n t t r e a t m e n t : • P a t i e n t r e p o rts s u bj e c tive i m p rove m e n t A m b u l a t o ry, with o u t l o n g - s u ffe r i n g o r t h o s t a s i s R e s ti n g H R < 1 0 0 b p m Sys t o l i c B P > 8 0 m m H g N e t u r i n e o u t p u t > 1 , 0 0 0 m L a n d n o n ew d e c r e a s e i n u r i n e o u t p u t < 3 0 m U h r (o r < 0 . 5 m U k g / h r) R o o m a i r S a o 2 > 9 0 % (u n l e ss o n h o m e 0 2) A l l CK - M B < 8 . B n g / m L , a n d t r o p o n i n T < 0 . 1 f.L g/ L N o i s c h e m i c - type c h e s t p a i n N o n ew c l i n i c a l ly s i g n i f i c a n t a r r hyth m i a Sta b l e e l e ct r o lyte p r o f i l e CK - M B , m u s c l e a n d b r o 1 n typ es of c r e a t m e k m a s e ; H R . h e a rt r a t e , S a o , , o r t e r 1 a l oxyg e n s a t u r a ti o n ' E x c e p t a s a p p r o p r i a t e 1 n t h e e n d - sta g e p a l l 1 at1ve - c a r e c o h o rt.

CHAPTER 6

•

H E A RT F A I L U R E A N D A C U T E P U L M O N A R Y E D E M A

References

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hemodynamic correlations in chronic congestive heart failure: con­ flicting results may lead to inappropriate care. Am J Med 1991 ;90:3 5 3 . 1 8 . Kono T, Suwa M , Hanada H, e t al. Clinical significance o f normal cardiac silhouette in dilated cardiomyopathy-evaluation based upon echocardiography and magnetic resonance imaging. Jpn Cin

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1 13

J Kidney Dis 2003;41(3) : 5 7 1 -579. 25. Vickery S, Price CP, John RI, et al. B-type natriuretic peptide (BNP) and amino-terminal proBNP in patients with CKD : Relationship to renal function and left ventricular hypertrophy.

Am J Kidney Dis 2005;46 : 6 1 0-62 0. 2 6 . Krauser P, Lloyd-Jones DM, Chae CU, et a!. Effect of body mass index on natriuretic peptide levels in patients with acute congestive heart failure: A ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) substudy. Am Heatt J 2005 ; 1 49:744-750. 27. Mueller C, Scholer A, Laule-Kilian K, et a!. Use of B-type natri­ uretic peptide in the evaluation and management of acute dyspnea.

N Eng! J Med 2 004; 3 50:647-654. 28. Harrison A, Morrison LK, Krishnaswamy P, et a!. B-type natriuretic peptide predict future cardiac events in patients presenting to the emergency deparrment with dyspnea. Ann Emerg Med 2002 ;3 9 : 1 3 1 . 29. Fonarow GC, Peacock WF, Phillips CO, et a!. Admission B-type natriuretic peptide levels and in-hospital mortality in acute decom­ pensated heart failure. J Am Col! Cardio/ 2007;49: 1 943-1 950. 30. Peacock WF, Summers RL, Vogel J, et a!. Impact of impedance cardiography on diagnosis and therapy of emergent dyspnea: the ED-IMPACT Trial. Acad Emerg Med 2 006; 1 3 (4): 3 65-3 7 1 . 3 0a. Masip J , Betbese AJ, Paez J , et a!. Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomised trial. Lancet 2 000; 3 56:2 1 2 6-2 1 3 2 . 3 1 . Mehta S, Jay GD , Woolard RH, et a!. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. O'"it Care Med 1 997;2 5 :62 0-62 8 . 3 1 a. Collins SP, Mielniczuk LM, Whittingham HA, e t a ! . The use of noninvasive ventilation in emergency department: a systematic review. Ann Emerg Med 2 006;48 :2 60-2 69. 3 2 . Silvers SM, Howell JM, Kosowsky JM, et a!. Clinical policy: criti­ cal issues in the evaluation and management of adult patients pre­ senting to the emergency department with acute heart failure syn­ dromes. Ann Eme1'g Med 2 007;49:62 7-669. 3 3 . Koga Y, Wada T, Toshima H, et a!. Prognostic significance of elec­ trocardiographic findings in patients with dilated cardiomyopathy.

Heart Ves 1 993 ; 8 : 3 7-4 1 . 34. Peacock WF Emerman CL, D oleh, M , et a!. A retrospective ,

review: the incidence of non-ST segment elevation MI in emer­ gency deparunent patients presenting with decompensated heart failure. Congest Hem7 Failure 2003;9(6) : 3 03-3 0 8 . 3 5 . VMAC Investigators. Intravenous nesiritide vs. nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. ]AMA 2 002 ;2 87 : 1 5 3 1 . 3 6 . Bumetadine, i n 1 9 9 8 Physicirm :r Desk Reje1'ence. Montvale, NJ : Medical Economics Company, 1 998:244 1 -2443 . 3 7 . Peacock WF rv; Remer EE, Aponte J, et al. Effective observation unit treatment of decompensated heart failure. Congest Heart

Failzn-e 2 002 ;8:68. 38. Le Conte P, Coutant V, N'Guyen JM, e t a!. Prognostic factors in acute cardiogenic pulmonary edema. Am] Erne1!S Med 1 999; 1 7 : 3 2 9 . 3 9 . Turpie A G . Thrombosis prophylaxis i n the acutely i l l medical 40.

41. 42 .

43 . 44.

patient: insights from the prophylaxis in MEDical patients with ENOXaparin (MEDENOX) trial. Am J Cardiol 2 000;86:48M. Abraham WT, Lowes BD, Ferguson DA, et al. Systemic hemody­ namic, neurohormonal, and renal effects of a steady-state infusion of human brain natriuretic peptide in patients with hemodynami­ cally decompensated heart failure. ] Cardiac Failun 1 998;4: 3 7 . Peacock WF Emerman C L , Young J . Nesiritide i n congestive heart failure associated with acute coronary syndromes: a pilot study of safety and efficacy. J Cardiac Failzwe 2 004; 1 0(2) : 1 2 0- 1 2 5 . Marcus L S , Hart D, Packer M , e t al. Hemodynamic and renal excretory effects of human brain natriuretic peptide infusion in patients with congestive heart failure. A double-blind, placebo con­ trolled, randomized crossover trial. Cinulation 1 996;94: 3 1 84-3 1 89. Yoshimura M, Yasue H, Ogawa H. Pathophysiological significance and clinical application of ANP and BNP in patients with heart failure. Can J Physiol Pharmaco/ 2 00 1 ; 79:730-7 3 5 . Sackner-Bernstein JD, Skopicki HA, Aaronson KD . Risk o f wors­ ening renal function with nesiritide in patients with acutely decom­ pensated heart failure. Circulation 2005; 1 1 1 : 1 487-149 1 . ,

1 14

PEACOCK

45. Sackner-Bernstein JD, Kowalski M, Fox M. Short-term risk of death after treatment with nesiritide for decompensated heart fail­ ure: a pooled analysis of randomized controlled trials. JAMA 2 005 ; 2 9 3 ( 1 5): 1 900-1905. 46. Mentzer RM, Oz MC, Sladen RN , et al on behalf of the NAPA Investigators. Effects of perioperative nesiritide in patients with left ventricular dysfunction w1dergoing cardiac surgery: the NAPA trial. ] Am Colt Cardio/ 2007;49(6) : 7 1 6-72 6 . 47. Yancy CW, Krum H, Massie B M , et a l , the FUSION II Investigators. The Second Follow-up Serial Infusions of Nesiritide (FUSION II) trial for advanced heart failure: study rationale and design. Am Hem1: J 2007; 1 5 3 (4):47 8-484. 48. Colucci WS , Elkayam U, Horton DP, et al. for the Nesiritide Study Group. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. N Eng! J Med 2 000; 343 :246-2 5 3 . 49. Francis G , Cohn J, for the V-HeFT VA Cooperative Studies Group. Plasma norepinephrine, plasma renin activity and conges­ tive heart failure. Cinulation 1 993 ;87 :41-48. 50. SOLVD Investigators. Effect of enalapril on survival in patients with reduced ventricular ejection fraction and congestive heart fail­ ure. N Eng! J Med 1 99 1 ; 3 2 5 :293 . 5 1 . Cohn JN, Johnson G, Ziesche S, et al. A comparison of enlapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Eng! J Med 1 99 1 ;3 2 5 : 303-3 1 0 . 5 2 . The CONSENSUS Trial Study Group. Effects o f enlapril o n mor­ tality in severe congestive heart failure: results of the Cooperative North Scandinavian Enlapril Survival Study (CONSENSUS). N Eng! ] Med 1 98 7; 3 1 5 : 1 42 9- 1 43 5 . 5 3 . McKelvie R , Yusuf S , Pericak D , e t al. Comparison o f candesartan, enlapril, and their combination in congestive heart failure : Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD pilot study) (abstract) . Em· Heart J 1 998; 1 9(Suppl): 1 3 3 . 54. Pitt B , Segal R , Martinez FA, e t a l o n behalf o f Elite Study Investigators . Randomized trial of losartan versus captopril in patients over 65 with heart failure (Evaluation of Losartan in the Elderly Study, ELITE). Lancet 1 997;349: 747-7 5 2 . 5 5 . McMurray]], YoungJB, Dunlap ME, et a!. CHARM Investigators. Relationship of dose of background angiotensin-converting enzyme inhibitor to the benefits of candesartan in the Candesartan in Heart failure: Assessment of Reduction in Mortality and mor­ bidity (CHARM)-Added trial. Arn Hem1: J 2006; 1 5 1 (5):98 5-99 1 . 56. ACC/AHA Task Force. Guidelines for the evaluation and manage­ ment of heart failure: report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee of Evaluation and Management of Heart Failure). Ci1·culation 1 995 ;92 : 2 7 64-2 784. 57. Cohn JN, Johnson G, Ziesche S , et al. A comparison of enlapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Eng! J Med 1 99 1 ; 3 2 5 : 3 03-3 1 0 . 5 8 . Cohn JN, Archibald D G , Ziesche S , e t a!. Effect o f vasodilator therapy on mortality in chronic congestive heart failure: results of the Veterans Administration Cooperative Study. N Eng! J Med 1 986;3 14: 1 547-1 5 5 2 . 59. Tsuyuki RT, Yusuf S, Rouleau JL, e t a!. Combination neurohornwnal blockade with ACE inhibitors, Angiotensin II antagonists and beta-blockers in patients with congestive heart failure: design of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study. Can J Cm�dio/ 1 997; 1 3 : 1 1 66-1 1 74. 60. MERIT-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure: metoprolol CR/XL randomized intervention trial in congestive heart failure. Lancet 1 999;3 5 3 : 2 00 1 . 6 1 . Colucci WS, Packer M, Bristow MR, et al. For the U.S . Carvedilol Study Group. Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure. Circulation 1 996;94:2 800-2 806. 62. CIBIS Investigators and Committees. A randomized trial of �­ blockade in heart failure: the Cardiac Insufficiency Bisoprolol Study (CIBIS). Circulation 1 994;90: 1 765-1 7 6 7 . 6 3 . Bristow MR, Gilbert EM, Abraham WT, e t a l For the MOCHA Investigators. Carvedilol produces dose-related improvements in left ventricular function and survival in subjects with chronic heart failure. Cimdation 1 996;94:2 807-2 8 1 6. 64. RALES Study Investigators. The effect of spironolactone on mor­ bidity and mortality in patients with severe heart failure. N Eng! J Med 1 999; 3 4 1 :709.

6 5 . Cioffi G, Pozzoli M, Forni G, et al. Systemic thromboembolism in chronic heart failure. A prospective study in 406 patients. Eur Hean J 1 996; 1 7 : 1 3 8 1- 1 3 89. 66. Baker DW, Wright RF. Management of heart failure. IV Anticoagulation for patients with heart failure due to left ventricu­ lar systolic dysfunction. JAMA 1 994;2 72 : 1 6 1 4-1 6 1 8. 67 . Elkayam U, Weber L, McKay C, et al. Spectrum of acute hemo­ dynamic effects of nifedipine in severe congestive heart failure. Am J Cm·dio/ 1 9 8 5 ; 5 6 : 5 60-5 66. 68. Barjon JN, Rouleau JL, Bichet D, et a!. Chronic renal and neuro­ humoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. J Am Colt Cm·dio/ 1 987 ;9:622-5 3 0 . 6 9 . Elkayam U , An1in J, Mehra A , e t a l . A prospective, randomized, double-blind, crossover study to compare the efficacy and safety of chronic nifedipine therapy with that of isosorbide dinitrate and their combination in the treatment of chronic congestive heart fail­ ure. Ci1'culation 1 990;82 : 1 954- 1 96 1 . 70. Goldstein RE, Boccuzzi SJ, Cruess D, e t a!. Diltiazem increase late-onset congestive heart failure in post-infarction patients with early reduction in ejection fraction. The Adverse Experience Committee and the Multicenter Diltiazem Post-infarction Research Group. Circulation 1 99 1 ; 8 3 : 52-60. 7 1 . Advisory Council to Improve Outcomes Nationwide in Heart Failure. Packer M, Cohn JN, eds. Consensus recommendations for the management of chronic heart failure. Arn J Cardia! 1 999; 8 3 : 54A. 7 2 . The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Eng! J Med 1 989; 3 2 1 :406-4 1 2 . 7 3 . The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of antiarrhythmic agent moricizine on survival after myocardial infarction. N Eng! J Med 1 992 ; 3 2 7 : 2 2 7-2 3 3 . 74. Doval HC, Nul DR, Grancelli HO, et a! for Grupo d e Estudio de Ia Sobrevida en Ia Insuficiencia Cardiaca en Argentina (GESICA). Randomised trial of low-dose amiodarone in severe congestive heart failure. Lancet 1 994; 3 44:493-498. 75. Doval HC, Nul DR, Grancelli HO, et a! for Grupo de Estudio de Ia Sobrevida en Ia Insuficiencia Cardiaca en Argentina (GESICA). Randomised trial of low-dose amiodarone in severe congestive heart failure. Lancet 1 994; 3 44:493-498. 76. Singh SN, Fletcher RD, Fisher SG, et a! for the Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure. Amiodarone in patients with congestive heart failure and asymptomatic ventric­ ular arrhythmias. N Eng! J Med 1 995 ; 3 3 3 : 7 7-8 2 . 77. Hobbs RE , Czerska MD. Congestive heart failure. Current and future strategies to decrease mortality. Postgrad Med 1 994;96: 1 67-1 72. 7 8 . Batsford WP, Mickleborough LL, Elefteriades JA. Ventricular arrhythmias in heart failure. Cardiol Clin 1 995 ; 1 3 : 8 7-9 1 . 79. Stevenson WG, Stevenson LW, Middlekauff HR, e t al. Sudden death prevention in patients with advanced ventricular dysfunc­ tion. Cinulation 1 993 ; 88(6) : 2 9 53 -2 96 1 . 80. The SOLVD Investigators. Effect of enlapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Eng! J Med 1 99 1 ; 3 2 5 :293-202 . 8 1 . Diercks DB, Kirk JD, Peacock WF et a!. Identification of emer­ gency department patients with decompensated heart failure at low risk for adverse events and prolonged hospitalization. J Cardiac Faihwe 2 004; l O(Suppl 4): S 1 1 8 . 82 . Burkhardt ], Peacock WF Emerman C L . Elevation i n blood urea nitrogen predicts a lower discharge rate from the observation nnit. Ann Emerg Med 2 004;44(Suppl 4):S99. 83. Fonarow GC, Heywood JT, Heidenreich PA, et a!. Risk stratification for in-hospital mortality in acutely decompensated heart failure: clas­ sification and regression tree analysis. JAMA 2 005;2 93(5):5 72-580. 84. Peacock WF rv; Albert NM. Observation unit management of heart failure. Enzerg Med Clin Nm-tb Am 2 00 1 ; 1 9 : 2 09. 8 5 . Silver MA, Maisel A, Yancy CW, et al. BNP Consensus Panel 2 004: A clinical approach for the diagnostic, prognostic, screening, treat­ ment monitoring, and therapeutic roles of natriuretic peptides in cardiovascular disease. Congest Hem't Fail 2 004; 1 0(5) : S 3 . 86. Peacock WF The B-type natriuretic peptide assay: a rapid test for heart failure. Cleve Clin J Med 2 002;69:243 . 8 7 . Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal Pro-BNP Investigation of Dyspnea in the Emergency Department (PRIDE) study. Am J Cm,dio/ 2 005;95 :948-954. ,

,

.

Chapter 7 Cardiogenic Shock Complicating Acute Coronary Syndromes John M . Field Patients with cardiogenic shock and STEM! should be primarily transported or secondarily transferred (with a door-to-departure time of within 30 minutes) to facilities capable of invasive strategies such as insertion of an intra-aortic balloon pump (IABP) , percutaneous coronary intervention (PC I) , and coronary artery bypass grafting ( CABG) . Recent trial data have shown an improved prognosis for survivors of cardiogenic shock who benefit from an early invasive strategy . Thus an aggressive approach to achieve early and complete reperfusion of the infarct related artery (IRA) , to prevent or correct mechanical complications of MI , and to provide pharmacologic and mechanical interventions to favorably influence early infarct remodeling are warranted in patients with cardiogenic shock or at high-risk for this complication . The incidence of cardiogenic shock had largely remained unchanged but appears to be decreasing in parallel with increasing rates of primary PCI for STEMI. And mortality is now, in the modern era, �50% below historical levels of 80% to 90%. • Right ventricular ( RV) shock (usually found in association with inferior wall M I ) has a high mortality rate, similar to that of left ventricular ( LV) shock. • An invasive strategy is recommended for patients 60 % . 5• 22

Pathophysiology and Hemodynamics of Cardiogenic Shock MI may result in hemodynamic instability and congestive heart failure (CHF). As described above, cardiogenic shock classically has been defined as a "pump" problem due to "massive" heart attack. In this context, cardiac output and ventricular ejection fraction fall due to severe left ventricu­ lar dysfunction. Heart rate increases to compensate for the fall in stroke volume in a reflex compensatory effort to main­ tain cardiac output. If the patient survives initially, ventricu­ lar dilation and remodeling occur over days to months, resulting in an increase in end-diastolic volume (increased ventricular preload), which may help to maintain stroke vol­ ume despite the fall in ejection fraction. In cardiogenic shock, the degree of myocardial dysfunc­ tion is often severe. But in many case this severe impairment of contractility does not lead to shock, and LV ejection frac­ tion (LVEF) may only be moderately depressed. 2 3 In the SHOCK trial, mean ejection fraction was 3 0 % . 2 4 In addi­ tion, LVEF is similar in the acute phase and 2 weeks later, when shock has resolved in survivors. Approximately half of patients with cardiogenic shock have small or normal LV size representing failure of an adaptive mechanism of acute dilation to maintain stroke volume early in MI. 2 5 Paradoxically, reduced ejection fraction and ventricular dilation are prognos­ tic indicators of increased survival in septic shock syndrome. 2 6 �

Iatrogenic Cardiac Shock The majority of patients with cardiogenic shock following MI develop shock after the first 2 4 hours. In some patients at high risk for cardiogenic shock, medications contribute to the development of shock, including beta-blocking agents, angiotensin converting enzyme inhibitors (ACEis), and other vasodilators such as nitrates and morphine2 7-30 (Fig. 7 - 1 ). In acute pulmonary edema, intravascular volume is redis­ tributed to the extravascular pulmonary interstitial space in the lungs . A tachycardia may be largely compensatory for depressed myocardial function and tenuous intravascular vol­ ume. Beta-blocking agents may decrease heart rate diminish­ ing stroke volume and vasodilators or diuretics may further redistribute blood volume or cause a poorly tolerated diuresis, precipitating a low output state. Low-dose diuretics should be initially used and nitrates added cautiously. Noninvasive positive-pressure ventilation may be useful if tolerated. IV ACEis are contraindicated early in MI. Oral ACEis should be

1 18

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F I G U R E 7 - 1 • P a t h o p hys i o l o g y of i a t r o g e n i c s h o c k . A c u t e p u l m o n a ry e d e m a is a s t a t e o f r e d i str i b u t i o n o f i n tr ava s c u l a r vo l u m e i n t o e x t r a c e l l u l a r s p a c e i n t h e l u n g s ( c e n t e r p a t hway) . W h e n h e m o dyn a m i c sta b i l i ty i s te n u o u s , t h e a d d i t i o n a l d e c r e a s e i n p l a s m a vo l u m e c a u s e d b y d i u r e t i c s i n p a t i e nts with o u t p r i o r h e a r t fa i l u r e m ay i n d u c e s h o c k . T a c h yc a r d i a i s o f t e n c o m p e n s a t o ry f o r l ower stro k e vo l u m e b u t i s n o t a p p r e c i a t e d a s s u c h ( l e ft- s i d e d p a t hway) . T r e a t m e n t with b e t a ­ b l o c k a d e l owers h e a rt r o t e a n d s t r o k e vo l u m e , l e a d i n g to s h o c k . D e c o m p e n s a t i o n m ay a l s o o c c u r wh e n p a t i e nts w h o a r e r e l i a n t o n c o m p e n s a t o ry va s o c o n st r i c ti o n a r e a g g r essively t r e a t e d w i t h a n g i o t e n s i n - c o nverti n g e n zym e i n h i b i t o r s , p a r ­ t i c u l a r ly i n tr ave n o u s l y a n d ve ry e a rly b e f o r e t h ey h ave h e m o dyn a m i c a l ly st a b i l i z e d . N i t r a te s wo u l d b e e x p e c t e d to h ave a s i m i l a r effect b u t d i d n o t i n t h e o n ly syst e m a t i c stu dy, wh i c h u s e d o r a l l ow- d o s e t r e a t m e n t . Vo l u m e e x p a n s i o n m ay b e d e l et e r i o u s w h e n u s e d to e x c ess o r w h e n R V f i l l i n g p r e ss u r e i s a l r e a dy e l eva t e d , b e c a u s e t h e R V m ay b e c o m e vo l u m e ove r l o a d e d with s h ift o f t h e s e p t u m , c a u s i n g i m p a i r m e n t i n LV fi l l i n g a n d c o n t r a c t i o n (r i g h t - s i d e d p a thway) . CVP , c e n t r a l ve n o u s p r essu r e ; HTN , hyp e r te n s i o n ; P CW P , p u l m o n a ry c a p i l l a ry we d g e p r essu r e ; RVE D P , R V e n d - d i a sto l i c p r essu r e ; RVE DV, RV e n d - d i a s to l i c vo l u m e . ( F r o m R eyn o l d s H R , H o c h m a n JS. Circulation 2 0 0 8 ; 1 1 7 [ 5 ) : 6 8 6-6 9 7 , w i t h p e r m issi o n . )

deferred until patients are hemodynamically stable. In ISIS-4, the only significant side effect of captopril was hypotension. 2 8 In this trial, patients who developed hypotension were at increased risk for the development of cardiogenic shock and tended to have lower blood pressures and higher heart rates. It is important to note that MI may lead to pulmonary edema without the development of shock. An initial effect of ischemia is a decrease in LV compliance, and pulmonary edema initially may mimic diastolic heart failure.

tant myocardium and extend the infarct area. In patients without acute heart failure, a reduction in heart rate with beta-blockade improves outcome mainly by decreasing episodes of fatal ventricular fibrillation. Blockade of excess sympathetic and neurohumoral stimulation reduces myocar­ dial oxygen consumption. But in compensatory tachycardia, beta-blockade can be life-threatening, as in cardiogenic shock or severe heart failure, when the stroke volume is crit­ ically dependent on the tachycardia (Fig. 7-2) (see Chapter 5).

Beta,Blockade and Heart Failure-Updated Guidelines

Hemodynamic Parameters of Cardiogenic Shock

As noted, tachycardia may help maintain cardiac output despite the fall in ejection fraction and stroke volume. But all compensatory changes are likely to increase myocardial oxy­ gen consumption. They can worsen ischemia in viable or dis-

When LV end-diastolic pressure increases substantially (>2 5-3 0 mm Hg), interstitial and then pulmonary edema develops. If RV end-diastolic pressure increases, peripheral

CHAPTER 7

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F I G U R E 7 - 3 • C l a s s i c s h o c k p a r a d i g m , as i l l u s t r a t e d by S . H o l l e n b e r g , i s s h own i n b l a c k . T h e i n f l u e n c e o f t h e i n fl a m m a t o ry r e s p o n s e syn d r o m e i n i t i a t e d by a l a r g e M I i s i l l u s t r a t e d i n r e d . LVE D P i n d i c a te s l e ft ve n ­ t r i c u l a r e n d - d i a sto l i c p r e ss u r e . ( F r o m H o c h m a n JS. Card i o g e n i c shock c o m p l icating a c u t e myo c a r d i a l i n f a r c ti o n : e x p a n d i n g t h e p a r a d i g m . Circulation 2 0 0 3 ; 1 0 7 : 2 9 9 8-3 0 0 2 , with p e r m issi o n . )

1 20

FIELD

impair perfusion of the gut, enabling transmigration of bacte­ ria. SIRS is more common with increasing duration of shock. 35 Investigation of inflammatory markers and mediators of SIRS may provide further targets for therapeutic intervention.

Treatment of Cardiogenic

Shock Associated With Acute Myocardial Infarction The mortality rate and occurrence of death from cardia­ genic shock has been variably reported. In patients with per­ sistent ST-segment elevation, failure of fibrinolytic therapy or persistent occlusion of an IRA after attempted primary PCI shock develops with a median time of 1 0 to 1 2 hours and most within 48 hours of infarction. 3'5 , 36 , 37

therapies. In selected patients, mechanical circulatory assis­ tance with intra-aortic balloon counterpulsation is an effec­ tive adjunct with reperfusion therapy (Fig. 7 -4).

Echocardiography The differential diagnosis of shock includes mechanical com­ plications of MI, including acute mitral regurgitation due to papillary muscle rupture or dysfunction, ventricular septal defect, subacute left ventricular free wall rupture, and RV infarction. Echocardiography can provide valuable informa­ tion to guide therapy in patients with undifferentiated shock and in those with cardiogenic shock. Echocardiography should be performed early and can be done at the bedside in the emergency department (see Chapter 8).

lntra�aortic Balloon Counterpulsation

Initial therapy for LV dysfunction without shock includes oxygen administration, IV administration of nitrates to reduce cardiac preload and afterload, and diuresis. Morphine is an excellent adjunctive agent if the STEM! patient has continuing ischemia. If SBP is < 1 00 mm Hg, nitrates and morphine should be used with caution if at all. Wilen SBP is 1 00

m m Hg

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>1 00 mm H g and Not 90- 1 00 mm Hg) and the patient has no serious signs or symptoms of shock, then IV nitro­ glycerin is the drug of choice for acute pulmonary edema. Nitroglycerin reduces pulmonary congestion by dilating the venous capacitance vessels, reducing preload. It also dilates systemic arteries, decreasing systemic vascular resistance. This effect can reduce afterload and increase cardiac output. Nitroglycerin may initially be administered by sublin­ gual tablets, oral spray (isosorbide oral spray is an acceptable alternative), or the IV route. A standard 0.4-mg tablet can be given every 5 to 1 0 minutes provided that SBP remains >90 to 1 00 mm Hg and the patient has no clinical signs of tissue hypoperfusion (shock). Nitroglycerin is contraindicated in hypotensive patients with signs of shock. Typically these patients cannot tolerate vasodilatation because of impaired cardiac output. They can­ not compensate for the nitrate-induced tachycardia with increased stroke volume, which is one reason why tachycardia is a contraindication to nitroglycerin. Patients with RV infarc­ tion are preload-dependent. Nitrates are also contraindicated in patients who have used a phosphodiesterase inhibitor within the previous 24 hours (tadalafil within 48 hours). In these patients nitroglycerin can cause severe hypotension refractory to vasopressors. Use nitroglycerin with caution (if at all) if the patient has an inferior wall AMI with possible RV involve­ ment. Patients with RV dysfunction are very dependent on maintenance of RV filling pressures to maintain cardiac output and blood pressure.

Oxygen and Possible Intubation

Furosemide

Deliver oxygen at high flow rates, starting at 5 or 6 L/min by mask. Nonrebreathing masks with reservoir bags can provide oxygen concentrations of 90% to near 1 00 % . A bag­ mask may be used to provide assisted ventilation if the patient's ventilation is inadequate. If the patient is breathing spontaneously, consider continuous positive airway pressure by mask (BiPAP). Be prepared to intubate the patient who has significant respiratory distress or respiratory failure. A need for intuba-

Furosemide has long been a mainstay in the treatment of acute pulmonary edema. It has a biphasic action. First, within approximately 5 minutes, it causes an immediate decrease in venous tone and an increase in venous capaci­ tance. These changes lead to a fall in LV filling pressure (preload) that may improve clinical symptoms . S econd, furosemide produces diuresis within 5 to 10 minutes of IV administration. The diuresis need not be marked to be effec­ tive. If the patient is not already taking furosemide, a small

First.-Line Actions If signs of acute pulmonary edema are present, proceed with first-line actions if low blood pressure and shock are absent: • • •

•

Supplementary oxygen and NIV!intubation as needed Nitroglycerin SL, then IV Furosemide IV 0 . 5 to 1 mg/kg Morphine IV 2 to 4 mg

1 26

FIELD

titrated dose is given as a slow IV bolus over 1 to 2 minutes. If the response to this dose is inadequate after about 2 0 min­ utes, a bolus of 2 mg/kg is administered. If the patient is already taking oral furosemide, a clinical rule of thumb is to administer an initial dose that is twice the daily oral dose. If no effect occurs within about 20 minutes, double the initial dose. Higher doses may be required if the patient has mas­ sive fluid retention, refractory heart failure, or renal insuffi­ ciency. Use caution in patients who may be volume-depend­ ent or who are at high risk for cardiogenic shock (see above). Recommendations for initial dosing are as follows : •

•

•

Administer furosemide < 0 . 5 mg/kg IV bolus for new onset acute pulmonary edema without hypovolemia. Use caution in patients who are at high risk for cardiogenic shock or who may be preload-dependent. Give 0 . 5 -1 .0 mg/kg for acute or chronic volume overload. Give 1 mglkg to patients with underlying renal insufficiency.

Clinical trials have been conducted with nesiritide, a recombinant human brain natriuretic peptide, in patients hospitalized with decompensated CHF. Compared with placebo and "standard therapy, " nesiritide was associated with improved hemodynamic function, decreased dyspnea and fatigue, and better global clinical status.57

Morphine Sulfate Morphine sulfate remains a part of the therapy for acute pul­ monary edema, although some question its effectiveness, espe­ cially in place of nitrates outside the hospital.58 Morphine dilates the capacitance vessels of the peripheral venous bed. This dilatation reduces venous return to the central circulation and diminishes ventricular preload. Morphine also reduces afterload by causing mild arterial vasodilatation. It also has a sedative effect. More effective vasodilators are now available, so morphine is considered an acceptable adjunct rather than a drug of choice for acute pulmonary edema. Use with caution in NSTEMI patients and those who are at high risk for car­ diogenic shock or who may be preload-dependent. 2 7

Agents to Optimize Initial Blood Pressure First-line actions also include the administration of agents to optimize blood pressure. Patients with acute pulmonary edema have excess adrenergic drive, and many have preex­ isting hypertension. These patients can present with high blood pressures or accelerated hypertension. Often treat­ ment of the pulmonary edema itself will resolve high blood pressure. But initial therapy may include the use of IV nitro­ glycerin as an antihypertensive agent as well as a venodila­ tor. Nitrates will reduce both preload and afterload to achieve this goal. In these patients the goal is to reduce blood pressure by no more than 30 mm Hg below the pres­ entation blood pressure by titration of nitrates. IV nitro­ glycerin is initiated at 10 meg/min and titrated to this target goal. As mentioned, patients may respond to initial therapy with resolution of their elevated blood pressure, decreasing or eliminating the need for IV nitrates. Use caution to avoid precipitating hypotension, because this may aggravate car­ diac ischemia or precipitate organ ischemia in other vascu­ lar beds (e.g., brain, kidneys, or gut).

Second ..Line Actions Patients who respond to first-line actions for pulmonary edema may not require additional therapy unless otherwise indicated (ACEis). If additional therapy is indicated, second­ line actions are based on the patient's SBP and clinical response.

Patients Not in Shock With SBP > 1 00 mm Hg If SBP is > 1 00 mm Hg and not < 3 0 mm Hg below base­ line, an ACEI is given to reduce afterload and attenuate LV remodeling in STEMI patients. ACEis are generally admin­ istered after reperfusion therapy has been achieved and the patient is hemodynamically stable. Other agents can be used as indicated and tailored to the patient's clinical profile. Nitrates can be continued with the precautions noted under first-line actions. Tachyphylaxis (tolerance) to nitrates occurs in about 24 hours, so other agents are considered once the patient is stable. Avoid long-acting and topical prepara­ tions in hemodynamically unstable or potentially unstable patients. Avoid use of nitroglycerin in patients who have taken phosphodiesterase inhitors within the previous 24 hours (48 hours with tildalafil) with hypotension (SBP 2 0 mm maximal thickness), and "very large" (>2 0 mm maximal thickness with cardiac compression)Y The problem with this classification system is that it is most applicable to patients with long-standing or slowly evolving pericardia! effusions. Rapidly forming pericardia! effusions can cause tamponade physiology with circumferential effu­ sions of less than 1 0 mm, especially in patients with car­ diomyopathy dependent on high filling pressures. 3 2 •33 Thus, in assessing an acutely unstable patient without the benefit of prior studies or known cardiac history, the clinician may be better served by the categories of "noncircumferential! physiologic" (see Fig. 8-5 and Video Clip 8-9); "circumfer­ ential, < 1 0 mm maximal thickness" (see Fig. 8-6 and Video Clip 8-6); and "circumferential, > 1 0 mm maximal thickness" (see Fig. 8-7 and Video Clip 8- 1 0), with a further determi­ nation made in each case as to the presence or absence of tamponade (Fig. 8-8 and Video Clips 8- 1 1 and 8- 1 2). Tamponade occurs when the intrapericardial pressure equals or exceeds diastolic filling pressures. The more rapid the accumulation of pericardia! fluid, the smaller the volume necessary to cause tamponade. 2 7•3 2 •3 3 Intrapericardial pres­ sure can rise abruptly with the acute accumulation of as little as 80 to 2 00 mL of fluid. 3 2 Right ventricular diastolic

F I G U R E 8 - 5 • T h i s p a r a s te r n a l s h o r t a x i s vi ew s h ows a n o n ­ c i r c u m f e r e n ti a l p e r i c a r d i a ! effu s i o n (P . E . ) with a p l e u r a l effu s i o n b e h i n d i t . T h e s l i g h tly t h i c k e n e d m i t r a l va lve l e a f l ets i n t h e i r c h a r ­ a ct e r i s t i c l o c a t i o n a r e i n d i c a t e d b y a r r ows. (RV, r i g h t v e n tr i c l e) .

CHAPTER 8

F I G U R E 8 - 6 • T h i s p a raste r n a l s h o r t a x i s view s h ows a m o d e r a t e c i r c u m fe r e n t i a l effu s i o n (arrows) with m e a s u r e d t h i c k n ess o f 9 . 4 mm.

collapse (RVDC) has been shown to b e the most accurate finding in tamponade (Fig. 8-8 and Video Clips 8- 1 1 and 81 2). 34·35 Right atrial collapse is more sensitive but less spe­ cific. 3 5· 3 6 Left ventricular collapse may also occur. 3 5 ·3 7 Subxiphoid and apical four-chamber windows provide good views of the right heart, although the former may be easier to obtain. If cineloop is available, a good image should be obtained, frozen, and the motion of the right ventricular free wall carefully reviewed frame by frame, since RVDC may be fleeting in the tachycardic heart. False-positive diagnoses of pericardia! effusions have been caused by misidentification of epicardial fat, pleural

F I G U R E 8 - 7 • T h i s a p i c a l f o u r c h a m b e r v i ew in a p a t i e n t with c h r o n i c l iver f a i l u r e s h ows a m a ss ive c i r c u m fe r e n t i a l effu s i o n o f u p to m o r e th a n 3 e m i n t h i c k n e s s .

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F I G U R E 8 - 8 • A s s e ss m e n t o f t a m p o n a d e s h o u l d b e d o n e dyn a m i ­ c a l ly, h oweve r t h i s s u b x i p h o i d i m a g e c a u g h t i n d i asto l e s h ows c o l l a p s e of r i g h t a t r i a l (RA) , l e ft a t r i a l (LA) , a n d r i g h t ve n t r i c u l a r (RV) wa l l s .

effusions, and vessels posterior to the heart (e.g., descending aorta, pulmonary vessels, or coronary sinus). 38 Epicardial fat is noncircumferential, localized, has an irregular outline, tends to lie along the paths of the coronary vessels (inter­ ventricular and interatrial grooves), and with optimal gain adjustment demonstrates internal echoes (see Video Clip 8- 1 3). In contrast to effusions it usually gets thinner towards the apex. The distinction between pericardia! and pleural fluid can be made by the conforming shape of the pericar­ dia! sac. Such an apparently obvious distinction may be chal­ lenging in the setting of an unstable patient with limited time, suboptimal cardiac windows, and poor patient posi­ tioning. Efforts should be made to image the fluid in the axillary or scapular lines, looking for the characteristic wedge shape of pleural fluid in the costophrenic sulci. In parasternal views, pericardia! fluid will appear anterior to the descending aorta, while pleural fluid will appear to be sur­ rounding or posterior to it (Video Clip 8-14). The descend­ ing aorta itself can be mistaken for pericardia! fluid when seen longitudinally, but its tubular structure should be apparent in an orthogonal plane (Video Clips 8- 1 5a and b). Severe hypovolemia can also cause diastolic ventricular collapse, but other clinical findings usually clarify the situa­ tion. 33 · 39 If there is any doubt, the IVC should be checked, and if it is not plethoric and with minimal or no respiratory collapse, tamponade is excluded. Conversely, tamponade may occur without RVDC in conditions causing elevated right heart pressures (e.g., pulmonary hypertension). 36 The "sniff test" may help to identify tamponade in this setting: the IVC should collapse by 5 0 % or more of its diameter with sudden inspiration, but will fail to do so with tamponade. Absence of IVC collapse with "sniff" is highly sensitive for tamponade, but since it occurs in many other conditions, it is very nonspecific. Acutely clotting blood (usually in traumatic tamponade) may be mistaken for thickened myocardium, although gain

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mania. The latter three are discussed in the section on the evaluation of acute dyspnea. This section considers the use of bedside ultrasound in the evaluation of acute ischemia and dissection.

Assessment of Cardiac Ischemia

F I G U R E 8 - 9 • T h i s u l t r a s o u n d to k e n l e s s th a n 1 5 m i n u t e s a ft e r t h o r a c i c t r a u m a c a u s e d P E A a r r est f r o m t a m p o n a d e s h ows a t h i c k I oyer of a l r e a dy c l o tt e d b l o o d (C) b e tw e e n t h e e p i c a r d i u m (black arrows) a n d t h e p e r i c a r d i u m (white arrows) , with a t h i n l ayer o f (bla ck) u n c l o t t e d b l o o d b e l ow t h e a n t e r i o r p e r i c a r d i u m . (RV, r i g h t ve n t r i c l e ; LV , l e ft ve n t r i c l e) .

optimization reveals heterogeneous echodensities reflecting blood at different stages of thrombosis (Fig. 8-9).40 While there are a number of echocardiographic findings that, con­ sidered in isolation, can be misleading, their significance is usually clarified by consideration of the clinical context (Fig. 8-8).

B edside Ultrasound in the

Evaluation of Acute Chest Pain: Clinical Scenario

A 76-year-old presents to the ED complaining of approxi­ mately 2 hours' midsternal pressure and shortness of breath. He has no prior cardiac history. At one point he felt as if he were going to "pass out." He smokes and has mild hyperten­ sion. His vital signs reveal a BP of 1 48/88 mm Hg, a pulse of 88, and a pulse oximetry of 98 % . His exam is remarkable only for his anxiety, discomfort, and pallor. His electrocardiogram (ECG) with ongoing symptoms shows a sinus rhythm with left ventricular hypertrophy (LVH) and nonspecific ST-T wave abnormalities. The patient has no prior ECGs for com­ parison.

Indications for Sonography In view of the multiple risk factors, this patient's symptoms are probably due to acute coronary syndrome (ACS). Other, less likely causes of chest pain include aortic dissection, pul­ monary embolism, spontaneous pneumothorax, and pneu-

Several studies have evaluated the ability of echocardiogra­ phy to stratify patients presenting with acute chest pain according to their risk for cardiac events.41-43 The overall predictive value of a positive echocardiogram (identification of wall motion abnormalities) varies with disease prevalence in the study population. In studies where the observed cardiac event rate is high, the predictive value of a positive study is 90% or greater.44-47 Conversely, the absence of wall motion abnormalities predicts that the likelihood of infarct or active ischemia is low but not so low as to reliably exclude the pres­ ence of acute ischemia with negative predictive value (NPV) ranging from 5 7 % to 9 3 % . In groups of low-risk patients with overall event rates of less than 2 0 % , a positive echocar­ diogram is less predictive of subsequent cardiac events, with positive predictive value (PPV) ranging from 3 4 % to 44% .41 •4 2 •48 In this group, the absence of regional wall motion abnormalities identifies low-risk patients, with an NPV of 93 % to 98 % . Although reassuring, this may still not be sufficient to allow safe discharge from the ED . Thus, a resting echocardiogram cam1ot be used alone as the basis for decisions about the disposition of patients with possible ischemic chest pain. The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines on the clinical use of echocardiography give the diagnosis of suspected acute ischemia or infarction a class I recommendation for patients with suspected acute myocardial ischemia when baseline ECG and laboratory markers are nondiagnostic and when the study can be performed during pain or within minutes of its abatement.49•50 The studies of transthoracic echocardiog­ raphy (TTE) in the evaluation of chest pain were performed and interpreted by trained echocardiologists with American Society of Echocardiography level 3 training, a requirement that, given the complexity of wall motion analysis, is unlikely to change. These conditions are met only at the minority of institutions in which echocardiologists are available on a stat basis for image interpretation at all times. 5 1 TTE i s directed t o the detection of segmental wall motion abnormalities, which occur at the onset of myocar­ dial ischemia and may precede clinical symptoms and ECG changes. The location of these abnormalities correlates well with the vessel involved and will reflect changes in regional perfusion in response to therapy. 5 2 • 5 3 In addition to the challenge of performing the test prior to the resolution of symptoms , there are several factors that limit the utility of echocardiography in the s etting of acute ischemia . Segmental wall motion abnormalities are no t specific for acute ischemia, since they can also be caused by myocardi­ tis and cardiomyopathies as well as scarring from prior myocardial infarction. In addition to ischemia, paradoxi­ cal motion of the septum can be due to conduction abnor­ malities , right ventricular (RV) pressure, and volume

CHAPTER 8

overload a n d c a n a l s o b e a sequela of sternotomy. Evaluation of wall motion is particularly dependent on image quality and precisely obtained scanning planes. This frequently limits its usefulness in technically challenging patients, including those with chest wall deformities, obesity, and lung disease. The variety of impediments to wall motion assessment makes it one of the most challenging skills in echocardiography. 54 Most of the studies on this topic have used unen­ hanced TTE. Advances in sonographic technology-such as harmonic imaging, tissue characterization, and use of myocardial contrast agents-improve the overall image quality and possibly the predictive value for ischemic events. 5 5-60 More recent studies have found improved per­ formance when myocardial contrast is used to enhance visualization of the ventricular cavity and assess overall myocardial perfusion. The contrast agents us ed are microbubbles, which have a distinct echogenicity and per­ fus e not only the ventricular cavity but also the myocardium. Studies using myocardial contrast to identify segmental wall motion abnormalities and myocardial per­ fusion demonstrate greater diagnostic accuracy than using unenhanced 2D echo . 5 5-5 8 The impact of echocardiography i n the assessment o f patients witl1 chest pain has n o t been studied i n large-scale prospective trials. Smaller studies have suggested that the benefits include confirmation of clinical impression, espe­ cially among patients at low risk for cardiac disease, and identification of nonischemic cardiac conditions including critical aortic stenosis, hypertrophic cardiomyopathy, and pericardia! disease as well as noncardiac diagnoses such as hemodynamically significant PE and aortic dissection. While sonographic evaluation of the heart by echocardiolo­ gists may be useful in the management of a patient with undifferentiated chest pain, there are currently no large­ scale studies describing the impact of bedside ultrasound in this setting. At this time, the role of noncardiologist, clini­ cian-performed bedside TTE in the evaluation of acute chest pain is not certain.

Aortic Dissection Although one of the less common causes of undifferenti­ ated chest pain, aortic dissection needs to be considered due to its life-threatening nature and the fact that if it is unrecognized, anticoagulation could be catastrophic. TTE for the diagnosis of aortic dissection was first described in 1 972 .61 Since then, studies have suggested a sensitivity of 6 7 % to 80% and a specificity of 99% to 1 00 % using the identification of an undulating intimal flap by TTE or transabdominal ultrasound (Fig. 8 - 1 OA and B and Video Clip 8 - 1 6).6 2 -63 Thus, in cases with a low pretest probabil­ ity of diss ection, ultrasound can b e us ed to screen for disease and confirm the clinical impression, usually in favor of an alternative diagnosis . In cases where the index of suspicion is high, ultrasound cannot reliably exclude the presence of disease. Some patients may have a pericardia! effusion as a clue to the presence of a proximal dissection. To reliably exclude dissection in p atients at high risk,

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A

B F I G U R E 8 - 1 0 • A. A s u p r a s te r n a l t r a n sv e r s e i m a g e o f t h e a o rt i c a r c h (o u t l i n e d by arrows) . B. T h e i n ti m a l f l a p (arrowh e a ds , b o t h i m a g es) c a n b e s e e n e x te n d i n g i n t o t h e a b d o m i n a l a o rt a (l o n g i ­ tu d i n a l vi ew) .

either a transesophageal echocardiogram (TEE) or an alternative imaging modality such as CT or MRI will be necessary.

B edside Ultrasound in the Evaluation of Unexplained Dyspnea: Clinical Scenario

A 5 8 -year-old woman presents to the ED with progressive shortness of breath, productive cough, and chest heaviness. She is 5 feet 2 inches tall and weighs 1 00 kg. She is unable to give a detailed history, but her medications include oral hypoglycemics , antihypertensives , bronchodilators, and steroids. She states she has home oxygen at night and has had problems with "fluid round the heart." Her HR is 1 1 8 , her BP 1 1 2/56, her respiratory rate 3 0 , and she speaks in short, broken sentences. Her breath sounds are distant, with

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rhonchi and possible scattered rales. Her heart sounds are distant, with a 3/6 systolic murmur in the precordium. Her ECG shows sinus tachycardia with low voltages and non­ specific ST-T-wave abnormalities. A portable chest radi­ ograph of poor quality suggests bilateral pleural effusions, and shows no pneumothorax.

Indications for Sonography Several potentially critical disease processes could be caus­ ing the symptoms of this patient. These include ACS , con­ gestive heart failure (CHF)/acute pulmonary edema, cardiac tamponade, PE, pneumonia, massive pleural effusions, and pneumothorax. Each of these entities has described sono­ graphic findings, some of which are sensitive and specific; others are less reliably and consistently found. Bedside ultra­ sound may also guide therapy. Both pulmonary edema and ACS may be caused by, or be the cause of, mitral regurgita­ tion. The patient's murmur may be due to critical aortic stenosis. Management will vary depending on whether the patient has a hypertrophic left ventricle with an ej ection fraction of 7 5 % , or an effaced and dilated one with an EF of 1 0 % , or obvious regions of focal wall motion abnormality. Furthermore, tl1e interventions needed to treat some of the diagnoses in this patient's differential are contraindicated and potentially harmful for others : volume resuscitation, which is needed if this patient has pneumonia and incipient sepsis, would be deleterious if the patient has CHF. Similarly, the anticoagulation that is called for in PE or ACS would be contraindicated if the patient has a large pericar­ dia! effusion with or without tamponade.

Congestive Heart Failure In most cases, the emergent diagnosis and management of pul­ monary edema can be made on clinical grounds without the assistance of ultrasound. However an ultrasound evaluation of mild heart failure or previously unrecognized heart disease in patients presenting solely with undifferentiated dyspnea may lead to the recognition of an unsuspected cardiac etiology such as peripartum cardiomyopathy or viral myocarditis. S everal sonographic parameters are used in routine echocardiography to identify, measure, and detect aspects of cardiac failure. These include diastolic filling velocities, wave­ forms, pressures, and volumes, assessed on both the right and left side of the heart. Cardiac output, tissue Doppler wave­ forms, EF, pulmonary artery pressures, and the IVC are also evaluated. Many of these echocardiographic findings require both time and skills that are not available to most clinician sonographers performing bedside ultrasonography on the critically ill. Of this list, EF has been most extensively studied in bedside sonography, and is most likely to be of use in the first minutes or hours of an acute episode of CHF. As previously noted, qualitative estimates of EF by non­ cardiologists can categorize a patient's cardiac function as "normal" (5 0 % -7 5 % ), "moderately depressed" (3 0%-50% ), and "severely depressed" (< 3 0 % ) (see Video Clips 8-4, 8-Sa and b, 8-6, 8-7a and b, and 8-8).2 1-2 6 In critically ill patients, accurate assessment of EF is possible even when

the exam is abbreviated by limitations of time or lack of access to cardiac windows.57 Two other parameters that can be readily assessed in a focused bedside evaluation for CHF but which, at this time, have not been widely used by inten­ sivist sonologists are mitral valve (MV) inflow velocity and septal velocity measured by tissue Doppler imaging (TDI). Both measurements are made using an apical four-chamber view. The inflow velocity is measured at the tips of the MV and in normal health shows a dual positive deflection due to passive filling in early diastole ("E wave"), followed by a second, smaller, late-diastolic deflection caused by atrial contraction ("A wave ") (Fig. 8 - l l A) . With decrease d myocardial compliance, which is often the result of diastolic dysfunction, there is reversal of the usual E/A

A

B F I G U R E 8 - 1 1 • A a n d B. E (arrowh e a ds) a n d A wove (diago n a l arrows) i n f l ow p a tt e r n s . A. A n o r m a l p a t i e n t i n wh o m E / A i s > 1 . B. D i a s to l i c dysfu n c t i o n i s s u g g e s t e d by t h e E / A r a t i o o f < 1 . A t t h e t o p o f p o rts A a n d B , B - m o d e a p i c a l fo u r - c h a m b e r vi ews (s e e n m o r e c l e a rly in B) o r e s e e n s h owi n g t h e D o p p l e r p a t h (long lin e) and gate (p arallel transverse lin es) , with f l ow a n g l e c o r r e c ­ t i o n (s e e n o n ly i n A ; s e e t e x t) .

CHAPTER 8

ratio > 1 , resulting in an E/A < 1 (Fig. 8 - l l B). With increas­ ing left atrial pressure (LAP) and diminishing effect of the atrial kick, there is "pseudonormalization , " with the E/A returning to > 1 . This can progress to "late stage" dysfunc­ tion, when very high LAP causes E> >A. One of the ways that pseudonormalization can be rec­ ognized is by the use of TDI, a feature found on an increas­ ing number of bedside ultrasound machines. This technol­ ogy applies Doppler principles traditionally used to measure blood flow to the motion of solid tissues. The tissue Doppler gate is placed on the septum (or lateral wall) adjacent to the MV annulus, and a waveform is recorded. Like the MV inflow waveform, the waveform of the normal septum shows a dual deflection in diastole. The first deflection is known as the " e ' ("E prime") wave" (Fig. 8- 1 2). The ratio E/e ' is then calculated. Normal LV filling pressures and intravascular volume are reflected by E/e ' < 8 ; increased left ventricular filling pressures by an E/e ' > 1 5 .63-66 Values between 8 and 1 5 are of indeterminate significance. The use of Doppler and TDI in the hands of nonechocardiologists has not been widely reported.67 However, the relative speed and simplic­ ity of the test make it likely that this technique will be of use to intensivist bedside sonographers, especially in patients with dilated IVCs, which might be clinically suspected of being due to factors other than fluid overload, such as pul­ monary hypertension and right heart failure or severe tri­ cuspid insufficiency. In patients with clinical failure, an assessment of gross cardiac size and wall thickness may also be helpful. Nomograms based on gender, age, and habitus have been developed but are unlikely to be accessible in caring for a critically ill patient. The range of normal end-diastolic

F I G U R E 8 - 1 2 • M o t i o n o f the s e p t u m i s away f r o m t h e t r a n s ­ d u c e r i n d i a s to l e , s o t h a t t h e wave f o r m o f i t s m o t i o n i s r e p r e ­ s e n t e d i n a n e g a tive d i r e c ti o n . T h e e ' waves a r e i n d i c a t e d b y a r r owh e a d s . T h e a ' wave s , wh i c h o r e f r e q u e n tly n o t c l e a r ly s e e n , a r e i n d i c a t e d by d i a g o n a l a r r ows.

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dimensions (measured from septum to posterior free wall at the level of the mitral leaflets) is 3 5 to 60 mm.68 Normal diastolic LV wall thickness (measured on the septum or pos­ terior free wall at the level of the distal mitral leaflets) ranges from 8 to 1 2 . 5 mm.68 Low ventricular volumes and thick­ ened ventricular walls in the setting of failure suggest hyper­ trophy and luseotropic failure. Conversely, a dilated ventri­ cle with effaced ventricular walls suggests likely primary forward failure. Focal wall motion abnormalities may sug­ gest unrecognized cardiac ischemia.

Pulmonary Embolus PE sufficient to cause hemodynamic instability results in gross, readily identifiable echocardiographic abnormali­ ties.69-73 Several parameters that can be readily assessed by a bedside clinician sonographer have been used, including right ventricular (RV) to LV dimension ratio, intracardiac thrombus , septal wall flattening, abnormal septal wall motion, and loss of the normal IVC collapse index.73 Other sonographic findings, such as tricuspid regurgitant peak flow velocities and pulmonary artery hypertension, require time­ consuming color-flow and spectral Doppler analysis that is beyond the expertise of most critical care bedside sonogra­ phers. 74 Reports of the accuracy of echocardiography in the evaluation of stable patients with PE are inconsistent, so that this modality should be used only to exclude PE in patients with hemodynamic instability. The following dis­ cussion focuses on this group. The normal RV end-diastolic dimension, measured at the tips of the tricuspid leaflets in the apical four-chamber view (or subxiphoid if that is not possible) should be less than 2 7 mm.7; This RV dimension will be exceeded in hemody­ namically significant PE as well as many other causes of car­ diac dilatation. Another index of RV enlargement-which can be obtained without the time-consuming process of caliper measurement does not require the memorization of arbitrary numbers and will not be falsely positive in the case of global dilated cardiomyopathy-is the right-to-left ventricular ratio, usually estimated at end-diastole. This is normally < 60% . In patients with acute PE, the ratio is almost always > 1 00% (see Video Clips 8- 1 7a and b and 8 - 1 8 , and 8- 1 9). 1 6 Chronic pulmonary hypertension also causes RV dilation but is likely to be accompanied by a thickened ventricular wall, whereas in PE the RV wall is effaced ( 7 5 % a n d p o ss i b l e e n d - systo l i c collapse.

I n te r p r e t a ti o n

P o t e n ti a l ly Reve r s i b l e E ti o l o g i e s

I n te rve n t i o n

U n d e r fi l l e d ve n t r i c l e , hypovo l e m i a

I n travasc u l a r hypovo l e m i a

P u l m o n a ry hyp e r t e n s i o n (a c u te)

P u l m o n a ry e m b o l i s m

F l u i d s , c o n s i d e r lyt i c t h e r a py

P e r i c a r d i a ! ta m p o n a d e

Myo c a r d i a l r u p tu r e , m a l i g n a n cy, i n fe c ti o u s

Peric o r diocentesis

Ca r d i o g e n i c s h o c k

AMI

E n d -sta g e c a r d i o myo p a thy

Co n s i d e r t o x i c a n d m e ta b o l i c c a u s e s : CCB a n d B B ove r d o s e , hyp e r k a l e m i a , e t c .

I n o t r o p i c t h e r a py, I A B P , PTCA

Ca r d i a c sta n d s ti l l

M a ss ive M I

E l e c tr o m e c h a n i c a l dissociation

E l e c tr o lyte (hyp e r k a l e m i a)

Vo l u m e r e p l a c e m e n t Search for sources of bleeding

S l i t- l i k e IVC M a x IVC d i a m e t e r 7 5 % (s e e t e x t) RV > LV Paradoxical septal m otion D i l a t e d IVC with b l u n te d r e s p i r a to ry va r i a t i o n Pericardia! effusi o n , RV c o l l a pse D i l a t e d IVC w i t h b l u n te d r e s p i r a to ry va r i a t i o n G r o ssly hyp o c o n tr a c ti l e ve n t r i c l e s D i l a t e d IVC with b l u n t e d r e s p i r a to ry va r i a t i o n N o wa l l m ove m e n t , r e g u l a r c a r d i a c r hyth m

Specific therapies

A M I , a c u t e myo c a r d 1 a l l nfarct1 o n ; B B , b e ta - b l o c k e r , CCB , c a l c 1 u m c h a n n e l b l o c k e r ; I A B P , 1 n t r a - a o rt 1 c b a l l o o n p u m p , IVC, m f e n o r v e n a c ava , IVC-CI , 1 n f e n o r v e n a c ava c o l l a p se 1 n d e x ; LV. l e ft ventr i c l e ; PTCA , p e r c u t a n e o u s t r a n s l u m 1 n a l c o r o n ary a n g 1 o p l a sty; RV. r 1 g h t ventr i c l e .

CHAPTER 8

o f intracardiac thrombus, may guide the termination resus­ citative efforts following ACLS guidelines, thus minimizing the Uflll e cessary expenditure of health -care resources (Video Clip 8-26a and b). 105 The risks and costs of routine performance of ultra­ sound in PEA arrest are minimal, although a potential draw­ back is the interruption of CPR while the study is per­ formed. In the patient who has a witnessed arrest in the presence of health-care providers, sonography can be per­ formed as part of the initial "look, listen, and feel" assess­ ment. For the majority of patients, resuscitative efforts are well under way by the time they can be assessed sonograph­ ically, and interruptions in CPR should be minimal.98 In a manikin study, Breitkreutz evaluated sonography performed by a dedicated rescuer as part of a resuscitation algorithm after a minimum of five cycles of high-quality CPR. 108 The ultrasound exam was done in 5 seconds or less using the sub­ xiphoid window, and the quality of the CPR was compared with a standard approach without ultrasound. They found that sonography did not affect no-flow intervals and that adherence to recommended CPR cycles was actually improved. The authors demonstrated that this algorithm can be taught in an 8-hour course, which includes acquisi­ tion of images within the 5-second time frame and accurate interpretation of 5 -second video clips of normal and patho­ logic conditions, including pericardia! effusion, asystole, hypovolemia, and reduced LV function.

B edside Ultrasound as an

Adjunct to Invasive Procedures Indications for Ultrasound

Many invasive procedures are performed in the resuscitation of the critically ill. Ultrasound has been described as an adjunct in the performance of almost all of them, including peripheral and central venous access and thora-, pericardia- , and para­ centesis. While some of these techniques are beyond the scope of this chapter, the prima facie validity of the concept that an invasive procedure would be safer with visual guidance than without it means that several of these techniques have not been evaluated by randomized prospective trials and that such trials may never be undertaken. It is probable that the use of ultra­ sound as an adjunct in invasive procedures will continue to grow as sonography becomes more widespread and clinician sonographers gain skill and experience. The following discus­ sion focuses on those procedures that at this time are com­ monly performed with the ultrasound guidance.

Central Line Placement With increasing focus on health-care safety and the reduc­ tion of medical errors, ultrasound guidance for central vein cannulation has been recommended by the U. S . Department of Health and Human Services. In a report prepared in 2 00 1 by the Agency for Health Care Research and Quality, ultra-

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sound guidance for central vein cannulation was listed as one of the 1 1 most highly rated safety practices. 109 This report was based on a meta-analysis of all prospective studies in the English language medical literature on this topic. A similar review, coming to similar conclusions, was published by the National Institute for Clinical Excellence (NICE) in 2003 Y0 There has been some debate over these recommen­ dations, and implementation 6 years later is far from univer­ sal. 1 1 1 · 1 1 2 However, the increasing availability of inexpensive ultrasound equipment, the intuitive advantages of direct visualization, and the difficulty of attaining the experience required for expertise in the landmark technique are likely to make ultrasonography increasingly widely used for cen­ tral venous access. Placement of a central line in an unstable patient may be compromised by hypotension, other ongoing resuscita­ tive efforts, and the patient's inability to cooperate. Bedside ultrasound has been shown to improve the likelihood of suc­ cessful central vein cannulation and to reduce the number of complications. These advantages are likely to be com­ pounded in unstable patients as well as those with poor anatomic landmarks, prior failed attempts at blind cannula­ tion, and prior central lines. The primary role of ultrasound in central vein cannula­ tion is to locate the vessel, ensure patency, and document placement of the catheter within the lumen. Whether the actual cannulation of the vein is observed sonographically is up to the individual practitioner. Typically one will watch for evidence of the needle's proximity to the vein, which will cause the vein to indent. As the vein is entered, it will briefly collapse and then rapidly rebound once cannulated. At this point blood will be aspirated into the syringe and the catheter placement continues "blindly. " Prior to actually using the catheter for infusion, it should be visualized within the lumen of the vessel. Central vein localization and can­ nulation can be readily accomplished using either transverse or longitudinal imaging planes. More experienced sonogra­ phers find the longitudinal view allows for more accurate localization of the needle tip.

Internal Jugular Vein Cannulation of the internal jugular vein, when performed under sonographic guidance, has been shown to require fewer attempts and is less likely to be complicated by carotid puncture, brachial plexus injury, or hematoma. 1 1 3-1 16 The relationship between the internal jugular vein and the carotid artery is highly variable and changes with head rota­ tion, which often causes the vein to lie directly anterior to the artery. Knowledge of the patient's anatomy prior to puncture reduces the chance of inadvertent carotid punc­ ture. l l 7· 1 1 8 In addition to locating the vessel, ultrasound can be used to identify its depth, size, and patency and to show changes in response to Valsalva and Trendelenburg. Unless precluded by clinical circumstances, every attempt should be made to position the patient in Trendelenburg. The internal jugular vein and carotid artery will appear as relatively superficial structures. When viewed in the transverse plane, the internal jugular vein is a thin-walled

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ovoid anechoic structure anterior and lateral to the carotid artery, which, unless the patient is in full arrest, will collapse much more easily than the artery (Fig. 8- l SA and B). The entire course of the vein and artery in the neck should be reviewed and the optimal head position and the most con­ venient location for cannulation chosen.

Femoral Vein As with cannulation of the internal jugular vein, the use of sonographic guidance in femoral vein catheterization leads to a greater chance of success and fewer complications com­ pared with standard landmark-guided technique. 1 1 9•1 2 0 Hilty found that in patients undergoing CPR, ultrasound-guided femoral venous access had a success rate of 90 % , with no arterial punctures, compared with rates of 6 5 % success and a 2 0 % femoral artery puncture in patients using the tradi­ tional landmark technique. 1 2 0 When viewed in the transverse plane, the femoral artery and vein will appear as superficial anechoic circular struc­ tures. High in the femoral triangle, the vein is found in its traditionally described location, medial to the artery.

A

However, within centimeters o f the inguinal crease, i t trav­ els posterior to the artery, precluding direct access. The vein can usually be recognized by it location, its thinner walls, its compressibility, and its larger size (the last two are unreliable in cardiac arrest). All central veins are subject to venous pul­ sations, so this finding should be used with caution in dis­ tinguishing it from the artery, especially in patients under­ going CPR, where pulsations will be seen primarily in the vein. 1 2 1 The vessel's size can be increased by reverse Trendelenburg or applied inguinal pressure proximal to the intended site of cannulation.

Subclavian Vein The subclavian vein (SCV) is a commonly used site for cen­ tral venous access during resuscitative efforts because the anatomic landmarks are clear, the vein is tethered by mus­ culoskeletal structures, and access can be performed without interruption of airway management or CPR. The procedure is not without complications, including arterial puncture and pneumothorax. The benefits of ultrasound guidance in SCV catheterization are not as clear cut as those in accessing the internal jugular vein, although some studies have shown that sonographic guidance improves the likelihood of successful placement, reduces the number of attempts needed, and decreases complications, including arterial puncture, hematoma, pneumothorax, and catheter malposition. 1 10•1 22 The SCV can be visualized by using either a supra- or infra­ clavicular window. If the supraclavicular approach is used, the ultrasound probe is placed parallel to and above the clavicle. The internal jugular vein is identified and then followed down to where it joins the subclavian vein. When the infraclavicular approach is planned, the probe is placed parallel and inferior to the most lateral aspect of the clavicle (Fig. 8- 1 6A and B). The SCV usually lies anterior to the artery in this plane and can be identified by typical venous features of respiratory variation, thin wall, dilation with Valsalva, and compressibility. Both approaches to the subclavian may be limited by the size of available linear array transducers, since a wider probe (e.g., 5-7 em) may preclude simultaneous visualization and access to the skin for the procedure. If a narrower-footprint transducer is not available, many experienced clinicians will access the distal axillary vein, lateral to the deltopectoral groove.

P ericardiocentesis

B F I G U R E 8 - 1 5 • A. I n t h i s t r a n sverse vi ew t h e b e a m o f t h e u l t r a ­ s o u n d i n te r s e cts t h e c a r o t i d a rt e ry a n d t h e i n t e r n a l j u g u l a r v e i n i n a t r a n sverse p l a n e . B . A s t h e n e e d l e a p p r o a c h es t h e ve i n , i t wi l l i n d e n t t h e ve i n . A n a l t e r n a tive a p p r o a c h i s to i m a g e t h e ve i n i n t h e l o n g i tu d i n a l vi ew. T h e p o t e n ti a l b e n efits i n c l u d e m i n i m i z i n g t h e r i s k o f p u n ct u r e o f t h e p o ste r i o r wa l l .

The role of bedside sonography in the management of patients with suspected pericardia! effusion is to establish the diagnosis and directly visualize placement of the aspirating needle or catheter within the pericardia! sac. Prior to the use of sonography, aspiration of the pericardia! sac was usu­ ally performed as a last resort effort in patients with PEA. The traditional approach involves a blind stick from the subxiphoid region through the left lobe of the liver. This technique is associated with a variety of complications, including liver injury, lung puncture, pneumothorax, and laceration of the myocardium or coronary vessels . Over the past decade, ultrasound guidance has become standard in

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much lower complication rates and higher success rates. 1 2 3 , 1 2 6 , 1 2 7 The patient is placed with the head of the bed slightly elevated, in a semidecubitus position on the left side to max­ imize cardiac contact with the chest wall. The rib space where the effusion is thickest and most directly accessible below the probe is located. Ideally, a site more than 5 em from the left sternal border is found to avoid the internal mammary artery. The sonographer analyzes and memorizes the planned angle and direction of the pericardiocentesis needle. The needle is directed along the predetermined tra­ j ectory into the pericardia! sac. Real-time sonographic information can be obtained from an adjacent window, but this is rarely practical in the management of critically ill patients. If pericardia! drainage is not successful or stops, the location of the catheter can be checked by direct visualiza­ tion or by use of a bedside sonographic contrast agent. This can be created by squirting 5 to 1 0 mL of saline back and forth between two partly filled syringes by way of a three­ way stopcock. This aerated solution is then introduced through the catheter. If it is in the correct location, the con­ trast agent will be seen entering the pericardium (Video Clip 8-27). Complications of ultrasound-guided pericardiocente­ sis in large series are very rare. 1 2 3 • 1 2 8• 1 2 9 They include hemothorax, pneumothorax, b acterial p ericarditis, and failure of drainage. A technique using a probe-mounted needle has also been shown to be equally successful, but such equipment is often unavailable in critical care settings . 1 3 0

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B F I G U R E 8 - 1 6 • A. To vis u a l i z e t h e s u b c l avi a n a rt e ry a n d ve i n , t h e p r o b e i s p l a c e d t r a n sversely j u st b e l ow t h e d i s t a l c l avi c l e . B. T h e a r t e ry wi l l a p p e a r a s a s m a l l , n o n c o m p r essi b l e vess e l w i t h p u l ­ s a t i l e f l ow i f c o l o r f l ow D o p p l e r is u s e d . T h e a dj a c e n t ve i n , wh i c h i s u s u a l ly l o c a t e d a b ove t h e a rtery, wi l l b e t h i n -wa l l e d a n d r e a d i ly c o l l a ps e u n d e r p r essu r e . I n t h i s i m a g e , c o l o r - f l ow e n h a n c e m e n t c l e a r ly i d e ntifies t h e ve i n (blue) a n d t h e a rtery (red) .

the aspiration of pericardia! effusion in the stable patient and is often p erformed at the bedside as a temporizing measure prior to definitive management. 1 02 • 1 2 3-1 2 5 In the critically ill, the indication is usually massive effusion or tamponade. With the advent of bedside ultrasonography, this procedure is not indicated unless a pericardia! effusion is identified. The best window is that which identifies a direct needle path to the effusion. Ideally tl1is path should be short and removed from the liver, lungs, and myocardium. Except in patients with advanced emphysema, it is extremely unusual to have difficulty establishing a direct sonographic and pro­ cedural pathway to large p ericardia! effusions from the parasternal rib spaces of the anterior chest wall . Thus , except in unusual circumstances, ultrasound guided pericar­ diocentesis employs a direct transthoracic approach rather than the traditional subxiphoid transhepatic metlwd, with

Thoracentesis The use of ultrasound to guide aspiration is routine in the management of pleural effusions. Complications includ­ ing pneumothorax, dry aspiration, inadvertent liver or splenic lacerations, and subcutaneous hemorrhage. These are reduced when the procedure is performed under sonographic guidance . m · 1 3 2 In addition, ultrasound can distinguish between tissue masses, fluid, and loculations in cases where these cannot be distinguished on chest radi­ ography. The optimal position for thoracentesis is with the patient seated comfortably with the arms supported by a table and the back exposed to the physician. 1 3 3 In most cases where there are no loculations, this will allow the effusion to collect in the most dependent space in the thorax: the posterior costophrenic sulcus. If the patient is unable to sit, tl1e procedure can be performed supine, although this makes it technically more challenging and precludes an eval­ uation of the posterior costophrenic sulcus. A site should be located at the point of greatest depth of the effusion and where there is a surrounding area free of overlying lung and diaphragm throughout the respiratory cycle. Thoracentesis should probably be avoided if the depth of the effusion is < 1 5 mm from the parietal to the visceral pleura throughout the respiratory cycle and if the effusion does not extend at

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least one rib space above and below the site of needle entry. Scanning through transverse and longitudinal planes around the site of the planned thoracentesis should be performed to identify nearby lung, heart, and diaphragm. For larger effusions, pleurocentesis can be performed as a two-step procedure. In the first step , the site is iden­ tified by ultrasound, the distance between the skin surface and the parietal pleura is measured so that the distance to which the needle will have to be inserted is known, and the skin is marked, with care that mobile skin folds are not dis­ placed by the ultrasound probe. The patient should be kept still while the area is prepped and draped and stan­ dard sterile thoracentesis is accomplished, usually within 1 minute . If the fluid pocket is small, a one-step technique is used in which the chest wall is punctured with real-time guidance from the ultrasound probe, protected by a ster­ ile cover and located immediately adj acent to the thora­ centesis needle.

strate that the sonographic impression of capture correlates with hemodynamic improvement. 13 8

I ssues of Training and Skill Acquisition

As this chapter demonstrates, clinicians have found uses for a wide range of ultrasound applications in their resuscitation of the critically ill. Common to all these applications is that they are limited in scope andfocused by the need to answer spe­ cific clinical questions. Despite these limitations, clinician­ performed bedside ultrasonography, like the history and physical exam, is an operator-dependent diagnostic modal­ ity that can be mastered only through a combination of training and experience. For this reason, training and prac­ tice guidelines for bedside ultrasonography have been devel­ oped by the specialty societies of the clinicians who use it.

Transvenous Pacemaker Insertion Transvenous cardiac pacing is often required for the patient with symptomatic bradycardia or heart block for whom trans­ cutaneous pacing fails to provide consistent capture or is poorly tolerated by the patient. Under optimal conditions, for­ ward flow will float the catheter into the right ventricle and ensure contact with the right ventricular wall, conditions that may not be met in patients who are hemodynamically com­ promised or who require emergent pacing. Success rates for blind transvenous pacemaker insertion with capture of the heart are highly variable, ranging from 1 0 % to 90% . Bedside sonography can readily demonstrate the passage of the pacing wire into the right ventricle, confirm contact with the right ventricular myocardium, and verify successful capture of the ventricle. Pacing catheter wires are highly reflective of sound waves and appear as bright linear echoes within the heart (Video Clip 8-28). The pacing wire can be tracked passing into the right ventricle and maneuvered under direct visualization into the ventricular apex. Myocardial capture is demonstrated sonographically as rhythmic contractions of the heart at the paced rate. Complications of pacemaker placement, including malposition and septal perforation, can also be identified by ultrasound. 134-137

Assessment of Capture by Transthoracic Pacemaker Although application of a transthoracic pacemaker is rela­ tively straightforward, it may be difficult to ascertain whether there is ventricular capture. The large currents generated by the pacemaker and skeletal muscle contraction may make rhythm strips difficult to interpret. Additionally, many devices have special damping circuits that make the pacer spikes hard to identify. Ultrasound can confirm capture by identifying ventricular contractions occurring at the paced rate. This can be tested by monitoring cardiac activity in response to changes of rate and output (Video Clip 8-29). Studies describ­ ing the role of ultrasound in this setting are small but demon-

·�····· ······························································································ S e e W e b s i t e f o r A CE P Cl i n i c a l P o l i cy o n

'V'

U l t r a s o u n d G u i d e l i n e s . A S E / A CC p o l i cy sta t e ­ m e n t o n e c h o c a r d i o g r a p hy i n e m e r g e n cy medicine.

Ultrasound assessment o f the heart has traditionally been the purview of echocardiologists. As noted in the dis­ cussion of chest pain above, American S ociety of Echocardiography (ASE) level 2 and 3 echocardiographic studies exceed most of the focused limited questions being asked during resuscitation and require expertise and experi­ ence beyond that available to most general intensivists. 1 3 9 Furthermore, echocardiologists with these skills are rarely available around the clock to perform or interpret such exams. 5 1 As noted previously, studies have shown that bed­ side ultrasonography significantly enhances the ability of a clinician, regardless of specialty or level of training, to eval­ uate and treat patients .54 •93 · 140-144 Although a complete echocardiographic examination may provide additional information about the patient's condition, this information is likely to be moot until the patient's condition has stabi­ lized. 1 3 9 The training necessary for this level of sonographic evaluation has been a topic of debate between and within specialty societies. 145-148 The ASE considers that the most basic sonographic evaluation of the heart (level I) requires 3 months of training, including 7 5 exams performed and an additional 7 5 exams interpreted. 149 VVhether these training requirements are appropriate for clinicians in emergency or critical care fields continues to be scrutinized by those spe­ cialty societies as they develop training and practice guide­ lines tailored to their practice domains. 147 · 1 50-1 54 Training programs in bedside ultrasonography typically start with cognitive and visual pattern-recognition skills. Since clinician sonographers cannot rely on technicians to obtain their images, they require practical training in

CHAPTER 8

"knobology" and the acquisition of images. This psychomo­ tor skill can be attained only by physical practice and expe­ rience, so that proctored hands-on training sessions are . . d , usua IIy as part o f a b as1c trammg . . course. 154-155 Th.I S reqmre is followed by a period of monitored practice. The scope and length of training programs as well as methods for assessing competence continue to be debatedY5 It is likely that as resuscitation techniques evolve, so too will the clinical and sonographic skills needed to support them. These will man­ date evolving skill sets and training. With this in mind, the clinician sonographer, regardless of experience, is always aware of the focused limited nature of the bedside ultra­ sonographic examination and, in equivocal cases, of the need for more definitive testing, often by imaging specialists.

Acknowledgment The authors would like to express their gratitude to James N. Kirkpatrick for assistance in the preparation of parts of this manuscript.

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2 006; 1 1 4(9) :945-9 5 2 . 4 0 . Choo MH, Chia B L , Chia FK, e t a l . Penetrating cardiac injury evaluated by two-dimensional echocardiography. Arn Heal't J 1 984; 1 08(2):41 7-42 0. 41. Sabia P, Afrookteh A, Touchstone DA, et al. Value of regional wall motion abnormality in the emergency room diagnosis of acute myocardial infarction. A prospective study using two-dimen­ sional echocardiography. Circulation 1 9 9 1 ;4:I8 5-I92 . 42 . Kontos MC, Arrowood JA, Paulsen WHJ, et al. Early echocar­ diography can predict cardiac events in emergency department patients with chest pain. Ann Eme1•g Med 1 99 8 ; 3 1 : 5 5 0-5 5 7 . 43 . Levitt MA, Promes S B , Bullock S , e t al. Combined cardiac marker approach with adjunct two-dimensional echocardiogra­ phy to diagnose acute myocardial infarction in the emergency department. Ann Eme1·g Med 1 996;2 7 : 1-7. 44. Peels CH, Visser CA, Kupper AJ , et al. Usefulness of two­ dimensional echocardiography for immediate detection of myocardial ischemia in the emergency room. American Joumal of

Cardiology 1 990;65(1 1) :687-69 1 . 45. Mohler ER, Ryan T, Segar D S , et al. Clinical utility of troponin T levels and echocardiography in the emergency department. Am Heart ] 1 998; 1 3 5 : 2 5 3-2 60. 46. Sasaki H, Charuzi Y, Beeder C, et al. Utility of echocardiography for the early assessment of patients with nondiagnostic chest pain.

Am Heart J 1 986; 1 2 :494-497 . 47. Horowitz R S , Morganroth J, Parrotta C, e t a l . Immediate diag­ nosis of acute myocardial infarction by two-dimensional echocar­ diography. Cimt!ation 1 982;65(2) : 3 2 3-3 2 9. 47a. Horowitz RS, Morgan roth ]. Immediate detection of early high­ risk patients with acute myocardial infarction using two-dimen­ sional echocardiographic evaluation of left ventricular regional wall motion abnormalities. American Heart Joumal 1 9 82 ; 1 03 (5):

8 1 4-82 2 . 4 8 . Kontos MC, Arrowood JA, Jesse RL, e t al. Comparison between 2 -dimensional echocardiography and myocardial imaging in the emergency department in patients with possible myocardial ischemia. Am Heart J 1 998; 1 3 6:724-7 3 3 . 49. B raunwal d E , Amman EM, B easley JW, e t a l . American College of Cardiology. American Heart Association. Committee on the Management of Patients With Unstable Angina. ACC/AHA 2 002 guideline update for the manage­ ment of patients with unstable angina and non-ST-segment elevation myocardial infarction-summary article : a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina) . JAm Colt

Cardio/ 2 002 ;40(7) : 1 3 66- 1 3 74. 50. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2 003 guideline update for the clinical applica­ tion of echocardiography-summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1 997 Guidelines for the Clinical Application of Echocardiography). J Am Colt Cardiol 2 003 ;42 (5):954-970. 5 1 . Beaulieu Y. Bedside echocardiography in the assessment of the critically ill. Crit Cm•e Med 2007 ; 3 5 (5 Suppl):S2 3 5-S249. 5 2 . Hauser A.J\1., Gangadharan V, Ramos RG, et al. S equence of mechanical, electrocardiographic and clinical effects of repeated coronary artery occlusion in human beings: echocardiographic observations during coronary angioplasty. J Am Colt Cardiol

1 9 8 5 ; 5 : 1 93-197. 53. Lundgren C, Bourdillon PD, Dillon JC, et al. Comparison of contrast angiography and two-dimensional echocardiography for

2 000; 1 3 (4) : 3 3 1-342 . 60. Kalvaitis S, Kaul S, Tong KL, et al. Effect of time delay on the diagnostic use of contrast echocardiography in patients pre­ senting to the emergency department with chest pain and no S­ T segment elevation. J Arn Soc Echocadiog1• 2 006; 1 9 ( 1 2 ) :

1 488-1493 . 6 1 . Millward DK, Robinson NJ, Craige E. Dissecting aortic aneurysm diagnosed by echocardiography in a patient with rup­ ture of the aneurysm into the right atrium; rare cause for contin­ uous murmur. American Journal of Cardiology 1 972 ; 3 0(4):42 7 -4 3 1 . 62 . Cobbs BW Jr, Nicholson WJ . Diagnosis of dissecting aortic aneurysm with suprasternal echocardiography. Arn J Cardiol

1 980;45(1): 1 83-1 84. 6 3 . Victor MF, Mintz GS, Kotler MN, et al. Two dimensional echocardiographic diagnosis of aortic dissection. Am J Cardiol 1 9 8 1 ;48(6) : 1 1 5 5-1 1 5 9. 63 a. Nagueh SF, Middleton KJ, Kopelen HA , et al. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricu­ lar relaxation and estimation of filling pressures. JAm Colt Cardiol

1 997;3 0(6) : 1 52 7- 1 5 3 3 . 64. Nagueh SF, Lakkis NM, Middleton KJ, e t al. Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation 1 999;99(2):254-2 6 1 . 6 5 . Ommen SR, Nishimura RA, Appleton CP, e t al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the esti­ mation of left ventricular filling pressures: a comparative simulta­ neous Doppler-catheterization study. Circulation 2 000; 1 0 2 ( 1 5):

1 7 88- 1 7 94. 66. Kasner M, Westermann D, Steendijk P, et a!. Utility of Doppler echocardiography and tissue Doppler imaging in the estimation of diastolic function in heart failure with normal ejection fraction: a comparative Doppler-conductance catheterization study.

Circulation 2007; 1 1 6(6):63 7-647. 67. D ean A, Hayden G, Mark D , et al. Bedside ultrasonography assessment of mitral valve inflow velocity and tissue Doppler are similar to echocardiology measurements. Acad Emerg Med 2 007;

1 4: 5 1 0 1-5 1 02 . 68. O h JK, Seward JB, Tajik AJ, et a!, eds. The Echo Manual, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 1 999, appendix. 69. Torbicki A. Imaging venous thromboembolism with emphasis on ultrasound, chest CT, angiography and echocardiography.

Th1•omb Haenwst 1 999;82(2):907-9 1 2 . 7 0 . Frazee B W, Snoey ER. Diagnostic role o f E D ultrasound i n deep venous thrombosis and pulmonary embolism. Am J Enterg Med 1 999; 1 7(3):2 7 1 -2 7 8 . 7 1 . Rudoni RR, Jackson RE, Godfrey G W, e t a l . Use o f two-dimen­ sional echocardiography in the diagnosis of pulmonary embolus.

J Emerg Med 1 998; 1 6(1):5-8. 72. Lualdi JC, Goldhaber SZ. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. Am Hem·t J 1 995; 1 3 0 : 1 2 76-1 2 8 2 . 7 3 . Weston MJ, Wilde P. Echocardiographic diagnosis o f massive pulmonary embolism. B1· ] Radiol 1 989;62 (740):75 1-7 5 3 . 74. Grifoni S, Olivotto I , Cecchini P, e t al. Utility o f a n integrated clinical, echocardiographic, and venous ultrasonographic

CHAPTER 8

approach for triage of patients with suspected pulmonary embolism. Am J Cardia/ 1 998;82 ( 1 0) : 1 2 3 0- 1 2 3 5 . 7 5 . Cheriex E C , Sreeram N , Eussen YF, e t a!. Cross sectional Doppler echocardiography as the initial technique for the diag­ nosis of acute pulmonary embolism. B•· Heart J 1 994;72(1): 52-5 7 . 76. Kasper W, Meinertz T, Kersting F, e t a!. Echocardiography in assessing acute pulmonary hypertension due to pulmonary embolism. Am J Cardio/ 1 980;45(3):5 67-5 7 2 . 7 7 . Goldberger JJ, Himelman R B , Wolfe CL, et a!. Right ventricular infarction: recognition and assessment of its hemodynamic sig­ nificance by two-dimensional echocardiography. J Anz Soc

Echoca.-diogr 1 9 9 1 ;4(2): 1 40-146. 78. Sharkey SW, Shelley W, Carlyle PF, et al. M-mode and two­ dimensional echocardiographic analysis of the seprum in experi­ mental right ventricular infarction: correlation with hemody­ namic alterations. Ant Heart J 1 9 8 5 ; 1 1 0(6): 1 2 1 0-1 2 1 8 . 79. Kinch JW, Ryan TJ. Right ventricular infarction. N Eng! J Med

1 994; 3 3 0( 1 7): 1 2 1 1 -1 2 1 7 . 8 0 . Steiner P, Lund GK, Debatin JF, e t a ! . Acute pulmonary embolism: value of transthoracic and transesophageal echocardio­ g-raphy in comparison with helical CT. AJD 1 996; 1 67:93 1-93 6. 80a. Agricola E, Bove T, Oppizzi M, et a!. Ultrasound comet-tail images: a marker of pulmonary edema: a comparative srudy with wedge pressure and extravascular lung water. Chest 2 005 ; 1 2 7(5):

1 690- 1 69 5 . 8 1 . Bedetti G , Gargani L, Corbisiero A , et a!. Evaluation o f ultra­ sound lung comets by hand-held echocardiography. Cm,diovasc Ultrasound 2 006;4: 34. 82 . Soldati G, Rossi M. "Wet" and "dry" lungs: a useful sonographic distinction. Crit Care 1 999;3 (Suppl 1): 1 24-1 2 5 . 8 3 . Lichtenstein D , Meziere G , Biderman P, e t al. The comet-tail artifact. An ultrasound sign of alveolar-interstitial syndrome. Am J Resph· Crit Cfm Med 1 997; 1 5 6(5): 1 640-1 646. 84. Lichtenstein D , Goldstein I, Mourgeon E, et a!. Comparative diagnostic performances of auscultation, chest radiography, and lung ultrasonography in acute respiratory distress syndrome.

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97. Nolan JP, Deakin CD, Soar J, et a!. European Resuscitation Council guidelines for resuscitation 2 0 0 5 : S ection 4. Adult advanced life support. Resuscitation 2 005;67(Suppl 1 ) : S 3 9-S 86. 98. Hazinski MF, Nadkarni VM, Hickey RW, et a!. Major changes in the 2 005 AHA Guidelines for CPR and ECC: reaching the tipping point for change. Cin·ulation 2 0 0 5 ; 1 1 2 (24 Suppl) : IV2 06-IV2 1 1 . 99. AHA/ECC Guidelines 2 000 for cardiopulmonary resuscitation and emergency cardiovascular care. Cin:ulation 2 000; 1 02 (Suppl 1):11 50-1 1 5 2 . 1 00. Cummins R O , e d . A CLS P1'ovider Manual. Dallas : American Heart Association, 2 00 1 :2 0 1 . 1 0 1 . Niendorff D F. Rapid cardiac ultrasow1d o f inpatients suffering PEA arrest performed by nonexpert sonographers. Resuscitation 2005; 67(1): 8 1 -8 7 . 1 0 2 . Blaivas M, Fox ]C. Outcome o f cardiac arrest patients found to have cardiac standstill on the bedside emergency department echocardiogram. Acad Enze1·g Med 2 00 1 ; 8(6):6 1 6-62 1 . 1 0 3 . Salen P, O'Connor R, Sierzenski P, et a!. Can cardiac sonography and capnography be used independently and in combination to pre­ dict resuscitation outcomes? Acad Enzerg Med 200 1 ;8(6):610-6 1 5 . 1 04. Salen P, Melniker L , Chooljian C, e t a!. Does the presence or absence of sonographically identified cardiac activity predict resuscitation outcomes of cardiac arrest patients? Anz J Enze1'g

Med 2005;2 3 (4) :45 9-462 . 1 0 5 . Varriale P, Maldonado JM. Echocardiographic observations dur­ ing in-hospital cardiopulmonary resuscitation. Crit Care Med 1 997;2 5 ( 1 0) : 1 7 1 7 - 1 720. 1 06. Tayal VS, Kline JA. Emergency echocardiography to detect peri­ cardia! effusion in patients in PEA and near PEA states.

Resuscitation 2 003 ;59: 3 1 5-3 1 8. 1 0 7 . Bocka J], Overton DT, Hauser A. Electromechanical dissociation in human beings: an echocardiographic evaluation. Ann Enzerg Med 1 988; 1 7 :45 0-45 2 . 1 0 8 . Breitkreutz R , Walcher F, Seeger FH. Focused echocardio­

Anesthesiology 2 004; 1 00(1):9- 1 5 . 8 5 . Volpicelli G , Mussa A , Garofalo G , et a!. Bedside lung ultrasound in the assessment of alveolar-interstitial syndrome. Am J Ernerg Med 2006;24(6) :689-696. 86. Reissig A, Kroegel C . Transthoracic sonography of diffuse

1 09.

parenchymal lung disease : the role of comet tail artifacts.

J Ultmsound Med 2 003 ;22(2): 1 7 3-1 80.

1 1 0.

8 7 . Jambrik Z, Monti S , Coppola V, et a!. Usefulness of ultrasound lung comets as a nonradiologic sign of extravascular lung water.

Am ] Cardio/ 2 004;93 ( 1 0): 1 2 65-1270. 8 8 . Picano E, Frassi F, Agricola E, et a!. Ultrasound lung comets: a clinically useful sign of extravascular lung water. J Am Soc Echocardiogr 2 006; 1 9(3): 3 5 6-3 6 3 . 8 9 . Lichtenstein DA, Lascols N , Meziere G , e t al. Ultrasound diag­ nosis of alveolar consolidation in the critically ill. !ntens Cm•e Med 2 004; 3 0(2):27 6-2 8 1 . 90. Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill: lung sliding. Chest 1 995 ; 1 08 : 1 3 45- 1 3 48 . 9 1 . Lichtenstein D , Meziere G , Biderman P, et a!. The "lung point": an ultrasound sign specific to pneumothorax. Intens Care Med 2 000;26(1 0) : 1434-1440. 92 . Lichtenstein D , Meziere G, Biderman P, et al. The comet-tail artifact: an ultrasound sign ruling out pneumothorax. lntens Care Med 1 999;2 5 : 3 83-3 8 8 . 93 . Kirkpatrick AW, Sirois M, Laupland KB, e t al. Hand-held tho­ racic sonography for detecting post-traumatic pneumothoraces: the Extended Focused Assessment with Sonography for Trauma (EFAST). J Ii'aunza lnj Infect Crit Can 2 004; 5 7(2):2 88-2 9 5 . 94. Dean A . Ultrasound evaluation o f the thorax a s a component of the focused assessment with sonography in trauma. Acad Enzerg

Med 2007; 1 4:e6. 9 5 . Ball CG, Kirkpatrick AW, Laupland KB, et a!. Factors related to the failure of radiographic recognition of occult posttraumatic pneumothoraces. Anz J Szt1·g 2 005 ; 1 89(5) :541-546. 96. Hendrickson RG, Dean AJ, Costantino TG. A novel use of ultrasound in pulseless electrical activity: the diagnosis of an acute abdominal aortic aneurysm ruprure. J Enze1-g Med 2 00 1 ;

2 1 (2 ) : 1 4 1 - 1 44.

1 147

1 1 1. 1 12. 1 13. 1 1 4.

1 15. 1 1 6.

1 17.

graphic evaluation in resuscitation management: concept of an advanced life support-conformed algorithm. O·it Care Med 2007; 3 5 (5 Suppl) : S 1 5 0-S 1 6 1 . Rothschild JM. Ultrasound guidance of central vein catheterization: making health care safer: a critical analysis of patient safety practices (Agency for Healthcare Research and Quality Web site). Publication No. 0 1 -E05 8. Available at http:lwww.allrq.gov/clinic/ptsafety. Calvert N, Hind D, McWilliams RG, et a!. The effectiveness and cost-effectiveness of ultrasound locating devices for central venous access: a systematic review and economic evaluation. Health Techno! Asse;)· (Winchester, UK). 2003 ;7(12): 1 -84. Muhm M. Ultrasound guided central venous access. [editorial; see comment] . BMJ 2 002 ; 3 2 5(7 3 7 7) : 1 3 73-1 3 74. Chalmers N. Ultrasound guided central venous access. NICE has taken sledgehammer to crack nut. BMJ 2 003 ; 3 2 6(7 3 9 1 ):7 1 2 . Denys B G , Uretsky BF, Reddy P S . Ultrasound-assisted cannula­ tion of the internal jugular vein. A prospective comparison to the external landmark-guided technique. Circulation 1 9 9 3 ; 8 7 : 1 5 5 7 . Leung J, Duffy M , Finckh A , et a!. Real-time ultrasound guided internal jugular vein catherterization in emergency department increases success rate and reduces complications : a prospective srudy. Ann Enzerg Med 2 006;48;540. Hrics P, Wilber S, Blanda M, et al. Ultrasound-assisted internal jugular vein catheterization in the ED. Am J Enzerg Med1998; 1 6:40 1 . Milling TJ, Rose M , Briggs WM , e t al. Randomized, controlled clinical trial of point of care limited ultrasonography assistance of central venous cannulation: The Third Sonography Outcomes Assessment Program (SOAP-3) trial. O'it Can Med2 005 ; 3 3 : 1 764. Denys BG, Uretsky BF. Anatomical variations of internal jugular vein location: impact on central venous access. O•it Care Med

1 99 1 ; 1 9 : 1 5 16. 1 1 8 . Troianos CA, Kuwik RJ, Pasqua! JR, e t a ! . Internal jugular vein and carotid artery anatomic relation as determined by ultra­ sonography. Anesthesiology 1 996;85 :4 3 . 1 1 9. Kwon TH, Kim YL , Cho DK. Ultrasound-guided cannulation of the femoral vein for acute haemodialysis. Nephrol Dial Ii'ansplant

1 997; 1 2 : 1 009. 120. Hilty WM, Hudson PA, Levitt MA, et a!. Real-time ultrasound­

guided femoral vein catheterization during cardiopulmonary resuscitation. Erne1'g Med Ann 1 997;29:3 3 1 .

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1 2 1 . Coletti RH, Hartjen B, Gozdziewski S , et al. Origin of canine femoral pulses during standard CPR. Crit Care Med 1 98 3 ; 1 1 :2 1 8 . 1 2 2 . Gualtieri E, Deppe SA, Sipperly ME, et al. Subclavian venous catheterization: greater success rate for less experienced opera­ tors using ultrasound guidance. C,'it Care Med 1 995;2 3 : 692 . 1 2 3 . Tsang TS, Freeman WK, Sinak LJ, et al. Echocardiographically guided pericardiocentesis: evolution and state-of-the-art tech­ nique. Mayo Clin Proc 1 998;73 (7):647-6 5 2 . 1 24. Mandavia DP, Hoffner RJ, Mahaney K , e t al. Bedside echocardio­ graphy by emergency physicians. Ann Enzerg Med 2 00 1 ; 3 8 : 3 7 7 . 1 2 5 . Mazurek B, Jehle D , Martin M. Emergency department echocar­ diography in the diagnosis and therapy of cardiac tamponade. J Enze1'g Med 1 9 9 1 ; 9 : 2 7 . 1 2 6. S alem K , Mulji A , Lonn E. Echocardiographically guided peri­ cardiocentesis: the gold standard for the management of peri­ cardia! effusion and cardiac tamponade. Can J Cm·diol 1 999; 1 5(1 1): 1 2 5 1-1 2 5 5 . 1 2 7 . Caspari G , Bartel T, Muhlenkamp S , e t al. Contrast medium echocardiography-assisted pericardia! drainage. Herz 2 0 0 0 ; 2 5(8) : 7 5 5-760. 128. Callahan JA, Seward JB, Nishimura RA, et al. Two-dimensional echocardiographically guided pericardiocentesis: experience in 1 1 7 consecutive patients. Am J Cm,dio/ 1 9 8 5 ; 5 5 (4):4 7 6-4 79. 129. Susini G, Pepi M, Sisillo E, et al. Percutaneous pericardiocente­ sis versus subxiphoid pericardiotomy in cardiac tamponade due to postoperative pericardia! effusion. J Cm,diothomc Vase Anesth 1 993 ;7(2): 1 7 8-1 8 3 . 1 3 0. Maggiolini S , Bozzano A , Russo P, e t al. Echocardiography­ guided pericardiocentesis with probe-mounted needle: report of 53 cases. J Am Soc Echocardiogr 2 00 1 ; 1 4(8):82 1-824. 1 3 1 . Diacon AH, Brutsche MH, Soler M. Accuracy of pleural punc­ ture sites: a prospective comparison of clinical examination with ultrasound. Chest 2003 ; 1 2 3 (2) :43 6-44 1 . 1 3 2 . Mayo PH, Goltz HR, 'Iafreshi M , e t al. Safety o f ultrasound­ guided thoracentesis in patients receiving mechanical ventilation. Chest 2 004; 1 2 5(3) : 1 05 9- 1 062 . 1 3 3 . Mayo PH, Doelken P. Pleural ultrasonography. Clin Chest Med 2 006;2 7(2):2 1 5-2 2 7 . 1 3 4. Meier B, Feiner JM. Two-dimensional echocardiographic evalu­ ation of intracardiac transvenous pacemaker leads. J Clin Ultmsozmd 1 9 82 ; 1 0:42 1-42 5 . 1 3 5 . Aguilera PA, Durham BA, Riley DA. Emergency transvenous car­ diac pacing placement using ultrasound guidance. Ann Eme1'g Med 2000; 3 6:224-2 2 7 . 1 3 6. Syverud S, Daisey W, Hedges J , e t al. Radiographic assessment of transvenous pacemaker placement during CPR. Ann Enzerg iVIed 1 986; 1 5 : 1 3 1- 1 3 7 . 1 3 7 . Macedo W Jr, Sturmann K, Kim]M, e t al. Ultrasonographic guid­ ance of transvenous pacemaker insertion in the emergency depart­ ment: a report of three cases. J Eme1'g Med 1 999; 1 7 (3):49 1-496. 1 3 8 . Holger JS, Minnigan HJ, Lamon RP, et a!. The utility of ultra­ sound to determine ventricular external cardiac pacing. Am J Enzerg Med 2 00 1 ; 1 9 : 1 3 4-1 3 6 . 1 3 9. Goodkin GM, Spevack DM, Tunick PA, e t a l . How useful is hand-carried bedside echocardiography in critically ill patients? J Am Col/ Cardio/ 2 00 1 ; 3 7(8) :2 0 1 9-2 02 2 . 140. Fedson S , Neithardt G , Thomas P, e t al. Unsuspected clinically important findings detected with a small portable ultrasound device in patients admitted to a general medicine service. J Am Soc Echocardiogr 2003 ; 1 6(9):90 1 -90 5 .

141 . Kronzon I . The hand-carried ultrasound revolution. Echocardiography 2003;2 0(5):45 3-454. 1 42 . Mark DG, Ku BS, Carr BG, et al. Directed bedside transthoracic echocardiography: preferred cardiac window for left ventricular ejection fraction estimation in critically ill patients. Am J Ernerg Med 2 007;2 5 (8):894-900. 1 43 . DeCara JM, Lang RM Koch R, et al. The use of small personal ultrasound devices by internists without formal training in echocardiography. Eur J Echocardiogr 2 003 ;4(2): 1 4 1-147. 1 44. Manasia AR, Nagaraj HM, Kodali RB, et al. Feasibility and potential clinical utility of goal-directed transthoracic echocar­ diography performed by noncardiologist intensivists using a small hand-carried device (SonoHeart) in critically ill patients . J Cardiothomc Vase Anesth 2 005 ; 1 9(2) : 1 5 5- 1 5 9 . 1 4 5 . Stewart WJ, Douglas P S , Sagar K , e t a ! . Echocardiography in emergency medicine: a policy statement by the American Society of Echocardiography and the American College of Cardiology. Task Force on Echocardiography in Emergency Medicine of the American Society of Echocardiography and the Echocardiography and Technology and Practice Executive Committees of the American College of Cardiology. J Am Coli Cardio/ 1 999; 3 3 (2 ) : 5 86-5 8 8 . 1 46. Krause RS. Echocardiography i n emergency medicine: A policy statement by the American Society of Echocardiology and the American College of Cardiology. Joumal of American Society of Echocardiogmphy 1 999; 1 2 (7): 607-608. 1 4 7 . Beaulieu Y. Specific skill set and goals of focused echocardiogra­ phy for critical care clinicians. C,'it Care Med 2007; 3 5 (5 Suppl): S 1 44-1 49. 148. Seward JB, Douglas PS, Erbet R, et al. Hand-carried cardiac ultra­ sound (HCU) device: Recommendations regarding new technol­ ogy. A report from the Echocardiography Task Force on New Technology of the Nomenclature and Standards Committee of the American Society of Echocardiography. J Am Soc Echocardiogr 2002 ; 1 5 : 3 69-3 7 3 . 1 49. Quinones MA, Douglas P S , Foster E , e t al. American Society of Echocardiography. Society of Cardiovascular Anesthesiologists. Society of Pediatric Echocardiography. ACC/AHA clinical com­ petence statement on echocardiography: a report of the American College of Cardiology/An1erican Heart Association/An1erican College of Physicians-American Society of Internal Medicine Task Force on clinical competence. J Am Soc Echocm'diogr 2003 ; 1 6(4) : 3 79-402 . 1 5 0. Neri L, Storti E, Lichtenstein D. Toward an ultrasound curricu­ lum for critical care medicine. Crit Care Med 2007; 3 5 (5 Suppl): S2 90-S 3 04. 1 5 1 . Mazraeshahi RM Farmer JC, Porembka DT. A suggested cur­ riculum in echocardiography for critical care physicians. C,'it Care Med 2 007 ; 3 5 (8 Suppl) : S43 1-S43 3 . 1 5 2 . Langlois Sle P. Focused ultrasound training for clinicians. C,'it Care Med 2007; 3 5 (5 Suppl) : S l 3 8-143 . 1 5 3 . American College of Emergency Physicians. Emergency ultra­ sound imaging criteria compendium. American College of Emergency Physicians. Ann Eme1'g Med 2006;48(4):48 7-5 1 0 . 1 54. American College o f Emergency Physicians. ACEP emergency ultrasound guidelines-2 00 1 . Ann Eme1'g Med 2 00 1 ; 3 8 (4) : 470-48 1 . 1 5 5 . Nair, Siu SC, Sloggett CE, Biclar L , et al. The assessment of technical and interpretative proficiency in echocardiography. J Am Soc Echocardiogr 2 006; 1 9(7):924-93 1 . ,

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. . . . . . . Iw.o.

Basic Life Support

Karl B . Kern The mechanism of blood-flow generation during cardiopulmonary resuscitation (CPR) is complex and depends on body habitus , the duration of CPR and the CPR technique utilized. Cardiac compression predominates as the mechanism early in CPR , with the thoracic pump mechanism more predominant as time progresses . •

Current concepts of the physiology of blood flow during CPR and their clinical implications

Coronary perfusion pressure as a maj or determinant of resuscitation outcome • Mechanisms for optimizing coronary perfusion pressure during CPR • Cardiac dysfunction and the CPR stunned myocardium: implications for management as part of the post-circulatory arrest syndrome •

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t r.o.du.c.ti on

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.

Cardiac arrest causes the complete cessation of forward blood flow, with resultant global ischemia affecting the entire organism. Various tissues have different tolerances to such global ischemia, but all will eventually succumb if blood flow is not restored in a timely fashion. The most prominent injuries occur in the central nervous system, which initially responds to ischemia with loss of consciousness after only 7 to 1 0 seconds of an circula­ tory arrest. Likewise, once the myocardial cells become globally ischemic, cellular nmc­ tion, including contraction, stops; if blood flow is not restored, myocytes begin to autoin­ farct. The duration of no blood flow is crucial in these responses; hence the importance of CPR for restoring at least some modicum of flow during cardiac arrest. CPR restores only a portion of normal blood flow previously generated by a contracting heart. Nonetheless, such support is crucial for the survival of both the central nervous system and the myocardium.

1 49

150

KERN

The Mechanism of Blood

Flow During CPR

The mechanism of blood flow produced during CPR has been a controversial and debated topic for several decades. Just how blood flow is produced became an important issue in trying to determine the optimal external chest compres­ sion rate. In 1 9 7 7 , Taylor and colleagues suggested that within the range of 40 to 80 compressions per minute, the duration of chest compression was more important than the rate of compression. 1 This ratio of the duration of compres­ sion to decompression is the "duty cycle." A duty cycle of 5 0 % (50% of the time the chest is compressed and 5 0 % decompressed, generally by passive recoil) with 60 compres­ sions per minute was initially thought optimal. In opposition to this concept, investigators at Duke University found that a higher chest compression rate produced better blood flow during closed chest CPR, up to a maximum rate of 1 40 compressions per minute. 2 Above a compression rate of 1 40/min, the relaxation or diastolic period for coronary fill­ ing is compromised to the point where total myocardial blood flow diminishes. In recognition of these findings, the National Conference on CPR in 1 9 8 5 recommended increasing the chest compressions to 80 to 1 00/min. 3

Cardiac or Thoracic Pump Mechanism? Physicians and scientists alike have assumed that external chest compression produces temporary blood flow by compressing the heart between the sternum and the vertebral column.

marked increases in their anterior-posterior chest diameter and relatively small hearts could nonetheless be resuscitated by sternal compression. Finally, they observed that during conventional CPR, the compression cycle that followed ven­ tilation often resulted in an increased blood pressure and carotid blood flow. To them, these observations appeared inconsistent with direct cardiac compression from external chest compression, and a new potential mechanism for blood-flow generation during CPR was developed. The "thoracic pump" mechanism of blood-flow generation sug­ gested that forward blood flow occurring during CPR was due to an increase in intrathoracic pressure compared with extrathoracic pressure. This theory was also supported by the work of Criley et al. on "cough CPR. "6

Cough Cardiopulmonary Resuscitation Cough CPR consists of having a patient with a recent onset of asystole or ventricular fibrillation forcefully cough every second.7 Since no hands are placed on the patient, this is an excellent example of the power of the thoracic pump mech­ anism to produce blood flow during CPR. If the patient coughs forcefully every second, significant aortic systolic pressures can occur. These pressures are often enough to perfuse the brain and consciousness can be preserved. The obvious disadvantage of this technique is that it must be ini­ tiated before unconsciousness occurs. Cough CPR has been most successfully employed in the cardiac catheterization suite, where Criley et al. have reported examples of patients sustaining consciousness for up to 40 seconds after the onset of ventricular fibrillation.6 Although some lay publications have touted this technique as a way to perform CPR on one­ self, cough CPR has generally failed to meet its initial expec­ tations outside the cardiac catheterization laboratory.8

The Thoracic Pump Mechanism Physicians and scientists alike have assumed that external chest compression produces temporary blood flow by com­ pressing the heart, similar to the manner of open chest inter­ nal cardiac massage, with the heart being squeezed between the sternum and the vertebral column. Indeed, a famous illustration by Frank Netter suggests such a mechanism, with the heart being squeezed between the sternum and the vertebral column and competent, functional valves directing the resultant blood flow out the aortic valve and to the body. It has been assumed that with such cardiac compression and competent mitral and aortic valves, blood moved in an ante­ grade fashion from the left ventricle into the aorta. This widely held concept was challenged in the late 1 97 0s and early 1 980s.4 Some investigators felt that the concept of car­ diac compression and competent valvular function was inconsistent with the number of observations during resus­ citation. They noted that when sternal compression was per­ formed in a patient with a flail chest, no arterial blood pres­ sure was recorded until the chest was bound to prevent paradoxical expansion. 5 They also observed that patients with severe chronic obstructive pulmonary disease with

An important rediscovery was that blood pressures in the aorta and right atrium were often similar during external chest compressions. This observation was initially reported by Weal and Rockwell-] ackson in 1 962 but at the time received little attention.9 Nearly two decades later, investi­ gators at Johns Hopkins noted that during external chest compressions, central venous and aortic pressures were often similar; indeed, pressures in all cardiac chambers and the intrapleural space were nearly equal. If the cardiac com­ pression mechanism is responsible for blood flow during CPR, the fluid-filled systems of the heart and great vessels must contain a pressure gradient across a resistance for the production of forward blood flow. Under the normal physi­ ology occurring during sinus rhythm, there is a large pres­ sure gradient involving the aorta, right atrium, and central venous systems. The lack of such a gradient during external chest compression suggests the heart is not functioning strictly as a pump but that the entire thorax was indeed the pump . 1 0 In contrast to the intrathoracic structures with similar pressures, the investigators at Johns Hopkins found a

CHAPTER 9

significant pressure difference between the extrathoracic carotid artery and the intrathoracic cardiac chambers and the right atrium and the extrathoracic jugular veins. This pressure gradient was thought to be responsible for produc­ ing the forward cerebral blood flow. It is at this time that Criley et al. demonstrated that the jugular venous valves were operative during cough CPR. 1 1 Indeed, early anatomists had also appreciated the presence of internal jugular venous valves and had described them in the 1 950sY Further supports for the theory that increases in intrathoracic pressure create forward blood flow during external chest compression came in the 1 980s from echocar­ diographic studies of clinical CPR. 1 3-14 Two different two­ dimensional echocardiographic studies performed late in a protracted resuscitation effort, showed that the mitral valve was not competent and did not close in a consistent fashion and that the left ventricular internal diameter was not deformed with chest compressions. 1 3-14 These findings sug­ gest that increased intrathoracic pressure in some patients, not cardiac compression, accounted for forward blood flow during chest compressions. Nonetheless, cardiac compression does occur in some humans.5 In a few patients studied at Johns Hopkins, central venous pressures were significantly lower than arterial pres­ sure during external chest compression, indicating a pres­ sure gradient and the possibility that in these patients a car­ diac compression mechanism for blood flow during CPR was possible. Based on this new theory for blood-flow generation during external chest compression, the investigators at Purdue University attempted to apply this concept to improving alternative techniques to conventional CPR. The group explored two basic strategies, simultaneous chest compression and ventilation, as well as abdominal binding. 1 5 Increased intrathoracic pressure could be obtained by clamping the endotracheal tube during chest compressions; however, the initial increase in pressure and flow dissipated rapidly, secondary to the inhibition of venous return by high intrathoracic pressure. Maintaining inflated lungs during external chest compressions, these investigators found sig­ nificant increases in arterial pressure and carotid flow over those observed with conventional CPR. 1 0 Of particular interest, in their experimental model large animals (i . e . , canines), treatment with simultaneous high-pressure venti­ lation and chest compressions produced significant systolic flows in the carotid arteries. However, the same was not true in smaller dogs . 1 6 In the smaller dogs, cardiac compression evidently occurs with relatively good blood-flow generation, and the addition of simultaneous high-pressure ventilation did not appear to improve these hemodynamics. However, in large animals, in which cardiac compression plays a smaller role, if any, the addition of simultaneous ventilation clearly improved the peripheral circulation during CPR. 10 Abdominal binding was shown by Redding et al. to improve hemodynamics during CPR. 1 7 Unfortunately, further inves­ tigations of this technique reported increases in liver lacera­ tions secondary to the abdominal binding, and the technique fell out of favor. It was also noted that abdominal binding had a detrimental effect on coronary perfusion pressure by

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15 1

the consistent increase in right atrial pressure both in systole and diastole. The ultimate test for the presence and efficacy of the "thoracic pump mechanism" as employed using simulta­ neous chest compressions and high-pressure ventilation with or without abdominal binding is its effect on survival. In an effort to evaluate this effect on survival, simultane­ ous chest compression and ventilation CPR with abdomi­ nal binding was compared with standard CPR in a labora­ tory experiment at the University of Arizona. 1 8 Survival in the control group of canines receiving standard CPR was 5 out of 6 , whereas none of the 6 animals undergoing simultaneous chest compression and high-pressure venti­ lation had return of spontaneous circulation in spite of intensive efforts. 1 8 A clinical trial with simultaneous com­ pression-ventilation CPR was also performed . 1 9 This clini­ cal study enrolled nearly a thousand patients in an out­ of-hospital cardiac arrest trial where ambulance staff were randomly assigned to use simultaneous compression­ ventilation CPR or conventional CPR. Both hospital admis­ sion and survival to discharge were greater in the conven­ tional CPR group than in the experimental group receiving simultaneous compression-ventilation CPR (P :s: 0 . 0 1 ) . In the subset of adult patients with nontraumatic witnessed car­ diac arrest, survival was 3 5 % of 3 3 7 versus 2 3 % of 3 6 5 (P :s: 0.00 1 ) . These two studies have dampened enthusiasm for simultaneous chest compression-ventilation CPR, and this technique is not currently recommended. Other investigators were less convinced about the importance of the thoracic pump mechanism for blood-flow generation during resuscitation efforts . Rankin and col­ leagues at Duke University were convinced, from their own clinical experience, that rapid chest compression rates were more effective than slower rates and that this reflected a car­ diac compression mechanism for blood-flow generation. These investigators studied the effects of varying manual chest compression rates, force, and durations in large chron­ ically instrumented dogs. 2 •2 0 In their model, they found that the relative contribution of thoracic pump and direct cardiac compression mechanisms to blood flow varied depending on the method of CPR being performed. During high-impulse (increased frequency) CPR, direct cardiac compression seems to be the predominant mechanism, while during low­ momentum compression techniques, the thoracic pump mechanism seemed to predominate. At tl1e same time, new echocardiographic experimental studies by Weil et al. sup­ ported the cardiac/vascular compression theory of CPR­ generated blood flow. 2 1 In fact, echocardiographic studies in anesthetized minipigs demonstrated incompetent cardiac valve motion with a clear change in left ventricular dimen­ sions during the early phases of cardiac arrest with closed­ chest CPR. The investigators interpreted these data as fur­ ther evidence for direct cardiac compression in the early phases of cardiac arrest and resuscitation efforts. Since that time, additional transesophageal echocardiographic studies in experimental models of cardiac arresrl 2 and clinical cases 2 3 have also shown left ventricular compression in competent mitral valve function, again suggesting a cardiac compres­ sion mechanism for blood flow.

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Current Concepts on Blood Flow During CPR As in most disagreements, there appears to be truth on both sides of this controversy. Cardiac compression clearly occurs at times, while the thoracic pump mechanism for blood-flow generation during CPR also appears to be operational, par­ ticularly later in the resuscitation effort. Open-chest cardiac massage and high-impulse closed-chest compression in small subj ects undoubtedly produce blood flow predomi­ nantly by cardiac or vascular compression. "\Nhereas cough and "vest CPR" forms of CPR, both of which produce very little thoracic compression, but rather large fluctuations in intrathoracic pressure, appear to produce blood flow via the thoracic pump mechanism. The authors examined this at the University of Arizona using our large database of experimental CPR studies. On sub­ jects undergoing open-chest cardiac compression, the authors observed that there is a large difference between the aortic and right atrial systolic pressures. In contrast, the authors found lit­ tle or no difference in systolic pressure between the aorta and right atrium in experimental subjects in whom blood is gener­ ated by the thoracic pump mechanism during vest CPR. This led to the conclusion that the absolute difference between aor­ tic and right atrial systolic pressure, which we termed the sys­ tolic pressure gradient, could actually indicate the mechanism of blood flow in real time. The authors reviewed 63 experi­ ments using a variety of CPR techniques and animal sizes. Each underwent 3 minutes of untreated ventricular fibrillation and then one of the five different types of CPR was initiated. Systolic pressure gradients between the aortic and right atrium were measured at 1 , 7, and 1 7 minutes of the resuscitation effort. 2 4 The systolic pressure gradient was greatest during open-chest cardiac massage (true cardiac compression), inter­ mediate with external mechanical or manual standard CPR, and lowest with CPR performed with a vest apparatus (pre­ dominantly thoracic pump). Wrth open-chest cardiac massage, this gradient was 60 to 65 mm Hg; with standard CPR in small animals, it was 2 8 to 3 0 mm Hg; and in larger animals, it was 1 5 to 20 mm Hg. Wrth vest CPR, the gradient was only 2 to 5 mm Hg. In this particular series, it was also noted that 24-hour survival was greatest in those animals where cardiac compres­ sion mechanisms seemed to be the predominant mechanism of blood-flow generation. This is of interest in light of a report from Deshmukh and associates using 2D echocardiography to evaluate eight rninipigs during CPR. 2 1 They found aortic and mitral valves demonstrating competency (not wide open with constant leakage) during the first 5 minutes of CPR in all ani­ mals. In the three successfully resuscitated animals, valve com­ petency persisted for the full 1 2 minutes of CPR. It appears that the mechanism ofbloodflow during CPR can vary accorded to the CPR technique utilized and the duration of cardiac arrest.

It appears that the mechanism of blood flow during car­ diopulmonary resuscitation can vary accorded to the CPR

technique utilized. Cardiac/vascular compression is greatest with open-chest cardiac massage or high-impulse CPR, par­ ticularly in smaller subj ects, while it is lowest with cough CPR or vest CPR. The mechanism of blood-flow generation also seems to vary with the duration of CPR efforts. Cardiac compression predominates as the mechanism early in CPR, with the thoracic pump mechanism more predominant as time progresses. This is consistent with the reported clinical echocardiographic reports noted earlier. l l , l4,2 3 In summary, the mechanism of blood-flow generation during CPR depends on body habitus, the duration of CPR, and the CPR technique utilized. Both mechanisms appear feasible and are probably present in each subject resuscitated.

Importance of Coronary

Perfusion Pressure

"The basic problem, then, in resuscitations seems to us to be that of securing some means ofsome infusion-a coronary pressure, approximately amounting to 30 to 40 mm Hg. "

Experimental work in resuscitation research in the 1 970s and 1 980s seemingly focused on the physiologic mechanisms for creating systemic blood flow during closed-chest resuscita­ tion. 2 5•2 6 During that era, the importance of blood flow to sus­ tain the myocardium and central nervous system during CPR became evident. Using microsphere techniques to measure blood flow, investigators found that regional perfusion of vital organs occurs with closed-chest compression CPR, but at substantially lower levels than during normal sinus rhythmY-2 9 Central nervous system flows average about 3 0 % o f normal with good anteroposterior chest compressions. Myocardial blood flows achieved with external chest com­ pressions average even less, generally only 1 0 % to 2 0 % of normal. Peripheral perfusion is almost nonexistent during CPR. Nevertheless, good CPR efforts can temporarily pro­ vide at least some perfusion to the myocardium and cerebrum until more definitive treatment (i. e. , defibrillation) can be accomplished. Myocardial perfusion during cardiac arrest can be esti­ mated by measuring "coronary perfusion pressure" during the resuscitation effort. This perfusion pressure gradient correlates well with resultant cerebral and myocardial blood flows generated with CPR, and with the subsequent possi­ bility of successful defibrillation and resuscitation. 2 7• 2 8

Determinants of Coronary Perfusion Pressure During Cardiopulmonary Resuscitation Adequate Perfusion Pressure The importance of an adequate perfusion pressure for suc­ cessful resuscitation was first described by Crile and Dolley in 1 906.30 "\Nhile studying means of reversing cardiorespira-

CHAPTER 9

tory arrest i n dogs and cats asphyxiated with the anesthetics of that time (chloroform and ether), they noted that "the basic problem, then, in resuscitations seems to us to be that of securing some means of some infusion-a coronary pres­ sure, approximately amounting to 30 to 40 mm Hg. " This concept was further developed through the work of Redding and Pearson . 1 7•3 1-3 3 These investigators showed that when aortic diastolic pressure during resuscitation was :::::: 40 mm Hg, animals could be successfully revived from cardiac arrest; but this was not possible if that level of diastolic pressure was not achieved. From their early work they deduced that the mechanism of action for epinephrine and other alpha­ adrenergic agonists during cardiac arrest was to cause peripheral vasoconstriction, which raised the central aortic diastolic pressure and thereby increased coronary perfusion. Otto and coworkers confirmed this mechanism. By using selective blockade, these investigators evaluated the role of the alpha- and beta-adrenergic receptors during resuscita­ tion. Animals that were blocked with the former had diffi­ culty in responding to epinephrine (i. e . , diastolic aortic pres­ sure did not increase and they were not resuscitated). In contrast, those that were blocked with the latter were suc­ cessfully resuscitated and exhibited peripheral vasoconstric­ tion with elevated aortic diastolic pressures in response to adrenergic agonists. 34-36

Perfusion Pressure Gradient Other investigators have confirmed not only the importance of a perfusion pressure (i. e . , the aortic diastolic pressure) but also of a defined perfusion pressure gradient, which included a "downstream" pressure from the myocardial venous sys­ tem acting as an impedance to forward flow. Voorhees et al.-measuring regional blood flow to the brain, heart, and other peripheral tissues-noted that the arteriovenous gra­ dient was important during the compression phase of CPR for cerebral blood flow and postulated that the same arteri­ ovenous gradient during the relaxation component of CPR was important for myocardial blood flow. 37 Both Niemann et al. 38 and Ditchey et al. 39 suggested that coronary perfusion during CPR results from the difference in mean pressure of the aorta and that of the right atrium. Ditchey et al. found that coronary blood flow during CPR was a linear function of the pressure difference generated across the coronary cir­ culation (i . e . , the mean pressure difference between the ascending aortic and right atrial pressures) .39

Measurement of Coronary Perfusion Pressure No standard method for measuring coronary perfusion pres­ sure during CPR has been agreed upon. Some investigators have suggested subtracting the middiastolic right atrial pres­ sure from simultaneously obtained middiastolic aortic pres­ sure, 1 8• 2 7 whereas others have suggested that coronary per­ fusion pressure be obtained by measuring the peak positive diastolic pressure gradient between the aorta and the right atrium.40 Another approach has been to calculate the coro-

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nary perfusion pressure gradient by subtracting the mean right atrial diastolic pressure from the mean diastolic aortic pressure. 2 8• 2 9 To address this uncertainty, the Utstein-style guidelines for reporting laboratory CPR research specify that the point just before compression be used as the refer­ ence point for measurement of coronary perfusion pressure. This point was selected because it is easily identified and more likely to be consistent among investigators.41 Nonetheless, multiple techniques for calculating coronary perfusion pressure during CPR are still in use. See ILCOR Utstein-style Guidelines for reporting laboratory data. An interesting alternative for calculating coronary per­ fusion pressure by measuring the integrated area under the aortic diastolic pressure minus the right atrial diastolic pres­ sure curves during each minute of CPR was reported by investigators at the University of ArizonaY This technique was developed to account for the effect of interrupting chest compression/relaxation cycles during the resuscitation effort. Since chest compression/relaxation cycles (i.e ., the relaxation phase specifically) are responsible for generating blood flow to the heart, a decrease in delivered chest com­ pression cycles can markedly decrease the total amount of myocardial perfusion generated with the resuscitation effort. Calculating coronary perfusion pressure in the usual fashion (end-diastolic aortic minus right atrial pressures) does not account for periods of chest compression interruptions. A more accurate method is to use the integrated area coronary perfusion pressure (iCPP) over each minute. The effect of chest compressions interruptions-for example, for rescue breathing-on coronary perfusion pressure becomes readily apparent, typically resulting in a 40 % decrease in cumulative coronary perfusion (Fig. 9- 1 A, B).

Clinical Implications Interruption of chest compression/relaxation has direct effects on the amount of coronary perfusion pressure gener­ ated during the period of consecutive compression cycles ( 1 5/min previously and 3 0/min currently). We found that at the beginning of each cycle of 1 5 , the first 5 to 1 0 compres­ sions/relaxations are "building up" the coronary perfusion gradient and that it is not optimal until at least one third of the series is completedY Then with cessation of chest com­ pressions/relaxations, this diastolic gradient falls off rapidly, often returning to near zero within 5 seconds. When chest compressions do resume, the coronary perfusion gradient must be rebuilt, usually starting from near zero (Fig. 9-2). Does antegrade coronary flow occur during the com­ pression phase or only during the relaxation phase of CPR? Schleien et al. suggested that forward coronary flow may occur during the compression phase of CPR when epineph­ rine infusions are used because of a net positive pressure gra­ dient from the aorta to the right atrium even during the compression phase. They concluded that the diastolic gradi­ ent as an index of coronary blood flow during CPR may be incomplete.44 Subsequent work has shown that many meth­ ods of CPR routinely generate some degree of pressure difference from the aorta to the right atrium during the

154

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F I G U R E 9 - 1 • A o r t i c a n d r i g h t a t r i a l p r es s u r e tr a c i n g s d e m o nstr a ti n g t h e c o r o n a ry p e rf u s i o n p r es s u r e g r a d i e n t d u r ­ i n g t h e r e l a x a t i o n p h a s e o f c h est c o m p r e ss i o n s . N o te t h e m a r k e d d i ffe r e n c e i n c u m u l a tive a r e a u n d e r t h e c u rve (yel­ low) for c o r o n a ry p e rf u s i o n p r essu r e (CP P) wh e n c o n ti n u o u s c h est c o m p r essi o n s (A) a r e d o n e ve r s u s i n t e r r u p t e d c h est c o m p r essi o n s , in this case i n t e r r u p t e d for ve n t i l a t i o n s (B) . E a c h p a n e l i l l u s t r a t e s a o rt i c a n d r i g h t a t r i a l p r essu r e d a t a d u r i n g 1 3 . 5 s e c o n d s o f C P R . A r e a u n d e r t h e c u rve (ye l l ow) m e a s u r e m e n t o f " i n t e g r a te d CP P " was 5 9 , 2 2 3 m m H g * d t s e c o n d s i n A ( c o n t i n u o u s c h est c o m p r e ssi o n s) a n d 3 5 , 7 3 7 m m H g * d t s e c o n d s i n B (i n t e r r u p te d c h est c o m p ressi o n s) . T h i s c a l c u l a te s t o a 4 0 % d e c r e a s e i n t h e i n t e g r a t e d a r e a C P P (iCPP) with t h e i n t e r r u p te d c h est c o m p r e ss i o n s .

CHAPTER 9

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P AT H O P H Y S I O L O G Y O F C A R D I A C A R R E S T

155

F I G U R E 9 - 2 • A o rt i c a n d r i g h t a t r i a l p r e s s u r e t r a c i n g s d e m o n s tr a t i n g t h e c o r o n a ry p e r fu s i o n p r e ss u r e g r a d i e n t d u r i n g t h e r e l a x a t i o n p h a s e o f c h est c o m p r e s s i o n s . N o te t h e r a p i d f a l l o f f i n t h e d i a s to l i c g r a d i e n t with t h e c e s s a t i o n o f c h est c o m p r e ss i o n s , and the time r e q u i r e d to " r e b u i l d " a m a x i m a l C P P a f t e r such i n t e r r u p t i o n .

compression phase, either positive o r negative; hence the potential for antegrade or retrograde coronary blood flow exists during chest compression or CPR systole. Total "net" flow during CPR may require consideration of the entire cardiac cycle (the compression phase and the relaxation phase). This hypothesis has been tested using an intracoro­ nary Doppler flow catheter to determine the relationship between systolic or compression phase coronary perfusion pressure as well as diastolic or relaxation-phase coronary perfusion and the direction of coronary blood flow in the proximal left anterior coronary artery.45 Retrograde coro­ nary artery blood flow (flow from the left main coronary artery back into the ascending aorta) occurred routinely dur­ ing the compression phase of manual CPR, regardless of the measured pressure gradient from the aorta to the right atrium. Even in circumstances where the aortic pressure exceeded right atrial pressure during compressions, no ante­ grade coronary blood flow occurred. Rather, such antegrade coronary blood flow occurred exclusively during the relax­ ation phase of chest compression and correlated only with a positive "diastolic" or relaxation-phase perfusion pressure gradient between the aorta and the right atrium. The greater

the gradient, the greater the antegrade coronary blood-flow velocity produced. Positive systolic coronary perfusion gra­ dients occurring during the compression phase do not sig­ nificantly improve antegrade blood flow and, indeed, can be associated with significant amounts of retrograde coronary flow. Hence diastolic perfusion pressure gradients account for the vast majority of cases of myocardial perfusion.

Myocardial Blood Flow and

Coronary Perfusion Pressure During Cardiopulmonary Resuscitation

Aortic and right atrial pressures can be easily measured in the experimental laboratory but require great effort in the clini­ cal setting. During the relaxation phase of chest compres­ sions, aortic pressure largely depends upon intrinsic arterial tone. Right atrial pressure during the relaxation phase of

156

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CPR i s largely determined by central venous return and venous capacitance. A significant correlation has been estab­ lished between coronary perfusion pressure and simultane­ ously measured myocardial blood flow during CPR. 2 7-2 9•46 Correlation coefficients vary from 0.82 to 0.89. Ralston et a!. found a correlation coefficient of 0.89 in dogs where no epi­ nephrine was used and of 0 . 8 5 when epinephrine was usedY Using epinephrine, Michael et a!. found a correlation coeffi­ cient of 0 . 842 8 and Halperin et a!. , from the same laboratory at Johns Hopkins, found a correlation coefficient with multi­ ple forms of CPR of 0.88. 2 9 Finally, Kern et a!. reported a correlation coefficient of 0.82 between the coronary perfu­ sion pressure achieved and the resultant myocardial blood flow to the anterior left ventricular wall (Fig. 9-3).46 The generally low coronary perfusion pressures gener­ ated with standard CPR ( 1 0 to 20 mm Hg) produce only small amounts of myocardial blood flow. With a coronary perfusion pressure of 1 0 to 20 mm Hg, Ralston et a!. found left ventricular flows of 1 5 to 2 0 mL/min/1 00 g. 2 7 Michael et a!. found flows of 5 to 40 mL/min/1 00 g, 2 8 Halperin et a!. found flows of 5 to 25 mL/min/1 00 g, 2 9 and Taylor et a!. found flows of 10 to 1 5 mL/min/1 00 g.47 However, these studies also demonstrated that if perfusion pressures are in the range of 40 to 60 mm Hg, excellent myocardial blood flow levels can result. Such perfusion pressure gradients pro­ duce myocardial blood flows of 40 to 200 mL/min/kgY-2 9•46

Myocardial Blood Flow and Coronary Artery Stenosis All of this previously described work correlating myocardial blood flow and coronary perfusion pressure was performed on experimental animals with normal coronary arteries and normal left ventricular function. To examine the effect of coronary artery lesions on the relationship between coro­ nary perfusion pressure and myocardial blood flow during

CPR, investigators at the University of Arizona evaluated a closed-chest porcine model of fixed artificial coronary artery stenoses.46 In a closed-chest model with minimal collateral circulation, coronary artery lesions were found to have major effects on regional myocardial blood flow measured during CPR. Coronary stenoses greatly decrease the amount of distal coronary blood flow for any given coronary perfu­ sion pressure produced. As expected, where few collateral vessels exist, complete coronary occlusion results in negligi­ ble distal myocardial perfusion, regardless of the coronary perfusion pressure. Where patent 3 3 % diameter stenoses existed, myocardial blood flow measured during CPR con­ tinued to show a high correlation with coronary perfusion pressure, albeit with less myocardial blood flow for every increment in coronary perfusion pressure. With coronary perfusion pressure of 3 0 to 60 mm Hg, coronary stenosis resulted in an approximate 5 0 % reduction in distal blood flow. For any given coronary perfusion pressure generated with CPR, a significant reduction in myocardial blood flow distal to the stenosis was seen. Therefore, even minimal or previously considered "insignificant" coronary lesions may have a profound effect on distal myocardial blood flow dur­ ing the performance of CPR.48

Resuscitation Duration Coronary perfusion pressure declines with lengthy resusci­ tation efforts .49 The highest pressure gradients and the greatest myocardial perfusion occur during the first minutes of resuscitation. This decline occurs from the gradual loss of arterial tone and increase in right heart pressures. The effect of "no-flow time" (period of cardiac arrest without support where no blood flow is being generated) on subsequent coronary perfusion pressure generated during CPR was studied by Duggal et a!. 5° They found no particu­ lar compromise in what level of coronary perfusion pressure could be generated after extending the downtime from 9 minutes to 1 5 minutes of untreated ventricular fibrillation. However, they did note that the previously established threshold levels of coronary perfusion pressure for resus­ citability were not valid after the longer downtimes (i.e ., a higher coronary perfusion pressure was needed after lengthy "downtimes" to ensure successful outcome).

Coronary Perfusion Pressure, Resuscitation, and Survival Coronary perfusion pressure correlates with myocardial blood flow during CPR but has also been shown to be predictive of successful resuscitation (i.e., restoration of spontaneous circu­ lation [ROSC] , short-term outcome, and long-term survival). Both Ralston et alY and Michael et a!. 2 8 showed that increased coronary perfusion pressure produced not only increased myocardial blood flow but also better outcomes. Other experimental studies have confirmed the predictive

CHAPTER 9

value o f the myocardial perfusion gradient and longer-term survival rates up to 7 days. 2 7-2 9•5 1 The use of coronary perfu­ sion pressure to monitor the effectiveness of resuscitation makes it attractive for use in clinical cardiac arrest. Over the last two decades there have been more than 200 patients who had coronary perfusion pressure measured during the performance of CPR. 5 2 -61 Important lessons have been learned. It is feasible to measure coronary perfusion pressure in victims of clinical cardiac arrest. The necessary instrumentation, including cannulation of the ascending aorta and right atrium, can be accomplished safely even dur­ ing resuscitation efforts. Usually, however, by the time the pressure-measuring catheters are in place, the patient is rel­ atively late in the course of cardiac arrest. In most cases, the information obtained so late is not useful for making any survival enhancing changes . Occasionally, cardiac arrest occurs in patients who already have a pulmonary artery catheter or an arterial line. Such patients can more easily be monitored for coronary perfusion pressure during CPR by the appropriate use of these pressures. The majority of measurements obtained during clinical cardiac arrest demonstrate very poor coronary perfusion pressures. The mean coronary perfusion pressures reported in human series range from zero to 1 5 mm Hg. Consistent with these low values, most humans monitored for coronary perfusion pressure during CPR have not survived. However, some data exist for survivors. McDonald 53 reported that 1 of his 1 2 patients survived. That patient had the highest coro­ nary perfusion pressure from his series ( 1 6 mm Hg). Paradis et al.59 reported on 1 00 patients, of whom 24 had return of spontaneous circulation. When coronary perfusion pressures between survivors and nonsurvivors were compared, there was a statistically significant difference in initial and maximal coronary perfusion pressure measurements. Patients without return of spontaneous circulation had a mean initial coronary perfusion pressure of 2 mm Hg; those in whom spontaneous circulation returned had mean initial perfusion pressure of 1 3 mm Hg. Likewise, maximal coronary perfusion pressures were significantly different between the two groups: 8 mm Hg versus 2 6 mm Hg. This series in particular substantiates the experimental data from animal models, showing that coronary perfusion pressure can be a predictor of the return of spontaneous circulation. Paradis et al. noted that in patients with prolonged cardiac arrest, coronary perfusion pressure was a better predictor of resuscitation outcome than was aortic pressure alone. 59 A coronary perfusion pressure of 1 5 mm Hg appeared to be the minimum required to obtain successful return of spontaneous circulation.

After Restoration of Spontaneous Circulation Once spontaneous circulation is restored a new challenge arises. Many times the lack of blood flow during untreated cardiac arrest and the resultant reperfusion can result in a postresuscitation syndrome. The myocardium is especially

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vulnerable. Postresuscitation myocardial dysfunction has become increasingly recognized as a major contributor to the poor long-term outcome results with current resuscitation efforts. Both systolic and diastolic left ventricular abnormal­ ities are readily identified following successful resuscitation. The global myocardial stunning seen during this period can be severe and unless supported can lead to death. Although the exact mechanism of postresuscitation global myocardial dysfunction is not yet known, a number of factors that con­ tribute have been identified, as well as several potential treat­ ment strategies (see also Chapter 2 9).

Postresuscitation myocardial dysfunction has become increasingly recognized as a major contributor to the poor long-term outcome results with current resuscitation efforts.

Experimental evidence of the postresuscitation syn­ drome was first reported in detail by University of Pittsburgh resuscitation researchers. 62 In their experimental canine model of prolonged cardiac arrest and resuscitation, they found elevated myocardial filling pressures with decreased cardiac outputs postresuscitation. Weil and colleagues at the Institute for Critical Care Medicine have shown, in isolated perfused hearts of Sprague­ Dawley rats, decreases in myocardial contractile function and left ventricular compliance following resuscitation from ven­ tricular fibrillation cardiac arrestY Further studies by this group in a large animal porcine model of cardiac arrest revealed similar findings.64 Pressure-volume relationships postresuscita­ tion showed strikingly reduced myocardial contractility accom­ panied by decreased stroke volume and ejection fraction. The University of Arizona Resuscitation Research Group studied invasive and noninvasive measurements of ventricular function before and after 10 or 1 5 minutes of untreated cardiac arrest in a swine model of ventricular fib­ rillation and subsequent resuscitation. 65 Left ventricular ej ection fraction showed a significant reduction 30 minutes after resuscitation, which progressively worsened through the first 5 hours postresuscitation. Partial recovery was seen by 2 4 hours, and full recovery was seen by 48 hours. The sys­ tolic left ventricular dysfunction was a diffuse, global process with wall motion abnormalities seen in all ventricular walls. Hemodynamic changes seen after resuscitation included a dramatic rise in left ventricular end-diastolic pressure, a fall in cardiac output, and an increase in isovolumic relaxation time ("tau") . These changes demonstrate significant dias­ tolic left ventricular dysfunction as well as the systolic dys­ function seen by the angiographic measurements. Transthoracic echocardiographic studies showed similar results, with diminished systolic ventricular function and diminished diastolic ventricular function postresuscitation. This was the first report in an in vivo model of cardiac arrest to elucidate the time course of left ventricular systolic and diastolic dysfunction after successful CPR. Maximal dysfunction was seen at 6 hours, with partial resolution by 24 hours and full recovery by 48 hours, indicating a true "stunning" phenomenon.

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Clinical Evidence for Postresuscitation Myocardial Dysfunction Clinical reports and studies have recently collaborated the experimental evidence for postresuscitation myocardial dysfunction. Several case reports of global left ventricular failure after successful resuscitation from prolonged cardiac arrest of different etiologies have appeared in the litera­ ture.66-68 Investigators in Paris reported on a series of successfully resuscitated out-of-hospital cardiac arrest victims, approxi­ mately half of whom developed myocardial dysfunction.6 Among 1 48 consecutive patients admitted after successful resuscitation from out-of-hospital cardiac arrest, 73 (49 %) developed myocardial failure manifested as hypotension and shock. Those who developed myocardial dysfunction had significantly lower ejection fractions at initial testing (pre­ sumably worse left ventricular function prior to cardiac arrest), significantly longer basic life support efforts, more defibrillation shocks, and more epinephrine administered. All of these features suggest a more difficult and longer resuscitation effort before circulation was restored. Similar to the experimental data, these clinical investi­ gators found that the left ventricular dysfunction or shock was generally transient, indicating global myocardial stun­ ning rather than permanent scarring. At 8 hours postresus­ citation, the average cardiac index postresuscitation among the 7 3 patients who developed shock was 2 . 1 L/min/m 2 (range 1 .4-2 .9). This improved to 3 . 2 L/min/m 2 (range 2 . 7-4.2) by 24 hours and to 3 . 8 Llmin/m< (range 3 .0-4.5) by 72 hours. However, although most postresuscitation shock was reversible, not all improved. Nearly 2 0 % ( 1 4 of 7 3 ) shock patients did not improve and subsequently died of persistent shock. Early death from multiple organ failure was associated with a persistently low cardiac index at 2 4 hours (2 . 6 Llmin/m 2 [range 2 . 3 -3 .0] vs . 3 . 3 Llmin/m 2 [range 2 .9-4. 3 ] ; P 4 Jlkg (as high

CHAPTER 1 3

as 9 ]/kg) have effectively defibrillated children 141 · 142 and p ediatri c animal models143 with no significant advers e effects . Based on adult clinical data96•144 and pediatric ani­ mal models, 145 biphasic shocks appear to be at least as effec­ tive as monophasic shocks and less harmful. Recommended manual defibrillation (monophasic or biphasic) doses are 2 ]/kg for the first attempt and 4 ]/kg for subsequent attempts . 145 , 146

Automated External Defibrillators Many AEDs now have pediatric capability, which means that they can deliver lower-energy shocks for use in children. Different models have different mechanisms to achieve this function-some use special cables with an in-line resistance and others alter the energy output of the device. These AEDs can accurately differentiate shockable from non­ shockable rhythms with a high degree of sensitivity and specificity in children.58 · 59 The FDA has approved a number of these modified devices or electrodes for use in children 1 to 8 years of age. For children 1 to 8 years of age the rescuer should use a pediatric device if one is available. 142 ·147· 148 If the provider initiates CPR to a child in cardiac arrest but does not have an AED with a pediatric attenuator system, she or he should use a standard adult AED . There are insufficient data to make a recommendation for or against the use of AEDs for infants < 1 year of age. 149

ln ..Hospital Use of Automated

External Defibrillators

The expectation and perhaps assumption among the med­ ical and lay-communities is that treatment of cardiac arrest is much better inside hospitals than outside. 150 Yet a report from the AHA National Registry of Cardiopulmonary Resuscitation/ 5 1 a voluntary registry and database of in­ hospital cardiac arrests from 3 69 hospitals, raises con­ cerns. This report found an overall survival-to-discharge rate from VF and pulseless VT of 3 4 % . The median time from recognition of arrest to shock delivery was an impressive 1 minute, but it was >2 minutes in 3 0 % of cases. D elay in defibrillation was associated with decreased survival. 1 5 2 D e fibrillation is more likely to be delayed when patients develop SCA in unmonitored hospital beds and in outpatient and diagnostic facilities. In such areas, several minutes may elapse before centralized response teams arrive with the defibrillator, attach it, and deliver shocks. This prompted consideration for use of AEDs . In-hospital AED use has been associated with increased survival rates from VF arrest. 1 5 3 · 1 54 D espite limited evidence, AED s should be considered for the hospital setting as a way to facilitate early defibrillation (a goal of :s 3 minutes from collapse) , especially in areas where staff have no rhythm­ recognition skills or defibrillators are used infrequently.

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Early defibrillation capability should be available i n ambu­ latory care facilities as well as throughout hospital inpa­ tient areas. When hospitals deploy AEDs, an effective system for rapid response and training and retraining of initial responders should be in place . 1 5 5 Hospitals should moni­ tor collapse- to-first-shock intervals and resus citation outcomes.

L ay..Responder Public Access Defibrillation Programs

Automated external defibrillators (AEDs) have the capacity to save lives. This has recently been confirmed by a large retrospective review reporting that bystander use of CPR combined with the use of an AED actually more than dou­ bled the chances of survival of out-of-hospital cardiac arrest. When CPR was done and the AED delivered a shock, survival increased to 3 6 % , which was approximately four times greater than with CPR alone. 1 56 However, the potential benefit of AEDs is fully realized only if they are used and used promptly and effectively by on-site respon­ ders. The implementation of a quality public access defib­ rillation (PAD) program with medical direction oversight is fundamental and will increase the likelihood of bystanders performing CPR and using the AED .

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S e e W e b s i t e f o r A H A S c i e n c e A dvi s o ry Sta t e m e n t-Lay R e s c u e r ( P u b l i c A c c e ss) A u t o m a t i c E x t e r n a l D e fi b r i l l a t i o n P r o g r a m s

A system approach integrating an AED program can have an impact beyond just early defibrillation. Although a critical goal, early defibrillation is integrated in a system that provides committed and increased provider training, early system activation, and advanced life support (Fig. 1 3 -9). The cost-effectiveness of PAD programs is difficult to evaluate because of the variability in potential costs and the determination of all incremental costs. One study estimated a median incremental cost of $44,000 per additional quality­ adjusted life year (QALY) for on-site lay-responders and $27 , 2 00 per QALY for police responders. 157 Another analy­ sis reported that the cost per QALY in casinos was $ 5 6 , 7 00 . 1 58 These studies noted that the primary factors influencing cost were frequency of arrest and the number of defibrillators deployed. The following section provides an overview of impor­ tant elements in developing and maintaining an effective PAD program.

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Col lapse

Dispatch of EMS units Time to C P R

T i m e t o defibril lation

Start of defibrillation

Return of perfusing rhythm Time to defi nitive care Arrival of ful l ACLS support

F I G U R E 1 3 - 9 • A n A E D p r o g r a m a c c o m p l i s h e s very e a r ly d e fi b r i l l a t i o n i n t h e setti n g of t r a i n e d p r ovi d e r s i n i n c r e a s e d n u m ­ b e r s a n d e a r ly a ctiva t i o n o f a d d i ti o n a l c o m p o n e n ts o f t h e c h a i n o f s u rviva l . P r e p l o n n i n g p r ovi d e s a syste m str u c t u r e a n d q u o l 1 ty r ev1 ew, a n d d e b r i e fi n g m a i n t a i n s q u a l i ty a n d i m p r ove c o r e .

Types of Automated External Defibrillator Programs

In some communities, the local EMS has provided consulta­ tion or program coordination services for these programs.

There are different types of PAD programs, mainly related to the specific site, population, or purpose, such as those described below.

Home (Residential) and Personal

Community/Neighborhood These are community-wide programs typically with desig­ nated first responders dispatched through the local 9 1 1 center. Typical first responders are firefighters (especially in urban areas with fire departments staffed with in-house crews) and police officers (more common in suburban areas). A national survey found that about 80% of local law enforcement agen­ cies responded to medical emergencies, with about 3 9 % of those equipped with AEDs.35 In many rural areas, volunteers often serve on an on-call basis as part of a quick response serv­ ice (QRS). All of these prehospital defibrillation programs are usually integrated as part of the local EMS system. S ome neighborhoods and gated communities have developed PAD programs for their well-defined small areas. These have utilized AEDs deployed by on-site security per­ sonnel when available or placed in central areas, often with a lock-box type of system. This model shares characteristics of a community and an on-site program.

On,Site for Public and Private Nonresidential Locations These programs comprise specific buildings or a defined loca­ tion such as office buildings, industrial plants, schools, churches, and public squares or parks. Such programs are often run by the site owner or management firm and not directly owned and operated by local EMS. However, these programs should be coordinated with local EMS and the 9 1 1 call center.

A newer concept is the deployment of AEDs in private resi­ dences and vehicles. This concept has garnered attention because 7 5 % to 80% of all SCAs occur at home. However, many of these are unwitnessed or occur during sleep, hence are unrecognized. Additional concerns regarding the effectiveness of this strategy are whether family members or others would be willing and able to promptly use the AED and that attention to the AED would not lead to delay or failure to call 9 1 1 . A mul­ ticenter trial that studied this concept in 700 1 patients with myocardial infarction found that overall mortality (about 6. 5%) did not differ between subjects who were provided AEDs and those who were not. Four of 3 2 patients on whom AED was used survived and no inappropriate shocks were reported. 159 However, use of a home defibrillator may still be a con­ sideration for the small group of persons with risk factors for SCA but who are not candidates for an implanted defibrillator. Some "worried well" individuals have deployed AEDs not only in their private residences but also their personal vehicles, planes, and vacation homes. Currently there is one AED model (Home Defibrillator, Philips Medical Systems, Andover, MA) with FDA approval for sale without a prescription. The similar components among these types of pro­ grams allow for a general format to set up and maintain any PAD program. The components that are different provide specifics that make a particular PAD program successful.

Liability and Regulatory Issues All states have some form of "good Samaritan" AED legis­ lation. In general, these laws provide immunity from legal

CHAPTER 1 3

liability for those who use and deploy AEDs without gross negligence or willful and wanton misconduct, but the details vary from state to state . Some states require train­ ing by nationally recognized training organizations, coordination with EMS , medical direction, and record keeping. The National Cardiac Arrest Survival Act provides liability protection for good Samaritans in states without such legislation. Now that all states do have this in place, whether the federal statute provides any additional pro­ tections is unclear and likely will depend on court inter­ pretations . This information can be accessed via the Internet at many different Web sites, such as the AHA, American Red Cross, Sudden Cardiac Arrest Association, as well as state­ based legislative Web sites.

Critical Elements of a Quality Public Access Defibrillation Program Coordination and Leadership Leadership is critical for the development and maintenance of a quality PAD program. There must be someone pas­ sionate and dedicated to making the program work, prefer­ ably someone in a leadership position in the organization or empowered by leadership. This person can make sure that the necessary resources are available and can motivate other individuals when necessary. A key part of leadership is medical direction oversight. This element is like an insurance policy, making sure that all the components are in place and functioning properly. The medical director is ideally a physician with interest and expert­ ise in prehospital care or resuscitation medicine. For the majority of AEDs a prescription is required in order to pur­ chase the device, which is considered a class III medical device by the FDA 01ttp://www.fda.gov/cdrhldevadvice/3 1 3 .html). A good knowledge base of the different AEDs available in the market is useful, since AEDs have differing options that make some better for PAD programs (such as the need for a basic AED) versus medical or advanced use by professional respon­ ders, such as an EMS agency or cardiac testing facility (where the need for visualization of the real-time ECG, manual over­ ride of preset energy levels, or pacing capabilities may be required). Medical direction oversight helps to assure protec­ tive legal steps are addressed, such as the use of checklists for expiration dates, battery-life status, and equipment require­ ments. Other components of a medical direction oversight program are listed below. The medical direction oversight team is composed of the physician and at least one coordinator, such as a nurse, EMT, EMT-P, or anyone knowledgeable about AED s . Having a medical background i s helpful but not necessary in the role of coordinator. This team provides the prescription, standard operating guidelines (SOG), and possibly training; it can also offer consultation on the need for PAD programs. Leadership is important, so that awareness of AEDs can be promoted, proper use of AEDs-in conjunction with

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CPR-can b e recommended, providing a source o f support to all involved for consistency and comfort of both the lay­ public and the medical personnel. Another key person is someone at the site who is will­ ing and able to be responsible for the AED and SOG, and serve as liaison between the site and medical direction over­ sight team. This person is called the on-site coordinator. If there is a safety committee or emergency response team already on-site, this is a good source to use. If there is secu­ rity on-site, as at the entrance to the site/building, this is not only a good location to place the AED but a good source to use for the daily equipment check, since such security is probably going to be making rounds and will be a consistent presence on-site. It is important to notify the local EMS agency that an AED is on-site. EMS also provides a source of support, information and possibly training. This also promotes com­ munication and awareness between the general public and the local EMS agency.

Response Planning and Device Deployment Assessment of the Site and/or Facility This is an impor­ tant step in any PAD program so the site can be visually inspected for its size and scope, entrances to buildings, access for EMS, deterrents that may hinder response time (such as automatically locking doors in stairways), location of elevators and stairs, and any other emergency equipment on-site. Two other components to assess would be the form of communication (overhead public access system, pagers, cell phones, walkie-talkies/radios, or nothing) and the cur­ rent emergency response plan. An emerging goal, based on published studies and expert opinion, is to deploy devices such that they can be retrieved and brought to the victim within 3 minutes . This step should actually be walked through and timed with a stopwatch from the furthest point from the AED location. Information collected on the site assessment will help to determine how many AEDs are ideal for the site as well as placement and location for storage and signage to direct the responder to the AED in the timeliest manner. The most central, easily accessed, and visual location is the optimal location for the AED . Written Standard Operating Guidelines This i s a key element, since it basically ties all the elements of the PAD program together. The chain of survival is a good model for any emergency response plan. The links include calling 9 1 1 , performing CPR, obtaining and using the AED , and EMS arrival. An emergency response plan should address the fol­ lowing elements: •

•

•

Recognition of possible cardiac arrest. How to call 9 1 1 : - Is it a direct line or must an outside line be dialed first? - How is the public made aware of this information (sign by the phones, stickers on the phone)? What is the form of communication on-site to alert oth­ ers of an emergency?

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How is the public made aware of this information (forms posted at key locations, frequent reminders at staff meetings)? Wbat is the location of the AED (or AEDs)? Statement that the AED should be brought to all events. EMS access (designated entrance, hold the elevator, unlock any doors)

The standard operating guidelines (SOG) serve as the blueprint that will guide and maintain organization of the PAD program for both the medical direction oversight team and the site itself. Components of the SOG include the jus­ tification for the AED by using current knowledge and sta­ tistics on how CPR and AED use affect the survival of the victim. Other components would be the emergency response plan, a list of the exact location of the AED(s) on-site, AED manufacturer and model number, CPR and AED "how to" steps, listing of ownership, responsibilities of the different entities involved (such as the medical direction oversight team, on-site coordinator, and responders). Contact infor­ mation for key persons should be included. Information spe­ cific to the AED 's functioning should be outlined. Helpful hints for troubleshooting are valuable and should be specific to the AED, including technical support contact information and referral to the manufacturer's owner's manual. Checklists for checking the AED 's state-of-readiness indicator as well as checking the equipment for expiration dates and lot num­ bers, battery-life status, and that all required equipment is intact. Event documentation forms are important for event data collection and quality-assurance review. This process must be outlined to detail who will collect data, in what time frame, and what equipment is necessary to obtain event data from the AED device. Quality assurance should include review of the entire event, time sequence and role of respon­ ders, AED event review for initial rhythm, rhythm at each analysis, rhythm at each shock or "no shock advised" assess­ ment, and final rhythm. This also presents the opportunity to provide feedback to the program personnel.

Personnel and Training All responding personnel should be trained in CPR and AED use. It is important to document and maintain this training. Some sites have designated response teams or safety committees of which all of those members should be trained. Another helpful training aspect is an in-service on the site on the specifics of the AED(s) by providing infor­ mation and a demonstration. It is optimal to do this at time of initial deployment and as review. A mock drill is another way to evaluate the PAD program, providing staff involve­ ment and teaching with the post-mock-drill review. Another option is the AHA's Heartsaver AED Anytime" self-training, which allows for viewing a DVD while practicing on the manikin provided, and then having an AHA instructor eval­ uate the procedure at a later time to be certified as having passed the AHA Heartsaver course.

Equipment and Supplies The suggested equipment that should be considered for storage with the AED includes the following:

•

•

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Battery (installed) Two sets of adult pads Carry case to hold the above in an organized and safe manner (recommended is a carry case specifically made for the AED , since it holds the AED firmly and has slots for extra supplies; this is preferable to any other carry bag format) "CPR kit," which would include medical scissors, razor, towel, gloves, and barrier device (face shield or face mask) Event report form All this equipment allows for a grab-and-go concept, since all is encapsulated inside the carry case (AED , battery, pads) and attached to the handle (CPR kit), so that it can easily be carried from storage to the victim for optimal response time.

Other equipment to consider based on specific circum­ stances would include: • •

•

•

Pediatric pads Spare battery (refer to manufacturer's owner's manual and medical director for recommendation on specifics of spare battery location; generally spare needed only for rechargeable batteries or if under unusual stress) Paper pad and pen to make notes of event Farms such as the emergency response plan and the CPR and AED "how to" and Event Report form

Storage and Signage There are several options for stor­ age of the AED . Wall-mounted cabinets can be recessed, semirecessed, or in on-the-wall format. There are also stand-alone cabinets. The cabinet can have different alert systems, such as a local alarm system (usually audible and visual) or an autodial phone mechanism to alert the 9 1 1 cen­ ter and/or an on-site call center. The cabinet can house just the AED or also other first aid equipment. The cabinet is usually metal with a clear front so that the AED can easily be seen, including the state-of-readiness indicator. There are also options for temperature-controlled and security cabinets ideal for outdoor settings, such as parks and pools. The cabinet door generally should not be locked, so that anyone can pull the door open to access the AED when needed. A cabinet is best for public locations so that the AED can be visualized but still kept protected. Another storage mode for AEDs employs a wall bracket or hook. This would be appropriate for a location that is not accessed by the general public, such as a doctor's office. Sigt1age is very important to make everyone aware that there is an AED on-site and where it is located. It seems redundant, but having a 3D AED sign (one that protrudes from the wall versus being flat on the wall) above the cabi­ net is useful so that it can be more easily seen. Directional signage with words or arrows to help the responder reach the AED location may be warranted in some settings . Having a sign stating that there is an AED on the premises and where it is located within the site is also useful. Signs can usually be purchased from the manufacturer of the AED , or they can be custom-made or even printed out and laminated (the Sudden Cardiac Arrest Association Web site offers the option of printing out the universal AED symbol).

CHAPTER 1 3

Maintenance (Equipment and Program ) Most AEDs conduct self-checks, and this generates a readi­ ness indicator on the device. This information can be found in the manufacturer's owner's manual. Most AEDs will make a chirping sound similar to the sound a smoke detector makes when its battery is low. There is also a change with the state-of-readiness indicator. All this is important for the on-site coordinator to know and assess for when checking the state-of-readiness indicator. This should be done daily for most sites or at minimum on a weekly basis, such as at a church. Such a checkup is ideally done in the morning, since most AEDs do the self-check after midnight. Since the battery is being used every day by the AED so as to be maintained in a state-of-readiness, this will lead to wear on the battery. Hence the state-of-readiness indica­ tor and daily visible check are important for ensuring that the AED is in optimal ready-to-use format at all times. It is important to document in the SOG when the battery was first installed in the AED . It is recommended to place an insertion date on the battery pack, using a p ermanent marker. This date will help determine when the battery will need to be replaced within a safe time margin. For example, the Philips lithium battery is a 4-year battery, but it will need to be replaced after about 3 . 5 years. If the AED is used for an event, this also means wear on the battery. Some manufacturers replace the battery pack at the same time as the pads, as with the Medtronic CR Plus and Express . One of the AED self-checks is to check the status of the battery; it will alert if it is low according to the state-of-readiness indicator. The AED is still usable in a limited format even in this low-battery state for a certain number of shocks and certain amount of time. The battery must be replaced with a new battery (or recharged if it is a rechargeable battery) so that the AED is maintained in a state-of-readiness and is not left with a dead battery, in which case the AED is not operational. The pads also have expiration dates, usually 2 years, but some manufacturers are now providing longer expiration dates. The package in which the pads come is sealed and should remain sealed to maintain the optimal life span of the pads, specifically the conductivity of the gel on the pads. When the seal is broken and the gel is exposed to air, the time during which the pads are usable-with good conduc­ tivity and adherence to the skin-is reduced. The pads are designed for one-time use only and will need to be replaced after an event. It is important to have two sets of adult pads, so that if the first set is not placed properly or does not adhere adequately (for example, on a male victim with a hairy chest), the second set can be used. Pediatric pads are optional; usually just one set of these is needed. They are considered preferable for children 1 to 8 years of age who weigh < 5 5 lb (2 5 kg). Adult pads can be used in the anteroposterior location if pediatric pads are not available. Some of the materials from the CPR kit can be cleaned and reused and some, once used, must b e dis­ carded and replaced after the event. The medical scissors can be cleaned appropriately and reused. The razor, towel, gloves, and barrier device will have to be replaced. If the

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b arrier device i s a face mask, only the valve will need replacement. Some face masks can be cleaned appropri­ ately and reused. The SOG should include the procedure for restocking the AED after an event or when items expire. The medical direction oversight team may keep supplies in stock for quick turnover postevent. If there is an event, the coordina­ tor goes to the site to retrieve the necessary forms and down­ load the information from the AED . At this time the AED is restocked with supplies. After the event, the site is given an order form to reorder whatever additional supplies may be needed. This allows for quick turnover and consistency of supplies and maintenance.

Incident Follow,up Post-AED actions should include several important compo­ nents. Documentation of the event from the responder(s) on a designated form is recommended. Information should include the date and time, location, when CPR was initiated, whether the AED was used, what the AED advised, whether there were any problems with CPR or AED use, whether all necessary emergency equipment was available, EMS notifi­ cation and response, and any other anecdotal information. The recorded information from the AED is downloaded and made available to the appropriate medical personnel. A des­ ignated individual is then responsible for cleaning and restocking the AED . Postevent response from the medical direction over­ sight team would be for quality assurance purposes to review the event forms and AED ECG; obtain follow-up, if able, on the victim; and provide a report and feedback to the site. The event ECG should be forwarded to the appropriate medical personnel if that had not already been done, includ­ ing the victim's medical records. It is obviously very impor­ tant to do this in a timely fashion, especially if the victim sur­ vives, so that the physician can assess the event ECG to possibly help determine what occurred and plan for treat­ ment. The medical direction oversight program should have the means to do this, either by having the necessary equip­ ment (software, infrared cable, laptop, etc.) or having access to such equipment from another source (possibly local EMS agencies or local AED manufacturer sales or technical sup­ port representative).

Quality Improvement The quality-improvement program should comprise both system and individual incident review. The program should be reviewed annually by the medical direction oversight team by actually going to the site again, reviewing the SOG, visually inspecting the AEDs, and discussing the program with the on-site coordinator and then updating the SOG as needed to maintain it at an optimal level . This review should assure that responses are initiated to all potential S CAs. The medical oversight team should also review the responder actions and AED function for every response. This includes reviewing data collected from the AED .

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Summary of PAD Lay-rescuer PAD programs save lives. An organized and consistent approach to the PAD program fosters success. Success will promote the program and save more lives. Remember that the AED is easy to use and difficult to mis­ use. The AED has self-checks that provide alerts showing whether it is functioning appropriately, so performing a check is easy and takes little time. A quality medical direc­ tion oversight program as the foundation of the PAD pro­ gram enhances success.

1 8. 19. 20. 21. 22. 23.

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1 2 6 . Yoon RS, DeMonte TP, Hasanov KF, et al. Measurement of tho­

racic current flow in pigs for the study of defibrillation and car­ dioversion. IEEE Trans Biomed Eng 2003 ;50(10): 1 1 67-1 1 7 3 . 1 2 7 . van Alem AP, Vrenken RH, d e Vos R , e t al. Use o f automated external defibrillator by first responders in out of hospital car­ diac arrest: prospective controlled trial. BMJ 2003 ; 3 2 7(742 7):

13 12. 1 2 8 . Carpenter J , Rea TD, Murray JA, e t al. Defibrillation waveform and post-shock rhythm in out-of-hospital ventricular fibrillation cardiac arrest. Resuscitation 2 003 ;59(2): 1 89-1 96. 129. Morrison LJ, Dorian P, Long}, et a!. Out-of-hospital cardiac arrest rectilinear biphasic to monophasic damped sine defibrillation waveforms with advanced life support intervention trial (ORBIT). Resuscitation 2005;66(2) : 1 49-1 5 7 . 1 3 0. Kudenchuk PJ, Cobb LA, Copass MK, et a l . Transthoracic incremental monophasic verus biphasic defibrillation by emer­ gency responders (TIMBER) . Circulation 2 006; 1 1 4:2 0 1 0-2 0 1 8 . 1 3 1 . Weaver WD , Cobb LA, C opass MK, et a!. Ventricular defibrilla­ tion: a comparative trial using 1 7 5 -J and 3 2 0-J shocks. N Eng! J

Med 1 9 82 ; 3 07(1 8) : 1 1 0 1-1 1 06. 1 3 2 . Miller PH. Potential fire hazard in defibrillation. JAMA 1972; 2 2 1 (2): 1 92 . 1 3 3 . Fires from defibrillation during oxygen administration. Health Devices 1 994;2 3 (7):3 07-3 09. 1 3 4. Sparking during discharge testing on Physio-Control Lifepak 9 defibrillator/monitors. Health Devices 1 994;2 3 (3):98-99. 1 3 5 . Lefever J, Smith A. Risk of fire when using defibrillation in an oxygen enriched atmosphere. A1.edical Devices Agency Safety Notices 1 995 ; 3 : 1 -3 . 1 3 6. Theodorou AA , Gutierrez JA, Berg RA . Fire attributable to a defibrillation attempt in a neonate. Pediat7'ics 2 003 ; 1 1 2 (3 Pt 1): 67 7-679. 1 3 7 . Panacek EA, Munger MA, Rutherford WF, et al. Report of nitropatch explosions complicating defibrillation. Am J Eme1'g Med 1 992 ; 1 0(2) : 1 2 8- 1 2 9 . 1 3 8 . Monsieurs KG, Conraads VM, Goethals MP, e t a l . Semi-auto­

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D E F I B R I L L AT I O N : P R A C T I C E

22 1

1 44. van Alem AP, Chapman FW, Lank P, et al. A prospective, ran­ domised and blinded comparison of first shock success of monophasic and biphasic waveforms in out-of-hospital cardiac arrest. Resuscitation 2 003 ; 5 8(1): 1 7-24. 145. Berg RA, Chapman FW, Berg MD, et al. Attenuated adult bipha­ sic shocks compared with weight-based monophasic shocks in a swine model of prolonged pediatric ventricular fibrillation.

Resuscitation 2 004; 6 1 (2): 1 89- 1 9 7 . 1 4 6 . Gutgesell HP, Tacker WA, Geddes LA, e t a l . Energy dose for ventricular defibrillation of children. Pediatrics 1 9 7 6 ; 5 8(6) : 898-90 1 . 1 4 7 . Samson RA, Berg RA, Bingham R, et al. Use of automated exter­ nal defibrillators for children: an update: an advisory statement from the pediatric advanced life support task force, International Liaison Committee on Resuscitation. Cinulation 2 003 ; 1 07(2 5) :

3 2 5 0-3 2 5 5 . 148. Jorgenson D, Morgan C, Snyder D, et a!. Energy attenuator for pediatric application of an automated external defibrillator. Ctit Care Med 2 002 ; 3 0(4 Suppl) : S l 45-S l 4 7 . 1 49. Samson R , Berg R , Bingham R , e t al. Use of automated external defibrillators for children: an update. An advisory statement from the Pediatric Advanced Life Support Task Force, International Liaison Committee on Resuscitation. Resuscitation 2003 ; 5 7(3):

2 3 7-243 . 1 5 0. Saxon LA. Survival after tachyarrhythmic arrest-what are we waiting for? N Eng! J Med 2008;3 5 8(1): 77-79. 1 5 1 . Peberdy MA, Kaye W, Ornata JP, et a!. Cardiopulmonary resus­ citation of adults in the hospital: a report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation.

Resuscitation 2 003 ; 5 8(3):2 97-3 08. 152. Chan P S , Krumholz H M , Nichol G, et al. American Heart

matic external defibrillation and implanted cardiac pacemakers: understanding the interactions during resuscitation. Resuscitation

Association National Registry of Cardiopulmonary Resuscitation Investigators. N Eng! J Med 2 008;3 5 8(1 ):9-1 7 . 1 5 3 . Zafari AM , Zarter SK, Heggen V, e t a l . A program encouraging early defibrillation results in improved in-hospital resuscitation efficacy. J Am Colt Cardio/ 2 004;44(4): 846-8 5 2 . 1 54. Destro A , Marzaloni M , Sermasi S, e t a l . Automatic external defibrillators in the hospital as well? Resuscitation 1 996; 3 1 ( 1 ) :

1 995 ; 3 0(2): 1 2 7-1 3 1 . 1 3 9. Calle PA, Buylaert W. When an AED meets an lCD . . .

3 9-43 . 1 5 5 . Kaye W, Mancini ME, Richards N. Organizing and implement­

Automated external defibrillator. Implantable cardioverter defib­ rillator. Resuscitation 1 998;3 8(3): 1 7 7-1 8 3 . 1 40. Levine PA, Barold S S , Fletcher RD , e t al. Adverse acute and chronic effects of electrical defibrillation and cardioversion on implanted unipolar cardiac pacing systems. J Am Colt Cardiol

ing a hospital-wide first-responder automated external defibrilla­ tion program: strengthening the in-hospital chain of survival.

1 9 8 3 ; 1 (6): 1 4 1 3-142 2 . 1 4 1 . Gurnett CA, Atkins D L . Successful use o f a biphasic waveform automated external defibrillator in a high-risk child. Am J Cm,diol 2 000;86(9): 1 0 5 1 - 1 05 3 . 1 42 . Atkins DL, Jorgenson D B . Attenuated pediatric electrode pads for automated external defibrillator use in children. Resuscitation 2 005 ;66( 1 ) : 3 1-3 7 . 143 . B erg RA, Hilwig RW, Ewy GA, et a l . Precountershock car­ diopulmonary resuscitation improves initial response to defibril­ lation from prolonged ventricular fibrillation: a randomized, con­ trolled swine study. Crit Cm'e Med 2 004; 3 2 (6): 1 3 52-1 3 5 7 .

Resuscitation 1 995 ; 3 0(2): 1 5 1- 1 5 6. 1 5 6. Weisfeldt ML, Griffith C, Aufderheide TP, et al. for the ROC investigators . Abstract 1 8 1 0 : Bystander Administered AED Shock Improves Survival from Out of Hospital Cardiac Arrest in U. S. and Canada. Circulation 2 007; 1 1 6 : 3 8 5-3 86. ! 5 7 . Nichol G, Hallstrom AP, Ornata JP, et a!. Potential cost-effec­ tiveness of public access defibrillation in the United States .

Cin:ulation 1 998;97( 1 3 ) : 1 3 1 5- 1 3 2 0 . ! 5 8 . Nichol G , Valenzuela T, Roe D, e t al. Cost effectiveness o f defib­ rillation by targeted responders in public settings . Ci1'culation 2 003 ; 1 08( 6) :697-703 . 1 59. Bardy GH, Lee KL, Mark DB, et al. HAT Investigators. Home use of automated external defibrillators for sudden cardiac arrest.

N Eng/ J Med 2 008 ; 3 5 8 ( 1 7): 1 793-1 804.

Roger D . White and Richard E . Kerber In human studies increasing evidence supports the observation that ventricular fibrillation (VF) is very organized , consisting of large structured wavefronts with origins in one or only a few reentrant circuits rather than many simultaneously circulating reentrant circuits . 1 5 · 23-24 To terminate VF, a defibrillation shock must extinguish these circuits and at the same time not itself induce VF. The transition of biphasic waveforms from implantable cardioverters-defibrillators (I COs) to external defibrillators constituted a significant technological advance for transthoracic defibrillation . Two types of VF have been reported to occur: wandering wavelets and a mother rotor with "spinoff' daughter wavelets. • Defibrillation is dependent upon creating refractoriness in myocardial cells so that they cannot propagate fibrillation wavefronts.

•

•

Shock efficacy has been defined and accepted as termination of VF during the 5 seconds after shock delivery. Biphasic waveform defibrillation shocks have greater efficacy in the termination of VF than monophasic shocks.

•

Currently available research indicates that biphasic shock energies, regardless of waveform, for initial shocks of 1 20 to 200 J are safe and effective. More limited data are available on 3 00- to 3 60-J biphasic shocks because of the very high efficacy (90% ) of initial shocks with lower energies.

V entricular Fibrillation:

Electrophysiologic

The mechanisms that initiate and sustain ventricular fibrillation (VF) are still not fully understood. 1-8 A variety of experimental models have helped define mechanisms of VF and have been reviewed in detaiL9-1 1 New terminology is being used along with traditional terms to describe the activation patterns that launch and sustain VF. Two types ofVF have been reported to occur, type I, consisting of wandering wavelets, and type II, consisting of a mother rotor with "spinoff" daughter wavelets. 1 2 -14 Recent observations in human VF indicate that both of these mechanisms may be operative, even in the same patient. 15 The multiple-wavelet mechanism states that VF is main­ tained by multiple wandering wavelets with constantly changing patterns of activation. Self-sustaining reen­ trant circuits are formed from these wavelets, resulting in continuing VF. Once initiated, VF can be sustained 222

by the incessant recirculation of re-entrant activation fronts moving along randomly changing pathways at varying conduction velocities. Excitable myocardium in their path assures their survival. The unstable and fragmented activation characteristic of VF can be understood as the result of wavefronts that have been disrupted by interaction with refractory tails of other waves. As these wavefronts fracture, some may propa­ gate unchanged until they are annihilated by random collision with other waves, whereas others can create new wavefronts. The final result would be fragmenta­ tion into multiple daughter wavelets. In this manner, the "pernicious stability" of VF can be sustained. Another mechanism described in human hearts is the mother-rotor hypothesis recently described and illustrated.16 This description proposes that VF is sustained by a single rapid source of excitation that cannot maintain uniform conduction tluoughout the myocardium; as a result, the rotor generates fibrilla­ tory conduction with intermittent conduction block, leading to the formation of multiple patterns of irregular activation. Re-entry can also be understood within the hypothesis of virtual electrode polarization (VEP)Y-2 3

CHAPTER 1 4

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V E N T R I C U L A R F I B R I L L AT I 0 N A N 0 0 E F I B R I L L A T I 0 N

This hypothesis has been invoked to explain both success­ ful and failed defibrillation shocks as well as the greater efficacy of biphasic shocks . VEP describes a complex global myocardial polarization characterized by the simultaneous presence of positive and negative areas of polarization adja­ cent to each other. In virtual electrode terminology, "neg­ ative polarization" describes repolarization (hyperpolariza­ tion) and "positive polarization" describes depolarization. Shortening of action potential duration by negative polar­ ization is referred to as " de -excitation , " which can be understood to be equivalent to repolarization. Thus , in essence, " excitation" refers to shock-induced depolariza­ tion of de-excited (repolarized) tissue. VEP is a result of redistribution of charge between neighboring areas of myocardium. Re-entry can develop because of the proxim­ ity of areas of shock-induced positive and negative polar­ ization. In human studies, increasing evidence supports the observation that VF is very organized, consisting of large structured wavefronts with origins in one or only a few reen­ trant circuits rather than many simultaneously circulating reentrant circuits. 1 5• 2 4• 2 5 To terminate VF, a defibrillation shock must extinguish these circuits and at the same time not itself induce VF. The mechanisms by which this might be achieved are discussed in the next section.

Defibrillation: Hypotheses and Electrophysiologic Mechanisms The mechanisms by which an electric shock terminates car­ diac tachyarrhythmias have not been conclusively demon­ strated. Various hypotheses have been described and include the "critical mass" hypothesis and the "upper limit of vul­ nerability" hypothesis. 2 6-2 8 The hypotheses of "extension of refractoriness" and "virtual electrode polarization" are dis­ cussed in more detail because they provide insights into the mechanism of defibrillation with biphasic waveforms. These various hypotheses are not necessarily mutually exclusive. Some or all of them may be applicable at any one time. Also, it should be noted that these hypotheses have been derived specifically from studies of VF; their applicability to the atrial myocardium for cardioversion of atrial fibrillation (AF) is unknown. Kerber et al. have shown that more organized tachyarrhythmias, such as ventricular tachycardia and atrial flutter, require lower energy to terminate than do VF and AF. This may be because only regional depolarization in the pathway of an advancing waveform is required to terminate these arrhythmias. 2 9 D efibrillation is dependent upon creating refractori­ ness in myocardial cells so that they cannot propagate fib­ rillation wavefronts . This is achieved by depolarizing the cell membrane sufficiently to trigger an action potential, which propagates throughout the membrane and to adj a­ cent cells . Following an action potential, the cell mem-

223

brane becomes absolutely refractory. As it repolarizes toward its resting potential, it becomes first relatively refractory and then fully excitable. Myofibrils are oriented at a variety of angles with respect to any electrical field (voltage gradient) . Thus cell membranes vary in their sus­ ceptibility to depolarization by a local voltage gradient, in part due to the variation in the angle they subtend with respect to the electrical field. Also, some portions of the cell membrane will be oriented to the field in such a man­ ner that depolarization will occur while other portions of the cell membrane will be repolarized. 2 0 During VF, cells are unsynchronized so that some are in an absolute refractory state, some in various degrees of rel­ ative refractoriness, and some in a resting state, readily depolarized by a stimulus. All of these factors combine to create a range of responsiveness of cells to an electrical field. A monophasic shock of a given strength will depolarize some mass of myocardial cells . At sufficient strength, the vast majority of cells will be depolarized and defibrillation will be achieved. Biphasic shocks can defibrillate with local electri­ cal fields of less intensity than can monophasic shocks-for several reasons, which are discussed in the next section. As a result, at any given intensity, a biphasic shock can depolarize a larger portion of the myocardium than can a monophasic shock of the same strength and, therefore, is more likely to defibrillate. Most of what is known about VF and defibrillation has been derived from a wide variety of animal models. The complexity and duration of commonly present underlying structural heart disease in human VF, the typical substrate for arrhythmogenesis, makes extrapolation from these experimental studies challenging, and it must be done with caution. In long-duration VF degradation of VF amplitude, frequency, and conduction properties progressively impairs the likelihood that a defibrillation shock will restore an organized rhythm. It can be anticipated that advances in waveform design and energy delivery will increase the probability that human VF can be terminated with longer durations and various underlying myocardial substrates. Whether such advances will be translated into improved survival remains to be determined. Given the complexities of cardiac arrest and resuscitation, including multiple inter­ ventions in many events, survival as an outcome measure of defibrillation waveform performance will be difficult to confirm.

Mechanisms of Superior Efficacy of Biphasic Shocks It is well accepted that biphasic waveform defibrillation shocks have greater efficacy in the termination of VF than monophasic shocks. This greater efficacy resides in the abil­ ity of the second phase to achieve defibrillation more easily by creating a homogeneous distribution of postshock trans­ membrane voltage. As pointed out above, myocytes stimu­ lated by an extracellular electrical field are depolarized on one side and hyperpolarized on the other, depending upon

>

.s however, is not infal­ lible as a means of confirming tube placement, particularly during cardiac arrest. Evidence from a meta-analysis in adults42 indicated a range of results: • •

Positive predictive value (probability of endotracheal placement if C0 2 is detected) : 1 00 % Negative predictive value (probability of esophageal placement if no C0 2 is detected) : 2 0 % to 1 00 %

Therefore, exhaled carbon dioxide almost certainly indicates that ventilation of the lungs is occuring; however absence of exhaled carbon dioxide may be due to esophageal intubation or to cardic arrest with no pefusion of the lungs. The use of C02 detecting devices to determine the correct placement of other advanced airways (e . g . , Combitube, LMA) has not been adequately studied.

COLOR CHANGE WITH COLORIMETRIC DEVICE: KNOW YOUR DEVICE The 2 000 Guidelines for Advanced Cardiovascular Life Support (ACLS) and Pediatric Advanced Life Support (PALS) as well as associated training materials offer examples of how colorimetric C 02 detection devices work and suggest mnemonic s chemes for interpretation. Those details were meant to help providers remember the significance of specific colors indicating the relative concentration of C 02 present in the expired air. S ome of the materials, for example, link the color purple with a sign of low C 02 and yellow with high C 02 • New devices have been introduced on the market with new indicators and color schemes. The indicators in some commercially available devices respond to detection of increasing C 02 concentration by transitioning in color using one of the following schemes: • • •

Basic Principles The body eliminates carbon dioxide through ventilation . When blood passes through the lungs, carbon dioxide moves from the blood, across the alveolar capillary membrane into the alveoli and then into the airways and is exhaled. Alveolar Pco 2 should be approximately equal to pulmonary venous, left atrial and arterial Pco 2 • If there is a good match of ven­ tilation and perfusion in the lungs and there is no airway obstruction, exhaled C02 should correlate well with arterial Pco 2 > and exhaled carbon dioxide can be used to estimate arterial carbon dioxide tension. Carbon dioxide can be detected by either of two techniques: •

•

Capnometry is a qualitative method that detects the pres­ ence of C0 2 in exhaled air. Colorimetric capnometers are semiquantitative devices based on a chemical reaction between exhaled C0 2 and a chemical detector impreg­ nated in a strip of paper. These devices are used to iden­ tify the presence or absence of a sufficient quantity of C0 2 to produce a color change at a point in time. Capnography devices are quantitative devices that meas­ ure the concentration of C0 2 using infrared absorption detectors. Carbon dioxide concentration is typically dis­ played by these devices as a continuous exhaled C0 2 con­ centration waveform with a digital display of end-tidal C0 2 • This plot of C0 2 concentration against time is called a capnograph.

Capnometry A C0 2 concentration of > 2 % will react with the chemical reagent in a colorimetric C0 2 detector and change the color (Fig. 1 8- 1 ). If the endotracheal tube is actually in the tra­ chea, the C0 2 detector will turn a color determined by the manufacturer. In the absence of expired C0 2 , the color of the colorimetric indicator will remain unchanged. Health care providers commonly use this color change with a disposable device as a quick check to provide one method of device confirmation of the success or failure of endotracheal intubation.43

245

Purple-to-yellow Blue-to-yellow White-to-purple

Even more possibilities will likely appear on the market in the coming years. Clearly, any one mnemonic that relies on color will not fit all available devices.

The product inserts for some commercially available semiqualitative colorimetric capnometers recommend that after intubation, six positive-pressure breaths be provided by hand or mechanical ventilation before attempting to identify exhaled C0 2 • Six breaths will wash out any C0 2 that is present in the stomach or esophagus from bag-mask ventilation. Any C0 2 detected after six breaths can be pre­ sumed to be from the lungs.44•45 There is no need to con­ tinue ventilation attempts if the endotracheal tube is clearly misplaced. In patients who weigh > 2 kg with a perfusing rhythm (not in cardiac arrest), the sensitivity and specificity of col­ orimetric capnometry methods approaches 1 00 % if six ven­ tilations have been provided following intubation. This means that if the endotracheal tube is in the trachea of a patient with a perfusing rhythm, the colorimetric device will change color with few exceptions (see "False-Positive Results , " below) . If the tube is in the esophagus, there should be no C0 2 detected after six breaths, so a colorimet­ ric C0 2 detector should remain unchanged. False-Positive Results When exhaled C0 2 is detected (positive reading for C0 2 ) in cardiac arrest, it is usually a reliable indicator of tube position in the trachea. False­ positive readings (C0 2 is detected but the tube is located in the esophagus) have b e en observed in animals that ingested large amounts of carbonated liquids before the arrest.44 A color change is generally a reliable indicator of the presence of C0 2 and endotracheal intubation. False-positive color changes are uncommon but can occur when the tip of the tube is in the supraglottic area rather than in the trachea. A false-positive may also be possible following prolonged

246

SINZ

•

HIGH

bag-mask ventilation,8-1 0 which is why some manufacturers recommend that six ventilations be provided after intubation and before the check for exhaled C0 2 • Finally, if the colori­ metric detector is contaminated with acidic gastric contents or acidic drugs, such as endotracheal administration of epi­ nephrine, a colorimetric detector may remain unchanged during the entire respiratory cycle. False-Negative Results False-negative results occur if the tube is in the trachea but the colorimetric indicator remains unchanged. A false-negative result is most often associated with cardiac arrest (see below). False-negative results may also occur with severe airway obstruction or pulmonary edema, which can impair C0 2 elimination so that inadequate C0 2 is detected in exhaled gas. Administration of an intra­ venous (IV) bolus of epinephrine in patients with cardiac arrest or very low cardiac output may transiently reduce pul­ monary blood flow and reduce exhaled C0 2 .46 False-negative readings (in this context defined as fail­ ure to detect C0 2 despite tube placement in the trachea) may be present during cardiac arrest for several reasons. The most common explanation for false-negative readings dur­ ing CPR is that blood flow and delivery of C0 2 to the lungs are low. False-negative results have also been reported in association with pulmonary embolus because pulmonary blood flow is reduced. In addition, elimination and detection of C02 can be drastically reduced with severe airway obstruc­ tion (e.g., status asthmaticus) and pulmonary edema.47 For these reasons, if C0 2 is not detected, the AHA 2 005 guide­ lines recommend that a second metlwd be used to confirm endotracheal tube placement, such as auscultation of the lungs, direct visualization of the tube passing through the vocal cords with a laryngoscope, or the esophageal detector device.

Capnography Some capnography devices are infrared devices in which a light-emitting diode is used to measure the intensity of light transmitted across a short distance, usually the diameter of an endotracheal tube. The measured light absorption varies inversely with the concentration of C0 2 passing through the endotracheal tube. When attached to the end of an endotra­ cheal tube, these infrared devices are called mainstream cap­ nometers. These devices readily reveal low exhaled C0 2 indicative of esophageal intubation, and they can provide estimates of the adequacy of ventilation and the effectiveness of circulation during CPR. Conversely, sidestream capnome­ ters draw a small sample of gas from the airway through a small tube to measure the C0 2 concentration in a device detached from the airway and the patient. Capnography devices provide a continuous readout of the concentration of C02 . They are used to monitor the quality of ventilation in nonarrest patients. Because of their high degree of sensitivity to expired COz, however, capnographs can often detect a sufficient quantity of C02 to indicate the presence of an endotracheal tube in the trachea even when cardiac arrest is present. Continuous capnography monitoring devices can identify and signal a fall in exhaled C02 consistent with endo-

tracheal tube dislodgment. This may be very helpful when patients are being moved or during emergencies.

Capnometry and Capnography in Cardiac Arrest End-tidal C02 monitoring is a safe and effective noninvasive indicator of cardiac output during CPR capnography may be an early indicator of return of spontaneous circulation (ROSC) in intubated patients because an increase in exhaled C02 typi­ cally occurs when cardiac output increases and perfusion of the lungs improves. During cardiac arrest, C02 continues to be generated throughout the body; however, there is little pul­ monary blood flow, and the level of C02 in exhaled gas may be too low to produce a color change or a graphic exhaled C02 waveform. In such situations, when a colorimetric device is attached to the distal end of a properly placed endotracheal tube, the color remains unchanged or the C02 level remains very low. Because the unchanged color and lack of exhaled C02 may also indicate that the tube has been placed in the esopha­ gus, the health care provider must decide whether the lack of carbon dioxide indicates esophageal intubation or reflects the absence of blood flow to the lungs. The major determinant of C02 excretion is its rate of delivery from the peripheral pro­ duction sites to the lungs. In the low-flow state during CPR, ventilation is relatively high compared with blood flow, so the end-tidal C02 concentration is low. If ventilation is reasonably constant, then changes in end-tidal C02 concentration reflect changes in cardiac output. Patients who are successfully resus­ citated from cardiac arrest have significantly higher end-tidal C02 levels than those who cannot be resuscitated.

References 1. Kern KB, Hilwig RW, Berg RA, et a!. Importance of continuous chest compressions during cardiopulmonary resuscitation: improved outcome during a simulated single lay-rescuer scenario. Cinttlation 2 002 ; 1 05(5):645-649. 2 . von Planta M, Wei! MH, Gazmuri RJ, et al. Myocardial acidosis associated with C02 production during cardiac arrest and resus­ citation. Cimtlation 1 989;80(3) :684-692 . 3 . Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest. Resuscitation 2005;64(3 ) : 3 63-3 7 2 . 4 . Aufderheide TP, Pirrallo RG, Yannopoulos D, e t al. Incomplete chest wall decompression: A clinical evaluation of CPR perform­ ance by trained laypersons and an assessment of alternative man­ ual chest compression-decompression techniques. Resuscitation 2 006; 7 1 (3) : 3 4 1-3 5 1 . 5 . Yannopoulos D , Aufderheide TP, McKnite S , et al. Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs. Resuscitation 2 006;69(3):487-494. 6. Baskett P, Nolan J, Parr M. Tidal volumes which are perceived to be adequate for resuscitation. Resuscitation 1 996; 3 1 (3):2 3 1 -2 3 4. 7 . Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation­ induced hypotension during cardiopulmonary resuscitation. Cimtlation 2 004; 109( 1 6): 1 960-1 965. 8. Paradis NA, Martin GB, Goetting MG, et al. Simultaneous aortic, jugular bulb, and right attial pressures during cardiopulmonary resuscitation in humans. Insights into mechanisms. Cinulation 1 989; 80(2) : 3 6 1-368. 9. Idris AH , Staples ED, O'Brien DJ, et al. Effect of ventilation on acid-base balance and oxygenation in low blood-flow states. Crit Cm'e Med 1 994;2 2 ( 1 1 ) : 1 82 7- 1 8 34.

CHAPTER 1 6

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M 0 N I T 0 R I N G A N 0 M A I N T A I N I N G A P AT E N T A I R W A Y

1 0 . Idris A, Wenzel V, Banner MJ, et al. Smaller tidal volumes mini­ mize gastric inflation during CPR with an unprotected airway. Circulation 1 995;92(suppl):I-7 59. 1 1 . Idris A, Gabrielli A, Caruso L. Smaller tidal volume is safe and effec­ tive for bag-valve-ventilation, but not for mouth-to-mouth ventila­ tion: an animal model for basic life support. Ci1·culation 1 999; 1 00 (suppl I):I-644. 1 2 . Dorph E, Wik L, Steen PA. Arterial blood gases with 700 ml tidal volumes during out-of-hospital CPR. Resuscitation 2 004;6 1 ( 1 ) :

35. 36. 37. 38.

2 3-2 7 . 1 3 . Winkler M , Mauritz W, Hackl W, e t al. Effects o f half the tidal vol­ unle during cardiopulmonary resuscitation on acid-base balance and haemodynamics in pigs. Eur J Emerg Med 1 998;5(2): 2 0 1 -206. 14. Babbs CF, Kern KB . Optimum compression to ventilation ratios in CPR under realistic, practical conditions: a physiological and mathematical analysis. Resuscitation 2 002 ; 54(2) : 1 47-1 5 7 . 1 5 . Greingor J L . Quality o f cardiac massage with ratio compres­ sion-ventilation 5/1 and 1 5/2 . Resuscitation 2002 ; 5 5 (3):263-267. 1 6 . Kern KB , Hilwig RW, Berg RA , e t a l . Efficacy o f chest compres­ sion-only BLS CPR in the presence of an occluded airway.

Resuscitation 1 998;39(3): 1 79- 1 88 . 1 7 . Wik L, Kramer-] ohansen J, Myklebust H, e t a l . Quality o f car­ diopulmonary resuscitation during out-of-hospital cardiac arrest.

39.

tube misplacement with the colorimetric carbon dioxide detector during anesthesia. Chung Hua I Hsueh Tsa Chih 1 993 ; 5 1 (6):41 5-

1 8 . Ornata JP, Hallagan LF, McMahan SB, et al. Attitudes of BCLS

(4) : 1 907-1 9 1 5 . 2 2 . Hallstrom AP. Dispatcher-assisted "phone" cardiopulmonary re­ suscitation by chest compression alone or with mouth-to-mouth ventilation. Orit Care Med 2 000;2 8(1 1 Suppl): N1 90-N192. 23. Waalewijn RA , Tijssen JG, Koster RW. Bystander initiated actions in out-of-hospital cardiopulmonary resuscitation: results from the An1sterdam Resuscitation Study (ARRESUST). Resuscitation 2 00 1 ;

services personnel, physicians, medical students, and medical laypersons. Ann Emerg Med 1 999; 3 4(6):720-729. Safar P, Escarraga LA, Chang F. Upper airway obstruction i n the unconscious patient. J Appl Physio/ 1 9 59; 14:7 60-7 64. Carlson KA, Jahr JS. An update on pulse oximetry. Part II: limita­ tions and future applications. Anesthesia! Rev 1 994;2 1 (2):41-46. Aughey K, Hess D, Eitel D, et al. An evaluation of pulse oximetry in prehospital care. Ann Eme1'g Med 1 9 9 1 ;2 0(8):887-8 9 1 . Bota GW, Rowe BH. Continuous monitoring o f oxygen satura­ tion in prehospital patients with severe illness: the problem of unrecognized hypoxemia. J Emerg Med 1 995 ; 1 3 (3):3 05-3 1 1 . Brown LH, Manring EA, Kornegay HB, et al. Can prehospital personnel detect hypoxemia without the aid of pulse oximeters?

Am ] Enmg Med 1 996; 1 4(1):43-44. 40. Valko PC, Campbeii JP, McCarty DL, et al. Prehospital use of pulse oximetry in rotary-wing aircraft. P1·ehosp Disast Med 1 9 9 1 ; 6(4) : 42 1 -42 8 . 41 . Wahr JA, Tremper KK. Noninvasive oxygen monitoring tech­ niques. Crit Care Clin 1 995 ; 1 1 ( 1): 1 99-2 1 7 . 42 . Li J. Capnography alone i s imperfect for endotracheal tube place­ ment confirmation during emergency intubation. J Eme1'g Med 2001 ;20(3):22 3-2 2 9 . 43 . Chow LH, Lui P W, Cheung EL, e t al. Verification o f endotracheal

JAMA 2005;293 (3):299-3 04. instructors about mouth-to-mouth resuscitation during the AID S epidemic. Ann Emerg Med 1 990; 1 9(2): 1 5 1- 1 5 6. 1 9 . Brenner BE, Van DC, Cheng D, et al. Determinants of reluctance to perform CPR among residents and applicants: the impact of experience on helping behavior. Resuscitation 1 997;3 5(3):203-2 1 1 . 20. Hew P, Brenner B , Kaufman ] . Reluctance of paramedics and emergency medical technicians to perform mouth-to-mouth resuscitation. J Enze1'g Med 1 997; 1 5 (3):279-2 84. 2 1 . Berg RA, Kern KB, Sanders AB , et al. Bystander cardiopulmonary resuscitation. Is ventilation necessary? Circulation 1 99 3 ; 8 8(pt 1)

24 7

418. 44. Sum Ping ST, Mehta M P, Symreng T. Accuracy o f the FEF C02 detector in the assessment of endotracheal tube placement. Anesth Analg 1 992 ;74(3):41 5-4 1 9 . 45 . Ornata JP, Shipley JB, Racht EM, e t a l . Multicenter study o f a portable, hand-size, colorimetric end-tidal carbon dioxide detec­ tion device. Ann Enmg Med 1 992 ; 2 1 (5): 5 1 8-52 3 . 46. CantineauJP, Merckx P, Lambert Y, et al. Effect of epinephrine on end-tidal carbon dioxide pressure during prehospital cardiopul­ monary resuscitation. Am J Ernerg Med 1 994; 1 2 (3): 2 67-2 70. 47. Ward KR, Yealy DM. End-tidal carbon dioxide monitoring in emergency medicine. Part 2 : clinical applications. Acad Emerg Med

improve outcome in a porcine model of single-rescuer bystander cardiopulmonary resuscitation. Circulation 1 997;95(6): 1 63 5-

1 998;5(6) :63 7-646. 48. Thomas M, Malmcrona R, Shillingford ]. Haemodynamic effects of oxygen in patients with acute myocardial infarction. Br Heart J 1 965 ;27 :40 1 -407 . 4 9 . Daly \V], Cline D, Bondurant S . Effects o f breathing oxygen on atrioventricular conduction. Am Hem1: J 1 963;66:32 1-324. 50. Daly \V], Behnke RH. Hemodynamic consequences of oxygen breathing in left ventricular failure. Circulation 1 96 3 ; 2 7 : 2 52-2 5 6. 5 1 . Kenmure AC, Murdoch WR, Beattie AD, et al. Circulatory and metabolic effects of oxygen in myocardial infarction. Br Med J 1 968;4(5 627):3 60-3 64. 5 2 . Foster GL, Casten GG, Reeves TJ. The effects of oxygen breath­ ing in patients with acute myocardial infarction. Cardiovasc Res 1 969;3 (2): 1 79-1 89. 53. Bourassa MG, Campeau L, Bois MA, et al. The effects of inhala­ tion of 1 00 percent oxygen on myocardial lactate metabolism in coronary heart disease. Am J Cardio/ 1 969;24(2) : 1 72 - 1 7 7 . 5 4 . Sukwnalchantra Y, Levy S, Danzig R , e t a l . Correcting arterial

1 641 . 2 8 . Berg RA, Kern KB, Hilwig RW, et al. Assisted ventilation during

hypoxemia by oxygen therapy in patients with acute myocardial infarction. Effect on ventilation and hemodynamics. Am J Cm·diol

"bystander" CPR in a swine acute myocardial infarction model does not improve outcome. Cimtlation 1 997;96(1 2): 43 64-43 7 1 . Deakin CD, O'Neill JF, Tabor T. Does compression-only car­ diopulmonary resuscitation generate adequate passive ventilation during cardiac arrest? Remscitation 2007; 75( 1 ) : 5 3-59. Wei! MH, Rackow EC, Trevino R, et al. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Eng! J Med 1 986;3 1 5(3): 1 53-1 56. Koster RW, Deakin CD, Bottiger BW, et al. Chest-compression­ only or full cardiopulmonary resuscitation? Lancet 2007; 3 69 (95 7 7) : 1 924; author reply 1 92 5 . Eberle B, Dick WF, Schneider T, e t al. Checking the carotid pulse check: diagnostic accuracy of first responders in patients with and without a pulse. Resuscitation 1 996; 3 3 (2): 1 07-1 1 6 . Bahr J, Klingler H, Panzer W, e t al. Skills o f lay people i n check­ ing the carotid pulse. Resuscitation 1 997; 3 5 (1):2 3-2 6 . Ruppert M, Reith M W, Widmann J H , e t a l . Checking for breath­ ing: evaluation of the diagnostic capability of emergency medical

1 969;24(6) : 8 3 8-8 5 2 . 5 5 . Neill WA. Effects o f arterial hypoxemia and hyperoxia o n oxygen

50(3):273-2 79. 24. Van Hoeyweghen RJ, Bossaert LL, Mullie A, et al. Quality and efficiency of bystander CPR. Belgian Cerebral Resuscitation Study Group. Resuscitation 1 993;2 6(1) :47-52 . 2 5 . Chandra NC, Gruben KG, Tsitlik JE, e t al. Observations o f ven­ tilation during resuscitation in a canine model. Cinulation 1 994;

90(6) : 3 070-3 0 7 5 . 2 6 . Tim g W, Wei! MH, Sun S , e t a l . Cardiopulmonary resuscitation by precordial compression but without mechanical ventilation.

Am J Respi1• Crit Care Med 1 994; 1 5 0(6 pt 1): 1 709-1 7 1 3 . 2 7 . Berg RA, Kern KB , Hilwig RW, et al. Assisted ventilation does not

29. 30. 31. 32. 33. 34.

56. 57. 58. 59. 60.

availability for myocardial metabolism. Patients with and without coronary heart disease. Am ] Cardio/ 1 969;24(2) : 1 66-1 7 1 . Madias JE, Hood WB Jr. Reduction of precordial ST-segment ele­ vation in patients with anterior myocardial infarction by oxygen breathing. Circulation 1 976; 5 3 (3 Suppl) : I l 9 8-I2 00. Madias JE, Madias NE, Hood WB Jr. Precordial ST-segment map­ ping. 2. Effects of oxygen inhalation on ischemic injury in patients with acute myocardial infarction. Circulation 1 976; 5 3 (3):41 1-4 1 7 . Madias JE, Hood WB Jr. Precordial ST-segment mapping. 4 . Experience with mapping o f ST-segment depression i n anterior transmural myocardial infarction. J Electrocardio/ 1 976;9(4):3 1 5-3 20. Rawles JM, Kenmure AC. Controlled trial of oxygen in uncom­ plicated myocardial infarction. Br Med] 1 976; 1 (60 1 8): 1 1 2 1 -1 1 2 3 . Nicholson C. A systematic review o f the effectiveness o f oxygen in reducing acute myocardial ischaemia. J Clin Nurs 2 004; 1 3 (8):

996-1 007.

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6 1 . Amman EM, Anbe DT, Armstrong PW, et a!. ACC/AHA guide­ lines for the management of patients with ST-eievation myocar­ dial infarction; A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1 999 Guidelines for the Management of patients with acute myocardial infarction). J Am Colt Cardia!

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J Am Col! Cm,diol 2 007;50(7) : e 1 -e 1 5 7 . 63 . Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guide­ lines for the management of patients with unstable angina/ non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2 002 Guidelines for the Management of Patients With Unstable Angina/ Non ST-Elevation Myocar(lial Infarction): developed in collabora­ tion with the American College of Emergency Physicians, the Society for Caf(liovascnlar Angiography and Interventions, and the Society of Thoracic Surgeons: endorsed by the An1erican Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. Circulation 2007; 1 1 6(7):e148-3 04. 64. Davies AE, Kidd D, Stone SP, et al. Pharyngeal sensation and gag reflex in healthy subjects. Lancet 1 995;345 (8948):487-488 . 6 5 . Bleach NR. The gag reflex and aspiration: a retrospective analysis of 1 2 0 patients assessed by videofluoroscopy. Clin Otolmyngol

Allied Sci 1 993 ; 1 8(4) : 3 03-3 0 7 . 66. Gallagher W'J, Pearce A C , Power SJ . Assessment of a new nasopharyngeal airway. Br J Anaesth 1 988;60(1): 1 1 2-1 1 5 . 6 7 . Feldman SA, Fauvel NJ , Ooi R . The cuffed pharyngeal airway. Eu1' J Anaesthesio/ 1 99 1 ; 8(4) : 2 9 1 -2 9 5 . 68. Ellis DY, Lambert C, Shirley P. Intracranial placement o f nasopharyngeal airways: i s i t all that rare? Emerg Med J 2006;2 3 (8):66 1 . 69. Muzzi DA, Losasso TJ, Cucchiara RF. Complication from a nasopharyngeal airway in a patient with a basilar skull fracture.

Anesthesiology 1 9 9 1 ; 74(2):3 66-3 68. 70. Schade K, Borzotta A, Michaels A. Intracranial malposition of nasopharyngeal airway. J Trauma 2 000;49(5):967-968 . 7 1 . Martin J E , Mehta R , Aarabi B , e t a l . Intracranial insertion o f a nasopharyngeal airway in a patient with craniofacial trauma. Mil Med 2 004; 1 69(6) :496-497 . 7 2 . Simons RW, Rea T D , Becker LJ, e t a l . The incidence and signif­ icance of emesis associated with out-of-hospital cardiac arrest.

Resuscitation 2007;74(3 ):42 7-43 1 . 7 3 . Kozak RJ, Ginther BE, Bean WS . Difficulties with portable suc­ tion equipment used for prehospital advanced airway procedures.

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Med 1 995 ; 1 5 5 (9) :93 8-943 . 76. Bretmer BE, Kauffman ]. Reluctance of internists and medical nurses to perform mouth-to-mouth resuscitation. Arch Intern Med 1 993 ; 1 5 3 ( 1 5) : 1 763-1 769. 77. Brenner B, Stark B, Kauffman ]. The reluctance of house staff to perform mouth-to-mouth resuscitation in the inpatient setting: what are the considerations? Resuscitation 1 994;2 8(3): 1 8 5-1 9 3 . 7 8 . Mejicano GC, Maki DG. Infections acquired during cardiopul­ monary resuscitation: estimating the risk and defining strategies for prevention. Ann Intem Med 1 998; 1 2 9 ( 1 0) : 8 1 3-82 8 . 79. Axelsson A , Thoren A , Holmberg S, e t a l . Attitudes o f trained Swedish lay rescuers toward CPR performance in an emergency:

a survey of 1 0 1 2 recently trained CPR rescuers. Resuscitation 2 000; 44( 1 ) : 2 7-3 6.

80. Melanson SW, O'Gara K. EMS provider reluctance to perform mouth-to-mouth resuscitation. Prehosp Eme1'g Cm'e 2000;4(1):48-52. 8 1 . Rossi R, Lindner KH , Ahnefeld FW Devices for expired air re­ suscitation. hebosp Disast Med 1 99 3 ; 8(2) : 1 2 3- 1 2 6 . 82. Cydnlka RK, Connor PJ, Myers TF, e t al. Prevention o f oral bacte­ rial flora transmission by using mouth-to-mask ventilation during CPR. J Eme1'g Med 1991 ;9(5):3 1 7-32 1 . 8 3 . Lawrence PJ, Sivaneswaran N . Ventilation during cardiopulmonary resuscitation: which method? Med J Aust 1 985; 143 ( 1 0):443-446. 84. Harrison RR, Maull KI, Keenan RL, et al. Mouth-to-mask ventila­ tion: a superior method of rescue breathing. Ann Eme1x Med 1982;

1 1 (2): 74-76. 85. Seidelin PH, Stolarek IH, Littlewood DG. Comparison of six meth­ ods of emergency ventilation. Lancet 1 986;2(85 1 8) : 1 2 74-1 2 7 5 . 86. Thomas AN O'Sullivan K , Hyatt J, e t a l . A comparison o f bag ,

mask and mouth mask ventilation in anaesthetised patients.

Resuscitation 1 993 ;2 6(1 ): 1 3-2 1 . 87. Paal P, Falk M, Sumann G, et a!. Comparison of mouth-to-mouth, mouth-to-mask and mouth-to-face-shield ventilation by lay per­ sons. Resuscitation 2006;70(1): 1 1 7- 1 2 3 . 8 8 . Johannigman JA, Branson RD, Davis K Jr, e t al. Techniques of emergency ventilation: a model to evaluate tidal volume, airway pressure, and gastric insufflation. J Trauma 1 9 9 1 ; 3 1 (1):93-98. 89. Elling R, Politis ]. An evaluation of emergency medical techni­ cians' ability to use manual ventilation devices. Ann Emerg Med

1 9 8 3 ; 1 2 ( 1 2): 765-768. 90. Cummins RO, Austin D, Graves JR, et al. Ventilation skills of emergency medical technicians : a teaching challenge for emer­ gency medicine. Ann Eme1'g Med 1 986; 1 5 ( 1 0): 1 1 87-1 1 9 2 . 9 1 . Hess D, Baran C . Ventilatory volumes using mouth-to-mouth, mouth-to-mask, and bag-valve-mask techniques. Am J Enm'g Med

1 9 8 5 ; 3 (4) :2 92-296. 92 . De Regge M, Vogels C, Monsieurs KG, et al. Retention of venti­ lation skills of emergency nurses after training with the SMART BAG compared to a standard bag-valve-mask. Resuscitation 2006;

68(3):3 79-3 84. 93 . Walsh K, Loveday K, O'Rathaille M. A comparison of the effec­ tiveness of pre-hospital bag-valve-mask ventilation performed by Irish emergency medical technicians and anaesthetists working in a tertiary referral teaching hospital. 11, Med J 2003 ;96(3):77-79. 94. Osterwalder ]], Schuhwerk W Effectiveness of mask ventilation in a training mannikin. A comparison between the Oxylator EM 1 00 and the bag-valve device. Resuscitation 1 998;36(1):23-2 7 . 9 5 . Martin P D , Cyna Aivt: , Hunter WA, et a!. Training nursing staff in airway management for resuscitation: A clinical comparison of the facemask and laryngeal mask. Anaesthesia 1 993 ;48(1):3 3-3 7 . 9 6 . Alexander R , Hodgson P, Lomax D, e t a l . A comparison o f the laryngeal mask airway and Guedel airway, bag and face mask for manual ventilation following formal training. Anaesthesia 1 993 ;48

(3):2 3 1 -2 3 4. 97. Jesudian MC, Harrison RR, Keenan RL, et al. Bag-valve-mask ventilation; two rescuers are better than one: preliminary report.

Crit Crwe Med 1 9 8 5 ; 1 3 (2): 1 22-1 2 3 . 98. Davidovic L , LaCovey D , Pitetti RD . Comparison o f 1 - versus 2 person bag-valve-mask techniques for manikin ventilation of infants and children. Ann Emag Med 2 005 ;46(1):3 7-42 . 99. Dunkley CJ, Thomas AN Taylor RJ, et al. A comparison of stan­ dard and a modified method of two resuscitator adult cardiopul­ monary resuscitation: description of a new system for research into advanced life support skills. Resuscitation 1 998;38(1):7- 1 2 . 1 00. Wheatley S, Thomas AN Taylor RJ, e t al. A comparison o f three methods of bag valve mask ventilation. Resuscitation 1 997; 3 3 (3): ,

,

2 07-2 1 0 . ,

1 0 1 . Thomas AN Dang PT, Hyatt ], e t a l . A new technique for two­ hand bag valve mask ventilation. B1' J Anaesth 1 992 ;69(4):3 97-3 98. 102. Wenzel V, Idris AH , Dorges V, et al. The respiratory system during resuscitation: a review of the history, risk of infection during assisted ventilation, respiratory mechanics, and ventilation strategies for patients with an unprotected airway. Resuscitation 2 0 0 1 ;49(2):

1 2 3-1 34. 1 0 3 . Dorges V, Ocker H, Wenzel V, et al. Emergency airway manage­ ment by non-anaesthesia house officers-a comparison of three strategies. Enzerg Med J 2 00 1 ; 1 8(2):90-94.

CHAPTER 1 6

•

M 0 N I T 0 R I N G A N 0 M A I N T A I N I N G A P AT E N T A I R W A Y

1 04. Wenzel V, Keller C, Idris AH , et a!. Effects of smaller tidal volumes 105. 1 06. 107. 108.

during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk? Resuscitation 1 999;43 (1):2 5-29. Dorges V, Ocker H, Hagel berg S , et al. Smaller tidal volumes with room-air are not sufficient to ensure adequate oxygenation during bag-valve-mask ventilation. Resuscitation 2 000;44( 1 ) : 3 7-4 1 . Tourtier J P, Compain M , Petitjeans F, et a!. Acid aspiration pro­ phylaxis in obstetrics in France: a comparative survey of 1 998 vs. 1 9 8 8 French practice. Eur J Anaesthesio/ 2 004;2 1 (2): 89-94. Soreide E, Holst-Larsen H, Steen PA. Acid aspiration syndrome prophylaxis in gynaecological and obstetric patients. A Norwegian survey. Acta Anaesthesia! Scand 1 994; 3 8(8): 863-868. Schlesinger S, Blanchfield D . Modified rapid-sequence induction of anesthesia: a survey of current clinical practice. AANA J 2 00 1 ;

69(4) : 2 9 1 -298. 1 09. Morris J, Cook TM. Rapid sequence induction: a national survey of practice. Anaesthesia 2 00 1 ; 5 6(1 1): 1 090-1 097. 1 1 0. Kluger MT, Willemsen G. Anti-aspiration prophylaxis in New Zealand: a national survey. Anaesth Intens Care 1 998;26(1): 70-7 7 . 1 1 1 . Lawes E G , Campbell I, Mercer D . Inflation pressure, gastric insufflation and rapid sequence induction. Br J Anaesth 1 987;59 (3): 3 1 5-3 1 8 . 1 1 2 . Lawes EG, Rea TD . The incidence and rapid sequence induction. B1' J Anaesth 2 007; 74(3):3 1 5-3 1 8. 1 1 3 . Admani M, Yeh TF, Jain R, et al. Prevention of gastric inflation during mask ventilation in newborn infants. O·it Cm'e Med 1 9 8 5 ; 1 3 (7):592-593 . 1 1 4. Moynihan RJ, Brock-Utne JG, Archer JH, et a!. The effect of cricoid pressure on preventing gastric insufflation in infants and children. Anestbesiology 1993;7 8(4):652-656. 1 1 5 . Neilipovitz DT, Crosby ET No evidence for decreased incidence of aspiration after rapid sequence induction. Can J Anaesth 2 007;

54(9): 748-764. 1 1 6. Quigley P, Jeffrey P. Cricoid pressure: assessment of performance and effect of training in emergency department staff. Emerg Med Australas 2007; 1 9(3):2 1 8-2 2 2 . 1 1 7 . Howells TH, Chamney AR, Wraight "WJ, e t a!. The application of cricoid pressure. An assessment and a survey of its practice.

Anaestbesia 1 9 8 3 ; 3 8 (5) :45 7-460. 1 1 8 . Lawes EG, Duncan PW, Bland B , et a!. The cricoid yoke-a device for providing consistent and reproducible cricoid pressure.

Br J Anaesth 1 986;5 8(8):925-93 1 . 1 1 9 . Vanner RG, O'Dwyer JP, Pryle BJ, et al. Upper oesophageal sphinc­ ter pressure and the effect of cricoid pressure. AnaeJthesia 1 992 ; 47(2):95-1 00. 120. Ellis DY, Harris T, Zideman D . Cricoid Pressure in Emergency Department Rapid Sequence Tracheal Intubations: A risk-benefit analysis. Ann Eme1•g 1Wed 2007. 1 2 1 . Brimacombe JR, Berry AM . Cricoid pressure . Can J Anaesth

1 997;44(4):41 4-42 5 . 1 2 2 . Levitan RM , Kinkle WC, Levin "W], e t al. Laryngeal view during

laryngoscopy: a randomized trial comparing cricoid pressure, backward-upward-rightward pressure, and bimanual laryn­ goscopy. Ann Emerg Med 2 006;47(6):548-5 5 5 . 1 2 3 . Stone B . The use o f the laryngeal mask airway by nurses during cardiopulmonary resuscitation: Results of a multicentre trial.

Anaesthesia 1 994;49( 1): 3-7. 124. Stone BJ, Chantler PJ, Baskett PJ. The incidence of regurgitation during cardiopulmonary resuscitation: a comparison between the bag valve mask and laryngeal mask airway. Resuscitation 1 998;38(1):

3-6. 1 2 5 . Guly UM, Mitchell RG, Cook R, et al. Paramedics and techni­ cians are equally successful at managing cardiac arrest outside hos­ pital. BMJ 1 99 5 ; 3 1 0(6987) : 1 09 1 - 1 094. 1 2 6 . Stiell IG, Wells GA, Field B , et al. Advanced cardiac life support in out-of-hospital cardiac arrest. N Eng! J Med 2 004; 3 5 1 (7):

647-656. 127. Gausche M, Lewis RJ, Stratton SJ, et al. Effect of out-of-hospital pediatric endotracheal intubation on survival and neurological outcome: a controlled clinical trial. JAMA 2 000;2 8 3 (6) :783-790. 1 2 8 . Jones JH, Murphy MP, Dickson RL, et al. Emergency physician­ verified out-of-hospital intubation: miss rates by paramedics. A cad

Emag Med 2 004; 1 1 (6) :707-709. 1 2 9 . Sayre MR, Sakles JC, Mistler AF, et al. Field trial of endotracheal intubation by basic EMTs. Ann Emerg Med 1 998;3 1 (2):228-2 3 3 .

249

1 3 0. Katz SH, Falk JL. Misplaced endotracheal tubes by paramedics in an urban emergency medical services system. Ann Emerg Med 2 00 1 ; 3 7(1 ) : 3 2-3 7 . 1 3 1 . Dorges V, Wenzel V, Knacke P, e t a l . Comparison o f different air­ way management strategies to ventilate apneic, nonpreoxygenated patients. O'it Cm·e Med 2 003 ; 3 1 (3):800-804. 1 3 2 . Kurola JO, Turunen MJ, Laakso JP, et a!. A comparison of the laryngeal tube and bag-valve mask ventilation by emergency med­ ical technicians: a feasibility study in anesthetized patients. Anesth

Analg 2 005 ; 1 0 1 (5) : 1 477-148 1 . 1 3 3 . Kette F, Reffo I , Giordani G, et a!. The use of laryngeal tube by nurses in out-of-hospital emergencies: preliminary experience.

Resuscitation 2 005 ;66(1):2 1 -2 5 . 1 3 4. Vertongen VM, Ramsay MP, Herbison P. Skills retention for insertion of the Combitube and laryngeal mask airway. Emerg Med 2 003 ; 1 5 (5 -6) :45 9-464. 1 3 5 . Brimacombe J. A proposed classification system for extraglortic airway devices. Anesthesiology 2 004; 1 0 1 (2):559. 1 3 6. Jones J H , Murphy MP, Dickson RL, e t a l . Emergency physician­ verified out-of-hospital intubation: miss rates by paramedics. Acad Emerg Med 2 004; 1 1 (6) :707-709. 1 3 7 . Beyer AJ III, Land G, Zaritsky A. Nonphysician transport of intu­ bated pediatric patients: a system evaluation. O'it Care Med 1 992 ; 2 0(7):96 1 -966. 1 3 8 . Bradley JS, Billows GL, Olinger ML, et al. Prehospital oral endo­ tracheal intubation by rural basic emergency medical technicians.

Ann Emerg Med 1 998;32(1):2 6-3 2 . 1 3 9. Sayre MR, Sakles JC, Mistler AF, et a!. Field trial o f endotracheal intubation by basic EMTs. Ann Emerg Med 1 99 8; 3 1 (2 ) : 2 2 8233. 1 40. Miller DM. A proposed classification and scoring system for supragloTtic sealing airways: a brief review. Anesth Analg 2 004;99 (5): 1 5 5 3 - 1 5 59; table of contents. 1 4 1 . Soar ]. The I-gel supragloTtic airway and resuscitation-some ini­ tial thoughts. Resuscitation 2 007;74(1): 1 9 7 . 142 . 2 005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Cil'Clllation 2005; 1 1 2 (24 Suppl):IVl -203 . 14 3 . Brain AI. The development of the laryngeal mask-a brief history of the invention, early clinical studies and experimental work from which the La.ryngeal Mask evolved. Eu1' J Anaesthesia! Supp/ 1 99 1 ;

4:5- 1 7 . 1 44. Brain AI. The laryngeal mask-a new concept i n airway manage­ ment. Br J Anaesth 1 9 8 3 ; 5 5 (8):80 1 -805 . 145. Flaishon R, Sotrnan A, Ben-Abraham R, et al. Antichemical pro­ tective gear prolongs time to successful airway management: a ran­ domized, crossover study in humans. Anestbesiology 2 004; 1 00(2):

2 60-2 66. 146. Goldik Z, Bornstein J, Eden A, et a!. Airway management by physicians wearing anti-chemical warfare gear: comparison between laryngeal mask airway and endotracheal intubation. Ezw

J Anaestbesio/ 2 002 ; 1 9(3) : 1 66-1 69. 147. Pennant JH, Pace NA, Gajraj NM. Role of the laryngeal mask air­ way in the immobile cervical spine. ] Clin AneJtb 1 993;5(3):226-2 3 0 . 1 4 8 . Flaishon R , Sotrnan A , Ben-Abraham R , e t a l . Antichemical pro­ tective gear prolongs time to successful airway management: a randomized, crossover study in humans. Anesthesiology 2 004; 1 00

(2):2 60-2 66. 1 49. Davies PR, Tighe SQ, Greenslade GL, et al. Laryngeal mask air­ way and tracheal tube insertion by unskilled personnel. Lancet 1 990; 3 3 6(872 1):977-979. 1 50. Pennant JH, Walker MB. Comparison of the endotracheal tube and laryngeal mask in airway management by paramedical per­ sonnel. Anestb Analg 1 992 ;74(4) : 5 3 1-5 3 4. 1 5 1 . Reinhart DJ, Simmons G. Comparison of placement of the laryn­ geal mask airway with endotracheal tube by paramedics and respi­ ratory therapists. Ann Eme1-g Med 1 994;24(2):2 60-2 6 3 . 1 5 2 . Deakin C D , Peters R , Tomlinson P, e t al. Securing the prehospital airway: a comparison of laryngeal mask insertion and endotracheal intubation by UK paramedics. Eme1·g Med J 2005;22(1):64-67. 1 5 3 . Burgoyne L, Cyna A. Laryngeal mask vs intubating laryngeal mask: insertion and ventilation by inexperienced resuscitators.

Anaesth Intens Cm'e 2 00 1 ;2 9(6):604-608. 1 54. Coulson A, Brimacombe J, Keller C, et a!. A comparison of the ProSeal and classic laryngeal mask airways for airway management

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by inexperienced personnel after manikin-only training. Anaesth

Intens Cm·e 2003 ; 3 1 (3):2 86-2 89. 1 5 5 . Dingley ], Baynham P, Swart M, et al. Ease of insertion of the laryngeal mask airway by inexperienced personnel when using an introducer. Anaesthesia 1 997;52(8) : 7 5 6-760. 1 5 6. Roberts I, Allsop P, Dickinson M, et a!. Airway management train­ ing using the laryngeal mask airway: a comparison of two differ­ ent training programmes. Resuscitation 1 997;3 3 (3):2 1 1-2 1 4. 1 5 7 . Yardy N, Hancox D, Strang T. A comparison of two airway aids for emergency use by unskilled personnel: the Combitube and laryngeal mask. Anaesthesia 1 999;54(2): 1 8 1 - 1 8 3 . 1 5 8 . Verghese C, Prior-Willeard PF, Baskett PJ. Immediate manage­ ment of the airway during cardiopulmonary resuscitation in a hos­ pital without a resident anaesthesiologist. Eur J Euze1·g Med 1 994;

1 (3): 1 2 3- 1 2 5 . 1 59. Samarkandi AH , Seraj MA, e l Dawlatly A , e t al. The role o f laryn­ geal mask airway in cardiopulmonary resuscitation. Resuscitation 1 994;2 8(2): 1 0 3 - 1 06. 1 60. Kokkinis K. The use of the laryngeal mask airway in CPR. Resuscitation 1 994;2 7(1):9- 1 2 . 1 6 1 . Leach A , Alexander CA, Stone B . The laryngeal mask i n car­ diopulmonary resuscitation in a district general hospital: a prelim­ inary communication. Re.�uscitation 1 993 ; 2 5 (3) :245-248. 162. Carrillo Alvarez A, Lopez-Herce Cid ], Moral Torrero R, et al. [Evaluation of basic and advanced pediatric resuscitation courses] .

An Esp Pediatr 2 000; 5 3 (2): 1 2 5- 1 34. 1 6 3 . Grantham H, Phillips G, Gilligan ]£. The laryngeal mask in pre­ hospital emergency care. 1 994;6: 1 93-197. 1 64. Rumball CJ, MacDonald D . The PTL, Combitube, laryngeal mask, and oral airway: a randomized prehospital comparative study of ven­ tilatory device effectiveness and cost-effectiveness in 470 cases of cardiorespiratory arrest. Prehosp Enze-rg Care 1 997; 1 (1): 1-10. 165. Ho BY, Skinner HJ, Mahajan RP. Castro-oesophageal reflux dur­ ing day case gynaecological laparoscopy under positive pressure ventilation: laryngeal mask vs. tracheal intubation. Anaesthesia

1 998; 5 3 (9) :92 1-924. 1 66. Maltby JR, Beriault MT, Watson NC, et al. LMA-Classic and LMA-ProSeal are effective alternatives to endotracheal intubation for gynecologic laparoscopy. Can J Anaesth 2003 ;50(1):7 1-77. 167. Rewari W, Kaul HL. Regurgitation and aspiration during gynae­ cological laparoscopy: Comparison between laryngeal mask air­ way and tracheal intubation. Joumal of Anaesthesiology Clin

Pharmaco/ 1 999; 1 5 (1) :67-70. 168. Atherton GL, Johnson ]C. Ability of paramedics to use the Combitube in prehospital cardiac arrest. Ann Eum·g Med 1 99 3 ; 2 2 (8) : 1 263-1268. 1 69. Rabitsch W, Schellongowski P, Staudinger T, et a!. Comparison of a conventional tracheal airway witl1 the Combitube in an urban emergency medical services system run by physicians. Resuscitation

1 7 7 . Staudinger T, Brugger S, Watschinger B, Roggla M, Dielacher C, Lobi T, Fink D, Klauser R, Frass M. Emergency intubation with the Combitube: comparison with the endotracheal airway. Ann

Eme1•g Med 1 993 ; 2 2 ( 1 0): 1 5 73-1 5 7 5 . 1 7 8 . Lefrancois DP, Dufour D G . Use o f m e esophageal tracheal com­ bitube by basic emergency medical technicians. Resuscitation 2002 ; 5 2 ( 1 ) : 7 7-8 3 . 1 79. Tanigawa K, Shigematsu A . Choice o f airway devices for 1 2 ,020 cases of nontraumatic cardiac arrest in Japan. Prehosp Eum·g Cm-e 1 998;2(2):96- 1 00. 1 80. Oczenski W, Krenn H, Dahaba AA, Binder M, El-S chahawi­

Kienzl I, Kohout S, Schwarz S, Fitzgerald RD . Complications fol­ lowing me use of me Combitube, tracheal tube and laryngeal mask airway. Anaesthesia 1 999;54(12): 1 1 6 1 -1 1 6 5 . 1 8 1 . Rabitsch W, Krafft P, Lackner FX, Frenzer R , Hofbauer R , Sherif C, Frass M. Evaluation of me oesophageal-tracheal double-lumen tube (Combitube) during general anaesthesia. Wien Klin Wochensch1·

2 004; 1 1 6(3):90-93 . 1 82 . Vezina D, Lessard MR, Bussieres J, Topping C, Trepanier CA. Complications associated with the use of the Esophageal-Tracheal Combitube. Can J Anaesth 1 998;45(1):76-80. 1 8 3 . Stoppacher R, Teggatz JR, Jentzen JM. Esophageal and pharyn­ geal injuries associated wim the use of the esophageal-tracheal Combitube. J F01·ens Sci 2 004;49(3):5 86-59 1 . 1 84. Urtubia R..l\1 , Aguila CM, Cumsille MA. Combitube: a study for proper use. Anesth Analg 2 000;90(4):958-962 . 1 8 5 . Hagberg CA, Vartazarian TN, Chelly JE, Ovassapian A. The inci­ dence of gastroesophageal reflux and tracheal aspiration detected wim pH electrodes is similar with the Laryngeal Mask Airway and Esophageal Tracheal Combitube-a pilot study. Can J Anaesth

2 004; 5 1 (3) :243-249. 1 86. Mercer MH. An assessment of protection of me airway from aspi­ ration of oropharyngeal contents using the Combitube airway.

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2003 ;96(2) : 6 1 8-62 1 . 1 89. Ochs M, Viike GM, Chan TC, Moats T, Buchanan ]. Successful prehospital airway management by EMT-Ds using me combitube.

hehosp Emerg Care 2000;4(4) : 3 3 3-3 3 7 .

1 90. Genzwuerker Hv, Dhonau S, Ellinger K. Use o fm e laryngeal tube for out-of-hospital resuscitation. Resuscitation 2 002 ; 5 2 (2):22 1-224. 1 9 1 . Asai T, Hidaka I, Kawachi S. Efficacy of the laryngeal tube by inexperienced personnel. Resuscitation 2002 ; 5 5 (2): 1 7 1 - 1 7 5 . 1 92 . Cook TM, McCormick B , Asai T. Randomized comparison of

( 1 3):412-4 1 5 . 1 7 1 . Rumball C, Macdonald D , B arber P, Wong H, Smecher C .

laryngeal tube with classic laryngeal mask airway for anaesthesia with controlled ventilation. B1· J Anaesth 2 003 ;9 1 (3):3 7 3 -3 7 8 . 1 9 3 . Ocker H , Wenzel V, Schmucker P, Steinfath M , Dorges V. A com­ parison of the laryngeal tube with the laryngeal mask airway during routine surgical procedures. Anesth Analg 2002;95(4) : 1 094-- 1 097. 1 94. Asai T, Moriyama S, Nishita Y, Kawachi S. Use of the laryngeal tube during cardiopulmonary resuscitation by paramedical staff.

Endotracheal intubation and esophageal tracheal Combitube insertion by regular ambulance attendants: a comparative trial.

Anaesthesia 2 003 ; 5 8(4) : 3 9 3 -3 94. 195. Genzwurker H, Finteis T, Hinkelbein J, Ellinger K. [First clinical

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experiences wim me new LTS. A laryngeal tube wim an oesophageal drain] . Anaesthesirt 2003 ;52(8):697-702 . 1 96. Gaitini LA, Vaida SJ, Somri M, Kaplan V, Yanovski B, Markovits R, Hagberg CA. An evaluation of the laryngeal tube during gen­ eral anesthesia using mechanical ventilation. Anestb Analg 2003;

2003 ; 5 7(1):2 7-3 2 . 1 70. Staudinger T, Brugger S , Roggla M , e t a!. [Comparison o f the Combitube with the endotracheal tube in cardiopulmonary resus­ citation in the prehospital phase] . Wien Klin Wochensch1· 1 994; 106

Combitube as a salvage airway device for paramedic rapid sequence intubation. Ann Eme1•g Med 2 003 ;42 (5):697-704. 1 7 3 . Ochs M, D avis D, Hoyt D, Bailey D, Marshall L, Rosen P. Paramedic-performed rapid sequence intubation of patients with severe head injuries. Ann Emerg Med 2 002 ;40(2) : 1 5 9- 1 6 7 . 1 74. Frass M , Frenzer R , Zdrahal F, Hoflehner G , Porges P, Lackner F. The esophageal tracheal combitube : preliminary results with a new airway for CPR. Ann Eme1-g Med 1 987; 1 6(7) : 768-772 . 1 7 5 . Frass M, Frenzer R, Iii as W, Lackner F, Hoflehner G, Losert U. [The esophageal tracheal Combitube (ETC): animal experiment results with a new emergency tube] . Anasth Intensivther Notfallmed

1 987;22(3) : 1 42-144. 1 76. Frass M, Frenzer R, Rauscha F, Schuster E, Glogar D . Ventilation with the esophageal tracheal combitube in cardiopulmonary Resuscitation Promptness and effectiveness. Chest 1 98 8 ; 9 3 (4) :

7 8 1 -7 84.

96(6) : 1 7 5 0-1 7 5 5 . 1 9 7 . Asai T, Murao K , Shingu K . Apparatus: efficacy o f the laryngeal tube during intermittent positive-pressure ventilation. Anaesthesia 2 000; 5 5 ( 1 1): 1 099-1 1 0 2 . 198. Kurola J, Harve H , Kettunen T, Laakso JP, Gorski ], Paakkonen H, Silfvast T. Airway management in cardiac arrest-comparison of the laryngeal tube, tracheal intubation and bag-valve mask ventilation in emergency medical training. Remscitation 2 004; 6 1 (2): 1 49- 1 5 3 . 1 99. Genzwuerker HV, Finteis T, Slabschi D, Groeschel J, Ellinger K. Assessment of the use of the laryngeal tube for cardiopulmonary resuscitation in a manikin. Resuscitation 2 00 1 ; 5 1 (3 ) : 2 9 1 -296. 200. Dorges V, Wenzel V, Neubert E, Schmucker P. Emergency airway management by intensive care unit nurses with the intubating

CHAPTER 1 6

201. 202. 203. 2 04. 205. 206.

207. 20 8 . 209.

2 1 0. 211. 2 12.

213. 2 1 4.

2 1 5. 2 1 6. 2 1 7.

2 1 8. 2 1 9. 220. 22 1 . 222. 223. 2 2 4. 225.

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laryngeal mask airway and the laryngeal tube. Crit Can 2 000;4 (6) : 3 69-3 76. Frass M, Frenzer R, Rauscha F, Weber H, Pacher R, Leithner C. Evaluation of esophageal tracheal Combitube in cardiopulmonary Resuscitation Crit Cm-e Med 1 9 8 7 ; 1 5 (6):609-6 1 1 . Pepe PE, Copass MK, Joyce TH. Prehospital endotracheal intu­ bation: rationale for training emergency medical personnel. Ann EnteJ'g Med 1 9 8 5 ; 1 4( 1 1 ) : 1 085-1 092 . Bowman FP, Menegazzi JJ, Check B D , Duckett TM. Lower esophageal sphincter pressure during prolonged cardiac arrest and resuscitation. Ann Ernerg Med 1 995;2 6(2):2 1 6-2 1 9 . Weiler N, Heinrichs W, Dick W. Assessment of pulmonary mechanics and gastric inflation pressure during mask ventilation. hehosp Disast Med 1 995 ; 1 0(2) : 1 0 1- 1 0 5 . Ruben H, Knudsen EJ, Carugati G . Gastric inflation i n relation to airway pressure. Acta Anaesth Scnnd 1 9 6 1 ; 5 : 1 07-1 14. Wenzel V, Idris AH , Banner MJ, Kubilis PS, Band R, WilliamsJL, Jr. , Lindner KH . Respiratory system compliance decreases after cardiopulmonary resuscitation and stomach inflation: impact of large and small tidal volumes on calculated peak airway pressure. Resuscitation 1 998;3 8(2): 1 1 3-1 1 8 . Stept WJ, Safar P. Rapid induction-intubation for prevention of gastric-content aspiration. Anesth Analg 1 9 70;49(4):63 3-6 3 6 . Wang H E , Sweeney TA, O'Connor RE, Rubinstein H. Failed pre­ hospital intubations: an analysis of emergency department courses and outcomes. P1'eho'p Enm-g Cm-e 2 00 1 ; 5 (2): 1 3 4- 1 4 1 . Wang HE, O'Connor RE, Megargel RE, Bitner M, Stuart R, Bratton-Heck B, Lamborn M, Tan L. The utilization of midazo­ lam as a pharmacologic adjunct to endotracheal intubation by paramedics. Preho'p Enzerg Cm-e 2 000;4(1): 1 4- 1 8 . Wayne MA, Slovis CM, Pirrallo RG. Management o f difficult air­ ways in the field. P1'ehosp Enze1'g Care 1 999; 3 (4) :2 90-2 96. Brownstein D , Shugerman R, Cummings P, Rivara F, Copass M. Prehospital endotracheal intubation of children by paramedics. Ann Emerg Med 1 996;2 8 ( 1 ) : 3 4-39. Ma OJ, Atchley RB, Hatley T, Green M, Young J, Brady W Intubation success rates improve for an air medical program after implementing the use of neuromuscular blocking agents. Anz J Emerg Med 1 998; 1 6(2) : 1 2 5- 1 2 7 . Kociszewski C, Thomas S H , Harrison T, Wedel SK. Etomidate versus succinylcholine for intubation in an air medical setting. Anz J Emerg Med 2 000; 1 8(7) : 7 5 7-7 6 3 . Syverud SA, Barron SW, Storer D L , Hedges J R , Dronen S C , Braunstein LT, Hubbard BJ. Prehospital u s e o f neuromuscular blocking agents in a helicopter ambulance program. Ann Enterg Med 1 98 8 ; 1 7(3): 2 3 6-242 . Walls R. The emergency airway algorithms. In: RS, ed. Manual of Entergency Airway Management. Philadelphia: Lippincott Williams & Wilkins, 2 000. Pace SA, Fuller FP. Out-of-hospital succinylcholine-assisted endo­ tracheal intubation by paramedics. Ann Ente�'g Med 2 000; 3 5 (6) : 5 68-5 7 2 . O'Connor RE, Swor RA . Verification o f endotracheal tube place­ ment following intubation. National Association of EMS Physicians Standards and Clinical Practice Committee. Prehosp Emerg Cm·e 1 999;3 (3):248-2 50. Wang HE, O'Connor RE, Domeier RM . Prehospital rapid­ sequence intubation. Pl-eho,p Emerg Cm-e 2 00 1 ; 5 ( 1 ) :40-48. Schneider RE WR Luten RC, Murphy MF. Manual of Enze1'gency Aimay Management. Philadelphia: Lippincott Williams & Wilkins; 2000. McGowan P, Skinner A. Preoxygenation-the importance of a good face mask seal. B1· J Anaesth 1 99 5 ; 7 5 (6) : 7 7 7-77 8 . Berthoud M , Read D H , Norman J. Pre-oxygenation: how long? Anaesthesia 1 9 8 3 ; 3 8(2):96- 1 0 2 . Nocera A . A flexible solution for emergency intubation difficul­ ties. Ann Emerg Med 1 996;2 7 (5):665-667 . Kidd JF, Dyson A , Latta IP. Successful difficult intubation. Use of the gum elastic bougie. Anaesthesia 1 98 8 ;43 (6):43 7-43 8 . Dogra S , Falconer R , Latto IP. Successful difficult intubation. Tracheal tube placement over a gum-elastic bougie. Anaesthesia 1 990;45(9) : 774-776. Nolan JP, Wilson ME. An evaluation of the gum elastic bougie. Intubation times and incidence of sore throat. Anaesthesia 1 992 ;47 ( 1 0) : 8 7 8-8 8 1 . ,

25 1

2 2 6 . Nolan JP, Wilson ME. Orotracheal intubation i n patients with potential cervical spine injuries. An indication for the gum elastic bougie. Anaesthesia 1 993 ;48(7) : 6 3 0-63 3 . 2 2 7 . Viswanathan S , Campbell C , Wood DG, et a!. The Eschmann Tracheal Tube Introducer. (Gum elastic bougie) . Anesthesia! Rev 1 992 ; 1 9(6):29-34. 2 2 8 . Hopkins PM. Use of suxamethonium in children. Br J Anaesth 1 99 5 ; 7 5 (6):67 5-67 7 . 2 2 9 . Morell R C , Berman JM, Royster RI, et a!. Revised label regarding use of succinylcholine in children and adolescents. Anesthesiology 1 994;80( 1):242-245. 230. Scheiber G, Ribeiro FC, Marichal A, et a!. Intubating conditions and onset of action after rocuronium, vecuronium, and atracurium in yorn1g children. Anesth Analg 1 996; 8 3 (2) : 3 2 0-324. 2 3 1 . McDonald PF, Sainsbury DA, Laing R]. Evaluation of the onset time and intubation conditions of rocuronium bromide in chil­ dren. Anaesth Intens Care 1 99 7 ; 2 5 (3):2 60-2 6 1 . 2 3 2 . Fuchs-Buder T, '"C"1ssonyi E . Intubating conditions and time course of rocuronium-induced neuromuscular block in children. Br J Anaesth 1 996;77(3) : 3 3 5-3 3 8. 2 3 3 . Maddineni VR, McCoy EP, Mirakur RK, McBride R]. Onset and duration of action and hemodynamic effects of rocuronium bro­ mide under balanced and volatile anesthesia. Acta Anaesthesia! Belg 1 994;45 (2):41-4 7 . 2 3 4 . Khuenl-Brady K S , Pomaroli A , Puhringer F, Mitterschiffthaler G, Koller ]. The use of rocuronium (ORG 942 6) in patients with chronic renal failure. Anaesthesia 1 993 ;48( 1 0) : 8 7 3-87 5 . 2 3 5 . Magarian T, Wood P, Caldwell J , Fisher D , S egredo V, Szenohradszky J, Sharma M, Gruenke L, Miller R. The pharma­ cokinetics and neuromuscular effects of rocuronium bromide in patients with liver disease. Anesth Analg 1 99 5; 80(4) : 7 54-7 59. 2 3 6 . Khalil M, D 'Honnenr G, Duvaldestin P, Slavov V, De Hys C, Gomeni R. Pharmacokinetics and pharmacodynamics of rocuro­ nium in patients with cirrhosis. Anesthesiology 1 994;80(6) : 1241-124 7. 2 3 7 . Ferres CJ, Crean PM, Mirakhur RK . An evaluation of Org NC 45 (vecuronium) in paediatric anaesthesia. Anaesthesia 1 9 8 3 ; 3 8 ( 1 0) : 943-947 . 2 3 8. Mirakhur RK, Ferres CJ, Clarke RS, Bali IM, Dundee JW Clinical evaluation of Org NC 45. Br ] Anae.rth 1 9 8 3 ; 5 5 (2): 1 1 9-1 24. 2 3 9. Lynam DP, Cronnelly R, Castagnoli KP, Canfell PC, Caldwell J, Arden J, Miller RD . The pharmacodynamics and pharmacokinet­ ics of vecuronium in patients anesthetized with isoflurane with nor­ mal renal function or with renal failure. Ane.rthesiology 1 988;69(2): 2 2 7-2 3 1 . 240. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1 9 6 1 ;2 :404-406. 2 4 1 . Grmec S. Comparison of three different methods to confirm tra­ cheal tube placement in emergency intubation. Intens Care Med 2 002 ;2 8(6):70 1-704. 242 . Anton WR Gordon RW, Jordan TM, Posner KL, Cheney FW A disposable end-tidal C02 detector to verify endotracheal intuba­ tion. Ann Ernerg Med 1 9 9 1 ;2 0(3):2 7 1 -2 7 5 . 2 43 . Bhende M S , Thompson AE. Evaluation o f a n end-tidal C02 detector during pediatric cardiopulmonary resuscitation. Pediatrics 1 995;95(3):3 95-3 99. 244. Bhende MS, Thompson AE, Cook DR, Saville AL. Validity of a dis­ posable end-tidal C02 detector in verifying endotracheal tube place­ ment in infants and children. Ann Enzerg Med 1 992;2 1 (2): 142-145. 245. Hayden SR, Sciammarella J, Viccellio P, Thode H, Delagi R. Colorimetric end-tidal C02 detector for verification of endotra­ cheal tube placement in out-of-hospital cardiac arrest. Acad ErneJ'g Med 1 99 5; 2 (6) :499-5 02 . 2 46. MacLeod BA, Heller MB, Gerard J, Yealy OM, Menegazzi J]. Verification of endotracheal tube placement with colorimetric end-tidal C02 detection. Ann Erne1'g Med 1 9 9 1 ;2 0(3):2 67-2 70. 247. Takeda T, llmigawa K, Tanaka H, Hayashi Y, Goto E, Tanaka K. The assessment of three methods to verify tracheal tube place­ ment in the emergency setting. Resuscitation 2003 ; 5 6(2) : 1 5 3 - 1 5 7 . 248. Tanigawa K , Takeda T, Goto E, Tanaka K . The efficacy of esophageal detector devices in verifying tracheal tube placement: a randomized cross-over study of out-of-hospital cardiac arrest patients. Anesth Analg 2 0 0 1 ;92(2) : 3 7 5-3 7 8 . 249. Varon AJ, Murrina J, Civetta JM. Clinical utility o f a colorimetric end-tidal C02 detector in cardiopulmonary resuscitation and emergency intubation. J Clin Manit 1 99 1 ;7(4):2 89-293 . ,

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2 50. Cantineau JP, Lambert Y, Merckx P, Reynaud P, Porte F, Bertrand C, Duvaldestin P. End-tidal carbon dioxide during cardiopul­ monary resuscitation in humans presenting mostly with asystole: a predictor of outcome. Crit Cm-e Med 1 996;2 4(5) :79 1-796. 2 5 1 . Hand IL, Shepard EK, Krauss AN , Auld PA. Discrepancies between transcutaneous and end-tidal carbon dioxide monitoring in the critically ill neonate with respiratory distress syndrome. Crit Care Med 1 989; 1 7(6) : 5 5 6-5 59. 252. Tobias JD, Meyer DJ. Noninvasive monitoring of carbon dioxide during respiratory failure in toddlers and infants: end-tidal versus transcutaneous carbon dioxide. Anestb Analg 1 99 7 ; 8 5 ( 1 ) : 5 5-5 8 . 2 5 3 . Pelucio M, Halligan L, Dhindsa H. Out-of-hospital experience with the syringe esophageal detector device. Acad Enzn-g Med 1 997;4(6) : 5 63-568. 2 54. Bozeman WP, Hexter D , Liang HK, Kelen GD. Esophageal detector device versus detection of end-tidal carbon dioxide level in emergency intubation. Ann Emerg Med 1 996;2 7(5) : 5 95-599. 2 5 5 . Sharieff GQ, Rodarte A, Wilton N, Silva PD, Bleyle D . The self­ inflating bulb as an esophageal detector device in children weigh­ ing more than twenty kilograms: A comparison of two techniques. Ann Enze1'g Med 2003;41 (5) :62 3-62 9. 2 5 6. Wee MY, Walker AK. The oesophageal detector device: an assess­ ment with uncuffed tubes in children. Anaestbesia 1 9 9 1 ;46(1 0):869-8 7 1 . 2 5 7 . Williams KN , Nunn JF. The oesophageal detector device: a prospective trial on 1 00 patients. Anaestbesia 1 989;44(5):412-424. 2 5 8 . Zaleski L, Abello D , Gold MI. The esophageal detector device. Does it work? Anestbesiology 1 99 3 ; 79(2):244-247. 259. Haynes SR, Morton NS. Use of the oesophageal detector device in children under one year of age. Anae;tbesia 1 990;45(12): 1 067-1069. 2 60. Baraka A, Khoury PJ, Siddik SS, Salem MR, Joseph NJ. Efficacy of the self-inflating bulb in differentiating esophageal from tra­ cheal intubation in the parturient undergoing cesarean section. Anestb Analg 1997;84(3 ) : 5 3 3-5 3 7 . 2 6 1 . Blanc VF, Tremblay NA. The complications o f tracheal intuba­ tion: a new classification with a review of the literature. Anestb Analg 1 974;5 3 (2):2 02-2 1 3 . 2 6 2 . Jones GO, Hale DE, Wasmuth CE, Homi J, Smith ER, Viljoen J. A survey of acute complications associated with endotracheal intu­ bation. Cleve Clin Q 1 968; 3 5 ( 1):2 3-3 1 . 2 6 3 . Taryle DA, Chandler JE, Good JTJ, Potts DE, Sahn SA. Emergenc.y room intubations: complications and survival. Cbest 1 979 ; 7 5(5): 541-543 . 2 64. Thompson DS, Read RC. Rupture of the trachea following endo­ tracheal intubation. JAMA 1 968;204( 1 1 ) :995-997. 2 6 5 . Wolff AP, Kuhn FA, Ogura JH. Pharyngeal-esophageal perfora­ tions associated with rapid oral endotracheal intubation. Ann Otol Rbinol Lmyngo/ 1 9 7 2 ; 8 1 (2):2 5 8-2 6 1 .

2 66. Stauffer JL, Petty TL. Accidental intubation o f the pyriform sinus: a complication of "roadside" resuscitation. JAMA 1 97 7;2 3 7 (2 1 ) : 2 3 2 4-2 3 2 5 . 2 6 7 . Pollard BJ, Junius F. Accidental intubation o f the oesophagus. Anaestb lntens Cm-e 1 9 80;8(2): 1 8 3 - 1 8 6 . 2 6 8 . Bernhard WN , Cottrell J E , Sivakumaran C, Patel K , Yost L, Turndorf H. Adjustment of intracuff pressure to prevent aspira­ tion. Anestbesiology 1 979;50(4) : 3 63-366. 2 69. Nordin U. The trachea and cuff-induced tracheal injury. An exper­ imental study on causative factors and prevention. Acta Otolmyngol Supp/ 1 9 7 7 ; 3 45 : 1-7 1 . 2 70. Cheney FW, Posner KL , Caplan RA. Adverse respiratory events infrequently leading to malpractice suits. A closed claims analysis. Anestbesiology 1 99 1 ; 7 5(6):93 2-9 3 9 . 2 7 1 . Cheney F W, Posner K , Caplan RA , Ward RJ. Standard o f care and anesthesia liability. JAMA 1 989;2 6 1 ( 1 1 ) : 1 5 99-1 603 . 2 7 2 . Caplan RA, Posner KL, Ward RJ, Cheney FW Adverse respira­ tory events in anesthesia: a closed claims analysis. Anestbesiology 1 990;72(5):82 8-8 3 3 . 2 7 3 . Cooper J B , Newbower RS, Kitz RJ. An analysis o f major errors and equipment failures in anesthesia management: considera­ tions for prevention and detection. Anestbesiology 1 9 84;60( 1 ) : 3 4-42 . 2 74. Cooper JB, Newbower RS, Long CD, McPeek B. Preventable anesthesia mishaps: a study of hun1an factors. Anestbesiology 1 9 7 8 ; 49(6) : 3 99-406. 275. Cooper JB, Cullen DJ, Nemeskal R, Hoaglin DC, Gevirtz CC, Csete M, Venable C. Effects of information feedback and pulse oximetry on ilie incidence of anesthesia complications. Anestbesiology 1987;67(5):686--694. 2 76. Cooper JB. Accidents and mishaps in anesthesia: how they occur; how to prevent them. Minm;a Anestesio/ 2 0 0 1 ;67(4) : 3 1 0-3 1 3 . 2 7 7 . Cooper JB. Towards patient safety in anaesthesia. Ann Acad Med Singapore 1 994;2 3 (4) : 5 52-5 5 7 . 2 7 8 . Florete O G . Airway management. In: Civetta JM, Taylor RW, Kirby RR, eds. O-itical Care. 2nd ed. Philadelphia: Lippincott, 1 992 : 1 43 0- 1 43 1 . 2 79. Brantigan CO, Grow JBS. Cricothyroidotomy: elective use in res­ piratory problems requiring tracheotomy. J Tbomc Crwdiovasc Surg 1 976; 7 1 ( 1 ) : 72-8 1 . 2 80. McGill J , Clinton JE, Ruiz E . Cricoiliyrotomy in the emergency department. Ann Enterg Med 1 9 82 ; 1 1 (7) : 3 6 1-3 64. 2 8 1 . Simon RR, Brenner BE, Rosen MA. Emergency cricothyroido­ tomy in the patient with massive neck swelling. Part 2: Clinical aspects. Crit Care Med 1 9 8 3 ; 1 1 (2): 1 1 9-1 2 3 . 2 8 2 . Simon RR, Brenner BE. Emergency cricothyroidotomy i n the patient with massive neck swelling: Part 1 : Anatomical aspects. C1'it Care Med 1 9 8 3 ; 1 1 (2): 1 1 4- 1 1 8 .

Chapter 1 7 Oxygen Administration and Supraglottic Airways Michael Shuster A first priority in treating any critical patient is assessment of the airway and the establishment of a patent airway if one is not already present. Endotracheal intubation requires skill , competence , and recurrent training. Bag- mask ventilation (BMV) is a fundamental skill of emergency airway management that has been taught to health care providers for more than 40 years , but effective BMV is difficult to perform . Supraglottic airways have been adopted both in and out of hospital because they are associated with ease of training, ease of skill maintenance , effectiveness , and paucity of serious complications . Indications and methods of administering supplementary oxygen Proper use and technique for supraglottic airways • Bag-mask versus supraglottic airway versus endotracheal intubation • •

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...

up.ple.me.ntary . . Oxygen ............ . .

Ventilation using exhaled air, whether mouth-to­ mo th or mouth-to-mask rescue breathing, can deliver only about 1 6 % to 1 7 % inspired oxygen con­ centration to the patient. Under ideal conditions, this can produce an alveolar oxygen tension of only about 80 mm Hg. In cardiac arrest, metabolic requirements may be reduced, but many factors such as low cardiac output, reduced peripheral oxygen delivery, and a wide arteriovenous oxygen difference or underlying respiratory disease and ventilation-perfusion mis­ match can contribute to decreased tissue perfusion. Untreated tissue hypoxia leads to anaerobic metabo­ lism, lactate production, and metabolic acidosis, which will blunt the beneficial effects of chemical and electrical therapy. Continued use of expired air will lead to lower and lower blood oxygen concentrations; therefore health care providers should give supple­ mentary 1 00 % inspired oxygen (Fi0 2 = 1 .0) as soon as it is available.

Myocardial Ischemia Supplementary oxygen is frequently administered in the care of patients encountered in emergency car­ diovascular care. For patients with chest discomfort of possible ischemic origin, the administration of oxy­ gen has become routine practice. There is, however, no evidence that supplemental oxygen has beneficial effect on myocardial ischemia in patients with normal

oxygen saturation, and some evidence suggests that supplemental oxygen may potentially cause harm. Hence, administration of oxygen for short periods during assessment of chest discomfort and other life­ threatening conditions is prudent, but continuing or long-term administration should be based on clear indications. A series of studies in the 1 960s showed that, in both normal patients and patients with myocardial infarction, high-flow oxygen increased arterial pres­ sure, increased systemic vascular resistance, and when oxygen saturation was >90 % , reduced cardiac out­ put. 1-6 In contrast, when arterial oxygen saturations were < 90 % , oxygen administration increased both oxygen content and cardiac output.l In another study, in patients with coronary artery disease, a fall in oxy­ gen saturation to between 7 0 % and 8 5 % produced anaerobic metabolism indicative of myocardial ischemia.8 In this same study, there was no evidence that hyperoxia relieved myocardial ischemia in patients with coronary artery disease.

FROM THE ACC AHA GUIDELINES No evidence is available to support the (routine continuing) administration of oxygen to all patients with acute coronary syndromes in the absence of signs of respiratory distress or arterial hypoxemia. Its use based on the evidence base can be limited to those with questionable respiratory status and documented hypoxemia. Nevertheless, it is the opinion of the Writing Committee that a short period of initial routine oxygen supplementation is reasonable during initial stabilization of the patient, given its safety and the potential for underrecognition of hypoxemia.

253

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In 1 97 6 , Madias et al. performed precordial ST-segment mapping in a controlled trial of 1 7 patients and concluded that oxygen administration may reduce ischemic injury; they demonstrated that administration of oxygen to patients expe­ riencing a myocardial infarction may reduce the sum of ST­ segment elevations as well as their number.9-1 1 Also in 1 976, a randomized, double-blind, controlled trial of oxygen therapy in the first 24 hours of uncomplicated myocardial infarction found that the group of 80 patients receiving 6 L/min of oxygen by mask for the initial 2 4-hour period had indications of greater myocardial damage than the group of 7 7 patients receiving room air. There was a greater proportion of deaths in the group receiving oxygen, 9 of 80 ( 1 1 . 3 o/o) versus 3 of 77 (3 . 9% ), but the difference did not reach statistical significance . 1 2 A systematic review of the evidence for the use of oxy­ gen to treat acute myocardial ischemia found only nine clin­ ical trials in human subj ects (randomized and nonrandom­ ized) and concluded that "any effect of oxygen is likely to be marginal so a suitably powered trial is necessary. " 1 3 Current guidelines recommend that supplemental oxygen be provided to patients during an initial period of stabilization and evaluation. Oxygen should be continued when oxygen sat­ uration is 6 L/min will increase the inspired oxygen concentration by 1 0 % . If oxygen inflow is adjusted to prevent collapse of the reservoir bag (flow rates of 1 0- 1 5 L/min), inspired oxygen concentrations of 90% to 9 5 % can be achieved provided that the mask is well sealed.

Venturi Mask The Venturi mask system entrains air into the mask at a spe­ cific ratio by passing oxygen through a calibrated opening under pressure. By varying the calibration of the opening, the Venturi mask delivers a reliable oxygen concentration of 24% to 5 0 % as long as the flow rate specified for each cal­ iber of opening is maintained.

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Airway Adjuncts Assessing and Establishing a Patent Airway The first priority in treating any critical patient is assessment of the airway and the establishment of a patent airway if one is not already present.

The first priority in treating any critically ill patient is assess­ ment of the airway and the establishment of a patent airway if one is not already present. Without adequate ventilation and oxygenation, circulation cannot be sustained. In the conscious patient, upper airway patency can be compro­ mised by obstruction from a swollen tongue or the soft tis­ sues surrounding the airway, from dentures or other foreign body, or by excessive bleeding or secretions (Fig. 1 7 -2). Obtundation, cyanosis, agitation, retractions, and stridorous or snoring respirations may all be signs of airway or ventila­ tory compromise. In the unconscious patient, upper airway obstruction results from loss of tone in the submandibular muscles which provide direct support to the tongue and indirect support to the epiglottis. Airway patency is often established simply by repositioning the head and neck but the maneuver may also require chin lift or jaw thrust and insertion of an oropharyngeal or nasopharyngeal airway. Once airway patency and ventilations are established, consideration must be given to the patient's ability to protect against aspiration of gastric contents, which can produce sig­ nificant morbidity and mortality. There is no evidence that the presence of the gag reflex corresponds to airway protec­ tive reflexes. 17 A gag reflex is an unreliable indicator of the ability to protect the airway as it may be absent in as many as 2 2 % to 3 7 % of normal adults . 1 6 • 1 7 The ability of the patient to swallow may be a more reliable indicator, but this is untested. In general, if a maneuver is needed to establish a patent airway, intubation should be considered.

Suspected Cervical Spine or Facial Injury Airway control and breathing remain top priorities in caring for patients with facial trauma or with suspected cervical spine injury, but the approach to airway management must be altered to minimize the potential for causing inadvertent harm through treatment. Although there is no published case of a spinal cord injury as a result of airway management, the poten­ tial for serious cord injury exists. Spine injury should be sus­ pected on the basis of the type and mechanism of injury, and in the presence of any suggestive injury (face, head, neck, mul­ tiple trauma) that is apparent. Airway control should be estab­ lished with in-line stabilization of the neck without a head tilt, using a jaw thrust or chin lift. With the head maintained in the neutral position by one rescuer and protected from excessive flexion, extension, or lateral movement, a second rescuer should perform whatever interventions are required to open the airway and ensure adequate ventilation (Fig. 1 7-3 ).

A

B F I G U R E 1 7 - 2 • O b str u c ti o n by the to n g u e a n d e p i g l o t t i s .

F I G U R E 1 7 - 3 • A. H e a d t i l t-c h i n l i ft . B. J aw t h r u st with o u t h e a d tilt.

CHAPTER 1 7

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0 X Y G E N A 0 M I N I S T R AT I 0 N A N 0 S U P R A G L 0 T T I C A I R WAY S

25 7

Maintaining a Patent Airway with an Airway Adjunct Oropharyngeal Airway

General Considerations The patient who is immobilized on his or her back, even if air­ way reflexes are intact, may not be able to cope with excessive salivation or oral bleeding. Suction should be immediately available if required and consideration should be given to how the patient might be safely turned to the side if necessary. If the patient is breathing spontaneously but unable to protect the airway or if ventilation must be controlled, an advanced airway should be established. Endotracheal or naso­ tracheal intubation were formerly the only options for advanced ai1way control short of cricothyrotomy, but excellent options now exist with the availability of supraglottic airways. Endotracheal intubation requires enough space behind the head for the rescuer to work and a sufficient view of the glot­ tis to be able to direct the tube. Endotracheal intubation may be extremely difficult in a patient where limited movement of the head and neck is possible and where bleeding or secretions may obscure the visual field. "Blind" nasotracheal intubation, once recommended only for expert providers, is rarely consid­ ered any longer: the failed insertion rate is high and the com­ plications are frequent and significant. Nasotracheal intuba­ tion can shear off turbinates, cause major nasal bleeding, or be misdirected into the brain or the retropharyngeal tissues. Supraglottic airways such as the Combitube or the laryngeal tube are considered to provide excellent protec­ tion from aspiration because of the dual cuffs sealing the air­ way from contamination from above and protecting the air­ way from regurgitated stomach contents from below. The laryngeal mask airway (LMA), once thought not to provide protection from regurgitation, has not been shown to increase the risk of aspiration compared with face-mask ven­ tilation. The supraglottic airways may be inserted with the rescuer in any position relative to the patient, and insertion requires little or no movement of the head and neck.

A

When submandibular muscles relax while a person is in a recumbent position, the tongue falls against the posterior pharyngeal wall and may obstruct the pharynx. The oropharyngeal airway (OPA) is designed to create a conduit through the oropharynx and posterior pharynx, keeping the airway open. The OPA is a rigid, comma-shaped device that has either a hollow inner channel or a solid core and hollow side channels (Fig. 1 7 -4) . Because the placement of the OPA stimulates the posterior pharynx, its use should be reserved for the unconscious and unresponsive patient with no cough or gag reflex. There are three methods for placing the OPA: ( 1 ) invert the device and rotate it into place when it reaches the posterior pharynx, or (2) turn the device 90 degrees and rotate it into place when it reaches the poste­ rior pharynx, or (3) insert it directly by following the curve of the tongue, with or without the help of a tongue depres­ sor. Whichever technique is chosen, care must be taken not to push the tongue into the posterior pharynx, thus causing airway obstruction. If there are problems ventilating the patient after insertion of the OPA, the device should be removed and reinserted. Although studies have not specifi­ cally addressed use of the OPA in cardiac arrest, clinical experience shows that it may aid ventilation with a bag­ mask device by preventing the tongue from occluding the airway.

Nasopharyngeal Airway The nasopharyngeal airway (NPA) is a soft rubber, Silastic, or plastic hollow tube that is inserted through the nose to the posterior pharynx, creating an op ening

B

F I G U R E 1 7 - 4 • O r o p h a ryn g e a l a i rways . A. F o u r o r o p h a ryn g e a l a i rway d evi c e s . B. O n e o r o p h a ryn g e a l a i rway d evi c e i n s e r te d .

258

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F I G U R E 1 7 - 5 • N a s o p h a ryn g e a l a i rways . A. T h r e e n a s o p h a ryn g e a l a i rway d evi c e s . B. O n e n a s o p h a ryn g e a l a i rway d evi c e i n s e r te d .

between the tongue and posterior pharyngeal wall (Fig. 1 7 - 5 ) . NPAs are particularly useful when conditions such as a clenched j aw prevent placement of an OPA. NPAs are less likely than OPAs to stimulate the gag reflex, so are a better choice in patients who are not deeply unconscious . In studies of anesthetized patients, 5 % to 3 0 % have bleed­ ing with insertion of an NPA. 1 8 • 1 9 To minimize or prevent bleeding, care must be taken to first lubricate the NPA well, then insert the airway with the beveled edge facing the septum pushing it into the nares while rotating the air­ way once it has passed the cartilaginous area of the sep­ tum, and directing it along the floor of the nose until the flared end of the NPA is against the nasal orifice. If avail­ able, a vasoconstricting nasal spray administered before placement may be helpful. Particular care must be taken when placing the NPA in patients with craniofacial injury: inadvertent intracranial placement of an NPA in patients with basilar skull fracture has been described in four case reports . 2 0-2 3 As with all adjunctive equipment, safe use of the NPA requires adequate training, practice, and retraining. Although studies have not specifically addressed the use of the NPA in cardiac arrest, clinical experience shows that it may aid ventilation with a bag-mask device by preventing the tongue from occluding the airway.

end of the delivery tube and a vacuum of > 3 00 mm Hg when the tube is clamped. The amount of suction should be adjustable to allow for use in children and intubated patients. Portable units should provide vacuum pressure and flow that is adequate for pharyngeal suction. The suction device should be fitted with large-bore, nonkinking suction tubing and semirigid pharyngeal tips of sufficient size to suction thick fluids and large particulate matter. Also, suc­ tion units must be checked regularly and maintained. When 5 1 paramedics from nine paramedic units were anonymously surveyed, 26 paramedics (5 1 % ) reported dif­ ficulties with the portable suction equipment. The diffi­ culty most commonly cited (2 1 times) was clogging of the tubing as a result of thick emesis. Poor suction power and battery problems were cited 1 3 times. As a result of fre­ quent problems with portable suction units, some emer­ gency medical services (EMS) systems may choose to carry both a battery-operated device and a manual hand-oper­ ated suction pump. 2 5 Both soft flexible and rigid suctioning catheters are available . Rigid catheters (e . g. , Yankauer) are used to suc­ tion the oropharynx. These are better for suctioning thick secretions and particulate matter (Fig. 1 7 -6). Soft, flexible catheters may be used in the mouth or nose. They can also be used for deep suctioning with an endotra­ cheal (ET) tube . Soft, flexible catheters come in sterile wrappers.

Suctioning Regurgitation is a frequent occurrence in cardiac arrest, and survival to hospital discharge after aspiration of regurgi­ tated materials is very low. 2 4 Suctioning is thus an essential aspect of airway management. Either a portable or installed suction device should be immediately available for resusci­ tation emergencies. An installed suction unit should be powerful enough to provide an airflow of >40 L/min at the

Several methods can be used to suction the upper air­ way and trachea. Central to each of these is the prevention both of hypoxia during the procedure and stimulation of reflexes leading to bradycardia and hypotension. Care must

CHAPTER 1 7

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O X Y G E N A D M I N I S T R AT I O N A N D S U P R A G L O T T I C A I RWAY S

TA B LE 1 7 - 2

Step

•

259

E n d o t r a c h e a l T u b e S u c ti o n i n g P r o c e d u r e

Action U s e s te r i l e t e c h n i q u e to r e d u c e t h e l i k e l i h o o d o f a i rway c o n ta m i n a ti o n .

2

G e n tly i n s e r t t h e c a t h e t e r i n to t h e E T tu b e . B e sure the side opening is n o t occluded d u r i n g i n s e r ti o n . I n s e r ti o n o f t h e c a t h e t e r b eyo n d t h e t i p o f t h e E T t u b e i s n o t r e c o m m e n d e d b e c a u s e i t m ay i nj u r e t h e e n d o t r a c h e a l m u c o s a o r s ti m u l a t e c o u g h i n g or bronchospasm.

3

A p p ly s u c t i o n b y o c c l u d i n g o n ly t h e s i d e o p e n i n g wh i l e wi t h d r awi n g t h e c a t h e t e r with a r o t a ti n g o r twi sti n g m o t i o n .

Suetion attempts should not exeeed 1 D seeonds. To avo i d hyp o x e m i a , p r e c e d e a n d fo l l ow s u c ti o n i n g a t te m p ts with a s h o r t p e r i o d o f a d m i n i s t r a ti o n o f 1 0 0 % o xyg e n .

F I G U R E 1 7 - 6 • R i g i d c a t h e t e r . R i g i d c a t h e t e r s (e . g . , Ya n k a u e r) a r e u s e d to s u c t i o n t h e o r o p h a ryn x . T h e s e a r e b e t t e r f o r s u c ti o n ­ i n g t h i c k s e c r e ti o n s a n d p a rt i c u l a t e m a tte r .

be taken to prevent damage t o the airway structures. During the procedure, the patient's heart rate, pulse, oxygen satura­ tion, and clinical appearance during suctioning should be monitored. If bradycardia develops, oxygen saturation drops, or the patient's clinical appearance deteriorates, suc­ tioning must be interrupted at once. High-flow oxygen is then administered until the heart rate returns to normal and the patient's clinical condition improves. Ventilation is assisted as needed. One method for suctioning the oropharynx and trachea through an endotracheal tube is given in Tables 1 7- 1 and 1 7-2 .

TA B LE 1 7 - 1

•

O r o p h a ryn g e a l S u c ti o n i n g P r o c e d u r e

G e n tly i n s e r t t h e s u c t i o n c a t h e t e r o r d evi c e i n to t h e o r o p h a ryn x b eyo n d t h e to n g u e . M e a s u r e t h e c a t h e t e r b e f o r e s u c ti o n i n g a n d d o n o t i n s e r t i t a ny f u r t h e r t h a n t h e esti m a t e d d i s ta n c e f r o m t h e t i p o f t h e n o s e to t h e e a r l o b e . 2

A p p ly s u c t i o n b y o c c l u d i n g t h e s i d e o p e n i n g wh i l e wi t h d r awi n g t h e c a t h e t e r with a r o t a ti n g o r twi sti n g m o t i o n .

JYpieally limit suetion attempts t o 1 0 seeonds or less. To avo i d hyp o x e m i a , p r e c e d e a n d fo l l ow s u c ti o n i n g a t te m p ts with a s h o r t p e r i o d o f a d m i n i s t r a ti o n o f 1 0 0 % o xyg e n .

T o h e l p r e m ove t h i c k m u c u s o r o t h e r m a t e r i a l f r o m t h e a i rway, i n s ti l l 1 o r 2 m L o f ste r i l e s a l i n e i n to t h e a i rway b e f o r e s u c ti o n i n g . P r ovi d e p o s i tive - p r e s s u r e ve n ti l a t i o n to d i s p e rs e t h e s a l i n e th r o u g h o u t t h e a i rways f o r m a x i m u m e f f e c t b e f o r e s u c ti o n i n g .

Mouth,to,Barrier Device (Face Shield, Tube, or Mask) For many years , mouth-to-mouth ventilation has been taught as the basic rescue ventilation technique. Mouth-to­ barrier-device has now superseded mouth-to-mouth as the basic ventilation technique recommended for training and for resuscitation, because the interposition of a protective barrier between rescuer and patient addresses a concern that rescuers may have about disease transmission. Although the risk of contagion is very low-there are only 1 5 reported cases of possible disease transmission during CPR and none during CPR training-surveys of both health care providers and the lay public have repeatedly cited the concern of con­ tagion as a factor affecting the respondent's expressed will· 2 6-34 Wh"l ingness to perform mouth -to-mouth vent!.1 ation. 1 e the interposition of a barrier device is likely to be more aesthetically pleasing to potential rescuers and will perhaps reduce their fears of contagion, whether rescuers actually undertake CPR more often when the device is available is unknown. Clearly, though, a barrier device can increase the likelihood of CPR performance only if health care providers and other potential rescuers carry such a device with them at all times. The three types of barrier devices are face shields, tubes, and masks (Fig. 1 7 -7). The devices are typically plas­ tic, they may be disposable or reusable, and they often incor­ porate a unidirectional valve that will direct the victim's expired air away from the rescuer. In addition, a one-way valve is available that fits to the inlet of a regular face mask,

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B F I G U R E 1 7 - 7 • A. F a c e s h i e l d . P l a c e t h e f a c e s h i e l d ove r t h e v i c t i m ' s m o u t h a n d n o s e , p o s i ti o n i n g t h e o p e n i n g a t t h e c e n t e r o f t h e s h i e l d o v e r t h e v i c t i m ' s m o u t h . T h e te c h n i q u e o f r e s c u e b r e a t h i n g w i t h a b a r r i e r d evi c e i s t h e s a m e a s t h a t f o r m o u t h - t o ­ m o u t h b r e a th i n g . B. P o c k e t f a c e m a s k .

so that the mask may be used for mouth-to-mask o r bag­ mask ventilation. Each of the devices has its own perform­ ance characteristics, and effectiveness in protecting against infection transmission varies from device to device. Drawbacks associated with some devices include the cre­ ation of inspiratory or expiratory resistance and valve leak-

age. One study that tested a variety of barrier devices found that few of them had low inspiratory and expiratory resist­ ances and that some of the one-way valves failed. 3 5 In another study, where cultures were performed after mock CPR, none of the masks with one-way valves were culture­ positive but one of three face shields that incorporated a one-way valve was culture positive and five of five face shields that did not have a one-way valve were contaminated with the victim's oral aerobic flora.36 It has not been proven that a barrier device will prevent disease transmission in real-world use, and, given the very low rate of disease trans­ mission that has been reported, it is unlikely that effective­ ness will be established. Mouth-to-barrier ventilation, like mouth-to-mouth ventilation, relies on the rescuer's expired air to ventilate the victim. Most rescuers will have the vital capacity necessary to provide the 5 to 6 L/min of air required for lung inflation but will be able to provide only 1 7 % oxygen, which is the approximate concentration of oxygen in expired air. If an oxygen source is available, the rescuer should wear a nasal cannula or should breathe from the oxygen source between rescue breaths. As soon as possible, the rescuer should switch to a barrier device that has an oxygen inlet, a bag-mask device with attached oxygen, or some other airway adjunct that will allow for the administration supplementary oxygen. Both tube and face-shield devices fit adults of all sizes, but any given mask fits people only within a particular size range, so the rescuer must have masks of different sizes avail­ able. If a mask is too big or too small for the given patient, an air leak will occur, which may reduce the effectiveness of ventilation. A leak can often be tolerated, however, since a full breath often provides more air than is required. The mouth-to-mask technique is easier than bag-mask ventila­ tion, since the rescuer is able to use two hands to correctly elevate the mandible, position the head, and seal the mask to the face. Studies on manikins have found that mouth-to­ mask ventilation is capable of delivering significantly larger tidal volumes than bag-mask ventilation, and a similar study on patients after induction of anesthesia endorsed mouth­ to-mask ventilation for its ease of use by inexperienced oper­ ators.37-40 No matter which barrier device is used, adequate training is important to ensure effective ventilationY Pocket face masks can be used effectively by a provider who is trained in their use and effectively maintains an open airway. Most have side ports for the administration of oxy­ gen. (Fig. 1 7 -8).

Bag�Mask Devices

Bag-mask ventilation (BMV) is a fundamental skill of emer­ gency airway management that has been taught to health care providers as part of both basic and advanced airway management for more than 40 years. Effective BMV is dif­ ficult to perform: in several studies, both inexperienced and experienced providers delivered inadequate tidal volumes

CHAPTER 1 7

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B

261

/

c

F I G U R E 1 7 - 8 • A. P o c k e t f a c e m a s k , l a t e r a l t e c h n i q u e . B. P o c k e t f a c e m a s k , c e p h a l i c te c h n i q u e . T h e r e s c u e r p l a c e s t h e thumb a n d thenar eminence o n top of the m ask. C. Pocket face m a s k , c e p h a l i c te c h n i q u e w i t h o xyg e n t u b e a t ta c h e d . T h e r e s ­ c u e r u s e s t h e " E - C " te c h n i q u e (th e " E " i s f o r m e d b y t h e t h r e e fi n g e r s a n d t h e " C " i s f o r m e d by t h e th u m b a n d f i r s t f i n g e r c u rv­ i n g a r o u n d t h e f a c e m a s k) .

when tested on manikins.42 -48 When tested on anesthetized subjects, where the face is more malleable and the lungs are more compliant than in a manikin, ventilation with a bag­ mask is still frequently inadequate: in a study of BMV use by 3 0 inexperienced nurses, the tidal volume averaged only 2 3 9 mL.49 ln another study, 1 0 nurses were able to adequately ventilate 1 00 patients only 4 3 % of the time. 50 Ventilation is unlikely to be performed any better under resuscitation con­ ditions than it is under the controlled conditions of a study. In order to provide effective ventilation with a bag­ mask, the head, neck, and mandible must be positioned so that the tongue does not obstruct the airway and a correctly sized mask must then be chosen so that a tight seal of the mask to the face can be achieved (Fig. 1 7 -9). Next, the bag

must b e squeezed in a deliberate, consistent manner over 1 second so as to avoid high inspiratory pressures and thus prevent gastric inflation. Each of these steps may pose diffi­ culty. The head must be tilted back and maintained in neu­ tral or slightly extended position while pulling the jaw for­ ward and pressing the mask down, all with one hand, while the second hand must hold and squeeze the bag (Fig. 1 7 -9A, Table 1 7- 3A). If the patient is edentulous or bearded, the mask seal will be more difficult to achieve. Maintaining a seal in the back of a moving ambulance can be especially challenging. To improve the mask seal and ensure that the hand squeezing the bag is large enough to hold and compress a sufficient volume of air from the bag, an effective strategy

262

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TA B LE 1 7 - 3 A

Step

•

One-Hand Mask Hold

Action P o s i t i o n yo u r s e l f d i r e c tly a b ove t h e p a t i e n t ' s h e a d .

2

P l a c e t h e m a s k o n t h e p a t i e n t ' s fa c e , u s i n g t h e b r i d g e o f t h e n o s e a s a g u i d e f o r c o r r e c t p o s i ti o n .

3

U s e t h e E - C c l a m p tech nique t o hold t h e m a s k in p l a c e wh i l e yo u l i ft the j aw to h o l d t h e a i rway o p e n :

A

4

•

Perform a head tilt.

•

Use the thumb and index finger of one hand to make a "C, " pressing the edges of the mask to the face.

•

U s e t h e r e m a i n i n g fi n g e rs to l i ft t h e a n g l e s o f t h e j aw (th r e e fi n g e r s f o r m a n " E " ) a n d o p e n t h e a i rway.

S q u e e z e t h e b a g to g ive b r e a t h s (1 s e c o n d e a ch) wh i l e watc h i n g f o r c h e s t rise. T h e d e l ive ry o f b r e a th s i s the s a m e w h e t h e r y o u u s e s u p p l e m e n ta ry o xyg e n or n o t .

B F I G U R E 1 7 - 9 • A. M o u th - t o - m a s k E - C c l a m p te c h n i q u e o f h o l d ­ i n g m a s k wh i l e l i fti n g t h e j aw. P o s i t i o n yo u r s e l f a t t h e v i c t i m ' s h e a d . Ci r c l e t h e th u m b a n d f i r s t fi n g e r a r o u n d t h e t o p of t h e m a s k (fo r m i n g a " C " ) wh i l e u s i n g t h e t h i r d , f o u r t h , a n d f i f t h fi n g e r s (fo r m i n g a n " E ") to l i ft t h e j aw. B. Two - r es c u e r u s e o f t h e b a g m a s k . T h e r e s c u e r a t t h e vi c ti m ' s h e a d t i l ts t h e v i c t i m ' s h e a d a n d s e a l s t h e m a s k a g a i nst t h e victi m ' s f a c e with t h e t h u m b a n d f i r s t fi n g e r o f e a c h h a n d c r e a ti n g a " C " t o p r ovi d e a c o m p l ete seal a r o u n d the e d g e s of the m ask. The rescu e r uses t h e r e m a i n i n g t h r e e fi n g e rs (t h e " E ") to l i ft t h e j aw (t h i s h o l d s t h e a i rway o p e n ) . T h e s e c o n d r e s c u e r s l owly s q u e e z e s t h e b a g (ov e r 1 s e c o n d) u n t i l t h e c h est r i s e s . B o t h r e s c u e r s s h o u l d o b s e rve c h est r i s e .

i s for one rescuer t o open the airway and seal the mask using both hands , while a second rescuer uses both hands to squeeze the bag. Two rescuers may provide more effective ventilation than one rescuer. When two rescuers use the bag-mask system, one rescuer opens the airway with a head tilt and jaw lift and holds the mask to the face while the other rescuer squeezes the bag (Fig. 1 7 -9B , Table 1 7 - 3 B) . Squeezing the bag requires minimal explanation and can typically be performed even by untrained assistants. Techniques for holding the mask are the same as those for the mouth-to-mask devices described above. 5 1-55 Peak inspiratory pressure is a key factor causing gas­ tric inflation, which in turn results in increased pulmonary compliance and hypoinflation of the lungs and an

TA B LE 1 7 - 3 B

Step

•

Two - H a n d M a s k H o l d

Action P o s i t i o n yo u r s e l f d i r e c tly a b ove the p a t i e n t ' s h e a d .

2

P l a c e t h e m a s k o n t h e p a t i e n t ' s fa c e , u s i n g t h e b r i d g e o f t h e n o s e a s a g u i d e f o r c o r r e c t p o s i ti o n .

3

U s e e i t h e r of t h e s e t e c h n i q u e s :

4

•

Lift t h e p a t i e n t ' s h e a d a n d s e a l t h e m a s k a g a i n s t t h e p a t i e n t ' s f a c e w i t h t h e th u m b a n d first fi n g e r o f e a c h h a n d , c r e a ti n g a " C " t o p r ovi d e a c o m p l e te s e a l a r o u n d t h e e d g e s o f t h e m a s k . U s e t h e r e m a i n i n g t h r e e f i n g e rs o f b o t h h a n d s (th e " E ") to l i ft t h e j aw.

•

H o l d the m a s k in p l a c e with the th u m b a n d t h e th e n a r p r o m i n e n c e o f t h e p a l m o f t h e h a n d s ; u s e t h e r e m a i n i n g fo u r fi n g e r s o f b o t h h a n d s t o l i ft t h e c h i n a n d o p e n t h e a i rway.

S q u e e z e the b a g to g ive b r e a t h s (1 s e c o n d e a ch) wh i l e watc h i n g f o r c h e s t rise. T h e d e l ive ry o f b r e a th s i s the s a m e w h e t h e r y o u u s e s u p p l e m e n ta ry o xyg e n or n o t .

CHAPTER 1 7

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O X Y G E N A D M I N ! S T R AT I O N A N 0 S U P R A G L O T T I C A I RWAY S

increased incidence of regurgitation. 56 It is possible to limit peak inspiratory pressure by controlling tidal vol­ ume , flow rate, and inflation time and maintaining an unobstructed airway: a bench study comparing a pediatric bag (700 mL) to an adult bag ( 1 , 5 00 mL) showed that the former produced comparable lung tidal volumes (2 45 ± 1 9 versus 2 7 1 ± 3 3 mL; P = NS); but a significantly (P < 0 . 0 0 1 ) lower gastric tidal volume ( 1 49 ± 1 1 versus 2 7 2 ± 2 4 mL). 5 7 A study comparing the two b a g sizes for ventilating adult patients undergoing anesthesia found that the pediatric bag resulted in less mean exhaled tidal volume (3 6 5 ± 5 5 versus 7 7 9 ± 2 2 mL; P < 0.000 1), lower peak airway pres­ sure (2 0 ± 2 versus 2 5 ± 5 em H2 0; P < 0. 000 1 ), and com­ parable oxygen saturation (97 % ± 1 % versus 98 ± 1 % ; NS); no patients experienced stomach inflation, whereas 5 of 40 patients ventilated with an adult bag did experience stomach inflation (P = 0 .054).58 It should be noted, however, that when small volumes are used to ventilate, oxygen saturation can be maintained only when supplemental oxygen is pro­ vided. 59 An advanced airway should be considered if the device can be inserted without significantly disrupting com­ pressiOns. Cricoid Pressure Cricoid pressure is widely used as a technique to reduce gastric inflation and prevent vomiting and regurgitation in patients undergoing rapid sequence induction and for resuscitation when being ventilated with a bag-mask. 60-64 Cricoid pressure is intended to displace the trachea posteriorly, causing the cricoid cartilage to compress the esophagus against the vertebrae, providing a barrier both to air being pushed down the esophagus into the stomach and stomach contents b eing pushed up and out of the esophagus (Fig. 1 7- 1 0) . Bag-mask ventilation, which pro­ duces only moderate peak inspiratory pressure, can still cause gastric inflation, which then predisposes to vomiting and regurgitation.65 Vomiting is a negative predictor of sur­ vival in cardiac arrest.66 When cricoid pressure is applied to anesthetized adults or children during bag-mask venti­ lation, even high peak inspiratory pressures do not cause gastric inflation.65 •67•68 However, a recent review of the lit­ erature failed to find confirmation that cricoid pressure is safe or evidence that it is an effective technique to decrease the risk of aspiration in rapid sequence induction.69 While cricoid pressure sounds easy to apply, studies show that it is difficult to estimate the optimal recommended pressure (3 0-44 newtons) .70-7 3 If too little pressure is used, the esophagus is incompletely occluded, while too much pres­ sure can distort the airway and make ventilation more dif­ ficult or impossible. In a review of cricoid pressure for emergency department rapid sequence intubation, Ellis notes that in 10 studies, functional occlusion of the airway occurred between 6% and 5 0 % of the time and that two studies of cricoid pressure observed cases of airway obstruction with the application of cricoid pressure.74 In the absence of evidence, it seems reasonable to apply cricoid pressure in patients requiring manual ventilation whenever there are sufficient rescuers available. However,

263

F I G U R E 1 7 - 1 0 • Cr i c o i d p r essu r e , or S e l l i c k ' s te c h n i q u e , is t h e a p p l i c a t i o n o f p r e ss u r e to t h e unresp o n sive p a t i e n t ' s c r i c o i d c a r ­ t i l a g e . T h e p r essu r e i s i n t e n d e d t o p u s h t h e t r a c h e a p o ste r i o r ly , c o m p r e ss i n g t h e e s o p h a g u s a g a i n st t h e c e rvi c a l verte b r a . Cr i c o i d p r e ss u r e i s effective i n p r eve n t i n g g a s t r i c i n f l a t i o n d u r i n g p o s i ­ tive - p r e s s u r e ve n ti l a t i o n o f unresp o nsive p a t i e n ts . S t e p 1 : Lo c a t e t h e thyr o i d c a r ti l a g e (A d a m ' s a p p l e) w i t h yo u r i n d e x fi n g e r . S t e p 2 : S l i d e yo u r i n d e x fi n g e r to t h e b o s e o f t h e thyr o i d c a r ti l a g e a n d p a l p a t e t h e p r o m i n e n t h o r i z o n t a l r i n g b e l ow t h e thyr o i d c a r ti l a g e (t h i s i s t h e c r i c o i d c a r ti l a g e) . S t e p 3 : U s i n g t h e t i p s o f yo u r t h u m b a n d i n d e x fi n g e r , a p p ly f i r m b a c kwa r d p r essu r e to t h e c r i c o i d c a r ti l a g e .

when performing bag-mask ventilation i n conjunction with cricoid pressure, the pressure should be adjusted, relaxed or released if it impedes ventilation. Cricoid pressure in con­ juction with laryngoscopy may make visualization of the vocal cords more difficult, and although there is little hard evidence, some studies have attributed failed intubation to cricoid pressure. 75•76 When intubating while applying cricoid pressure, the pressure should be maintained until the endotracheal tube is passed through the cords unless the pressure interferes with intubation, in which case cricoid pressure can be relaxed or released.

Ventilation with Supraglottic Airways Use of Bag,Mask versus Advanced Airway Bag-mask ventilation has long been considered a temporiz­ ing maneuver until either the patient was able to protect the airway and to breathe independently or a definitive airway­ endotracheal intubation-was employed. Bag-mask ventila­ tion was taught to virtually all health care providers, while only anesthetists at first, and then other physicians, and then specific categories of nonphysicians were permitted to

264

SHUSTER

perform endotracheal intubation (ETI). While BMV is cer­ tainly easier to perform than endotracheal intubation, it is clearly not without problems : not only do rescuers have dif­ ficulty delivering adequate ventilation with a bag-mask, but the bag-mask is difficult to use in certain physical situations (e.g., trapped in a car in a ditch or in a small overcrowded elevator) or with certain body types (edentulous, bearded). Other serious disadvantages of BMV are the need to inter­ rupt chest compressions during CPR and the increased like­ lihood of regurgitation. Recent studies suggest that not only advanced providers but also basic providers can safely use supraglottic airways in place of ETI and BMV In a multicenter prospective obser­ vational trial, nurses successfully used the LMA as the pri­ mary ventilation method in 56 of 1 64 (34%) patients and in 1 44 of 1 64 (88 % ) patients overall. The authors note that regurgitation occurred in 20 patients before LMA insertion (BMV had been used in 1 7 of 2 0) and in 3 cases during LMA use (BMV had been used in all three cases).77 In another prospective trial, 797 cardiac arrests occurring over 3 . 5 years were examined. The regurgitation rate was 1 2 .4% when BMV was the primary method of ventilation followed by endotracheal intubation, 1 1 . 8 % when BMV was the primary method of ventilation followed by LMA, and 3 . 5 % when LMA was the primary airway adjunct used.78 No prospective randomized trials have directly assessed the outcome of adult victims of cardiac arrest after bag-mask ventilation compared to those who had been treated with an advanced airway. Studies comparing outcomes of out-of-hos­ pital cardiac arrest in adults treated by either emergency med­ ical technicians or paramedics failed to show a link between long-term survival rates and various paramedic skills, includ­ ing intubation.79•80 One prospective randomized, controlled trial in an EMS system with short out-of-hospital transport intervals showed no survival advantage for endotracheal intu­ bation over bag-mask ventilation in children where providers had limited training and experience in intubation.81 Endotracheal intubation, once considered the optimal method of managing an airway in cardiac arrest, is no longer an automatic intervention. The change is due to the increasing recognition that the failure and complication rates of ETI are high, especially when performed by less experienced or less practiced practitioners, that adequate practitioner-training is time- and labor-intensive, and that many trained rescuers get inadequate experience with the device .8 2 -84 Trials of supraglottic airways have demonstrated that they can be successfully used by all levels of providers. 85-87 Supraglottic airways are quickly being adopted both in and out of hospital because they are associated with ease of training, ease of skill maintenance, effectiveness, and paucity of serious complications.88 Despite the positive aspects of these newer advanced airway devices, insertion can be diffi­ cult, failure can occur and practitioners must maintain their insertion skills through frequent experience or practice. 88 The optimal method of managing the airway during any particular cardiac arrest will vary according to provider experience, the characteristics of the EMS or health care sys­ tem, and the patient's condition.

S upraglottic Airways

" Supraglottic airway" is a term used to describe any airway that is "above the glottis"-the glottis, of course, being the space between the vocal cords. Supraglottic airways may also be referred to as "extraglottic" devices89 and are dis­ tinct from the endotracheal tube, which passes through the glottis to lie within the trachea. Although there is a long list of these devices, only a few have been studied in resus­ citation. While the endotracheal tub e is an effective airway, signifi cant complications, including death, occur as a result of its use . 90•91 Practitioners require considerable training and experience to become proficient in inserting the endotracheal tube as well as significant ongoing expe­ rience and practice to maintain their skills . There is a high failure rate in the hands of those who are less skilled or practiced.9 2 •93 Supraglottic airways were originally devel­ oped to avoid the problems of the endotracheal tube, and new versions continue to be developed in an effort to find the perfect airway. The perfect airway for use in resuscitation would be easy to insert in all patients and in all situations on the first attempt. The user would require little or no training to be proficient at insertion and would require no practice to maintain insertion skills. The device itself would be an inex­ pensive, single-use device that could effectively maintain air­ way patency and provide a conduit for ventilation regardless of the size of the patient, the pressures required to ventilate, or the presence of anatomic anomalies. This ideal airway would be easy to secure so it stayed in place during CPR and patient transport, yet its presence would not damage the tis­ sues, and it would protect against aspiration. The perfect air­ way does not yet exist. More than 2 5 supraglottic devices have so far been described and others are no doubt in devel­ opment. In an attempt to organize thinking about supraglottic airways , Miller has proposed a classification of these devices according to their sealing mechanism: cuffed peri­ laryngeal sealers (CPLS), cuffed pharyngeal sealers (CP S), and cuffless anatomically preshap ed s ealers (CAP S ) . 94 This classification is especially useful in a discussion about resuscitation, since the sealing mechanism of the supra­ glottic airway has implications for stability of the device during CPR and for protection from aspiration. The CAPS are the newest of the three classes of devices, and their use has been reported in resuscitation only once. 95 Initial reports of CAPS make them appear promising as airways , but their role in resuscitation has yet to be defined. Since the AHA's 2 000 guidelines regarding emergency cardiovascular care (ECC), both the laryngeal mask airway (LMA) (a cuffed perilaryngeal sealer device) and the Combitube (a cuffed pharyngeal sealer) have been recom­ mended for use in resuscitation, initially as an alternative to bag-valve-mask ventilation and then in the AHA's 2 00 5 Guidelines also a s an alternative to the endotracheal tube.96

CHAPTER 1 7

•

O X Y G E N A D M I N ! S T R AT I O N A N 0 S U P R A G L O T T I C A I RWAY S

·�····· ······························································································· S e e W e b s i t e f o r A H A g u i d e l i n e s o n a i rway V' i n t e rve n t i o n s : S u p r a g l o t t i s A i rways Laryngeal Mask Airway A laryngeal mask airway (LMA) is an advanced airway device that is an acceptable alternative to the endotracheal tube (ETT). The LMA is composed of a tube with a cuffed mask­ like projection at the end of the tube (Fig. 1 7- 1 1 ) . The LMA was designed by British anesthesiologist Archie Brain (and called the Brain airway); it has been used in general anesthesia since 1 988.97 ·98 Its chief advantages over bag-mask ventilation are that once it is inserted, it can be left in place and used "hands free" by a minimally trained rescuer to maintain a reliable conduit for ventilation. The LMA is designed to be inserted "blindly, " without use of a laryngoscope and without visualization of the vocal cords, so it can be quicker and easier to insert than the endotracheal tube, with less extensive train­ ing needed to develop competence. Another major advantage of the LMA is that it can be inserted without interrupting car­ diopulmonary resuscitation. The LMA may also have advan­ tages over the endotracheal tube when access to the patient is limited,99· 1 00 when the patient may have an unstable neck injury, 101 or when some other factor makes it impossible to appropriately position the patient for endotracheal intubation.

The LMA has been studied extensively in anesthesia as well as in direct comparison to bag-mask ventilation, to endo­ tracheal intubation, and to ventilation with other devices. In randomized controlled trials (RCTs) on anesthetized patients, the LMA is generally as easy or more easy to insert as com­ pared with the endotracheal tube, whether the users are experienced 102 -106 physicians, nurses, respiratory therapists, or EMS personnel. Inexperienced personnel were also quickly and easily taught to successfully insert the device into anesthetized patients in RCTs comparing tl1e LMA to bag-mask ventilation or another alternate airway (not com­ pared with the ETT). so,s 5 , 107-l l l

F I G U R E 1 7 - 1 1 • la ryn g e a l m a s k a i rway.

265

It is important that novice users or users with limited ongoing experience be able to use the airway quickly, reli­ ably, and safely. In nonrandomized studies of patients under­ going resuscitation, novice users successfully performed intubation and ventilation with LMA in a high proportion of adult patients. 1 1 2 -1 1 7 In a pseudorandomized study compar­ ing the LMA to bag-mask ventilation and to the Combitube, successful insertion and ventilation was accomplished in 7 3 % of patients randomized to LMA compared with 86% of patients randomized to Combitube. 1 1 8 The idea o f using the LMA i n resuscitation was ini­ tially treated skeptically because the LMA does not fully seal the airway. However, studies have not shown an increased incidence of aspiration with the LMA. In RCTs with anesthetized patients, there was no reflux on intuba­ tion or with intermittent positive pressure ventilation (IPPV) with the LMA as compared with four cases with the ETT (P = 0 . 1 1 ) . 1 1 9 There was no gastric distention1 2 0 and no aspiration when tested with methylene blue . 1 2 1 Resuscitation studies have yielded results similar to those of the anesthesia studies with regard to aspiration. In a multi­ center study of cardiac arrest ventilatory management by RNs in 1 64 patients, regurgitation was observed in 2 0 patients before the LMA was inserted and in three patients during LMA use. In only one case (not involving LMA use) was there clinical evidence of aspiration. Where the LMA was inserted mainly by junior anesthesia staff with no previous experience in its use in a series of 50 cardiac arrest cases, the LMA was inserted successfully in 98% of the patients and no signs of regurgitation or aspiration were detected. 1 14 In a study of 797 patients in cardiac arrest, when the LMA was used as the first­ line airway management device, the incidence of regurgita­ tion was significantly less than when bag-mask ventilation was used first (3 . 5 % versus 1 2 . 3 % ; P e by experienced providers is indicated. Importantly, on(y experienced and continually qualified individuals should perform endotracheal intubation after a care­ ful assessment of the risks and benefits in an emer­ gency setting. Urgent or emergent endotracheal intubation will pose additional challenges. Currently, advanced cardiac life support (ACLS) experts consider the cuffed endotracheal tube the venti­ lation adjunct of choice for providers who are skilled and experienced in its use. The cuffed endotracheal tube • •

•

•

•

• •

Keeps the airway patent Allows suctioning of airway secretions Ensures delivery of a high concentration of oxygen Provides a route for administration of certain drugs Facilitates delivery of a specific tidal volume Protects the airway from aspiration of gastric con­ tents Protects the airway from aspiration of blood and mucus from above the trachea . '

Indications Indications for insertion of an endotracheal tube in an emergency situation include cardiac arrest and acute respiratory insufficiency. General indications in these settings are:

•

•

Inability of the provider to ventilate the uncon­ scious patient with less invasive methods. In gen­ eral, attempt to provide oxygenation and ventila­ tion of the lungs with exhaled-air methods, simple airway adjuncts, or bag-mask ventilation before attempting endotracheal intubation. Inability of the patient to protect the airway (e.g., because of coma, absent reflexes, or cardiac arrest). To provide adequate lung inflation, rescuers often gener­ ate airway and esophageal pressures that exceed the closing pressure of the gastroesophageal junction. This can lead rapidly to gastric inflation and subse­ quent regurgitation. When the airway is unprotected, regurgitated gastric contents can enter the lungs. 2 -5 Prolonged need for chest compressions during resuscitation. Simple, noninvasive airway adjuncts may be used to maintain oxygenation and ventilation during cardiac arrest of short duration such as ven­ tricular fibrillation (VF) or pulseless ventricular tachycardia (VT) arrest responsive to defibrillation. When resuscitation is prolonged, however, gastric inflation often becomes problematic and airway con­ trol is needed. As soon as practical during tl1e resus­ citative effort, intubate the trachea or insert one of the two acceptable alternative advanced airways­ the laryngeal mask airway (LMA) or Combitube.

Endotracheal Intubation in �ardiac J\rrest

The principles of assessment and management o f airway emergencies are complex; th e specific approach required is influenced by the training, 273

274

HIGH

skills, and experience of emergency health care providers, the assistance and resources available in different clinical settings, and local protocols.

Rapid Sequence Intubation Versus "Crash Airway" ( Cardiac Arrest) Intubation "Rapid sequence intubation" (RSI) and "rapid sequence induction" both describe a sequential protocol for the rapid induction of anesthesia and intubation in patients at risk for aspiration of gastric contents. Peter Safar's pioneer descrip­ tion of such a protocol used both terms: "rapid induction/ intubation for prevention of gastric-content aspiration . "6 The more inclusive term "rapid sequence intubation" is preferred now because "induction" currently refers only to the step of "inducing" anesthesia via sedative agents.

Crash Airway Intubation for Cardiorespiratory Arrest Obvious differences exist between a patient who is breathing spontaneously-the usual candidate for RSI-and someone in cardiac (cardiorespiratory) arrest. The term "crash airway" describes patients who are unresponsive (no airway protec­ tive reflexes), without effective respirations or circulation.

Assess the Patient: The Primary and Secondary ABCD Surveys On arriving at the scene of a cardiac arrest or respiratory emergency in any setting, ACLS personnel follow the steps of the primary AB CD survey: assess/ manage airway, breathing, circulation, and ventricular fibrillation-with an automatic external defibrillator (AED) or conventional defibrillator. The steps of endotracheal intubation are part of the sec­ ondary ABCD survey. Correct performance of the primary ABCD survey, however, accomplishes a number of critical steps required for endotracheal intubation: • •

•

Open airway. If patient is unresponsive, insert oropharyn­ geal airway. Administer high-flow ( 1 0- 1 5 L/min) 1 00% oxygen. Provide positive-pressure ventilation with bag and mask if spontaneous ventilation is absent or inadequate (see "Preoxygenation," below).

If bag-mask ventilation is provided for the unresponsive patient (with no airway protective reflexes), provide cricoid pressure if personnel are available. Begin the secondary ABCD survey: • •

Designated intubator verifies effectiveness of ventilation and oxygenation and prepares to intubate (secondary A and B). D esignated N accessor/medication provider gains peripheral vein access (see Table 1 8- 1 ) to provide appro­ priate resuscitation medications and premedications for intubation if needed.

Initial Steps of Crash Airway ( Cardiac Arrest) Intubation The patient with a crash airway requires chest compressions and positive-pressure ventilation before and after endotra­ cheal intubation. In such circumstances several steps in the sequence of RSI-such as preoxygenation, premedication, defasciculation, and sedation-are either unnecessary or have a lower priority. When endotracheal intubation is per­ formed for the crash airway, the intubation steps (see below) are modified according to the following steps: Step 1 . Preparation per routine appropriate for the setting Step 2. Assessment Step 3. Preoxygenation, accomplished during resuscitation Step 4. P1'emedication, omitted because the "LOAD " agents (lidocaine, opioids, atropine, and defasciculating agents) add little if any clinical value to benefit the cardiac arrest patient Step 5. Induction of anesthesia and paralysis, omitted because the patient is already unresponsive and flaccid due to cerebral anoxia from lack of blood flow Use of Paralytic Agents With the Crash Airway Although the paralysis step is often omitted for patients with crash airway, residual muscle spasm and hypertonicity dur­ ing the first minutes after cardiac arrest may complicate attempted endotracheal intubation. In one emergency med­ ical services (EMS) system in which paramedics were not allowed to use paralytic agents, 49 % of failed intubations were due to "inadequate relaxation."7 Some EMS systems have initiated programs that train and protocols that author­ ize advanced life support (ALS) personnel to administer sedative agents, 8 paralytic agents,9 or both.10 Many such pro­ tocols are based on published experience in air medical transport systems, involving trauma patients 1 1-13 and others who require a crash airway. 14 Because most experience with RSI protocols using sedatives and paralytic agents in the pre­ hospital setting have actually involved management of the crash airway, the need for-and effects of-RSI medications has not been demonstrated. There have been no reports of outcomes of airway management by systems that have prospectively studied the use of paralytic agents in cardiac arrest.9 In fact, many published protocols for the use of suc­ cinylcholine specifically exclude patients in cardiac arrest. 15 Intubation of some victims of cardiac arrest may be facili­ tated by the use of neuromuscular blocking agents if proto­ cols and programs are based on the consensus guidelines of organizations such as the National Association of EMS Physicians. 1 6• 1 7

The "RAPIDS" Approach to Endotracheal Intubation for Crash Airway Patients 1 8 I n the crash airway situation usually presented t o health care responders, the patient is unresponsive without effective res­ piration (agonal gasps may be present) and no circulation.14 No monitoring or treatment action other than basic CPR is ongoing. The following approach is one method to rapidly intubate the trachea and control the airway.

CHAPTER 1 8

R: Resuscitate Patient-Continue CPR while planning to establish a definitive airway. •

•

•

Personnel. Two or preferably three persons are assigned to airway management. One person is designated in advance as the intubator; this person must have proper training and experience and documented intubation success. Equipment and medications. Regular (daily or every shift) review of the checklist is essential (see the pre-event checklist at the end of this chapter). Begin primary ABCD survey: assess and support

Airway: Insert oropharyngeal airway. Breathing: Administer supplementary oxygen. Provide bag-mask (or mouth-to-mask/shield) ventilation. Apply cricoid pressure (see Chapter 1 7) . Circulation: Ensure that adequate chest compressions are performed. Evaluate rhythm. Defibrillate: Attempt defibrillation as appropriate. A: Access-Establish peripheral venous access and start secondary ABCD survey. •

•

Establish peripheral vein access. Designated intubator prepares to intubate.

P: Position Patient-Align the respiratory axes to best facilitate laryngoscopy. •

•

Flex the neck relative to the thorax. Extend the head relative to the neck (see Fig. 1 8- 1 ).

1:

Intubate

•

Intubator makes one oral intubation attempt without using pharmacologic agents. If successful, see step D-"Determine tube location. " I f unsuccessful o n first attempt, resume bag-mask ventilation:

•

•

1 . Bag-mask ventilation: Consider: do the bag-mask ventilations produce effective chest rise per clinical evaluation? If yes, see step 2 ; further endotracheal tube attempts are OK. If no, make only one more attempt; then go to step 3 . 2 . Review relaxation/flaccidity: During the first intuba­ tion attempt, was there complete skeletal muscle relax­ ation? If yes, more intubation attempts are OK. If no, see step 3 : succinylcholine 1 . 5 mg/kg. 3 . Paralyze the patient: Administer succinylcholine 1 . 5 mg/kg to ensure complete relaxation of the patient for intubation.

•

M A N A G E M E N T O F T H E D I F F I C U LT A I RWAY

•

275

Perform confirmation with a device such as a C0 2 detec­ tor or esophageal detector device (EDD).

S: Secure Tube-To prevent dislodgment, use tape or a commercial tube holder. Monitor position of the tube frequently.

Rapid Sequence Intubation Initial Steps of Rapid Sequence Intubation RSI is used primarily for patients who need to be intubated but who are usually breathing spontaneously, are variably responsive to stimuli, have intact airway protective reflexes, and-most critically-may have a full stomach. Consequently the recommended RSI steps incorporate actions to prevent pain, anxiety, and distress; to blunt multiple adverse physio­ logic responses to laryngoscopy and endotracheal intubation; and to reduce the risk of aspiration of gastric contents. Step 1 is pre-event preparation. Step 2 is preoxygenation. A high concentration of inspired oxygen is administered to the spontaneously-breathing patient to maximize arterial and alveolar oxygen content. To prevent gasu·ic inflation, bag-mask ventilation is not routinely provided at this time. If adequate spontaneous ventilation is present.

A

A. Give one dose only; no sedative or anesthetic. B . After 30 to 40 seconds, check jaw and neck muscles for flaccidity. C. If flaccid, attempt endotracheal intubation. D: Determine Tube Location • Perform confirmation with physical examination and five point auscultation.

F I G U R E 1 8 - 1 • A l i g n i n g a x e s of u p p e r a i rway. 1 , o r a l a x i s ; 2 , p h a ryn g e a l a x i s ; 3 , tr a c h e a l a x i s . A . N o r m a l p o s i ti o n . B . N e c k f l e x e d o n t h e s h o u l d e rs to a l i g n a x i s 2 with a x i s 3 , a n d h e a d e x te n d e d o n t h e n e c k to a l i g n a x i s 1 w i t h a x e s 2 a n d 3 .

276

HIGH

Step 3 is premedication. Pharmaceutical agents are adminis­ tered to blunt specific reflex reactions to airway manipu­ lation. The Airway Course, an advanced emergency air­ way management course, 19 has developed the mnemonic "LOAD " as a memory aid for the premedication (pre­ treatment) agents: lidocaine, opioids, atropine, and defas­ ciculating agents. (See the next section for further infor­ mation about the use of these medications.) Step 4 is induction of anesthesia or sedation and paralysis.

One provider is typically assigned to establish vascular access. Vascular access will be needed during resuscitation to provide vasoactive and other medications and will be needed during intubation of the responsive patient if sedatives and paralytic agents are used during RSI. Inexperienced providers should use only those airway management devices for which they have adequate training. Providers who perform endotracheal intubation require either frequent experience or frequent retraining. 1 ,2 ° ,2 1 •

·�····· ······························································································· S e e W e b s i t e f o r A C E P p o l i cy s t a t e m e n t o n �

•

r a p i d s e q u e n c e i n t u b a ti o n .

The Seven "Ps" of Rapid Sequence Intubation

•

The "Seven P's of Rapid Sequence Intubation" was devel­ oped as a memory aid for advanced airway providers. 1 8 As modified for ACLS use, seven steps or "Ps" are as follows: l.

2. 3. 4. 5.

6. 7.

Pre-event Preparation. Prepare personnel, equipment, medications, and monitoring and begin primary ABCD survey. Note any history that will influence intubation procedure or choice of medication. This preparation will be influenced by the setting and acuity of the intubation procedure. Preoxygenate. Pretreatment/Premedication. Paralyze after sedation. Induce anesthesia. Protection/Positioning. Cricoid pressure applied: just as airway protective reflexes (cough, gag) are lost and before positive-pressure ventilation. Placement of endotracheal tube with both clinical con­ formation and a device. Postintubation management, including securing of tube and radiographic verification of tube placement; continuous monitoring of tube position, oxygenation, and ventilation.

Step 1 : Pre-event Preparation Multiple advanced resus­ citation interventions must be performed simultaneously during an intubation procedure . This is particularly true when intubation is required during resuscitation. Resuscitation teams should have predesignated responsibili­ ties so that in the event of an emergency, rescuers can act without waiting for instructions.

EMS systems should establish a system of quality improvement monitoring for intubation attempts, docu­ menting for each provider and patient the number of intu­ bations attempted, number of confirmed successful intuba­ tions, complications, and outcomes. One successful model for out-of-hospital response to cardiac arrest is a two-tier response: a two- to tl1ree-member BLS-D response team followed by a two-member ALS response team. In this system it is common for BLS respon­ ders to perform chest compressions, bag-mask ventilation, and defibrillation. One member of the two-person ALS team gains intravenous access and administers medications, and the other performs endotracheal intubation and airway management. This should be the default response model for emergencies both in and out of hospital. In the absence of procedural delays, one ALS provider should be ready to attempt intubation when the other ALS responder is ready to administer IV medications after ensuring chest.

Equipment CUFFED ENDOTRACHEAL TUBE

A typical cuffed endo­

tracheal tube •

•

•

Personnel Two or preferably three providers should be assigned to airway management, with one of the providers designated to perform intubation. As the designated provider prepares for the intubation attempt, the other "air­ way" providers perform bag-mask ventilation (see discussion of bag-mask ventilation in preceding pages) and assist with intubation.

Advanced skills are required to place an endotracheal tube and verify correct position. Delays in intubation or failure to intubate will adversely affect the outcome of cardiac arrest. Failure-to-intubate rates are as high as 50% in EMS systems with low patient volume and providers who perform intubation infrequently. 22 •2 3 Intubation attempts may produce serious complications that are more common when the provider is inexperienced. These potential complications include trauma to the oropharynx, hypoxia and hypercarbia from long interrup­ tions in ventilation, delayed or withheld chest compres­ sions, esophageal intubation, failure to secure the tube, and failure to recognize tube misplacement or displacement.

• •

Is open at both ends Is measured in length (em) from the distal end and marked at several intervals (in adults the tube depth mark visible at the front teeth should be approximately 2 0-2 2 em) Has size markings indicating the internal diameter of the tube in millimeters. For an average-sized woman, the tube size should be 7 mm; for an average-sized man, 8 mm. Has a standard 1 5 -mm/2 2 -mm end connector that will fit positive-pressure ventilation devices. Has a high-volume, low-pressure inflatable cuff attached to an inflating tube with a one-way valve for the cuff-infla­ tion syringe.

CHAPTER 1 8

•

Has a pilot balloon between the one-way valve and inflat­ ing syringe to indicate cuff inflation.

Always check the inflatable cuff for integrity by testing it just before insertion. Use the same syringe that will be used to inflate the cuff after insertion. STYLET A stylet is typically a plastic-coated, malleable metal rod that can be inserted through the endotracheal tube to curve and stiffen the tube to the desired configuration. This procedure will facilitate insertion of the tube into the larynx and trachea by allowing easier manipulation of the direction of the tube. Apply a water-soluble lubricant to the stylet before inserting it to a point 1 to 2 em from the end of the tube. Do not allow the end of the stylet to extend beyond the end of the tube, because it could injure the vocal cords and laryngeal mucosa. Once the stylet is properly positioned in the tube, bend the stylet over the edge of the connector to prevent inad­ vertent advance of the stylet during attempted intubation.

The Eschmann endotracheal tube introducer, more commonly called the gum elastic bougie, is another device used to assist with placement of the endo­ tracheal tube2 4 (Fig. 1 8-2). Currently the gum elastic bougie is used by trained providers only for difficult or unsuccessful oral intubations. It is a semirigid, resin-coated device, about 2 feet long (60 em), made of braided polyester. As seen in Figure 1 8-2 , use of the gum elastic bougie is quite analogous GUM ELASTIC BOUGIE

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277

t o the Seldinger wire technique for inserting intravascular catheters. The device is inserted with a laryngoscope, but only partial visualization of laryngeal structures is required. The small-diameter flexible device is inserted in the trachea largely by "feel"; the design allows the provider to feel the bumping of the tracheal rings when the device enters the trachea. Once the bougie has been passed into the trachea, it essentially acts as a "guidewire" over which an endotracheal tube is passed and advanced blindly into position in the trachea. The endo­ tracheal tube is then stabilized and the rescuer slides the bougie back out. 2 5-30 The tip of the endotracheal tube some­ times gets caught on laryngeal structures and cannot be advanced. In such cases, rotation of the tube with gentle pres­ sure will allow it to advance into the trachea. Some endotra­ cheal tubes (e.g., the Parker endotracheal tube) are designed to reduce this problem by having a curved bevel that causes the tip of the tube to more closely follow the introducer. LARYNGOSCOPE (HANDLE/BLADE-HOLDER PLUS CURVED

AND STRAIGHT BLADE)

The laryngoscope is used to expose the glottis and allow direct visualization of the vocal cords and the tracheal entrance (see Fig. 1 8-2). The laryngoscope consists of three parts: • •

•

The handle, which holds batteries for the light source The blade, which has a bulb in the distal third of the blade The fitting, whi ch is the connection point between the blade and the handle where electrical contact is made

Always check that the light is working. •

•

Attach the indentation of the blade to the bar of the handle. Elevate the blade to the point where it makes a right angle to the handle. The light should come on. If it does not, check the bulb or the batteries.

There are two common types of blades: • •

Curved (Fig. 1 8- 3A, the Macintosh design) S trai ght (s ee Fig. 1 8 -4A, the Miller design) . The choice of blade is a matter of p ersonal preference . Variations i n design usually alter the technique used by the operator.

Medications All medications that may be needed dur­ ing the intubation attempt should be prepared and at hand. These medications may include • •

Premedications ("LOAD " : lidocaine, opioids, atropine, and defasciculating agents) Paralyzing agents, sedatives, and anesthetics

Monitoring Before any attempted intubation, providers should establish appropriate monitoring based on the setting and the type of intubation to be performed. This monitor­ ing should include F I G U R E 1 8 - 2 • T h e g u m e l a s t i c b o u g i e is u s e d to a s s i s t e n d o ­ t r a c h e a l i n t u b a t i o n b y t h e o r a l r o u t e . (F i g u r e i s r e p r i n t e d with p e r m i ss i o n from Ann als o f Emerg e n cy Me dicin e . 1 9 9 6 ; 2 7 : 6 6 5- 6 6 7 . © 1 9 9 6 Ann als o f Emerg e n cy Me dicin e . )

• • •

Continuous electrocardiographic (ECG) rhythm moni­ toring Pulse oximetry Intermittent blood pressure measurements

278

HIGH

B

F I G U R E 1 8 - 3 • A. C u rved b l a d e atta c h e s to l a ryn g o s c o p e h a n ­ d l e . B . A tta c h e d t o l a ryn g o s c o p e h a n d l e . C. I n s e r t e d a g a i n st e p i g l o t t i s . D u r i n g l a ryn g o s c o py, the h a n d l e i s h e l d in the l e ft hand.

c

Continuous end-tidal C0 2 is valuable but not required. Always designate one provider to monitor the patient throughout the intubation attempt. This monitor should immediately inform the intubator if the patient's heart rate slows or becomes irregular or if there is any fall in the oxy­ hemoglobin saturation. Note that emergent monitoring of the cardiac arrest patient cannot include pulse oximetry. There is no pulsatile signal for the pulse oximeter to use to measure oxyhemo­ globin saturation. Cardiac monitoring is also distorted by artifact from chest compressions. Base assessment of how the patient is tolerating the intubation attempt on general appearance and on duration. Step 2 : Preoxygenation •

VVhen RSI is performed for a spontaneously breathing, adequately ventilated patient, provide preoxygenation by delivering 1 00 % oxygen through a well-fitted face mask

•

for at least 3 minutes. Preoxygenation maximizes hemo­ globin and arterial oxygen saturation and provides an oxy­ gen reservoir in the lungs. A typical preoxygenation period is not possible for victims of cardiac arrest who are apneic or lack adequate ventila­ tions or have no airway protective (cough and gag) reflexes. In this situation deliver high-flow 1 00 % oxygen by bag-mask ventilation plus cricoid pressure . See "Protect the Airway With Cricoid Pressure, " below.

Step 3 : Premedication Provide premedication to responsive patients. D o not provide premedication to an unresponsive, or " crash airway" (cardiac arrest) patient. Properly trained providers, in an appropriate setting, should administer the following "LOAD " medications when indications are present: •

Lidocaine 1 . 5 mglkg IV. Administer to patients with ele­ vated intracranial pressure or reactive airways disease. In

CHAPTER 1 8

•

M A N A G E M E N T O F T H E D I F F I C U LT A I RWAY

•

A

B F I G U R E 1 8 - 4 • A. S t r a i g h t - b l a d e l a ryn g o s c o p e . B. I n s e r t e d p a st e p i g l o t t i s . D u r i n g l a ryn g o s c o py, t h e h a n d l e is h e l d i n t h e l e ft hand.

•

•

patients with elevated intracranial pressure (ICP), lido­ caine prevents a reflex rise in intracranial pressure stimu­ lated by laryngoscopy and intubation. Lidocaine mitigates bronchospasm induced by laryngoscopy and intubation in reactive airways patients. Administer lidocaine 3 minutes before the paralytic agent. Opioids, most commonly fentanyl, 3 1-1g/kg Iv. Administer to patients who have no contraindications . Opioids blunt the catecholamine discharge that accompa­ nies laryngeal manipulation. Opioids are particularly use­ ful in patients with elevated ICP because any elevations in blood pressure would further elevate ICP. Opioids are also useful in patients for whom an increase in sympa­ thetic activity or in cardiovascular "shear" pressure would pose a risk (i. e . , those with ischemic heart disease, aortic dissection, or ruptured intracranial aneurysm). Like lido­ caine, opioids should be given 3 minutes before the para­ lytic agent. Atropine 0.02 mglkg; given Iv. Administer to patients who are bradycardic immediately before an intubation attempt (first rule out hypoxia); to all infants younger than 1 year of age and in children 1 to 5 years of age who are going to receive succinylcholine; and to all older children or adults who are to receive a second dose of succinyl­ choline. Atropine is also given 3 minutes before the para­ lytic agent.

279

Defasciculating agents (most often a nondepolarizing agent) given at 1 0 % of the usual paralytic dose. Administer to patients who are to receive succinylcholine and to those who could be harmed by the rise in intracra­ nial pressure that can accompany succinylcholine-induced fasciculations.

Step 4: Paralysis After Sedation Approximately 3 minutes after the last premedication (see above), induce deep sedation (to the point of anesthesia) by rapid IV administration of a benzodiazepine (such as midazolam) , or etomidate or one of several other types of anesthetic agents . Follow immediately with rapid IV administration of a paralytic agent (neuromuscular blocking agent) such as succinyl­ choline or vecuronium. The sedative agents rapidly induce loss of consciousness, loss of airway protective reflexes, and loss of muscle tone, thereby permitting rapid intubation. As the patient becomes unconscious , perform Sellick 's maneuver (firm pressure applied on the cricoid cartilage) to occlude the esophagus and prevent passive regurgita­ tion o f gastric contents (see Chapter 1 7 and Vi deo Clip 17 -8). Cricoid pressure must be timed to occur with the onset of deep sedation (loss of consciousness, loss of cough, gag, and airway protective reflexes) . Bag-mask ventilation can begin with the application of cricoid pressure. Maintain steady pressure on the cricoid while the endotracheal tube is inserted, correct tube placement is confirmed, and the cuff is inflated. The majority of crash airway patients will be unrespon­ sive to such a degree that step 4: paralysis after sedation, is unnecessary. Many patients, however, will maintain a degree of postarrest muscle tone and spasm such that bag-mask ven­ tilation and endotracheal intubation are difficult or even impossible. Administer one of the paralyzing agents to these hypertonic patients. Sedatives or the LOAD premedications are unnecessary.

Neuromuscular Blockade to Facilitate Endotrach eal Intubation in Cardiac Arrest For patients whose cardiac arrest has been witnessed, the intubation goal is to intubate every patient, on the first attempt, and within seconds. •

•

•

The first obj ective in achieving this goal is to paralyze the patient. Numerous studies have confirmed the value of effective paralysis, which facilitates the challenging task of aligning the airway axes in most cases and determines suc­ cess in others. The second objective is to paralyze the patient early and quickly, before positive-pressure ventilation induces gas­ tric inflation, regurgitation, and the devastating conse­ quences of aspiration. The third obj ective is to paralyze the patient briefly, so that, upon return of spontaneous circulation, the patient can resume spontaneous respirations as well.

Clinical indicators of adequate paralysis in the nonarrested patient include lack of spontaneous movements, respiratory effort, and blink reflex and j aw relaxation as manifested by

280

HIGH

the provider's ability to fully open the patient's mouth with­ out resistance. WHICH PARALYTIC AGENT TO USE? The ideal paralytic agent to use for endotracheal intubation would have the fol­ lowing characteristics: •

• •

Rapid onset of action Short duration of action Minimal adverse effects

No paralytic agent possesses all three of these charac­ teristics. Therefore, the final choice of paralytic agent depends on the setting (in hospital versus out of hospital) and the specific protocol (RSI versus cardiac arrest or crash airway). Neuromuscular blocking agents used in endotra­ cheal intubation during cardiac arrest are summarized in Table 1 8- 1 . Many experts consider succinylcholine the drug of choice for endotracheal intubation during both RSI and cardiac arrest. It is the only agent that meets two of the three crite­ ria for a paralytic agent: rapid onset of action (3 0-60 seconds) plus ultrashort duration (3-5 minutes). But succinylcholine does not meet the criterion for minimal adverse effects, because it possesses numerous, sometimes fatal, side effects (see below and Table 1 8-2). Two nondepolarizing agents, rocuronium and vecuro­ nium, also have rapid onset of action but more benign side effects than succinylcholine. Consequently these two drugs may be used in emergency departments and in-hospital set­ tings. Many experts prefer them as paralytic agents over suc­ cinylcholine. Rocuronium and vecuronium, however, do not fulfill the criterion of short duration of action. The slower onset and long duration of action of rocuronium and vecuro-

I TA B LE 1 8 - 1

Drug

•

nium render them unacceptable for use in the out-of-hospi­ tal setting. For appropriately trained prehospital personnel responding to out-of-hospital cardiac arrest, the general consensus is that succinylcholine remains the paralytic agent of choice. In the National Emergency Airway Registry project, a multicenter study of emergency department intubations, only a few of the more than 7 ,000 rapid sequence intuba­ tions reported were accomplished with any neuromuscular blocking agent. PHA.Ri\1.ACOLOGY OF SUCCINYLCHOLINE In the nonar­ rest patient, succinylcholine produces onset of paralysis within 30 to 6 0 s econds and almost universal e ffective (intubation-level) paralysis within 45 seconds. The effects of sudden complete loss of all tone and the onset of com­ plete flaccidity in all the muscles of the head, neck, and thorax are dramatic and obvious . Onset of action may be delayed in patients in cardiac arrest. The effects of suc­ cinylcholine may be difficult to ascertain in the patient in cardiac arrest because the arrest itself produces many of the same effects on muscle tone as succinylcholine-induced paralysis . However, the lack of spontaneous movements, respiratory effort and blink reflex, and jaw relaxation (the provider should be able to completely open the patient's mouth without resistance) indicate onset of action. An appropriate IV dose of succinylcholine is 1 . 5 mg/kg. Duration of action is normally about 3 to 5 minutes . Effective spontaneous respirations may not be possible for approximately 8 minutes . The advantage o f a n agent with a n ultrashort duration of action is that if the intubation attempt is unsuccessful, the agent will quickly wear off, and the patient may be able to

N e u r o m u s c u l a r B l o c k i n g A g e n ts U s e d i n E n d o t r a c h e a l I n t u b a t i o n D u r i n g Ca r d i a c A r r e s t

Dose0

R o u te

Duration of P a r a lys i s

S i d e E ff e c ts

IV, 1 Mb

3 - 5 m i n u te s

Muscle fasciculations

Depolarizing muscle relaxant

Rise in i n t r a o c u l a r , i n tr a g a str i c , i n tr a c r a n i a l pressure

R a p i d o n set; s h o r t d u r a t i o n of action R e n a l fa i l u r e , b u r n s , h i g h p o ta s s i u m l eve l a r e c o n tr a i n d i c a ti o n s

Life - t h r e a te n i n g h i g h l eve l o f p o ta s s i u m

Co n s i d e r d e f a s c i c u l a ti o n with n o n d e polarizing agent

Hyp e r t e n s i o n

D o n o t u s e f o r m a i n t e n a n c e o f p a r a lys i s

Co m m e n ts

N e u r o m u s c u l a r B l o c k i n g A g e n ts 1 to 2 m g / k g IV; 2 to 4 mg/kg I M

.,

0 . 1 -0 . 2 mg/kg

IV

3 0-6 0 m i n u te s

M i n i m a l c a r d i ova s c u l a r s i d e effects

Nondepolarizing agent O n s e t of a c ti o n : 2-3 m i n u t e s

0 . 6-1 . 2 mg/kg

IV

40+ m i n u te s

M i n i m a l c a r d i ova s c u l a r s i d e effects

Nondepolarizing agent R a p i d - a c ti o n o n s e t l i k e s u c c i nyl c h o l i n e

' D o s e s sh own a r e g U i d e l i n e s o n ly. 6 A c t u a l d o s m g m a y vary d e p e n d m g o n p a t i e n t ' s c l i n i c a l status.

CHAPTER 1 8

TA B LE 1 8 - 2

•

•

M A N A G E M E N T O F T H E D I F F I C U LT A I RWAY

281

S u c c i nyl c h o l i n e : A dverse E ff e c ts a n d R e l a tive Co n t r a i n d i c a t i o n s

A dverse E ffects

Co n t r a i n d i c o t i o n s

•

M u s c l e fasciculotions

•

D e n e rvoti o n syn d r o m e (str o k e , s p i n a l c o r d i nj u ry) > 7 2 h o u r s e a r l i e r

•

Muscle pain

•

Neuromuscular disorders

•

R h a b d o myolys i s

•

Increased intracranial pressure

•

Myo g l o b i n u r i a

•

O p e n i nj u ry o f t h e eye g l o b e

•

Hyp e r k a l e m i a

•

Glaucoma

•

Hyp e r t e n s i o n

•

H i s t o ry (p a t i e n t o r fa m i ly) o f m a l i g n a n t hyp e r th e r m i a

•

I n c r e a s e d i n tr a c r a n i a l p r e s s u r e

•

H i s t o ry o f p l a s m a c h o l i n e ste r a s e d e f i c i e n cy

•

I n c r e a s e d i n tr a o c u l a r p r e s s u r e

•

M aj o r c r u s h i nj u r i e s

•

I n creased intrag astric pressure

•

T r a u m a o r b u r n s > 4 8 h o u r s a f t e r i nj u ry

•

M a l i g n a n t hyp e r t h e r m i a

•

Hyp e r k a l e m i a

•

B r a dyca r d i a , a systo l e

•

R e n a l fa i l u r e

resume spontaneous ventilation, minimizing the period of bag-mask ventilation. Many patients, however, may have underlying disease that will prevent effective ventilation. So if intubation is unsuccessful, the provider should be pre­ pared to provide a prolonged period of bag-mask ventila­ tion, thereby negating the advantage of a short- acting agent. Succinylcholine has numerous contraindications and p otential side effects, which may occasionally be fatal (Table 1 8-2). Providers who use succinylcholine must be completely familiar with its potential dangers and con­ traindications and must carefully weigh its risk-benefit ratio against those of the nondepolarizing agents available. Because of its potential detrimental effects, succinylcholine should never be used to maintain paralysis after intuba­ tion. 3 1 , 3 2

Alternative Paralytics Rocuronium is an aminosteroid nondepolarizing agent with rapid onset and intermediate duration of action. Acceptable intubation conditions can be achieved within 60 seconds at doses of 0 . 6 to 1 . 2 mg/kg IV with a duration of >40 minutes . 3 3-3 5 At these doses rocuronium has minimal to no cardiovascular side effects . 3 6 It is safe to use in p ati ents with renal3 7 and hepatic failure, although the duration of neuromuscular blockade may be prolonged with liver disease. 38•3 9 Another advantage of rocuronium is that it is available as a premixed solution. Vecuronium is considerably more potent than rocuro­ nium. Because onset is inversely related to potency, vecuro­ nium has a slower onset. Doses of 0. 1 to 0.2 mg/kg IV will produce a level of muscle relaxation acceptable for intuba­ tion within 90 to 1 2 0 seconds and that can last from 3 0 min­ utes up to 1 hour.40•41 Higher doses produce more rapid onset but at the expense of prolonged duration of action.

Vecuronium also has minimal side effects and is safe for patients with renal and hepatic failure.42 Unlike rocuronium, vecuronium is supplied as a powder that must be reconsti­ tuted before it can be administered. Step 5: Protection of Airway with Cricoid Pressure (Sellick's Maneuver) and Positioning of Patient

Protect Airway With Cricoid Pressure Cricoid pressure occludes the esophagus, minimizing air entry into the stom­ ach. It should be provided before initiation of bag-mask ven­ tilation, so it may be necessary early in the preparation for intubation or later for an RSI sequence. If the victim is in cardiac arrest (crash airway), bag-mask ventilation is initiated as one of the first steps of resuscita­ tion. Sedatives are not administered and paralysis is seldom required before intubation. If adequate personnel are avail­ able, one rescuer should apply cricoid pressure before posi­ tive-pressure ventilation is provided and should maintain it until intubation is complete, the tube cuff is inflated, and correct tube placement is verified. In the prehospital setting, however, a third rescuer is often not available to provide cricoid pressure. In an RSI sequence, sedative and paralytic drugs are administered to a patient who is breathing spontaneously. Providers should apply cricoid pressure as soon as the patient becomes sedated (i. e. , loses consciousness with loss of airway protective and gag reflexes) and before bag-mask ventilation is initiated. VVhen possible, maintain cricoid pressure con­ tinuously until the endotracheal tube is successfully placed.43 Cricoid pressure during the intubation attempt can improve visualization of the vocal cords because the maneuver dis­ places the larynx back into visual alignment with the laryn­ goscope. The application of cricoid pressure will not prevent all regurgitation or aspiration. A portable suction device

282

HIGH

(battery powered) or access to a wall-vacuum source and an adequately sized suction catheter must be readily available (see Video Clip 1 7 -8).

Position the Patient: Align the Respiratory Axes to Best Facilitate Laryngoscopy •

•

Flex the neck relative to the thorax. Extend the head relative to the neck.

The most common cause of unsuccessful intubation is the intubator's inability to see the vocal cords through the laryngoscope (see Fig. 1 8- 5 C). The laryngoscope (Figs . 1 8 -2 and 1 8 - 3 ) is a rigid metal device that is not well designed for intubation; it allows the intubator to see the vocal cords only along a straight visual axis between the provider's eye and the vocal cords. The dif­ ficulties are created by the presence of three separate, angu­ lated lines of sight and by the patient's teeth, tongue, and uvula, which vary in size and consistency. Visualization is best accomplished by moving the patient's head, neck, and thorax into the "sniffing position" (see Fig 1 8-4). ALIGNJNG THE AIRWAY AXES

• •

•

Three axes-the oral, pharyngeal, and tracheal-must be aligned to achieve direct visualization of the larynx. To accomplish this, first flex the neck forward relative to the chest; then lift the chin (which extends the head backward relative to the neck). An exaggerated attempt to "sniff' (the sniffing position) duplicates the position needed. One recent study using cervical spine radiography concluded that precise "alignment of the axes" seldom if ever occurs. Do not allow the head to hang over the end of a bed or stretcher, because intubation is virtually impossible in that position.

For proper flexion of the neck, it is often helpful to place several towels under the patient's head to elevate it a few centimeters above the level of the bed. The intubator can then extend the head and visualize the vocal cords.

Step 6: Perform Oral Endotracheal Intubation and Confirmation of Endotracheal Placement • During cardiac arrest, the intubator typically makes one oral intubation attempt without using sedative or paralytic agents. • If successful, see step 7 . If unsuccessful, resume bag-mask ventilation. See Figure 1 8-8.

Peiform Oral Endotracheal Intubation DIRECTLY VISUALIZE THE VOCAL CORDS WITH THE LARYNGOSCOPE •

Open the patient's mouth with your right hand. If an assistant is applying cricoid pressure, he or she may retract the right corner of the mouth.

•

• • •

Hold the laryngoscope in your left hand. Insert the blade in the right side of the mouth, displacing the tongue to the left. Move the blade toward the midline and advance it to the base of the tongue. Simultaneously move the lower lip away from the blade with your right index finger. Be gentle and avoid applying pressure on the lips and teeth.

Using a curved blade (Fig. 1 8-5B), advance its tip into the vallecula (i. e. , the space between the base of the tongue and the pharyngeal surface of the epiglottis). Using a straight blade (Fig. 1 8-5A), insert its tip under the epiglottis. Expose the glottic opening by exerting upward trac­ tion on the handle . Do not use a prying motion, and do not use the upper teeth as a fulcrum. Point and firmly lift the end of the handle at an angle of 3 0 to 45 degrees above and toward the patient's feet. This helps to create the sniffing position and allows the best view of the vocal cords (Fig. 1 8 -4B) . •

• •

• • •

•

Keeping the vocal cords under direct vision, advance the tube from the right side of the mouth through the cords . Continue inserting the tube until the cuff appears and completely passes through the cords. Then advance the tube 1 .2 5 to 2 . 5 em further into the tra­ chea. The tip of the tube should now be about halfway between the vocal cords and the carina. In the average adult, this position will result in the front teeth aligning between the 1 9- and 2 3 -em depth markings on the tube. This position allows for some movement of the tip of the tube during neck flexion or extension without extubation or movement of the tip into a main bronchus. If you used a stylet, remove it now. Inflate the cuff with enough air to occlude the trachea (usually 1 0-2 0 mL). Note: Oxyhemoglobin saturation and oxygen delivery will quickly fall during an intubation attempt. Hypoxia develops rapidly because bag-mask ventilation and oxy­ gen delivery have stopped abruptly and no ventilations or chest compressions can b e provi d e d . Intubation attempts should, therefore, be expeditious but gentle, exposing the glottic opening as quickly as possible and placing the tube through the cords under direct vision in a controlled manner. It may be necessary to interrupt the intubation attempt to provi de oxygen if the patient's heart rate, oxyhemoglobin saturation, or clin­ ical appearance deteriorates significantly during the attempt. As soon as the tube is placed, inflate the cuff. Then: • Confirm tube position. Various approaches to confir­ mation of tube placement are acceptable provided one critical principle is always followed: a combination of both clinical (physical examination) and device (e.g. , capnometery or EDD) confirmation techniques must be used to confirm tub e placement. S e e " C onfirmation of Endotracheal Tub e Placement, " below.

CHAPTER 1 8

A

•

M A N A G E M E N T O F T H E D I F F I C U LT A I RWAY

283

B

�··· Ton g u e

c

•

F I G U R E 1 8 - 5 • Visu a l i z a t i o n o f vo c a l c o r d s . A. Vi ew of vo c a l c o r d s with s t r a i g h t - b l a d e l a ryn g o s c o p e (e p i g l ottis i s cove r e d by str a i g h t b l a d e and n o t vi s i b l e) . B . Vi ew o f t h e vo c a l c o r d s with c u rve d - b l a d e l a ryn g o s c o p e (e p i g l o t ­ tis i s vi s i b l e) . C. A n a to my.

Confirm effective seal of the trachea by the cuff with these steps: listen over the larynx with a stethoscope, pro­ vide a ventilation (normal tidal volume), and if an air leak is heard around the cuff, add more air from the syringe. Repeat this sequence of providing ventilations and adding air to the cuff until the audible air leak disappears.

Confirmation of Endotracheal Tube Placement A thor­ ough assessment of endotracheal tube position should be performed immediately after placement. For patients in car­ diac arrest, this assessment should not require interruption of chest compressions. Assessment by physical examination consists of visualizing chest expansion bilaterally and listen­ ing over the epigastrium (breath sounds should not be heard) and the lung fields bilaterally (breath sounds should be equal and adequate). A device should also be used to con­ firm correct placement in the trachea (see below). If there is

doubt about correct tube placement, use the laryngoscope to visualize the tube passing through the vocal cords. If still in doubt, remove the tube and provide bag-mask ventilation until the tube can be replaced.

Use of Devices to Confirm Tube Placement Providers should always use both clinical assessment and devices to confirm endotracheal tube location immediately after placement and each time the patient is moved. No study, however, has identified a single device as both sensi­ tive and specific for endotracheal tube placement in the trachea or esophagus . All confirmation devices should be considered adjuncts to other confirmation techniques. There are no data to quantify the capability of devices to monitor tube position after initial placement. False-positive and false-negative results can occur for a variety of reasons (Table 1 8-3).

284

HIGH

T A B LE 1 8 - 3

•

R e a s o n s f o r M i s l e a d i n g R e s u l ts U s i n g E n d - Ti d a l C0 2 D e t e c t o r a n d E s o p h a g e a l D e t e c t o r D evi c e

A : Co l o r i m e t r i c E n d - Ti d a l C0 2 D e t e c t o r Reading

A c t u a l Lo c a t i o n o f ETT: T r a c h e a

A c tu a l Lo c a ti o n o f ETT: E s o p h a g u s ( o r Hyp o p h a rynx)

Carbon Dioxide Detected

ETT in

Co l o r c h a n g e : p o s i tive C0 2 p r e s e n t ( o r a s s p e c i f i e d by m a n u fa c t u r e r)

P r o c e e d with ve n ti l a t i o n s .

Re11sons fo r 11pp11rent C02 detection despite tube in esopll11gus

=

tNclle•

Causes: D i s te n d e d sto m a c h , r e c e n t i n g e s ti o n o f c a r b o n a t e d b eve r a g e , n o n ­ p u l m o n a ry s o u r c e s o f C0 2 • Consequences: U n r e c o g n i z e d e s o p h a g e a l i n t u b a ti o n ; c a n l e a d to i a t r o g e n i c d e a t h .

No C02 Detected

N o C02 detection witll tube in tNclle•

No c o l o r c h a n g e : n e g a tive C0 2 a b s e n t (o r a s s p e c i f i e d b y m a n u fa c t u r e r) =

Causes: Low o r n o b l o o d f l ow state (e . g . , c a r d i a c a r r e s t) ; a ny c a r d i a c a r r e s t with n o , p r o l o n g e d , o r p o o r CPR. Consequences: Le a d s to u n n e c e s s a ry r e m ova l o f p r o p e r l y p l a c e d E n . R e i n t u b a t i o n a t te m p ts i n c r e a s e c h a n c e s o f o t h e r a dverse c o n s e q u e n c e s .

No C02 detection 11nd tube is not in tr•­ clle• (i. e., tube is in esopll11gus) Causes: R e s c u e r h a s i n s e r t e d E n i n e s o p h a g u s/hyp o p h a ryn x . A l i fe - t h r e a t e n ­ i n g a dve r s e eve n t h a s o c c u r r e d . Consequences: R e s c u e r r e c o g n i z e s E TT i s n o t i n tr a c h e a ; p r o p e r ly a n d r a p i d ly i d e n ­ t i fi e d ; t u b e i s r e m ove d a t o n c e ; p a t i e n t is reintuboted.

B : E s o p h a g e a l D e t e c t o r D ev1 c e Reading

A c tu a l Lo c a ti o n o f ETT: E s o p h a g u s

A c tu a l Lo c a t i o n o f ETT: T r a c h e a

Consistent With Tube in Esophagus

Device suggests tube in esopll11gus wlten it is in esopll11gus

Device suggests tube in esopll11gus wlten it is in tNclle•

Causes: R e s c u e r h a s i n s e r t e d t u b e i n e s o p h a g u s/hyp o p h a ryn x . A l i fe - th r e a t e n ­ i n g a dverse eve n t h a s o c c u r e d .

Causes: S e c r e ti o n s i n t r a c h e a (m u c u s , g a s t r i c c o n te n ts , a c u te p u l ­ m o n a ry e d e m a) ; i n s e r t i o n i n r i g h t m a i n b r o n c h u s ; p l i a b l e tra c h e a (m o r b i d o b e ­ s i ty, l a te - t e r m p r e g n a n cy) .

B u l b d o e s n o t r e fi l l or r e fi l l s s l owly ( > 5 s e c o n d s x 2) , o r syr i n g e c a n n o t b e a s p i r a te d , s u g g esti n g t h a t t i p o f E n i s i n eso p h a g u s

Consequences: R e s c u e r c o r r e ctly r e c o g ­ n i z e s E n i s i n e s o p h a g u s ; E TT i s r e m oved at once; patient is reintuboted.

Consistent with Tube i n Trachea B u l b f i l l s i m m e d i a t e ly or syr i n g e c o n b e a s p i r a te d , s u g g esti n g t h a t E n i s i n t r a ­ chea

Consequences: Le a d s to u n n e c e s s a ry r e m ova l of p r o p e r ly p l a c e d ETT. R e i n t u b a t i o n a t te m p ts i n c r e a s e c h a n c e s o f o t h e r a dverse c o n s e q u e n c e s .

Results suggest tll11t tube is NOT in esopll­ •gus (i. e., tll11t it is in tr11clle11) wit en tube IS in esopll11gus

Results suggest tll11t tube is NOT in tile esopll11gus (i. e., tll11t it is in tile tNclle•) wlten it IS in tile tNcllefl.

Causes: • Co n d i t i o n s t h a t c a u s e i n c r e a s e d l u n g e x p a n s i o n (e . g . , CO P D , s t a t u s o s t h m a t i c u s) . • Co n d i t i o n s t h a t fi l l sto m a c h with a i r (e . g . , r e c e n t b o g - m a s k ve n ti l a ti o n , m o u t h - to - m a s k o r m o u t h - to - m o u t h b r e a th i n g) . • Co n d i t i o n s t h a t c a u s e p o o r to n e i n eso p h a g e a l s p h i n cter or i n creased g a str i c p r e s s u r e ( l a t e p r e g n a n cy) .

E s o p h a g e a l d e t e c t o r d evi c e i n d i c a t e s E TT is i n t r a c h e a . P r o c e e d with ve n ti l a t i o n s .

Consequences: U n r e c o g n i z e d e s o p h a g e a l i n t u b a ti o n c o n l e a d to d e a t h .

CHAPTER 1 8

•

M A N A G E M E N T O F T H E D I F F I C U LT A I RWAY

•

-�..... .............................................................................................. . S e e W e b s i t e f o r A CE P p o l i cy s t a te m e n t o n V' c o n f i r m a t i o n o f e n d o tr a c h e a l t u b e p l a c e ­

Exhaled C 0 2 Detectors (Fig. 1 8 -6) D etection o f exhaled C0 2 i s one of several independent methods o f confirming endotracheal tube position. Given the simplic­ ity of the exhaled C0 2 detector, it can be used as the ini­ tial method for detecting correct tube placement even in the victim of cardiac arrest. D etection of exhaled C0 2 , however, is not infallible as a means of confirming tube placement, particularly during cardiac arrest. But evidence from one meta-analysis in adults,44 one prospective con­ trolled cohort study, 45 and s everal case s eries and reports46-54 indicates that exhaled C0 2 detectors (wave­ form, colorimetry, or digital) may be useful as adjuncts to confirm endotracheal tub e placement during cardiac arrest. The range of results obtained from the reviewed papers is as follows : Sensitivity (percentage of correct endotracheal placement detected when C0 2 is detected) : 3 3 % to 1 00% Specificity (percentage of incorrect esophageal place­ ments detected when no C0 2 is detected) : 97% to 1 00 % Positive predictive value (probability of endotracheal placement if C0 2 is detected) : 1 00 %

• •

A

Negative predictive value (probability of esophageal placement if no C0 2 is detected) : 2 0 % to 1 00 % .

When exhaled C0 2 is detected (positive reading for C0 2 ) in cardiac arrest, it is usually a reliable indicator of tube position in the trachea. False-positive readings (C0 2 is detected but the tube is located in the esophagus) have been observed in animals that ingested large amounts of carbon­ ated liquids before the arrest.55 False-negative readings (in this context defined as failure to detect C0 2 despite tube placement in the trachea) may be present during cardiac arrest for several reasons. The most common explanation for false-negative readings during CPR is that blood flow and delivery of C0 2 to the lungs is low. False-negative results have also been reported in association with pulmonary embolus because pulmonary blood flow to the lungs is reduced. If the detector is contaminated with gastric con­ tents or acidic drugs (e.g., endotracheally administered epi­ nephrine), a colorimetric device may display a constant color rather than breath-to-breath color change . In addition, elimination and detection of C0 2 can be drastically reduced following an intravenous bolus of epinephrine56 or with severe airway obstruction (e.g., status asthmaticus) and pul­ monary edema.46 •5 7-59 For these reasons, if C0 2 is not detected, a second method should be used to confirm endo­ tracheal tube placement, such as direct visualization or the esophageal detector device. Use of COrdetecting devices to determine the correct placement of other advanced airways (e . g . , Combitube, LMA) has not been adequately studied; however, the

ment.

•

285

B

F I G U R E 1 8 - 6 • C o n fi r m a t i o n o f e n d o t r a c h e a l t u b e p l a c e m e n t . A. E n d - t i d a l c o l o r i m e t r i c c a r b o n d i o x i d e i n d i c a t o r : p u r p l e c o l o r i n d i c a t e s l a c k o f c a r b o n d i o x i d e-p r o b a b ly i n t h e e s o p h a g u s . B . E n d - ti d a l c o l o r i m e t r i c c a r b o n d i o x i d e i n d i c a to r s : ye l l ow i n d i c a te s t h e p r e s e n c e o f c a r b o n d i o x i d e a n d t u b e i n t h e a i rway. N o t e t h a t t h e c a r b o n d i o x i d e d e t e c t i o n c a n n o t e n s u r e p r o p e r depth o f t u b e i n s e r ti o n . D i ffe r e n t m a n u fa c t u r e r s m ay u s e d i ff e r e n t c o l o r i n d i c a t o rs .

286

HIGH

presence of a C0 2 tracing using capnography is the standard of care for LMAs used in anesthesia consistent with lung ventilation. Esophageal Detector Devices The esophageal detector device (EDD) consists of a bulb that is compressed and attached to the endotracheal tube (Fig. 1 8-7). If the tube is in the esophagus (positive result for an EDD), the suction created by the EDD will collapse the lumen of the esopha­ gus or pull the esophageal tissue against the tip of the tube and the bulb will not re-expand. The EDD may also consist of a syringe attached to the endotracheal tube; the provider attempts to pull the barrel of the syringe. If the tube is in the esophagus, it will not be possible to pull the barrel (aspirate air) with the syringe. Eight studies of at least fair quality evaluated the accu­ racy of the EDD (self-inflating bulb or syringe), 5 2 •53 •60-65 but many suffer from small numbers and lack of a control group . The EDD was highly sensitive for detection of endo­ tracheal tubes that were misplaced in the esophagus (sensi­ tive for esophageal placement) in five case series.49-53 But in two studies5 2 •53 involving patients in cardiac arrest, the EDD had poor specificity for indicating endotracheal placement of an endotracheal tube. In these studies up to 3 0 % of cor­ rectly placed tubes may have been removed because the EDD suggested esophageal placement. 53 In the operating room, the EDD had poor sensitivity and specificity in 2 0 children < 1 year o f age.66 With these findings i n mind, use of the EDD should be considered as just one of several inde­ pendent methods for confirmation of correct endotracheal tube placement. The EDD may yield misleading results in patients with morbid obesity, late pregnancy, or status asthmaticus, or when there are copious endotracheal secretions,67 because

with these conditions the trachea tends to collapse. There is no evidence that the EDD is accurate for the continued monitoring of endotracheal tube placement.

Confirming Endotracheal Tube Placement When "Confirmation " Results Are Equivocal As a general rule , whenever there is doubt about the results from clinical and device confirmation, the best course of action is to remove the endotracheal tube and provide reoxygenation and venti­ lation with bag and mask. One or two reattempts at intuba­ tion may be appropriate, depending on available resources. The most experienced and highly skilled intubator available should reattempt intubation. If chest movement or breath sounds are asymmetric, particularly if breath sounds are heard over only one lung, consider whether inadvertent intubation of the right or left main bronchus has occurred. Do not wait for a chest radi­ ograph to determine proper tube position or whether intu­ bation of a main bronchus has occurred. Slowly withdraw the endotracheal tube centimeter by centimeter until equal breath sounds are heard bilaterally and chest expansion is symmetric.

Complications of Endotracheal Intubation The most fre­ quent complications of endotracheal intubation68-70 are described below. Trauma Trauma to the lips , mouth, teeth, or oral mucosa can easily occur during intubation. The lips or tongue can be compressed and lacerated between the blade of the laryngoscope and the teeth. The teeth themselves may be chipped. The tip of the tube or stylet may lacerate the pharyngeal or endotracheal mucosa, resulting in bleeding, hematoma, or formation of an abscess. Rupture of the tra­ chea has been reported.7 1 Avulsion of an arytenoid cartilage and injury to the vocal cords is also possible. Other compli­ cations are pharyngeal-esophageal perforation7 2 and intuba­ tion of the pyriform sinus. 73 Vomiting and Aspiration Vomiting can occur and gas­ tric contents may be aspirated into the lower airway. This complication is most likely to occur during emergent intu­ bation of the semiconscious patient who has preserved air­ way protective reflexes (cough and gag). Vomiting and stim­ ulation of a strong cough or gag reflex can also contribute to increased intracranial pressure. Reflex Sympathetic and Parasympathetic Stimulation

F I G U R E 1 8 - 7 • E s o p h a g e a l d e t e c t o r b u l b d evi c e : t h e a s p i r a t i o n te c h n i q u e . T h e t u b e s h o u l d b e h e l d i n p l a c e a n d t h e n s e c u r e d o n c e correct p ositi o n is verifi e d .

Patients who are not in circulatory arrest receive intense stimulation from laryngoscopy and endotracheal intubation. This adverse stimulation can trigger a complex series of sympathetic and parasympathetic reflexes, including release of high levels of catecholamines from the adrenals. Clinically this can lead to increased intracranial pressure, bron­ chospasm, hypertension, hypotension, bradycardias, tachy­ cardias, and other arrhythmias. 1 4 The use of lidocaine, opi­ oids, and atropine at the "premedication step" helps prevent these reactions. These reflexes are much less pronounced in

CHAPTER 1 8

the cardiac arrest patient because the absence of circulation dominates the clinical picture.

Main Bronchus Intubation Insertion of the endotra­ cheal tube into a main bronchus is a relatively common com­ plication. Auscultate the chest to check for bilateral breath sounds and examine it for equal expansion of both sides dur­ ing ventilation. Intubation of a bronchus can result in hypoxemia and atelectasis caused by underinflation of the other lung. Esophageal Intubation Unrecognized insertion of the endotracheal tube into the esophagus will result in ineffective ventilation and oxygenation. If this situation remains uncor­ rected for more than a few minutes, the result can be fatal. 74 Preventing Complications of Endotracheal Intubation To minimize complications of endotracheal intubation, follow these recommendations : •

•

•

•

Only properly trained personnel should perform endotra­ cheal intubation. This is the key to preventing complica­ tions. Try to limit intubation attempts to approximately 2 0 to 3 0 seconds per attempt. When the time limit i s reached o r if clinical deterioration occurs (e.g., significant bradycardia, hypoxia, or deterioration in color), provide bag-mask ven­ tilation with 1 00 % oxygen until the clinical appearance improves. Typically another attempt can be made approx­ imately 30 to 60 seconds later. If the provider has proper training, experience, and sup­ port and the patient is responsive with spontaneous ven­ tilation, consider use of the RSI sequence (with premed­ ication, sedation, and paralysis). Use endotracheal tubes with a high-volume, low-pressure cuff, which can be used for prolonged intubation after resuscitation. Measure intracuff pressure and adjust it to 2 5 to 3 5 em H2 0. The minimum intracuff pressure to prevent aspiration in adults appears to be 2 5 em H2 0/5 and the pressure that produces a decrease in mucosal cap­ illary blood flow (ischemia) in adults is >40 em H2 0.76

If Step 6 (First Intubation Attempt) Is Unsuccessful, Resume Bag-Mask Ventilation See Figure 1 8- 8 . Numbered boxes below refer to this figure.

"Successful" Bag-Mask Ventilation If the first endotra­ cheal intubation attempt does not succeed, immediately resume bag-mask ventilation (B ox 3 ) . If bag-mask ventila­ tion is "successful , " with return and maintenance of oxy­ gen saturation at a level 2:: 9 0 % (or good color for the patient with cardiac arrest), then proceed to clinical and device confirmation (Box 2 ) . "Unsuccessful" Bag-Mask Ventilation I f bag-mask ven­ tilation cannot achieve and maintain an oxygen saturation level 2:: 90% (or good color for the patient with cardiac arrest), attempt endotracheal intubation once more. But review the

•

M A N A G E M E N T O F T H E D I F F I C U LT A I RWAY

287

level of relaxation and flaccidity in the patient's neck and jaw muscles during the first intubation attempt (Box 4) before making the next attempt. This will determine whether the patient should be paralyzed before the next intubation attempt. If the second attempt is m1successful, the clinical sit­ uation has now become the dreaded "unable to oxygenate­ unable to ventilate" scenario (Box 7). 14 In many settings this is the major indication for initiating a surgical airway proto­ col (e.g., cricothyrotomy; see "Cricothyrotomy, " below). In other settings, most often in the prehospital setting or emergency department, this scenario represents the major indication for use of a temporizing airway adjunct, such as the Combitube or LMA (Box 8). The value of these two newly recommended devices (see "Alternative Advanced Airways") derives from the requirement for blind insertion only. The provider does not face the challenge of direct visu­ alization of the vocal cords.

Evaluate Relaxation/Flaccidity The intubator actually gathers this information during the first endotracheal intu­ bation attempt. It is only upon failure to intubate that the rescuer can determine if there was complete skeletal muscle relaxation. If j aw and neck muscle flaccidity was nearly absolute, then endotracheal intubation can be attempted again. If there was any resistance to intubation, paralysis is indicated (Box 6). Pamlyze the Patient When you administer succinyl­ choline 1 . 5 mg/kg rv; you should immediately resume the most effective bag-mask ventilations possible with 1 00 % oxygen. In many in-hospital settings, the person who per­ forms emergency intubations has already drawn up a syringe containing 1 00 mg of succinylcholine, an appropriate dose for a patient weighing 6 5 to 70 kg. This will ensure complete paralysis of the patient for intubation. A. If the patient is in cardiac arrest, give one dose (for a patient in cardiac arrest sedation is not necessary). B. Mter 3 0 to 40 seconds, check the jaw and neck muscles for flaccidity. C. If flaccid, attempt endotracheal intubation again. Step 7: Postintubation Management-Prevent Endotracheal Tube Dislodgment The endotracheal tube may be displaced if the tube is not secured, particularly in pre-hospital settings or during any transport of the patient. Maintenance of proper tube position requires fre­ quent assessment, not only immediately after intubation, but whenever the patient is moved. The endotracheal tube is secured with tape or a com­ mercial endotracheal tube holder (Fig. 1 8-9). It is acceptable to use locally derived, ad hoc tape-and-tie systems if they are supported by formal teaching and demonstrations or proto­ cols. The tube may still be displaced or dislodged, regardless of how it is secured, particularly during patient transfer. Continuous monitoring of end-tidal C0 2 and oxygen

288

HIGH

Placement of Endotracheal Tube (1 st Attempt) Successful? YES

2

NO

3

y Proceed to

Resume

• - C l i n ical confirmation

bag mask venti lation

• - Device confirmatio n

Maintains 02 S a t >90%?

If confirmation ind icates

NO

YES

unsuccessful attem pt, remove tube and resu m e bag-mask ventilation (see box to the rig ht)

7 "Cannot tube; cannot bag"

(patient needs LMA, combi­ tube, or surgical ai rway) Are these options ava i l a b l e ?

NO

8

4

• Reattempt endotracheal

State of muscle relaxation at 1 st endotracheal Intubation attem pt C o m p l ete relaxat i o n ? Review:

i ntubation •

If unsuccessfu l , then attempt LMA, combitube, or surg ical airway

NO

YES

6

Reattempt endotracheal i ntubation (up to 2 more attempts)

Pa ra lyze

Succi nylcholine 1 .5 mg/kg • E nsure effective oxygenation • Wait 30-40 sec • Check paralysis • Reattempt tracheal i ntubation

F I G U R E 1 8 - 8 • A c t i o n s for p r ovi d e r i f first a t t e m p t e d i n t u b a t i o n i s u n s u c c e ssfu l (s e e text for fu l l e x p l a n a t i o n ) . M aj o r a c t i o n s a r e t ry to p l a c e t u b e with f i r st o r a l i n t u b a t i o n a tte m p t , r e s u m e b a g - m a s k v e n t i l a t i o n s , r evi ew r e l a x a t i o n / f l a c c i d i ty, a n d p a r a lyz e t h e p a t i e n t .

saturation is recommended. I n the prehospital setting, immobilization of the cervical spine with a collar, backboard, or both can serve as an additional precaution, although the use and effect of these immobilizers on tube placement has not been reported.

Checklists for Endotracheal Intubation Checklists provide means to improve the performance of complex, psychomotor skills that are difficult to learn and remember. A variety of helpful checklists have been devel­ oped for advanced airway management, 77-79 particularly

CHAPTER 1 8

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289

endotracheal intubation. 79-84 The purpose of these checklists is to have all equipment and personnel in place and in work­ ing order before every intubation attempt. One of many pos­ sible Preparation-Action Checklists that lists actions, intu­ bation team members, and designated duties as shown here. This checklist for resuscitation personnel reviews areas and topics to be considered. Different settings, personnel, and resources will require different preparation-action check­ lists. Some items on this sample checklist must be completed before an actual clinical event occurs. Others are performed urgently, just before an endotracheal intubation attempt in cardiac arrest. F I G U R E 1 8 - 9 • A c t i o n s for resc u e r if first atte m p ted i n t u b a t i o n is u n s u c c essfu l (se e text for f u l l e x p l a n a t i o n ) . M aj o r a c t i o n s a r e try to p l a c e t u b e with first o r a l i n t u b a t i o n atte m p t , resu m e b a g - m a s k ve n ti l a ti o n s , r evi ew r e l a x a t i o n/fl a c c i d i ty, a n d p a r a lyz e t h e p a t i e n t .

Pre-Event Equipment Checklist for Endotracheal Intubation: Equipment and Drugs Recommended for Endotracheal Intubation Yes?

No?

D

D

Cardiac monitor

D

D

Automatic blood pressure cuff

D

D

Intravenous infusion equipment

D

D

Oxygen supply, equipment for connections to airway adjunct device

D

D

Esophageal detector device (aspiration technique)

D

D

Exhaled C0 2 detector device: capnometry (qualitative) or Exhaled C0 2 measuring device: capnography (continuous, quantitative)

Equipment

D

D

Pulse oximeters

D

D

Suction device and suction catheter (confirm working; catheter near patient head)

D

D

Bag-mask connected to high-flow oxygen source

D

D

Endotracheal tubes, proper size (all sizes should be available for emergent use; typically the size above and below anticipated size for the patient should be within reach during the attempt)

D

D

Endotracheal tube stylet

D

D

Laryngoscope blade (curved and straight available)

D

D

Laryngoscope handle with working light

D

D

Backup light source (another laryngoscope handle and blade)

D

D

5 - to 1 0-mL syringe to test-inflate endotracheal tube balloon (attached to pilot balloon)

D

D

Premedication agents: lidocaine, opioids (such as fentanyl), atropine, and defasciculating agents

D

D

Analgesic agents: opioids

D

D

Sedative/anesthetic agents: etomidate, propofol, methohexital, thiopental, midazolam, ketamine

D

D

Paralytic agents: succinylcholine, vancuronium, pancuronium

D

D

Commercial endotracheal tube holder if used instead of tape

D

D

Restraints for patient's hands if awake

D

D

Container for patient's dentures if needed

D

D

Towel or pad to place under patient's neck (to elevate neck 1 0 em)

Modify where appropriate. Modifications will depend on specific settings (e.g. , critical care unit versus paramedic-staffed ambulance). For intubation during cardiac arrest, adjunctive and analgesic agents are typically omitted. Paralytic agents, most often succinylcholine, may be the only medications used. This checklist can serve as a pre-event checklist for endotracheal intubation during cardiac arrest. In practice, similar checklists must be incorporated into the daily/every shift supply check or stocking rounds standard in emergency departments, critical care units and EMS .

290

HIGH

Sample Checklist for Personnel Preparation and Responsibilities During Endotracheal Intubation This sample checklist includes actions, intubation team members, and designated duties for intubation of the unresponsive patient with no spontaneous respirations and no spontaneous circulation. Some items on this checklist must be completed before an actual clinical event. Other actions are performed urgently, just before attempting endotracheal intubation in a cardiac arrest. The checklist concept provides a quality-improvement/assurance tool with the purpose of having all equip­ ment and personnel in place and in working order before every intubation attempt. Yes?

No?

D

D

-

D

D

Equipment

Assistant to intubator. At start of shift (before time of arrest), designate and identify an assistant to the intubator. These duties are assumed by intubator if no assistant is available. These duties include responsibility for equipment and devices, including the following: • Attach cardiac monitor; maintain continuous surveillance of rhythm before, during, and after intubation; announce any rhythm change • Attach and maintain automatic blood pressure device • Attach and maintain 0 saturation device; survey readings; announce drops in readings, 0 saturation; 2 2 state response to changes in Fi0 2 or in response to intubation attempt • Assess for signs of decompensation • Track periods without ventilation; announce any > 3 0 seconds in duration • Remove patient's dentures as needed before intubation attempt • Apply cricoid pressure when bag-mask ventilation begins; maintain throughout laryngoscopy and insertion of endotracheal tube until cuff inflated and primary and secondary confirmations completed • Perform or assist with clinical confirmation of tube placement (five-point auscultation, chest rise and fall, tube condensation) • Perform or assist with device confirmation of tube placement (colorimetric exhaled C0 2 device, esophageal detector device, quantitative exhaled C0 2 device) • For in-hospital intubation: call radiology for postintubation radiograph of chest after confirmation of tube placement

-

IV accessor/medications. At start of shift, designate person responsible for N access and administration of drugs; review her or his duties: Establish peripheral vein access • Verify ready availability of drugs most likely to be needed, administer agents when ordered (drugs used will vary by clinical setting and protocols) • Premedications: lidocaine, opioids-such as fentanyl, atropine •

• •

Defasciculating/paralytic agents: succinylcholine, vecuronium, rocuronium, etc. Sedative/hypnotic/anesthetic agents : fentanyl, etomidate, propofol, methohexital, thiopental, ketamine,

midazolam, diazepam D

D

Oxygen: locate oxygen source; make sure connecting tubing is in place; attach to bag mask (start at 1 5 L/rnin)

D

D

Endotracheal tube: select size (7 mm for average-size woman; 8 mm for average-size man); check volume

D

D

Laryngoscope: select blade (straight or curved); check that light is ON; confirm availability of backup light

D

D

Oral suction: confirm that wall suction source or battery-powered portable unit is available and in working order and that connecting tube is in place. Use Yankauer-type suction tip. • Start suction, place suction tip near patient's head (in hospital: under pillow)

D

D

Final steps before picking up laryngoscope and endotracheal tube:

of inflatable cuff; using syringe, inject that volume into balloon; check for leaks, deflate; leave syringe attached • Insert stylet into endotracheal tube (if needed) • Check that additional endotracheal tubes are available source

I.

2. 3. 4. 5. 6. 7.

Place a towel under patient's head to elevate it 1 0 em Check head positioning: neck is slightly flexed, head extended Review latest vital signs Identify rhythm on monitor Obtain oxygen saturation reading Ask if intubator assistant and IV accessor/medications are ready to start intubation Announce "I am ready to begin intubation "

CHAPTER 1 8

S urgical Airways

Cricothyrotomy Description

The term "cricothyrotomy" refers to the procedure of creat­ ing an opening in the cricothyroid membrane so that an air­ way tube can be inserted directly into the trachea (Fig. 1 8- 1 0). There are two acceptable techniques for the ACLS provider: • Percutaneous dilational cricothyrotomy. This is the preferred technique , using one of the prepackaged commercial cricothyrotomy kits to gain access to the trachea via a modified Seldinger technique. After a suitably sized open­ ing is produced with an introducer, guidewire, and dilator, a commercially produced cricothyrotomy tube is advanced over the guidewire.85 • Surgical cricothyrotomy. This technique makes use of a scalpel incision with ad hoc dilation of the opening by rotation of the scalpel handle and insertion of a pediatric­ sized endotracheal tube (without an inflatable cuff) or a cuffed tracheostomy tube. This technique is acceptable if a cricothyrotomy kit is unavailable. Use of the scalpel sur­ gical technique is discouraged, especially in emergency settings, where cricothyrotomies are rarely if ever per­ formed. 8 5-89 The ventilation through small-diameter tubes allows emergency oxygen administration but severely limits ventilation (C0 2 elimination). S afe performance of a cricothyrotomy requires spe­ cialized training. It should be performed by only highly

•

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skilled medical providers who encounter complete upper airway obstruction that is unresponsive to standard inter­ ventions .

Indications An invasive procedure, cricothyrotomy is indicated only when airway control is impossible by other available meth­ ods. These "difficult airway" situations are caused by upper airway obstruction by trauma, allergic reactions with swelling and angioedema, foreign bodies, anatomic varia­ tions, and bleeding.

Insertion Technique : Simple Cricothyrotomy • •

•

•

• • •

•

•

Position the patient supine with the neck extended and the larynx as anterior as possible. Palpate the prominent thyroid cartilage (Adam's apple) and locate the cricothyroid membrane with your gloved fingernail as the transverse indentation below the thyroid cartilage and above the cricoid cartilage. Clean the area with antiseptic solution. With the commercial cricothyrotomy kits, the general approach is to make a small horizontal opening in the cricothyroid membrane witl1 a scalpel. This allows easy insertion of the larger introducer needle, through which a Seldinger-like guidewire is introduced. The introducer needle is replaced by a dilator to enlarge the opening. Next, the kit's cricothyrotomy tube is inserted into the opening over the guidewire. The surgical technique requires a larger scalpel incision through the skin, through the cricothyroid membrane, and into the trachea. After enlarging the opening by rotation of the scalpel handle, insert the largest pediatric-sized endotracheal tube or tracheostomy tube that will fit through this opening. Attach a bag-mask device connected to the highest avail­ able oxygen concentration and begin ventilation.

Complications Possible complications are hemorrhage, false passage of the tube, perforation of the esophagus, and subcutaneous or mediastinal emphysema.

Tracheostomy Tracheostomy is familiar to most emergency health care providers but is rarely a procedure that even experienced ACLS providers should ever expect to perform.

Description

F I G U R E 1 8 - 1 0 • N e c k with c r i c o i d m e m b r a n e d i s p l aye d , with a n a r row i n d i c a t i n g l o c a t i o n f o r a n e m e r g e n cy c r i c o thyr o t o my.

The term "tracheostomy" refers to the procedure of surgi­ cally creating an opening through the cartilage rings of the trachea. This procedure is considerably more involved and complicated than a cricothyrotomy, which requires only a simple incision through the cricothyroid membrane.

292

HIGH

Indications and Prevention of Complications •

• • •

A patient becomes a candidate for a tracheostomy only after the airway is first secured with one of the following: an endotracheal tube inserted through a cricothyrotomy, an endotracheal tube inserted through the mouth and hypopharynx, or a translaryngeal catheter. A tracheostomy is a follow-up or secondary procedure. A tracheostomy is not appropriate for urgent situations such as airway obstruction or cardiac arrest. Surgical opening of the trachea and insertion of a tra­ cheostomy tube should be performed only under con­ trolled conditions in the operating room or emergency department by a health care professional skilled in the procedure.

References l. Pepe PE, Co pass MK, Joyce TH. Prehospital endotracheal intuba­

tion: rationale for training emergency medical personnel. Ann

Eme1'g Med 1 9 8 5 ; 14(1 1): 1 085-1 092 . 2 . Bowman FP, Menegazzi JJ, Check BD, et al. Lower esophageal sphincter pressure during prolonged cardiac arrest and resuscita­ tion. Ann Eme1'g Med 1 995;2 6(2):2 1 6-2 1 9 . 3 . Weiler N, Heinrichs W, Dick W. Assessment of pulmonary mechanics and gastric inflation pressure during mask ventilation. Prehosp Disaste7' Med 1 995 ; 1 0(2) : 1 0 1 - 1 0 5 . 4. Ruben H, Knudsen EJ, Carugati G. Gastric inflation i n relation to airway pressure. Acta Anaesth Scand 1 9 6 1 ; 5 : 1 07-1 14. 5 . Wenzel V, Idris AH, Banner MJ, et al. Respiratory system compli­ ance decreases after cardiopulmonary resuscitation and stomach inflation: impact of large and small tidal volumes on calculated peak airway pressure. Resuscitation 1 998;3 8(2) : 1 1 3-1 1 8 . 6 . Stept VV], Safar P. Rapid induction-intubation for prevention of gastric-content aspiration. Anesth Analg 1 9 70;49(4):63 3-6 3 6 . 7 . Wang HE, Sweeney TA, O'Connor RE, e t a l . Failed prehospital intubations: an analysis of emergency department courses and out­ comes. P1·ehosp Emerg Care 2 00 1 ; 5(2): 1 3 4- 1 4 1 . 8. Wang HE, O'Connor RE, Megargel RE, et al. The utilization of midazolam as a pharmacologic adjunct to endotracheal intubation by paramedics. Pnhosp Enm·g Can 2 000;4(1 ) : 1 4- 1 8 . 9. Wayne MA, Slovis CM, Pirrallo RG. Management o f difficult air­ ways in the field. Prehosp Emerg Care 1 999; 3 (4):2 90-2 96. 1 0 . Brownstein D, Shugerman R, Cummings P, et al. Prehospital endo­ tracheal intubation of children by paramedics. Ann Enze1•g Med 1 996;2 8 ( 1 ) : 3 4-3 9. 1 1 . Ma OJ, Atchley RB, Hatley T, et al. Intubation success rates improve for an air medical program after implementing the use of neuromuscular blocking agents . Am J Emerg Med 1 998; 1 6(2 ) : 1 2 5- 1 2 7 . 1 2 . Kociszewski C, Thomas S H , Harrison T, e t al. Etomidate versus succinylcholine for intubation in an air medical setting. Am J Eme1•g Med 2 000; 1 8(7) : 7 5 7-76 3 . 1 3 . Syverud SA, Borron S W, Storer D L , e t al. Prehospital use o f neu­ romuscular blocking agents in a helicopter ambulance program. Ann Emag Med 1 9 8 8 ; 1 7(3):2 3 6-242 . 14. Walls R. The emergency airway algorithms. In: Walls RN Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management. Philadelphia: Lippincott Williams & Wilkins, 2000. 15. Pace SA, Fuller FP. Out-of-hospital succinylcholine-assisted endotra­ cheal intubation by paramedics. Ann Emerg Med 2 000; 3 5 (6):5 68-5 7 2 . 1 6 . O'Connor RE, Swor RA . Verification o f endotracheal tube place­ ment following intubation. National Association of EMS Physicians Standards and Clinical Practice Committee. Prehosp Emerg Care 1 999; 3 (3):248-2 5 0 . 1 7 . Wang H E , O ' Connor RE, Domeier RM . Prehospital rapid­ sequence intubation. Prehosp Eme1•g Cm'e 2 00 1 ; 5 ( 1):40--48 . 1 8 . Walls RN Luten RC, Murphy MF, et al, eds. Manual ofEme1'gency Ainvay Management. Philadelphia: Lippincott Williams & Wilkins, 2000. ,

,

19. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/An1erican Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2 002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Eievation Myocardial Infarction): developed in col­ laboration with the An1erican College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society ofThoracic Surgeons: endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. Ci1,culation 2 007; 1 1 6(7):e1 48-e3 04. 2 0 . McGowan P, Skinner A. Preoxygenation-the importance of a good face mask seal. Br J Anaesth 1 99 5 ; 7 5 (6): 7 7 7-77 8 . 2 1 . Berthoud M , Read D H , Norman ]. Pre-oxygenation: how long' Anaesthesia 1 9 8 3 ; 3 8(2):96- 1 0 2 . 2 2 . Mejicano G C , Maki DG. Infections acquired during cardiopul­ monary resuscitation: estimating the risk and defining strategies for prevention. Ann Intem Med 1 998; 1 2 9( 1 0) : 8 1 3-82 8 . 2 3 . Axelsson A, Thoren A, Holmberg S, e t al. Attitudes o f trained Swedish lay rescuers toward CPR perfom1ance in an emergency: a survey of 1 0 1 2 recently trained CPR rescuers. Remscitation 2 000;44(1):27-3 6. 24. Melanson SW, O'Gara K. EMS provider reluctance to perform mouth-to-mouth resuscitation. Pnhosp Eme1'g Care 2000;4(1):48-52 . 2 5 . Nocera A . A flexible solution for emergency intubation difficulties. Ann Emerg Med 1 996;2 7 (5):665-667 . 2 6 . Kidd J F, Dyson A , Latta I P. Successful difficult intubation. Use of the gum elastic bougie. Anaesthesia 1 988;43 (6) :4 3 7--4 3 8 . 2 7 . Dogra S , Falconer R , Latto I P. Successful difficult intubation. Tracheal tube placement over a gum-elastic bougie. Anaesthesia 1 990;45(9): 7 74-776. 2 8 . Nolan JP, Wilson ME. An evaluation of the gum elastic bougie. Intubation times and incidence of sore throat. Anaesthesia 1 992 ;4 7 (1 0): 878-8 8 1 . 2 9 . Nolan JP, Wilson ME. Orotracheal intubation i n patients with potential cervical spine injuries. An indication for the gum elastic bougie. Anaesthesia 1 993 ;48(7) : 6 3 0-63 3 . 3 0 . Viswanathan S , Campbell C , Wood DG, e t al. The Eschmann Tracheal Tube Introducer. (Gum elastic bougie). Anesthesiol Rev 1 992 ; 1 9(6): 2 9-34. 3 1 . Hopkins PM. Use of suxamethonium in children. Br J Anaesth 1 99 5 ; 7 5 (6):675-67 7 . 3 2 . Morell R C , Berman JM, Royster RI, e t al. Revised label regarding use of succinylcholine in children and adolescents. Anesthesiology 1 994; 80(1):242-245. 3 3 . Scheiber G, Ribeiro FC, Marichal A, et al. Intubating conditions and onset of action after rocuronium, vecuronium, and atracurium in young children. Anesth Analg 1 996;8 3 (2) : 3 2 0-3 24. 34. McDonald PF, Sainsbury DA, Laing RJ. Evaluation of the onset time and intubation conditions of rocuronium bromide in children. Anaesth lntens Care 1 997;25(3):260-2 6 1 . 3 5 . Fuchs-Buder T, Tassonyi E . Intubating conditions and time course of rocuronium-induced neuromuscular block in children. Br J Anaesth 1 996;77(3): 3 3 5-3 3 8 . 3 6 . Maddineni VR , McCoy EP, Mirakur RK, e t al. Onset and duration of action and hemodynamic effects of rocuronium bromide under bal­ anced and volatile anesthesia. Acta Anaesthesiol Belg 1 994;45(2):41--47. 37. Khueni-Brady KS, Pomaroli A, Puhringer F, et al. The use of rocuronium (ORG 942 6) in patients with chronic renal failure. Anaesthesia 1 993 ;48(1 0): 8 7 3-87 5. 3 8 . Magarian T, Wood P, Caldwell ], et al. The pharmacokinetics and neuromuscular effects of rocuronium bromide in patients with liver disease. Anesth Analg 1 99 5 ;80(4) : 7 5 4-7 59. 3 9 . Khalil M, D'Honneur G, Duvaldestin P, et al. Pharmacokinetics and pharmacodynamics of rocuronium in patients with cirrhosis. Anestbesiology 1 994; 80(6): 1 2 4 1 - 1 247. 40. Ferres CJ, Crean PM, Mirakhur RK. An evaluation of Org NC 45 (vecuronium) in paediatric anaesthesia. Anaesthesia 1 9 8 3 ; 3 8 ( 1 0) : 943-947. 4 1 . Mirakhur RK, Ferres CJ, Clarke RS, et al. Clinical evaluation of Org NC 45. 81' J Anaestb 1 9 8 3 ; 5 5(2): 1 1 9-1 24. 42 . Lynam DP, Cronnelly R, Castagnoli KP, et al. The pharmacody­ namics and pharmacokinetics of vecuronium in patients anes­ thetized with isoflurane with normal renal function or with renal failure. Anesthesiology 1 988;69(2 ) : 2 2 7-2 3 1 .

CHAPTER 1 8

43 . Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1 96 1 ;2 :404-406. 44. Li ]. Capnography alone is imperfect for endotracheal tube place­ ment confirmation during emergency intubation. J Eme1'g Med 2 00 1 ;20(3):22 3-2 2 9 . 45. Grmec S . Comparison o f three different methods t o confirm tra­ cheal tube placement in emergency intubation. Intens Ca-re Med 2 002 ;2 8( 6): 70 1-704. 46. Ornata JP, Shipley JB, Racht EM, et al. Multicenter study of a portable, hand-size, colorimetric end-tidal carbon dioxide detec­ tion device. Ann Eme1'g Med 1 992;2 1 (5): 5 1 8-52 3 . 4 7 . Anton WR , Gordon RW, Jordan TM, e t a!. A disposable end-tidal C02 detector to verify endou·acheal intubation. Ann Eme1'g Med 1 9 9 1 ;2 0(3):2 7 1-2 7 5 . 4 8 . Bhende M S , Thompson AE. Evaluation of a n end-tidal C02 detector during pediatric cardiopulmonary resuscitation. Pediat1'ics 1 995;95(3):3 95-3 99. 49. Bhende MS, Thompson AE, Cook DR, et al. Validity of a dispos­ able end-tidal C02 detector in verifying endotracheal tube place­ ment in infants and children. Ann Eme1'g Med 1 992;2 1 (2): 1 42-145. 50. Hayden SR, SciammarellaJ, Viccellio P, et a!. Colorimetric end-tidal C02 detector for verification of endotracheal tube placement in out­ of-hospital cardiac arrest. Acad Eme1'g Med 1 995;2(6):499-502 . 5 1 . MacLeod BA, Heller MB, Gerard J, et al. Verification of endotra­ cheal tube placement with colorimetric end-tidal C02 detection. Ann Enze-rg Med 1 9 9 1 ;20(3):2 67-2 70. 5 2 . Takeda T, Tanigawa K, Tanaka H, et a!. The assessment of three methods to verify tracheal tube placement in the emergency set­ ting. Resuscitation 2 003 ; 5 6(2) : 1 5 3-1 5 7 . 5 3 . Tanigawa K , Takeda T, Goto E , e t al. The efficacy o f esophageal detector devices in verifying tracheal tube placement: a randomized cross-over study of out-of-hospital cardiac arrest patients. Anesth Analg 2 0 0 1 ;92(2):3 75-3 7 8 . 5 4 . Varon AJ, Morrina J, Civetta JM. Clinical utility o f a colorimetric end-tidal C02 detector in cardiopulmonary resuscitation and emergency intubation. J Clin Monit 1 99 1 ; 7(4):2 89-2 9 3 . 5 5 . Sum Ping ST, Mehta MP, Symreng T. Accuracy o f the FEF C02 detector in the assessment of endotracheal tube placement. Anesth Analg 1 992 ; 74(3 ) :4 1 5-4 1 9. 56. CantineauJP, Lambert Y, Merckx P, et al. End-tidal carbon dioxide dur­ ing cardiopulmonary resU5citation in humans presenting mostly with asystole: a predictor of outcome. Orit Ca-re Med 1 996;24(5):79 1-796. 5 7 . Ward KR, Yealy DM. End-tidal carbon dioxide monitoring in emergency medicine. Part 2: clinical applications. Acad Ente1'g Med 1 998;5(6) :63 7-646. 5 8 . Hand IL, Shepard EK, Krauss AN, et a!. Discrepancies between transcutaneous and end-tidal carbon dioxide monitoring in the critically ill neonate witl1 respiratory distress syndrome. Crit Cm'e

Med 1 989; 1 7(6) : 5 5 6-559. 59. Tobias JD, Meyer DJ. Noninvasive monitoring of carbon dioxide during respiratory failure in toddlers and infants: end-tidal versus transcutaneous carbon dioxide. Anesth Analg 1 99 7 ; 8 5 ( 1 ) : 5 5-5 8 . 6 0 . Pelucio M, Halligan L, Dhindsa H. Out-of-hospital experience with the syringe esophageal detector device. Acad Erne-rg Med 1 997 ;4(6) : 5 63-5 6 8 . 6 1 . Bozeman WP, Hexter D , Liang HK, Kelen GD . Esophageal detec­ tor device versus detection of end-tidal carbon dioxide level in emergency intubation. Ann Ernerg Med 1 996;2 7 (5) : 5 9 5-599. 62 . Sharieff GQ, Rodarte A, Wilton N, et al. The self-inflating bulb as an esophageal detector device in children weighing more than twenty kilograms: A comparison of two techniques. Ann Ente1'g Med 2 003 ;41 (5):623-629. 63. Wee MY, Walker AK. The oesophageal detector device: an assessment with uncuffed tubes in children. Anaesthesia 1991 ;46(1 0):869-87 1 . 64. Williams KN , Nunn J F The oesophageal detector device: a prospective trial on 1 00 patients. Anaesthesirt 1 989;44(5):41 2-424.

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65. Zaleski L, Abello D, Gold MI. The esophageal detector device. Does it work? Anesthesiology 1 99 3 ; 7 9(2):244-247. 66. Haynes SR, Morton NS. Use of the oesophageal detector device in children under one year of age. Anaesthesia 1 990;45 ( 1 2) : 1 067-1 069. 67. Baraka A, Khoury PJ, Siddik SS, et al. Efficacy of the self-inflating bulb in differentiating esophageal from tracheal intubation in the parturi­ ent undergoing cesarean section. Anesth Analg 1 997;84(3):533-5 3 7 . 68. Blanc VF, Tremblay NA. The complications o f tracheal intubation: a new classification with a review of the literature. Anesth Analg 1 974; 5 3 (2):2 02-2 1 3 . 69. Jones GO, Hale DE, Wasmuth CE, et al. A survey o f acute com­ plications associated with endotracheal intubation. Cleve Clin Q 1 96 8 ; 3 5 (1):2 3-3 1 . 70. Taryle DA, Chandler JE, Good JTJ, et a!. Emergency room intu­ bations: complications and survival. Chest 1 979;75(5):54 1-543 . 7 1 . Thompson DS, Read RC. Rupture of the trachea following endo­ tracheal intubation. JAMA 1 968;204( 1 1):995-997. 7 2 . Wolff AP, Kuhn FA, Ogura JH. Pharyngeal-esophageal perfora­ tions associated with rapid oral endotracheal intubation. Ann Otol

Rhino/ Lmynga/ 1 9 72 ; 8 1 (2):2 5 8-2 6 1 . 7 3 . Stauffer JL, Petty TL. Accidental intubation o f the pyrifom1 sinus: a complication of "roadside" resuscitation. JAMA 1 977;2 3 7 (2 1 ): 2 3 24-2 3 2 5 . 74. Pollard BJ, Junius F Accidental intubation o f the oesophagus. Anaesth Intens Care 1 980;8(2) : 1 83-1 86. 75. Bernhard WN, Cottrell JE, Sivakumaran C, et al. Adjusunent of intracuff pressure to prevent aspiration. Anesthesiology 1 979;50(4): 3 63-366. 76. Nordin U. The trachea and cuff-induced tracheal injury. An exper­ imental study on causative factors and prevention. Acta Otolmyngol

Supp/ 1 977;345 : 1-7 1 . 77. Cheney FW, Posner KL , Caplan RA. Adverse respiratory events infrequently leading to malpractice suits. A closed claims analysis.

Anesthesiology 1 99 1 ; 7 5 (6):93 2-9 3 9 . 7 8 . Cheney F W, Posner K , Caplan RA , e t a ! . Standard o f care and anesthesia liability. JAMA 1 989;2 6 1 ( 1 1 ) : 1 5 99-1 603 . 79. Caplan RA, Posner KL, Ward RJ, et a!. Adverse respiratory events in anesthesia: a closed claims analysis. Anesthesiology 1 990; 7 2 (5): 82 8-8 3 3 . 80. Cooper JB, Newbower RS, Kitz RJ. An analysis o f major errors and equipment failures in anesthesia management: considerations for prevention and detection. Anesthesiology 1 984;60( 1 ) : 3 4-42 . 8 1 . Cooper ]B, Newbower RS, Long CD, et al. Preventable anesthesia mishaps: a study of human factors . Anesthesiology 1 9 7 8 ;49(6) : 3 99-406. 82 . Cooper JB, Cullen DJ, Nemeskal R, et a!. Effects of information feedback and pulse oximetry on the incidence of anesthesia com­ plications. Anesthesiology 1 9 8 7;67(5):686-694. 8 3 . Cooper JB. Accidents and mishaps in anesthesia: how they occur; how to prevent them. Minerva Anestesio/ 2001 ;67(4) : 3 1 0-3 1 3 . 84. Cooper ]B. Towards patient safety in anaesthesia. Ann Acad Med Singapore 1 994;2 3 (4) : 5 52-5 5 7 . 8 5 . Florete O G . Airway management. I n Civetta JM, Taylor RW, Kirby RR, eds. O'itical Care, 2nd ed. Philadelphia: Lippincott, 1 992 : 1 43 0-143 1 . 86. Brantigan CO, Grow JBS. Cricothyroidotomy: elective use in res­ piratory problems requiring tracheotomy. J Thome Cardiovasc Su1'g 1 976;7 1 ( 1 ) : 72-8 1 . 87. McGill ], Clinton JE, Ruiz E . Cricothyrotomy in the emergency department. Ann Emerg Med 1 9 82 ; 1 1 (7): 3 6 1 -3 64. 88. Simon RR, Brenner BE, Rosen MA . Emergency cricothyroido­ tomy in the patient with massive neck swelling. Part 2: Clinical aspects. O'it Cm'e Med 1 9 8 3 ; 1 1 (2): 1 1 9-1 2 3 . 89. Simon RR, Brenner BE. Emergency cricothyroidotomy i n the patient with massive neck swelling: Part 1 : Anatomical aspects. O'it Care Med 1 9 8 3 ; 1 1 (2): 1 1 4-1 1 8 .

Arrhythmias

Peter ] . Kudenchuk If a patient is pulseless or in shock , a wide-complex tachycardia is best presumed to be ventricular tachycardia (VT) until proved otherwise . In a study of patients who presented with a wide-QRS­ complex tachycardia, if they said yes to two questions ( "Have you ever had a heart attack in the past? " and "Did [these kind of symptoms] start after your heart attack? " ) VT was the culprit arrhythmia in nearly all (28 of 29) cases . Evaluation and assessment of patients with life-threatening arrhythmias • Diagnostic clues in the 1 2 -lead electrocardiogram • • •

Triggers for actions and interventions Knowing when to call expert consultation for complicated rhythm interpretation or pharmacologic or management decisions

Basic Principles Cardiac arrhythmias present with a wide variety of symptoms, including palpitations, chest discomfort, dyspnea, dizziness, confusion, syncope, as well as unheralded collapse (cardiac arrest). These symptoms may be intermittent when caused by self-terminating (paroxys­ mal) arrhythmias and can range in severity from bothersome but not necessarily life-threat­ ening to catastrophic, requiring immediate intervention. The initial assessment of an arrhythmia should focus on the patient, her or his clinical status, and whether there is time to establish a rhythm diagnosis before treatment or before moving to immediate lifesaving measures-cardiopulmonary resuscitation (CPR) and electrical cardioversion or defibrilla­ tion-in the case of someone who is unconscious, markedly hypotensive, or pulseless. In presentations with a wide complex tachycardia (WCT), the hemodynamic stability (or instability) of the patient is singularly unhelpful in discriminating whether it represents a supraventricular or a ventricular tachycardia. 1 Typically heart rate, not the supraventric­ ular or ventricular etiology of the arrhythmia, is the single most important determinant of 295

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symptoms and their severity. From a hemodynamic stand­ point, arrhythmias are also generally better tolerated among patients with better underlying heart function than in those whose ventricular function is significantly impaired.

History A brief history focused on whether the patient has heart dis­ ease can be revealing. Ventricular arrhythmias predominate in patients with known structural heart disease as well in as older adults with other risk factors for heart disease. Supraventricular arrhythmias tend to be more common in younger, healthier patients and in those in whom arrhyth­ mias may have preceded their development of heart disease. In a study of conscious patients who presented with a wide­ QRS-complex tachycardia, an affirmative answer to two questions addressing these issues ("Have you ever had a heart attack in the past? " and "Did [tl1ese kind of symptoms] start after your heart attack? ") correctly identified VT as the culprit arrhythmia in nearly all (2 8 of 2 9) cases . 1 Comparison of a prior ECG (if available) with an ECG of the current arrhythmia can also be quite helpful.

infarction (AMI) or severe ischemia. Because the greatest risk for serious arrhythmias exists during the first hour after onset of symptoms of infarction or ischemia, health care profes­ sionals should start cardiac monitoring as soon as possible. All ECG and rhythm information should be interpreted in context of other available information about the patient, including ventilation, oxygenation, heart rate, blood pressure, level of consciousness, acid-base status, and medication use. In specific clinical settings, care providers should consider possi­ ble aggravation of arrhythmias by antiarrhythmic drugs (proarrhythmia), adverse drug effects from intentional or unintentional overdose, or drug toxicity occurring with nor­ mal dosing patterns or as a result of drug-drug interactions. With these principles in mind, care providers should: 1 . Recognize the symptoms and signs requiring immediate treatment of the patient with cardioversion or defibrilla­ tion. 2 . Understand the initial diagnostic, electrical, and pharma­ cologic treatment approaches for rhythms that are hemo­ dynamically unstable and those that are not. 3 . Know when to call expert consultation for complicated rhythm interpretation or pharmacologic or management decisions.

In a study of conscious patients who presented with a wide-QRS­ complex tachycardia, an affirmative answer to two questions ("Have you ever had a heart attack in the past?" and "Did {these kind of symptoms] start after your heart attack?') correctly identified VT as the culprit arrhythmia in nearly all (28 of29) cases.

Providers of acute cardia! life support (ACLS) should also participate in training and evaluation sessions that will establish their ability to detect and treat serious arrhythmias, including regular updates to enhance their expertise in rhythm interpretation and in using and troubleshooting ECG monitoring equipment.

Physical Examination

Arrhythmia Recognition and Classification

The physical examination of patients in arrhythmia should initially assess for signs of hemodynamic instability or evi­ dence that the arrhythmia is being poorly tolerated, including level of consciousness, heart rate, and blood pressure, fol­ lowed by evidence of heightened sympathetic drive, including skin pallor, cool extremities, and diaphoresis. Auscultation of lung fields may reveal diffuse crackles suggestive of pul­ monary edema. The pulse may be regular, irregularly irregu­ lar, thready, or absent. Variability in the intensity of the first heart sound (S 1) and cannon "A" waves in the jugular pulse are highly sensitive and specific indications of atrioventricular dissociation associated VT. Although these signs are helpful when detected, very often the rapid ventricular rate precludes making a rhythm diagnosis on the basis of physical findings alone. Documenting the rhythm through rhythm monitoring or an electrocardiogram (ECG) is required.

Electrocardiogram ECG monitoring should be instituted as soon as possible, ideally simultaneous with the initial assessment of the patient. In emergent or semiemergent circumstances, this can be done most efficiently by applying defibrillation elec­ trodes (from which the ECG can be monitored) or by use of the "quick-look paddles" feature available on most conven­ tional defibrillators. Early ECG monitoring is also important in high-risk patients, such as those with acute myocardial

Advanced providers and professionals should be able to dis­ tinguish true arrhythmias from normal heart rhythms occur­ ring at other than usual rates and from fictitious arrhythmias. Patients in acute distress are likely to manifest normal rhythms at more rapid rates, which should not be confused with a primary arrhythmia unless the rate is not appropriate for the clinical situation. Confusion can sometimes occur when the heart rate is sufficiently rapid that the P wave blends into the preceding T wave, making it difficult to see and, therefore, difficult to distinguish a supraventricular tachycar­ dia (SVT) from what is simply sinus tachycardia. Obtaining a 1 2 -lead ECG in this instance can be helpful because P waves may be more easily distinguished in some leads than in oth­ ers, making the rhythm diagnosis more apparent. Obtaining a 1 2-lead ECG can be helpful because P waves may be more easily distinguished in some leads than in others, making the rhythm diagnosis more apparent.

The following rhythms should be recognized by experienced health care professionals:

CHAPTER 1 9

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• •

• •

• • •

•

• •

•

•

E V A L U AT I O N , I D E N T I F I C AT I O N , A N D A S S E S S M E N T

Fictitious rhythms (artifact) Sinus rhythm (including smus bradycardia and smus tachycardia) Sinus pause and arrest Atrioventricular (AV) blocks of all degrees Premature atrial complexes (PACs) Supraventricular tachycardia (SVT) Preexcited arrhythmias (associated with an accessory pathway) Premature ventricular complexes (PVCs) Ventricular tachycardia (VT) Ventricular fibrillation (VF) Ventricular asystole Accelerated idioventricular rhythm

Fictitious Arrhythmias Fictitious arrhythmias are those generated by body motion, muscle artifact, electrical interference from nearby equip­ ment, loose electrodes, or loss of the ECG signal. 2 When motion artifact and electrical interference are superimposed upon a normal rhythm, both the appearance of QRS com­ plexes and the normal isoelectric baseline between QRS complexes are typically altered, creating the impression of a rapid tachycardia. Important clues to an apparent arrhyth­ mia being artifactual include the absence of associated symp­ toms and signs and failure to corroborate the presence of an arrhythmia by physical findings (pulse). Neither VF nor true asystole are associated with a normal level of consciousness, at least not for long! Another important clue as to the ficti­ tious nature of an arrhythmia is the ability to distinguish normal-appearing QRS complexes amid the baseline artifact with a rate and regularity that appear m1disturbed (as com­ pared with the preceding normal rhythm) by the apparent arrhythmia (Fig. 1 9 - 1 ) .

Another important clue as to the fictitious nature ofa n arrhythmia is the ability to distinguish normal-appearing QRS complexes amidst the baseline artifact with a rate and regularity that appears undisturbed (as compared with the preceding normal rhythm) by the apparent arrhythmia.

F I G U R E 1 9 - 1 • F i ctiti o u s a r r hyth m i a . T h e tra c i n g i l l u strates m o t i o n a rtifact. I n t h i s i n sta n c e t h e patient is b r u s h i n g h i s teeth wh i l e b e i n g m o n it o r e d and is i n n o r m a l sinus rhyt h m t h r o u g h o u t . T h e first s i n u s r hyt h m c o m p l e x o n t h e l eft a p p e a r s to c h a n g e to a n a p p a r e n t atri a l a r r hyth m i a (atr i a l f l u tter) , t h e n t o a n a p p a r e n t wi d e c o m p l e x t a c hyc a r d i a (ve n t r i c u l a r t a c hyca r d i a) . H oweve r , a s i n d i c a t e d by t h e a r r ows (sh own b e tween a l te r n a te QRS c o m p l ex e s) , o n e i s a b l e t o " m a r c h o u t " QRS c o m p l ex e s with o u t a c h a n g e i n t h e i r r a te o r r e g u l a r i ty th r o u g h o u t t h e a p p a r e n t a r r hyth m i a s , a t e l l ta l e s i g n t h a t t h e a p p a r e n t a r rhyt h m i a s a r e a rtifactu a l .

297

Classifying Tachycardias QRS Appearance Tachycardias can be classified in a number of ways. One use­ ful system is based on the width (or duration) of the QRS interval. The QRS interval reflects the time required for complete depolarization of the ventricles . This normally occurs within 80 to 1 00 milliseconds (0 .08-0 . 1 0 seconds) due to the rapid conduction of impulses through the His-Purkinj e system. Depolarization of the ventricles via the specialized conduction tissue compnsmg the His-Purkinje system is an order of magnitude faster than muscle-to-muscle conduction would be outside this conduc­ tion system. 3 Hence, any disruption in conduction in the His-Purkinj e system (as, for example, by right or left bun­ dle-branch block), results in the corresponding portion of the ventricles being depolarized by slower muscle-to-muscle conduction. The ventricular depolarization that now tran­ spires over a longer time interval results in widening of the QRS and is referred to as aberrant conduction, or aberrancy. Similarly, ventricular arrhythmias (VF and VT) are associ­ ated with a wide QRS because ventricular depolarization in this instance originates from muscle tissue outside the His-Purkinj e system and thereafter propagates by muscle­ to-muscle conduction throughout the ventricles. Notably, one should not confuse widening of the QRS (which repre­ sents the longer time required to depolarize the ventricles with each impulse) with the actual rate of a tachycardia (which represents how rapidly such impulses may come in succession) . Wide- or narrow-complex tachycardias can each be quite rapid.

Preexcitation Preexcited rhythms are also manifested by a wider than nor­ mal QRS.4 "Preexcitation" refers to early ventricular activation as a result of one or more congenitally acquired muscular con­ nections between the atria and ventricles. The atrioventricular node, which is ordinarily the only electrical connection between the atria and ventricles, transiently slows the conduc­ tion of impulses between the atria and ventricles, resulting in the typical PR interval of 0. 1 2 to 0.20 seconds between the onset of the P wave and begitming of the QRS complex. In contrast, conduction tl1rough an atrioventricular accessory pathway "bypasses" tl1e atrioventricular node and starts to excite the ventricles almost immediately after the P wave [rep­ resented by a foreshortened PR interval ( 0 . 1 2 seconds)? Is the ventricular rate regular or irregularly irregular? Are the QRS complexes preceded by P waves in a 1 : I fashion? Are PR intervals (when seen) constant or variable?

These questions, the rationale for which is further developed in subsequent chapters, allow the health care provider to break down the parts of the ECG and better separate rhythms into descriptive categories. Even if a rhythm diagnosis is not readily apparent from the answers, describing an arrhythmia in this fashion may better communicate its attributes to an expert who could assist with the diagnosis. For example, using this series of questions, were one to describe a narrow complex tachycardia (question I) that was regular at a rate of 1 5 0 bpm (question 2 ) , with two P waves for each Q R S (question 3 ) and unchanging P R intervals (question 4), a n expert might suggest a likely diagnosis of atrial flutter with 2 : 1 AV block. Alternatively, if one were to describe a wide-complex rhythm (question 1) that was regular at a rate of 40 bpm (question 2 ) , with more Ps than QRS complexes such that there was not a 1 : 1 correspondence between each P and each QRS (question 3) and widely variable PR intervals from beat-to-beat (question 4), a possible diagnosis might be third­ degree heart block.

Skill Development and Maintenance Many health care providers derive value from participation in regular training and evaluation sessions that increase their ability to recognize and treat serious arrhythmias. Experienced providers must also know how to use ECG monitoring equipment and be able to troubleshoot the most common technical problems . 1 Quality improvement can take the form of regular periodic reviews of difficult, missed, and misdiagnosed tracings from clinical cases . An expert provider in electrocardiography or electrophysiology can provide insightful guidance and education.

A Systematic Approach to Rhythm Analysis Every rhythm interpretation must be correlated with other signs of the patient's condition to properly assess and man­ age indicated interventions . A consistent approach to rhythm analysis is helpful and, when applied to every rhythm, is key to consistent and accurate interpretation.

Cardiac Monitoring: Monitoring Systems Cardiac monitoring systems generally consist of a monitor screen that displays the ECG and a recording system that transcribes the rhythm onto paper. Lights and tones may provide visual and audible signals of the heart rate. Monitor leads or electrodes may be attached to the patient's chest or

extremities. A 3 -lead ECG continues to be commonly used for monitoring, but 5 -lead ECG monitoring is a growing norm. The chest leads must be placed to show clearly the waves and complexes of the ECG strip and to leave the chest clear for defibrillation if necessary. The most common lead used to evaluate and monitor the cardiac rhythm is a modi­ fied lead II (Fig. 2 0-5). This lead parallels the direction (vec­ tor) of the P wave during normal activation of the atria from the sinus node and, therefore, provides the best display of atrial activity. Monitoring electrodes are color-coded for ease of appli­ cation and location. In the United States (a different color system is used in Europe), for a 3 -lead ECG the convention is for the right arm electrode to be colored white, the left arm electrode black and the left leg electrode red. For the 5 lead ECG, t o additional electrodes are provided, green for the right leg (ground), and brown for chest. These elec­ trodes can all be placed on the torso (they do not necessar­ ily have to be placed on the arms and legs), so long as they are oriented in such a manner that what is left is placed on the left side of the torso, what is right is placed on the right, and that an arm lead is placed above a leg lead (and vice versa) . Typically, the white electrode is placed below the clavicle on the right side, the black electrode below the clav­ icle on the left, and the red electrode on the left lower chest wall often adjacent to the cardiac apex. If a green electrode is provided, it can be placed on the right side of the lower chest opposite the red electrode; a brown or chest electrode

308

KUDENCHUK

can be placed anywhere a typical "V _/ ECG lead might be 1 located. See figure 2 0-5A. The popular mnemonics "white­ to-right, red-to-ribs, and black-on-top" and "white-to­ right, smoke [black] -over-the-fire [red] " are aids to remembering where to place the monitor electrodes for lead II when using a 3 or 5 lead ECG for monitoring.

Cardiac Monitoring: Key Points A :* .

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F I G U R E 2 0 - 5 • P l a c e m e n t o f ECG electrodes for best record i n g o f l e a d I I . Wh e n u s i n g a 3 - l e a d E C G sys t e m to m o n i t o r l e a d I I , o n ly t h e wh i t e , b l a c k a n d r e d e l e c tr o d e s a r e r e q u i r e d ; w h i t e i n t h i s i n s ta n c e i s t h e n e g a tive e l e ct r o d e , r e d i s p o s i tive , wh e r e a s t h e b l a c k e l e c t r o d e swi t c h e s p o l a r i ty d e p e n d i n g o n w h e t h e r l e a d I I o r a n o t h e r l e a d i s s e l e c t e d f o r m o n i t o r i n g . T h e g r e e n (r i g h t l e g o r g r o u n d a s d e n o t e d b y i t s sym b o l) a n d b r own ( c h e st) e l e c t r o d e s r e p r e s e n t t h o s e a p p l i e d to t h e c h est wh e n a 5 - l e a d E CG i s u s e d f o r m o n i to r i n g . T h e r e d t r i a n g l e i n t h e c e n t e r o f t h e c h est r e p r e ­ s e n ts " E i n th ove n ' s tr i a n g l e " wh i c h d e p i cts h ow t h e e l e c t r i c a l s i g n a l f r o m t h e h e a r t i s m o n i t e r e d b y t h e w h i t e (-) , b l a c k (-) a n d r e d (+) e l e c t r o d e s to c r e a t e t h e E CG s h own i n l e a d I I . I n E i n th ov e n ' s tr i a n g l e , t h e d o tt e d t h e r e d e l e c t r o d e r e p r es e n ts t h e " e l e c tr i c a l l o c a ti o n " o f t h e r e d e l e ct r o d e eve n t h o u g h i t i s p hys ­ i c a l ly l o c a t e d o n t h e l eft c h est wa l l . Le a d 2 u s u a l ly d i s p l ays u p r i g h t c o m p l e x e s f o r P wave , QRS c o m p l e x , a n d T wave .

1 . A prominent P wave should be displayed if organized atrial activity is present. Use lead II, which in most patients provides the clearest display of the P wave. 2 . The QRS amplitude should be sufficient to properly trig­ ger the rate meter. 3 . The patient's precordium must be kept exposed so that defibrillation paddles can be readily used if necessary. 4. Monitoring is for rhythm interpretation only. One should not try to read ST abnormalities or attempt more elaborate interpretation without obtaining a 1 2 -lead ECG. If such changes are observed on the monitored rhythm, a 1 2 -lead ECG should be obtained. 5 . Artifacts should be recognized and eliminated as much as possible. Loose electrodes, for example, may produce a per­ fectly straight line or a bizarre, wavy baseline that resembles ventricular fibrillation. The appearance of patient move­ ment and 60-cycle electrical interference on the monitor should be immediately recognizable and corrected.

References 1. Marriott H. Pmctical Electrocardiogmphy, 8th ed. Baltimore: Williams & Wilkins, 1 9 8 8 . 2 . Marriott H. Recognition o f cardiac arrhythmias and conduction dis­ mrbances. In Hurst JW, ed. The Hem1:, A11:e1·ies, and Veins, 7th ed. New York: McGraw-Hill, 1 990:489-5 34. 3. Smith W Mechanisms of cardiac arrhythmias and conduction dis­ mrbances. In Hurst JW, ed. The Hem1:, A11:eries and Veins, 7th ed. New York: McGraw-Hill, 1 990:47 3-488. 4. Zipes D . Genesis of cardiac arrhythmias : electrophysiological considerations. In Braunwald E, ed. Heart Disease: A Textbook of Ca1·diovasculm• Medicine, 4th ed. Philadelphia: Saunders, 1 992 : 5 88-62 7 . 5 . Task Force o f the Working Group o n Arrhythmias o f the European Society of Cardiology. The Sicilian gambit. A new approach to the classification of antiarrhythmic drugs based on their actions on arrhythmogenic mechanisms. Circulation 1 9 9 1 ;84: 1 8 3 1- 1 8 5 1 .

Peter ] . Kudenchuk The most critical interventions during the first minutes of a cardiac arrest are immediate bystander cardiopulmonary resuscitation (CPR) providing high-quality chest compressions with minimal interruption . •

Primary emphasis on high quality uninterrupted chest compressions and CPR

Immediate defibrillation for ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT) • Secondary emphasis on vasoactive agents and endotracheal intubation • Coordinated team approach with defined team leader •

P ulseless Arrest Due to Ventricular Fibrillation or

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Pulseless cardiac arrest is caused by four rhythms: VF, pu[seless VT asystole, or pulseless electrical activity (Fig. 2 1 - 1 ). The basic life support (BLS) algorithm is fo lowed (see Chapter 1 1 , Fig. 1 1 -2); an automatic elec­ trical defibrillator (AED) or manual defibrillator is placed as soon as possible and the rhythm determined (Fig. 2 1 - 1 , Box 2). Based upon rhythm analysis, a shockable or nonshockable rhythm is determined to be present and further interventions are based on the type of rhythm (Boxes 3 and 9). The 2005 AHA ECC guidelines gave renewed emphasis to the importance of high-quality, minimally interrupted CPR during the course of resuscitation. A single-shock strategy with subsequent shocks sepa­ rated by 2 minutes (five cycles) of CPR also displaced the former algorithm of three serial "stacked" shocks. This was recommended in part because it was recog­ nized that serial AED analyses and repeated shocks have limited yield and can deprive patients in cardiac arrest of needed CPR for protracted periods of time. 1•2 For similar reasons, it is now recommended that 2 minutes (five cycles) of CPR be interposed before rhythm and pulse checks following all interventions, including shock. In the current AHA ECC guidelines, pharmacologic therapies (epinephrine or vasopressin) to bolster coronary perfusion pressure are recom,

mended after failure of one or more shocks, and antiar­ rhythmic therapies for recurrent or resistant VFIVT are recommended after failure of rwo or more shocks to restore an organized perfusing rhythm. In particu­ lar, patients in whom a perfusing rhythm can be u·an­ siently restored but not successfully maintained berween repeated shocks (recurrent VFIVT) are appropriate candidates for early treatment with antiar­ rhythmic medications. In such patients the antiar­ rhythmics may facilitate and stabilize the return of cir­ culation that shock alone has failed to accomplish. As is true for virtually all interventions, the likelihood of benefit from antiarrhythmic drug therapies declines rapidly with the lengthening duration of cardiac arrest.

Defibrillation The optimal number of attempted defibrillatory shocks that should be administered for refractory VFNT before initiating pharmacologic therapy is unknown. Traditionally, given the established efficacy of early defibrillation, pharmacologic therapy was recommended after at least three precordial shocks failed to restore a stable perfusing rhythm. If VF/pulseless VT is present (Fig. 2 1 - 1 , Box 3), providers should deliver one shock (Box 4) and then resume CPR immediately, beginning with chest com­ pressions . If a biphasic defibrillator is available, providers should use the dose at which that defibril­ lator has been shown to be effective for terminating VF (typically a selected energy of 1 2 0-2 00 J). If the provider is unaware of the effective dose range of the device, a dose of 200 J for the first shock may be used and an equal or higher shock dose for the second and subsequent shocks . If a monophasic defibrillator is used, providers should deliver an initial shock of 3 60 J and use that dose for subsequent shocks. If VF is ini­ tially terminated by a shock but then recurs later in the arrest, subsequent shocks may be delivered at the previously successful energy level. 309

3 10

KUDENCHUK

1 •

•

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PULS ELESS ARREST B LS Algorithm : Call for help, give CPR G ive oxyge n when available Attach monitor/defibril lator when avail able 2

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Asystole/PEA

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(before or after the shock) amiodarone (300 mg IV/10 once, then consider add it ional 1 50 mg IV/10 once) or lidocaine (1 to 1 . 5 mglkg first dose, then 0.5 to 0.75 mg/kg IV/10, maximum 3 doses or 3 mglkg)

Consider magnesium, loading dose 1 to 2 g IV/10 for torsades de pointes After 5 cycles of CPR,• go to Sox 6 above

F I G U R E 2 1 - 1 • P u l s e l ess c a r d i a c a r r e st a l g o r i th m .

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•

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Rotate compressors every 2 minutes with rhythm checks Search for and treat poss i ble contributing factors: - Hypovolemia -

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- Hypo-/hyperkalemia - Hypoglycemia

- Hypothermia - Toxins - Tamponade, cardiac - Tension pneumothorax - Th rombosis (coronary or pulmonary) - Trauma

CHAPTER 2 1

Intravenous Access, Pharmacologic Therapy, and Endotracheal Intubation Establishing IV access is important (see below), but it should not interfere with CPR and the delivery of shocks . The pulseless arrest algorithm (Fig. 2 1 - 1 ) does not specify pre­ cisely when providers should accomplish endotracheal intu­ bation and gain access to the circulation except that these should be accomplished as soon as feasible in unconscious patients who are not responsive to shock and that these activities do not or only minimally interfere with CPR and defibrillation. Since administration of drugs requires intra­ venous or intraosseous access or endotracheal intubation (see Chapter 1 8), these interventions should ideally be per­ formed during the CPR interludes between shocks once skilled providers who are trained in such tasks are on scene. Importantly, efficacy studies of vasoactive agents and antiarrhythmic drugs in VFIVT arrest have addressed only short-term outcomes. Thus recommendations for their use are based on surrogate or immediate or intermediate out­ come measures (such as admission alive to hospital) that may

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20

Time (sec)

F I G U R E 2 1 - 2 • T h i s g r a p h i l l ustrates the c h a n g e in p r o b a b i l ity f o r s u ccessfu l d e fi b r i l l a t i o n w i t h retu r n o f s p o n t a n e o u s c i r c u l a t i o n (PRose) b a s e d o n t h e n u m b e r o f s e c o n d s wit h o u t CPR (" h a n d s off" p e r i o d) b e twe e n wh e n ECG a n a lysis was i n i t i a t e d and a s h o c k was a c tu a l ly a d m i n istered (a m e d i a n o f 20 s e c o n d s l a ter) to p a ti e n ts in c a r d i a c a r rest. I t uses a s u r r o g ate m e a s u r e for ROSC, PRosc(v) , w h i c h is d e r ived b a s e d o n a va r i e ty of factors t h a t c a n affect t h e E C G s i g n a l (ce n t r o i d f r e q u e n cy, p e a k p ower fr e q u e n cy, s p e c t r a l f l a t n ess a n d e n ergy f e a t u r e s o f t h e s i g n a l) a n d h a s b e e n u s e d t o p r e d i ct t h e l i k e l i h o o d o f R O S C a fter s h o c k . T h e g r a p h i l l ustrates t h e effect o f t h e p a u s e i n CPR u p o n t h e E CG s i g n a l f o r 3 g r o u p s o f p a t i e n ts , t h o s e whose a n a lyz e d ECG b e f o r e s h o c k (ti m e 0 o n t h e g r a p h) wo u l d h ave p r e d i cted a h i g h l i k e l i h o o d o f R O S C (4 0 to 1 0 0 % ; " [ b l a c k d o t ) " ) , t h o s e i n wh o m t h e i r ECG p r e d i cted a m o d e r a t e l i k e ­ l i h o o d o f R O S C (2 5 to 4 0 % : " * " ) a n d t h o s e w i t h a l ow l i k e l i h o o d (0 to 2 5% " x " ) . A m o n g p a t i e n ts in c a r d i a c a r rest in wh o m t h e i r ECG wo u l d h ave p r e d i cted a high o r m o d e r a t e l i k e l i h o o d o f ROSC (to p m ost l i n es i n t h e g r a p h) , s a w t h a t p r o b a b i l i ty ste a d i ly d e c l i n e d u r ­ i n g t h e 2 0 s e c o n d t i m e p e r i o d b e f o r e s h o c k w a s a ctu a l ly a d m i n i s ­ te r e d . I n p a t i e nts i n wh o m PRosc(v) was a l re a dy l ow (b o tto m m o st l i n e in the g r a p h) w h e n t h e i r ECG was fi rst a n a lyz e d , the effect of t i m e with o u t CPR on p r e d i cted o u t c o m e was l ess a p p a r e n t , p r o b a ­ b ly b e c a u s e t h e i r p r e d i cted o u t c o m e w a s a l r e a dy so p o o r a t t h e o u tset. (A d a p t e d f r o m E ftesto l T , S u n d e K , S t e e n P A . Effects o f i n te r r u p t i n g p r e c o r d i a l c o m p ressi o n s o n t h e c a l c u l a t e d p r o b a b i l i ty of d e fi b r i l l a t i o n s u c c ess d u r i n g o u t - o f - h o s p i t a l c a r d i a c a r rest. Circulation 2 0 0 2 ; 1 0 5 [ 1 9 ) : 2 2 7 0-2 2 7 3 , r evised with p e r m issi o n .)

•

PULSELESS CARDIAC ARREST

311

not correlate with the preferred outcome of neurologically intact survival to hospital discharge after the cardiac arrest. This is detailed in the subsequent sections with respect to antiarrhythmic agents.

Rhythm, Pulse Checks, and Team Coordination Rhythm checks should be brief, and pulse checks should gen­ erally be performed only if an organized rhythm is observed. If there is any doubt about the presence of a pulse, resume CPR. During treatment of VF/pulseless VT, health care providers must practice efficient coordination between CPR and shock delivery. VVhen VF is present for more than a few minutes, the myocardium is depleted of oxygen and metabolic substrates. A brief period of chest compressions can deliver oxygen and energy substrates, increasing the likelihood that a perfusing rhythm will return after shock delivery. 3 Analyses of VF waveform characteristics predictive of shock success have documented that the shorter the time between chest com­ pression and shock delivery, the more likely it is that the shock will be successful.3•4 Reduction in the interval from compres­ sion to shock delivery by even a few seconds can increase the probability of shock success4 (Fig. 2 1 -2).

Pulseless Arrest due to Asystole or Pulseless Electrical Activity (PEA) Definitions Asystole is defined as the absence of any electrical cardiac activ­ ity (either atrial or ventricular) for seconds to minutes or elec­ u·ical activity that is so profoundly slow (perhaps seen as only a single QRS complex) that for all practical purposes it is a "straight line" rhythm (Fig. 2 1 -3). It should be distinguished from bradycardia (in which successive QRS complexes at a definable albeit slow rate are seen), complete atrioventricular block with ventricular asystole (in which there is evidence of atrial electrical activity without either ventricular conduction or a ventricular escape rhythm), and pulseless electrical activity (an organized rhythm without a corresponding detectable pulse).

F I G U R E 2 1 - 3 • A syst o l e . A l th o u g h asysto l e is c o m m o n ly r e g a r d e d as t h e c o m p l ete a b s e n c e o f a ny e l e ct r i c a l a ctivity o n t h e ECG , it can a lso present i n the m a n n e r sh own here, with a r a r e QRS c o m p l e x . I n f a c t t h e i s o l ated Q R S c o m p l e x c o n f i r m s t h a t t h e b a s e l i n e is i n d ee d "flat" a n d d o e s n o t repres ent " f i n e " ve ntr i c u l a r fi b r i l l ati o n . B e c a use o n ly a s i n g l e QRS c o m p l e x is evi d e n t i n this i nsta n c e , n o rate can b e assi g n e d to this rhyt h m . The p r o t r a cted " stra i g h t l i n e " a p p e a r a n c e of t h e rhyt h m fo l l owi n g the Q R S b e s t c h a r a cterizes it as asysto l e .

312

KUDENCHUK

Pulseless electrical activity (PEA) (terminology that has displaced " electromechanical dissociation, " or EMD) is defined as the presence of an organized ventricular rhythm for which a corresponding pulse would ordinarily be expected but is noticeably absent. It does not refer to ven­ tricular fibrillation or pulseless ventricular tachycardia, for which the rapid rate and character of the arrhythmia explain the absence of a pulse . PEA can represent the complete absence of mechanical cardiac contraction in association with each QRS complex. It can also refer to poor mechanical con­ traction that is insufficient to create a discernible pulse but for which more sensitive methods demonstrate a blood pres­ sure (so-called pseudo-PEA), mechanical contraction that would be adequate were it not compromised by inadequate cardiac filling (such as that caused by pericardia! tamponade, tension pneumothorax, or exsanguination), or obstruction to outflow from the heart (such as a large pulmonary embolus).6 If rhythm analysis confirms asystole or PEA, resume CPR immediately. A vasopressor (epinephrine or vasopressin) may be administered at this time. Epinephrine can be admin­ istered approximately every 3 to 5 minutes during cardiac arrest; one dose of vasopressin may be substituted for either the first or second epinephrine dose (Fig. 2 1 - 1 , Box 1 0). For a patient in asystole or slow PEA, consider atropine. Do not interrupt CPR to deliver these medications. After drug delivery and approximately 5 cycles (or about 2 minutes) of CPR, recheck the rhythm (Fig. 2 1 - 1 , Box 1 1). If a shockable rhythm is present, deliver a shock (Box 4). If no rhythm is present or if there is no change in the appearance of the electrocardiogram, immediately resume CPR (Box 1 0). If an organized rhythm is present (Box 1 2), try to palpate a pulse. If no pulse is present (or if there is any doubt about the pres­ ence of a pulse), continue CPR (Box 1 0). If a pulse is present, the provider should identify the rhythm and treat appropriately.

Treatment and Prognosis Prognosis for cardiac arrest due to asystole or PEA is poor. Asystolic cardiac arrest is rarely salvaged unless found in asso­ ciation with a readily reversible problem, such as severe hyper­ kalemia. Cardiac arrest associated with PEA carries a better prognosis than asystole if its wider range of causes (see below) can be readily identified and corrected.7 From a practical standpoint, both rhythms are treated empirically with CPR, epinephrine, or vasopressin and/or atropine. Notably, transcu­ taneous pacing (which is recommended for symptomatic bradycardia when a pulse is present) is not recommended for either PEA or asystole because of poor efficacy and resulting distraction from performing CPR. Antiarrhythmic drugs have no benefit and in theory may be harmful because of their rhythm-suppression and hypotensive effects. Asystole and par­ ticularly PEA have a "differential diagnosis" in terms of what entities can produce these heterogenous rhythms (Table 2 1 - 1 ). Accordingly, particularly victims of PEA should be thought­ fully evaluated to discover a potential reversible cause.

Reversible Causes Underlying and potentially reversible causes of cardiac arrest should be considered regardless of the rhythm presentation.

TA B LE 2 1 - 1 • T h e M o s t Co m m o n C a u s e s of P u l s e l e s s E l e c t r i c a l A c tivity P r e s e n t e d a s H s a n d Ts Hs

Ts

Hyp ovo l e m i a

To x i n s

Hyp o x i a

Ta m p o n a d e (ca r d i a c)

Hyd r o g e n i o n (a c i d o s i s)

Te n s i o n p n e u m o t h o r a x

Hyp e r -/hyp o k a l e m i a

Th r o m b o s i s (c o r o n a ry a n d p u l m o n a ry)

Hyp o g lyc e m i a

Tra u m a

Hyp o t h e r m i a

VFNT may b e precipitated by acute myocardial ischemia or infarction, electrolyte abnormalities, hypoxia, or drug toxicity, recognition and correction of which may facilitate the success of defibrillation. Effective therapeutic options are far more lim­ ited when cardiac arrest stems from asystole or PEA, for which the successful restoration of circulation depends almost entirely on recognizing and treating a potentially reversible cause. As a memory aid, such causes can be classified as "the Hs and Ts." The "Hs" are: •

• •

• • •

Hypovolemia Hypoxia Hydrogen ion (acidosis) Hyperkalemia/hypokalemia and metabolic disorders Hypothermia Hypoglycemia

The "Ts"are: • • • •

•

Toxins/tablets (drug overdose, illicit drugs) Tamponade, cardiac Tension pneumothorax Thrombosis, coronary Thrombosis, pulmonary

References 1. Yu T, Wei! MH, Tang W, et al. Adverse outcomes of interrupted precordial compression during automated defibrillation. Cin:ulation 2002 ; 1 06(3 ) : 3 68-3 7 2 . 2 . Rea TD, Shah S, Kudenchuk PJ, et a!. Automated external defibril­ lators: to what extent does the algorithm delay CPR? Ann Enzerg Med 2 005 ;46(2) : 1 3 2 -1 4 1 . 3 . Eftestol T, Wik L, Sunde K , et a!. Effects o f cardiopulmonary resus­ citation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest. Cin:ulation 2 004; 1 1 0( 1 ) : 1 0- 1 5 . 4 . Eftestol T, Sunde K , Aase S O , e t al. Predicting outcome o f defibril­ lation by spectral characterization and nonparametric classification of ventricular fibrillation in patients with out-of-hospital cardiac arrest. Circulation 2 000; 1 02 ( 1 3): 1 5 2 3 - 1 529. 5 . Eftestol T, Sunde K, Steen PA. Effects of interrupting precordial com­ pressions on the calculated probability of defibrillation success during out-of-hospital cardiac arrest. Cinulation 2002 ; 1 0 5 ( 1 9):22 70-2 2 7 3 . 6. Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management: concept of an advanced life support-conformed algorithm. c,·it Care Med 2 00 7 ; 3 5 (5 Suppl) : S 1 5 0-S 1 6 1 . 7 . Cobb LA, Fahrenbruch CE, Olsufka M , et a!. Changing incidence of out-of-hospital ventricular fibrillation, 1 980-2 000. JAMA 2 002 ; 2 8 8 (2 3) : 3 008-3 0 1 3 .

Peter ] . Kudenchuk Guesses as to whether a wide-complex tachycardia is ventricular or supraventricular in origin are wrong as often they are right . Differentiating a wide-complex tachycardia that is supraventricular from one of ventricular origin is important because of the differing treatment and prognostic implications for the patient . The most common presumption is that a hemodynamically stable wide-complex tachycardia must be supraventricular (with aberrancy) in origin , whereas the hemodynamic characteristics of an arrhythmia have little to do with its site or origin . Accordingly , the clinician then proceeds to inappropriately treat a true VT with agents meant for SVT, which are not only ineffective but also expose the patient to adverse effects . •

Definition and approach to the patient with a tachycardia

Differential diagnosis of narrow-complex tachycardias • Emergency differential diagnosis of wide-complex tachycardias • Initial treatment, including "expert consultation advised" •

need for rapid intervention with electrical cardiover­ sion, whereas a hemodynamically stable tachycardia can be approached more deliberately with attention to the most probable rhythm diagnosis and treat­ ment, targeted at its likely origin and mechanism. Or such a patient can potentially be transported to a facility more capable of diagnosing the rhythm.

0 -=,ve.rview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

_ _ _ _

.

Although, convention tachycardia is defined as a heart ate 2: 1 00 bpm, abnormal tachycardias are somewhat arbitrarily defined by a resting rate of > 1 2 0 bpm. It should be recognized, however, that a normal rhythm (sinus tachycardia) may reach or exceed this resting rate under some conditions. Therefore, in light of the appearance and clinical circumstances surrounding the rhythm and rate, the provider must initially ascertain whether an abnormal tachycardia is actually present. Is it a real tachyarrhyth­ mia? (Fig. 2 2 - 1 , Box 1 .) If the rate and appearance of the tachycardia suggest that it truly represents an arrhythmia (rather than a normal rhythm at a faster rate, or an artifactual arrhythmia), the initial approach to its characterization is to assess the patient and determine if serious symptoms are present and due to the tachycardia (Fig. 2 2 - 1 , Box 2). If serious or significant symptoms are present, then is the patient hemodynamically stable (Fig. 2 2 - 1 , Box 3)? Unstable signs include altered mental status, ongoing chest pain, hypotension, or other signs of tissue hypoperfusion. A hemodynamically unstable tachycardia prompts the

INITIAL STEPS IN ASSESSING THE 12-LEAD ELECTROCARDIOGRAM 1 . Is the QRS complex narrow or wide (2'=0. 1 2 seconds)? 2 . Is the ventricular rate regular or irregularly irregular? 3 . Are the Q RS complexes preceded by P waves in a 1 : 1 fashion? 4. Are PR intervals (when seen) constant or variable?

The next steps in the evaluation of the patient with arrhythmia are to characterize the tachycardia as b eing wide (QRS 2: 0 . 1 2 seconds) or narrow in appearance (Fig. 2 2 - 1 , Boxes 6 and 1 2); whether it is regular or irregularly irregular in rate (Fig. 2 2 - 1 strat­ ification of rhythms shown below Boxes 6 and 1 2); and whether there is a 1 : 1 correspondence between each P wave and QRS complex. Finally, determining whether the PR intervals (when seen) are constant or variable can be helpful in determining whether P waves are being conducted to QRS complexes or are more randomly associated with them. Obtaining a 1 2 -lead ECG of the tachycardia is crucial. A rhythm obtained from a single lead (in which a portion of the QRS complex may be isoelectric and 3 13

3 14

KUDENCHUK

1 TAC H YCA R D IA With P u l ses 2 •

Ass e ss and suppo rt ABCs as needed Give oxygen Monitor ECG Qdentify rhythm), b l ood pressure, oxi metry Identify and treat revers ible causes

•

•

•

• •

!

3

5 Estab l ish IV access

Obtain 1 2- lead ECG

(when available) or rhythm strip Is Q RS narrow (48 hours. Oral amiodarone has rate slowing effects in preexcited atrial fibrillation. 1 1 5-1 1 7 IV amiodarone also increases the refractoriness and slows the conducting proper­ ties of accessory pathways.63 However, there have been case reports of accelerated heart rates when IV amiodarone was administered more rapidly and at higher than recommended initial loading doses to patients with preexcited atrial fibrilla­ tion." 8 · 1 1 9 This illustrates how the beneficial electrophysio­ logic properties of an antiarrhythmic drug may be mitigated by its acute hypotensive effects and result in destabilizing a marginally compensated patient. Such experience under­ scores the importance of viewing preexcited atrial fibrillation as an inherently unstable arrhythmia for which electrical car­ dioversion is likely the fastest and safest treatment. Anticoagulation Unless required for other reasons, patients who are cardioverted from atrial fibrillation or flutter within 48 hours of the arrhythmias' onset do not need to be antico­ agulated before or following the conversion. Conversely, if AF has been present for >48 hours, a risk of systemic emboliza­ tion exists with conversion to sinus rhythm unless patients are adequately anticoagulated for at least 3 weeks beforehand (fol­ lowed by a minimum of 4 weeks afterward). 1 2 0·1 2 1 Electrical cardioversion and the use of antiarrhythmic agents should be avoided unless the patient is unstable or hemodynamically compromised. In patients who are intolerant of atrial fibrilla­ tion or flutter and unable to wait for a 3 -week course of ther­ apeutic anticoagulation before cardioversion, acute heparinization and cardiology consultation with the use of transesophageal echocardiography to exclude atrial thrombi is indicated to assess the risk and benefits of acute conversion strategies. Such patients, however, still require ongoing and w1interrupted anticoagulation for a minimum of 4 weeks after cardioversion. Some experts initiate anticoagulation with hepain within the first 48 hours of onset of atrial fibrillation or flutter, in hope of extending the time window during which a patient can be safely cardioverted (from a thromboembolic standpoint). If such a patient is successfully cardioverted within 48 hours of rhythm onset, continued anticoagulation is not required; however if cardioverted >48 hours after onset of AF or flutter, anticoagulation should be continued for a minimum of an additional 4 weeks. Restoring Sinus Rhythm Electrical cardioversion is the technique of choice, with relatively low risk, for cardiover­ sion of patients with AF or atrial flutter to sinus rhythm. 1 22 The recommended initial energy settings are discussed in Chapter 24. The efficacy of biphasic shock waveforms for

335

cardioversion of AF and atrial flutter is greater and may allow for lower energy settings than for monophasic wave­ form shock. 1 2 3· 1 2 4 If electrical cardioversion is not feasible, desirable, or successful, a number of pharmacologic alternatives are available for cardioversion of patients, including IV ibu­ tilide, 1 2 5-1 2 8 IV procainamide, 1 1 3 · 1 2 5· 1 2 9-1 3 8 IV amio­ darone, 2 4,2 5 , 5 8-6 I, 65 , IOI - I os, I J 9- I 47 IV quinidine, I 48 IV flecainide (not available in the United States), 149 IV propafenone (not available in the United States), 150 IV sotalol (not available in the United States),67 and IV disopyramide (not available in the United States). 1 5 1 · 1 5 2 In patients with impaired LV func­ tion, the negative inotropic effects of flecainide, propafenone, sotalol, and procainamide as well as the poten­ tial proarrhythmic potential of ibutilide make these agents less desirable. IV amiodarone is a preferable agent in such circumstances. It should also be remembered that the likeli­ hood of successful pharmacologic conversion of atrial fibril­ lation or flutter with any antiarrythmic agent is variable and the precise timing of its occurrence is unpredictable, such that conversion may not necessarily be achieved within 48 hours of the arrhythmias' onset. Beyond 48 hours, anticoag­ ulation issues as discussed in the immediate preceding sec­ tion must be adequately addressed before cardioversion (electrical or pharmacologic) is performed. Finally, with respect to pharmacologic cardioversion of atrial flutter, an AV-nodal blocking drug (such as diltiazem or a beta-blocker) should be administered before antiarrhythmic agents, which may otherwise paradoxically accelerate ventricular rates. The mechanism for such acceleration is primarily due to a slowing of the atrial flutter rate (for example from 3 00-2 00 per minute) by antiarrhythmic drugs. A slower atrial rate may afford a higher proportion of atrial impulses being con­ ducted 1 : 1 rather than 2 : 1 across the atrioventricular node, paradoxically increasing the ventricular response (in the example cited, from 1 5 0-2 00 per minute) . Pretreatment with a calcium channel or beta-blocker reduces such risk by increasing the degree of AV block.

Accessory Pathway-Mediated Tachycardias The presence of one or more accessory pathways, linking the atria and ventricles via a muscular bridge, predisposes patients to arrhythmias that fall within the broad category of Wolff-Parkinson-"\Nhite syndrome. Among these arrhyth­ mias is paroxysmal supraventricular tachycardia (PSVT) due to atrioventricular reentry. A reentry circuit that involves the atrioventricular node as one limb and the atrioventricular accessory pathway as the other limb can result in PSVT. Most commonly, this reentry circuit "spins" in such a manner that ante grade (forward) con­ duction to the ventricles occurs via the atrioventricular node, and retrograde (backward) conduction from ventricle to atriwn occurs via the accessory pathway. This results in a reg­ ular narrow-complex tachycardia of abrupt onset that may be indistinguishable from atrioventricular nodal tachycardia (AVNRT), called orthodromic reciprocating tachycardia, and is treated in the same fashion. Rarely the reentry circuit "spins" in the opposite direction, such that antegrade (for­ ward) conduction to the ventricles occurs via the accessory pathway and retrograde (backward) conduction from the

336

KUDENCHUK

ventricle to atrium occurs via the atrioventricular node. In this instance, a wide-complex tachycardia results, called antidromic reciprocating tachycardia, which, apart from prior knowledge of the existence of an accessory pathway, may not be easily distinguishable from ventricular tachycardia. Both forms of AVRT, orthodromic and antidromic reciprocating TA B LE 2 2 - 6

•

U p d a t e d R e c o m m e n d a t i o n s for the A c u te M a n a g e m e n t o f H e m o dyn a m i c a l ly Sta b l e R e g u l a r T a c hyc a r d i a

ECG

Recommendation•

N a r r ow Q R S - c o m p l e x t a c hyc a r d i a (SVT)

Va g a l m a n e uvers Adenosine Ve r a p a m i l , d i l t i a z e m B e ta - b l o c k e r s Amiodarone Digoxin

Wi d e Q R S - c o m p l e x t a c hyc a r d i a • SVT a n d B B B • P r e e x c i t e d SVT/ A F "

•

tachycardia, are dependent upon conduction through the AV node as one limb of the circuit and will terminate with maneu­ vers or agents that block the atrioventricular node. This is the single scenario in Wolff-Parkinson-White syndrome where AV-nodal blocking agents (adenosine, calcium channel block­ ers, beta-blockers, and digoxin) are recommended.

Wi d e QRS - c o m p l e x t a c hyc a r d i a o f u n k n own o r i g i n

Wi d e QRS - c o m p l e x t a c hyc a r d i a o f u n k n own o r i g i n i n p a t i e n ts with p o o r LV fu n c t i o n

Cl a ssifi c a ti o n

I IIb lib IIb

S e e a b ove F l e c a i n i d eb I b u t i l i d eb P r o c a i n a m i d eb DC c a r d i oversi a n P r o c a i n a m i d eb Sata l a lb Amiodarone D C c a r d i aversi a n Li d o c a i n e A d e n o s i n e' B e ta - b l o c k e rsd Ver a p a m i l '

Leve l o f Ev1 d e n c e B A A c c c

B B B c

I lib lib III III

Amiodarone D C c a r d i ove rsi o n Li d o c a i n e

LEVE L O F EVI D E N C E : Leve l A (h i g h est) : d e rived f r o m m u l t i p l e r a n d o m i z e d c l i n i c a l tr i a l s ; Leve l B ( i n te r m e d i ate): d o t o o r e o n t h e b a s i s o f o l i m ­ i t e d n u m b e r o f r a n d o m i z e d t r i a l s . n o n r a n d o m i z e d stu d i e s , o r o b s e rva t i o n a l r e g istr i e s ; Level C (lowest) : p r i m a ry b a s i s f o r t h e r e c o m m e n d a ­ tion was expert consensus. CLASS I F I CATI O N Class 1 : C o n d i t i o n s for wh i c h t h e r e i s evi d e n c e for a n d / o r g e n e r a l a g r e e m e n t t h a t t h e p r o c e d u r e o r t r e a t m e n t i s u s e f u l a n d effective ; Class I I : Co n d i t i o n s for wh i c h t h e r e i s c o n f l i c t i n g evi d e n c e a n d / o r a dive r g e n c e o f o p i n i o n a b o u t t h e u s e fu l n ess/effi c a cy o f a p r o c e d u r e or t r e a t m e n t ; C l a s s II a: T h e w e i g h t of evi d e n c e or o p i n i o n is in favo r of t h e p r o c e d u r e or t r e a t m e n t ; C l a s s l i b : U s e f u l n ess/eff i ­ c a cy i s l e s s we l l esta b l i s h e d by evi d e n c e o r o p i n i o n ; Class I I I : Co n d i t i o n s f o r wh i c h t h e r e i s evi d e n c e a n d / o r g e n e r a l a g r e e m e n t t h a t t h e p r o c e d u r e o r t r e a t m e n t i s n o t u s e f u l /effective a n d i n s o m e c a s e s m ay b e h a r m fu l . A F , atri a l f i b r i l l a t i o n ; B B B . b u n d l e - b r a n c h b l o c k ; D C , d i r e ct c u r r e n t ; E C G , e l e c tr o c a r d i o g ra m ; LV, l e ft ventri c u l a r ; Q R S , ventr i c u l a r activa­ tion o n ECG; SVT , s u p r ave n tr i c u l a r . T h e o r d e r i n wh i c h t r e a t m e n t r e c o m m e n d a t i o n s a p p e a r i n t h i s t a b l e with i n e a c h c l a s s o f r e c o m m e n d a t i o n d o e s n o t n e cessa r i ly r e f l e c t a p r e f e r r e d s e q u e n c e of a d m i n i strati o n . F o r p e r t i n e n t d o s i n g i n f o r m a ti o n , p l e ase r e f e r to t h e A H A / A CC/ESC g u i d e l i n e s on t h e m a n a g e m e n t of p a t i e nts with atrial fi b r i l l a t i o n . ' A l l l i sted d r u g s a r e a d m i n i s t e r e d i n trave n o u sly ' S h o u l d not be t a k e n by p a t i ents with r e d u c e d LV f u n c t i o n . ' A d e n o s i n e s h o u l d b e u s e d with c a u t i o n i n p a t i e nts with severe c o r o n a ry a r t e ry d i s e a s e b e c a use vas o d i l a t i o n of n o r m a l c o r o n ary vess e l s m ay p r o d u c e i s c h e m i a i n vu l n e r a b l e t e r r i t o ry. I t s h o u l d b e u s e d o n ly w i t h f u l l r e s u s c i tative e q u i p m e n t ava i l a b l e . ' B e t a b l o c k e r s m ay b e u s e d a s first- l i n e t h e r a py f o r t h o s e w i t h c a te c h o l a m i n e - s e n s i tive tachyc a r d i a s s u c h a s r i g h t ventr i c u l a r o u tf l ow t e c hyc a r d i a 'Ve r a p a m i l m a y b e u s e d a s first- l i n e t h e r a py f o r t h o s e w i t h LV fasc i c u l a r VT. A d a pt e d f r o m B l o mstr o m - Lu n d qvist C, S c h e i n m a n M M , A l i o t E M , A l p e r t J S , Ca l k i n s H , C a m m AJ , C a m p b e l l WB , H a i n e s D E , K u c k K H , Le r m a n B B , M i l l e r D O , S h a effer CW, Steve n s o n WG , T o m a s e l l i G F . ACC/ A H A/ESC g u i d e l i n e s f o r t h e m a n a g e m e n t of p a t i e n ts with s u p r ave n tr i c u l a r a r r hyth ­ m i a s . A r e p o rt of t h e A m e r i c a n Co l l e g e of Card i o l o gy/A m e r i c a n H e a rt A ss o c i a t i o n T ask F o r c e on P r a c t i c e G u i d e l i n e s a n d t h e E u r o p e a n S o c i ety of C a r d i o l ogy C o m m ittee for P r a c t i c e G u i d e l i n e s . (Wr i t i n g C o m m ittee to Deve l o p G u i d e l i n e s f o r t h e M a n a g e m e n t of P a t i e n ts With S u p r ave n tr i c u l a r A r r hyth m i a s) . J A m Ca l l Co r d i a l 2 0 0 3 : 4 2 : 1 4 6 3 - 6 3 1 .

B B B B B c c

B B B B

CHAPTER 2 2

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TAC H Y C A R D I A W I T H P U L S E S : N AR R OW AN D W I D E

Conversely, patients with a n accessory pathway may also experience other atrial arrhythmias, including ectopic atrial tachycardia, multifocal atrial tachycardia, atrial fibrillation and atrial flutter. In such instances, conduction from the atria to the ventricles will likely occur over both the atri­ oventricular node and the accessory pathway, with a mixture of wide, narrow, and fused QRS complexes. Ventricular rates are likely to be rapid, and in some cases life-threatening, because the accessory pathway will conduct atrial impulses rapidly to the ventricles without the slowing that is usually afforded by conduction that is restricted to the atrioventric­ ular node. Such arrhythmias cannot and should not be treated with atrioventricular nodal blocking agents (such as digoxin, beta-blockers, or calcium channel blockers and also not with adenosine), which will not slow and may accelerate ventricular rates. Instead, if electrical cardioversion is not an immediate option, pharmacologic agents that have the abil­ ity to slow conduction in the muscular accessory pathway should be employed, as discussed in the preceding section; these include IV procainamide, IV amiodarone, IV fle­ cainide, IV propafenone, and IV sotalol (the latter drugs are not available in the United States).

Junctional Tachycardia In adults , true junctional tachycardia is rare. Apparent junctional tachycardia is most commonly due to misdiag­ nosed PSVT and should b e treated accordingly. True junctional tachycardia in adults is often a manifestation of digitalis toxicity (best treated by withdrawal of digitalis) or of exogenous catecholamines or theophylline (best treated with reduction or withdrawal of such infusions). If no apparent cause is found, symptomatic junctional tachy­ cardia may respond to IV amiodarone or to beta-blockers or calcium channel blockers. This recommendation, however, has no specific human evidence to provide support. Instead the recommendation is based on rational extrapolations from the known antisympathetic and nodal effects of beta­ blockers and calcium charmel blockers or experience with IV amiodarone for such arrhythmias in children. 1 5 3

Summary In summary, the diagnosis and management of narrow- and wide-complex tachycardias can be difficult and complex. Emergency cardiac care treatment is focused on the princi­ ple of identifying the symptomatic patient and immediately treating those who are hemodynamically unstable or immi­ nently so. Treatment of the stable symptomatic patient is also challenging. When the diagnosis is certain and the treatment specific, therapy can be initiated by providers familiar with initial agents used routinely to treat and termi­ nate the arrhythmia. When it is uncertain, treatment of stable patients is best left to experts familiar with the differential diagnosis and alternate therapies available to these patients (Table 2 2 -6). Shotgun therapy runs the risk of bad treatment, induction of unintended arrhythmias (proarrhytl1mia), and unanticipated side effects of drug-drug interactions.

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J Enzerg Med 1 990;8(1): 1 5-20.

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411

Arginine Vasopressin and its Pharmacologic Effects Peripheral effects of arginine vasopressin are mediated by different arginine vasopressin receptors; namely V a, Vn" and 1 v arginine vasopressin receptors. v,a receptors are located 2 on smooth muscle cells in arterial blood vessels and induce vasoconstriction by an increase in cytoplasmic ionized cal­ cium via the phosphatidyl-inositol-bisphosphonate cascade. I 9 On a molar basis, arginine vasopressin was shown to be a sev­ eralfold more potent vasoconstrictor than norepinephrine and angiotensin II. 2 0 In contrast to those of catecholamine­ mediated vasoconstriction, the effects of arginine vasopressin are preserved during hypoxia and severe acidosis. 2 1 Arginine vasopressin--mediated vascular effects differ substantially within particular vascular beds.

However, arginine vasopressin-mediated vascular effects differ substantially within particular vascular beds. Physiologically, most arterial beds exhibit vasoconstriction in response to arginine vasopressin. 22•2 3 Vasopressor effects are strongest in the muscular, adipose, cutaneous, and prob­ ably also the splanchnic vasculature . In a porcine CPR model, Voelckel et a1 . 2 4 found a significantly lower blood flow in the superior mesenteric artery in pigs resuscitated with arginine vasopressin when compared to epinephrine; there were no differences in hepatic or renal blood flow. Like oxytocin-mediated paradoxical vasodilatation of vascu­ lar smooth muscle, vasodilatation after arginine vasopressin has been described not only in the pulmonary, coronary, and vertebrobasilar circulation but, interestingly, also in the mesenteric vascular bed, suggesting a dose-dependent response. 2 5-28 The underlying mechanisms for such an argi­ nine vasopressin-mediated vasodilatation seem to be nitric oxide-dependent. 2 6 Russ and Walker reported that stimula­ tion of VI receptors can release nitric oxide, presumably from the endothelium of some vascular regions. 2 9 Recently, there is increasing evidence of hemodynamically relevant VI receptors on cardiomyocytes . In vitro and animal experi­ ments have demonstrated an increase of intracellular cal­ cium concentration and inotropy after stimulation of myocardial VI receptors. 30•3 I In the kidney, V receptors are located on distal rubules 2 and collecting ducts. Upon stimulation, they facilitate inte­ gration of aquaporines into the luminal cell membrane of the collecting ducts, leading to increased resorption of free water via an adenylate cyclase-dependent mechanism.3 2 Despite the antidiuretic effect of a continuous infusion of arginine vasopressin, a paradoxical increase of urine output has been reported in patients with advanced vasodilatory shock. 3 3-3 5 It is hypothesized that together with increased renal perfusion pressure, arginine vasopressin selectively constricts efferent glomerular arterioles whereas it dilates

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afferent vessels, thus increasing effective filtration pressure in the glomerulus. 3 3 V b receptors are located o n the anterior hypophysis; 1 stimulation induces liberation of ACTH and prolactin. 3 6 Accordingly, Kornberger e t al. 37 reported significantly higher serum ACTH and cortisol concentrations in animals resusci­ tated from cardiac arrest with arginine vasopressin as com­ pared with epinephrine. However, in patients with advanced vasodilatory shock, a continuous arginine vasopressin infu­ sion at dosages of 4 IU/hr affected neither serum ACTH nor cortisol concentrations . 3 8 A complex dysfunction of the hypophyseal-adrenal axis in critical illness may explain the lack of effects of the potent stimulator arginine vasopressin on ACTH-producing cells. Nonetheless, arginine vaso­ pressin seems to be able to promote prolactin excretion by stimulating V b receptors . Additional V b receptors are 1 1 expressed on pancreatic islet cells, where they enhance insulin secretion in the presence of high glycemic levels.39

Arginine Vasopressin During CPR In a porcine model simulating ventricular fibrillation, a dose-response investigation of three arginine vasopressin dosages (0 . 2 , 0.4, and 0 . 8 U/kg) compared with the maxi­ mum effective dose of 2 00 J.Lglkg of epinephrine showed that 0 . 8 U/kg of arginine vasopressin was most effective at increasing blood flow to vital organs40 (Figs. 2 7 -2 and 27 -3).

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FIGURE 27-3 • E ffects of d i ff e r e n t d o se s of a r g i n i n e va s o p r e s s i n ve r s u s h i g h d o s e e p i n e p h r i n e o n l e ft ve n tr i c u l a r b l o o d f l ow. D A =d r u g a d m i n ist r a t i o n (From Li n d n e r K H , P r e n g e l RW, P f e n n i n g e r E G , e t a l . Va s o p r e s s i n i m p r oves vi ta l o r g a n b l o o d f l ow d u r i n g c l o s e d - c h est c a r d i o p u l m o n a ry resuscitati o n i n p i g s . Circulation 1 9 9 5 ; 9 1 :2 1 5-2 2 1 , with p e r m issi o n . )

Correspondingly, arginine vasopressin significantly improved cerebral oxygen delivery during CPR when compared with a maximum dose of epinephrine4 1 (Fig. 2 7 -4) . Furthermore, the effects of arginine vasopressin on vital organ blood flow lasted longer after arginine vasopressin than after 50

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FIGURE 27- 2 • E f f e c ts of d i ffe r e n t d o s e s of a r g i n i n e va s o ­ p r e ss i n ve r s u s h i g h - d o s e e p i n e p h r i n e o n systo l i c a n d d i a s to l i c b l o o d p r e ss u r e . D R =d r u g a d m i n i s t r a ti o n . (F r o m Li n d n e r K H , P r e n g e l RW, P fe n n i n g e r E G , e t a l . Va s o p r e s s i n i m p r oves vi t a l o r g a n b l o o d f l ow d u r i n g c l o s e d - c h est c a r d i o p u l m o n a ry r e s u s c i t a ­ t i o n i n p i g s . Circulation 1 9 9 5 ; 9 1 : 2 1 5-2 2 1 , w i t h p e r m i s s i o n . )

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• E f f e c ts o f d i ffe r e n t d o s e s o f a r g i n i n e va s o ­ p r essi n v e r s u s h i g h - d o s e e p i n e p h r i n e o n t o t a l c e r e b r a l b l o o d f l ow a n d c e r e b r a l p e r f u s i o n p r e ss u r e . D R =d r u g a d m i n i s t r a ti o n . ( F r o m P r e n g e l RW, Li n d n e r K H , K e l l e r A . Ce r e b r a l o xyg e n a t i o n d u r i n g c a r ­ d i o p u l m o n a ry r e s u s c i t a t i o n w i t h e p i n e p h r i n e a n d v a s o p r e s s i n i n p i g s . Stroke 1 9 9 6 ; 2 7 : 1 2 4 1 - 1 2 4 8 , w i t h p e r m iss i o n . )

FIGURE 27-4

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� 7 0 % , hematocrit > 3 0 % or Hb > 8 g dL- I , lactate ::S 2 mmol/L, urine output ::::: 0 . 5 mL!kg/hr, and oxygen delivery index > 600 mL/min/m2 . The goals are achieved with the use of intravenous fluids, inotropes, vasopressors, and blood transfusion as required. The benefits of EGDT include mod­ ulation of inflammation, reduction of organ dysfunction, and reduction of health care resource consumption.9&-98 In severe sepsis, EGDT has also been shown to reduce mortality.96

Early hemodynamic optimization or early goal-directed therapy (EGD7) is an algorithmic approach to restoring and maintaining the balance between systemic oxygen delivery and demand. Monitoring and therapy are initiated as early as possible with the aim of achieving goals within hours ofpresentation.

The systemic ischemia-reperfusion response and myocar­ dial dysfunction of PCAS have many characteristics in com­ mon with sepsis. 7 2 Therefore, it has been hypothesized that early hemodynamic optimization might improve the out­ come of post-cardiac arrest patients. However, the benefit of this approach has not been studied in randomized prospec­ tive clinical trials. Moreover, the optimal goals and strategies to achieve those goals could be different in PCAS, given the concomitant presence of post-cardiac arrest brain injury, myocardial dysfunction, and persistent precipitating pathologies. Hemodynamic instability is common after cardiac arrest and manifests as dysrhythmias, hypotension, and a low cardiac index.63 Underlying mechanisms include intravascu­ lar volume depletion, impaired vasoregulation, and myocar­ dial dysfunction. Dysrhythmias are treated by maintaining normal electrolyte concentrations and using standard drug and electrical therapies. There is no evidence to support the prophylactic use of antiarrhythmic drugs after cardiac arrest. Dysrhythmias are commonly caused by focal cardiac ischemia, and early reperfusion treatment is probably the best antiarrhythmic therapy. Ultimately, survivors whose cardiac arrest is attributed to a primary dysrhythmia should be evaluated for pacemaker or an implantable or internal cardioverter defibrillator (ICD) placement. The first-line intervention for hypotension is to opti­ mize right heart filling pressures using intravenous fluid. In one study, 3 . 5 to 6 . 5 L intravenous crystalloid was required in the first 24 hours after out-of-hospital cardiac arrest to maintain right atrial pressures in the range of 8 to 1 3 mm Hg.63 In one study, out-of-hospital post-cardiac arrest patients had a positive fluid balance of 3 . 5 ::':: 1 .6 L in the first 24 hours, with a CVP goal of 8 to 12 mm Hg.6 The appro­ priate CVP for individual patients is highly variable; for example, those with right heart dysfunction or pulmonary embolism will require a much higher CVP than a patient whose primary problem is severe left ventricular dysfunc­ tion. The optimal MAP for post-cardiac arrest patients has not been defined by prospective clinical trials. These

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patients require an adequate MAP to perfuse the postis­ chemic brain but without subj ecting the postischemic heart to excessive afterload. The loss of cerebrovascular pressure autoregulation makes cerebral perfusion dependent on cere­ bral perfusion pressure (CPP MAP ICP). Since sus­ tained elevation of the ICP during the early post-cardiac arrest phase is uncommon, cerebral perfusion is predomi­ nantly dependent on MAP. If fixed or dynamic cerebral microvascular dysfunction is present, an elevated MAP could theoretically increase cerebral oxygen delivery. In one human study, the MAP during the first 2 hours after ROSC correlated positively with neurologic outcome.99 Good out­ comes have been achieved in published studies where the MAP target was as low as 65 to 75 mm Hg2 7 to as high as 90 to 1 00 mm Hg4•5 for patients admitted after out-of-hospital cardiac arrest. The optimal MAP in the post-cardiac arrest period might be dependent on the duration of cardiac arrest, with higher pressures needed to overcome the potential no­ reflow phenomenon observed with > 1 5 minutes of untreated cardiac arrest.34•35• 100 At the opposite end of the spectrum, a patient with an evolving acute myocardial infarction (AMI) or severe myocardial dysfunction might benefit from the lowest target MAP that will ensure ade­ quate cerebral oxygen delivery. Inotropes and vasopressors should be considered if hemodynamic goals are not achieved despite optimized pre­ load. Post-cardiac arrest global myocardial dysfunction is common;63 •67•7 2 although it is generally reversible and responsive to inotropes, the severity and duration of the myocardial dysfunction will affect surnval.63 Early echocar­ diography will enable the extent of myocardial dysfunction to be quantified and may guide therapy. Impaired vasoregu­ lation is also common in post-cardiac arrest patients; this may require treatment with vasopressors and is also reversible. Persistence of reversible vasopressor dependency has been reported for up to 72 hours after out-of-hospital cardiac arrest despite preload optimization and reversal of global myocardial dysfunction.63 No individual drug or combination of drugs has been demonstrated to be superior in the treatment of post-cardiac cardiovascular dysfunction. The choice of inotrope and/or vasopressor can be guided by blood pressure, heart rate, echocardiographic estimates of myocardial dysfunction, and surrogate measures of tissue oxygen delivery such as Scv0 , lactate clearance, and urine 2 output. If a pulmonary artery catheter (PAC) or some form of noninvasive cardiac output monitor is being used, therapy can be further guided by cardiac index and systemic vascular resistance. If volume expansion and treatment with vasoactive and inotropic drugs do not restore adequate organ perfusion, consider mechanical circulatory assistance. 101 •102 This treat­ ment can support the circulation for the period of transient severe myocardial dysfunction that often occurs after ROSC.63 The intra-aortic balloon pump (IABP) is the most readily available device to augment myocardial perfusion; it is generally easy to insert with or without radiologic imag­ ing, and its use after cardiac arrest is well documented.6•93 Monitoring of the balance between systemic oxygen delivery and consumption can be accomplished indirectly =

-

with Sv0 (mixed venous oxygen saturation) or Scv0 (cen­ 2 2 tral venous oxygen saturation) . However, use of PAC­ required for the measurement of Sv0 -is diminishing, the 2 optimal Scv0 goal for post-cardiac arrest patients has not 2 been defined, and the value of continuous Scv0 monitoring 2 is uncertain. Urine output and lactate clearance are surrogates for oxygen delivery. Although two EGDT trials used a urine output target of ::::: 0 . 5 mL/kg/hr,96•98 a higher urine output goal of > 1 mL/kg/hr is reasonable in post-arrest patients treated with therapeutic hypothermia, because this inter­ vention induces diuresis.6 A limitation is that urine output can be misleading in the presence of acute or chronic renal insufficiency. Lactate concentrations are elevated early after ROSC because of the total-body ischemia caused by cardiac arrest. This limits the utility of a single measurement during early hemodynamic optimization. Lactate clearance is asso­ ciated with outcome after out-of-hospital cardiac arrest; 1 03• 1 04 however, lactate clearance can be impaired by hepatic insufficiency and hypothermia. The optimal goal for hemoglobin concentration in the post-cardiac arrest phase has not been defined.6 In summary, based on the limited available evidence, reasonable goals for post-cardiac arrest syndrome include a MAP of 65 to 1 00 mm Hg (taking into consideration the patient's normal blood pressure, the cause of the arrest, and the severity of any myocardial dysfunction), S cv0 > 7 0 % 2 , urine output > 1 mL/kg/hr, and a normal o r decreasing serum lactate concentration. Goals for hemoglobin con­ centration during postresuscitation care remain to be defined.

Controlled Reoxygenation Existing guidelines emphasize the use of an inspired oxy­ gen concentration of 1 00 % during CPR, and clinicians will frequently maintain ventilation with 1 00 % oxygen for vari­ able p eriods after RO S C . Although it is important to ensure that patients are not hypoxemic, a growing body of preclinical evidence suggests that hyperoxia during the early stages of reperfusion harms postischemic neurons by causing excessive oxidative stress.47•48• 1 05• 1 06 Most relevant to post-cardiac arrest care, ventilation with 1 00 % oxygen for the first hour after ROS C in dogs resulted in worse neurologic outcome compared with immediate adjustment of the fractional inspired oxygen concentration (Fi0 ) to 2 produce an arterial oxygen saturation of 94% to 9 6 % .49 Thus, based on preclinical evidence alone, it is advisable to avoid unnecessary arterial hyperoxia, especially during the initial post-cardiac arrest period. This can be achieved by adjusting the Fi0 to produce an arterial oxygen saturation 2 of 94% to 96% .

Ventilation Although cerebral autoregulation is either absent or dys­ functional in most patients in the acute phase after cardiac

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arrest,40 cerebrovascular reactivity to changes in arterial car­ bon dioxide tension seems to be preserved.4 1 •43 • 1 07• 1 08 Cerebrovascular resistance may be elevated for at least 24 hours in comatose survivors of cardiac arrest.43 There are no data to support the targeting of a specific PaC0 after resus­ 2 citation from cardiac arrest; however, extrapolation from studies of other cohorts suggest ventilation to normocarbia is appropriate. Studies in brain-injured patients have shown that the cerebral vasoconstriction caused by hyperventilation may produce potentially harmful cerebral ischemia. 1 09-1 1 1 Hyperventilation also increases intrathoracic pressure, which will decrease cardiac output during and after cardiopul­ monary resuscitation. 1 12 • 1 1 3 Hypoventilation may also be harmful because hypoxemia and hypercarbia can increase intracranial pressure or compound metabolic acidosis, which is common shortly after ROSC. High tidal volumes cause barotrauma, volutrauma, 1 14 and biotrauma 1 1 5 in patients with acute lung injury. Recent evidence indicates that normal lungs can also be injured by ventilation with high tidal volumes. 1 16 Although there are no data to support use of a specific tidal volume during postre­ suscitation care, it would seem reasonable, if patients are considered to be at risk of acute lung injury, to avoid tidal volumes >8 mL/kg. In inducing therapeutic hypothermia, additional blood gases may be helpful to guide adjustment of tidal volumes, because cooling will decrease metabolism and, therefore, the tidal volumes required.

Sedation and Neuromuscular Blockade If patients do not show adequate signs of awakening within the first 5 to 1 0 minutes after ROSC, endotracheal intubation (if not already achieved), mechanical ventilation, and sedation will be required. Adequate sedation will reduce oxygen con­ sumption, which is further reduced with therapeutic hypothermia. Use of published sedation scales for monitoring these patients (e.g., the Richmond or Ramsay scale) may be helpful. 1 1 7• 1 1 8 Both opioids (analgesia) and hypnotics (e.g., propofol or benzodiazepines) should be used. In patients treated with therapeutic hypotl1ermia, optimal sedation can prevent shivering, which is most prominent during the induc­ tion phase, and reduce the time taken to achieve target tem­ perature. If shivering occurs despite deep sedation, neuro­ muscular blocking drugs (as an intravenous bolus or infusion) should be used with close monitoring of sedation and neuro­ logic status (e.g., seizures) . Because of the relatively high incidence of seizures after cardiac arrest, continuous elec­ troencephalographic (EEG) monitoring should be considered for patients requiring sustained neuromuscular blockade. 1 1 9

Therapeutic Hypothermia A period of hyperthermia is common in the first 48 hours after cardiac arrest,50• 12 0• 1 2 1 and the risk of a poor neurologic outcome increases for each degree of body temperature > 3 rc. 5 1 A retrospective study of patients admitted after out-of-hospital cardiac arrest reported that a maximal

433

recorded temperature > 3 7 . 8 °C was associated with increased in-hospital mortality (OR 2 . 7 ; 9 5 % CI 1 .2-6 . 3 ) .8 If therapeutic hypothermia (see below) is not feasible or is contraindicated, then, at a minimum, pyrexia must be pre­ vented. A period of hyperthermia is common in the first 48 hours after cardiac arrest, and the risk of a poor neurologic outcome increases for each degree of body temperature >37'C. There is good animal and human evidence to indicate that mild hypothermia, even when induced after ROSC, is neuroprotective and improves outcome after a period ofglobal cerebral hypoxia-ischemia.

There is good animal and human evidence to indicate that mild hypothermia, even when induced after ROSC, is neu­ roprotective and improves outcome after a period of global cerebral hypoxia-ischemia. 122 • 12 3 Cooling suppresses many of the pathways leading to delayed cell death. Hypothermia decreases the cerebral metabolic rate for oxygen (CMR0 ) 2 by about 6% for each 1 oc reduction in temperature/ 2 4 and this may reduce the release of excitatory amino acids and free radicals. 122 Hypothermia blocks the intracellular conse­ quences of excitotoxin exposure (high calcium and glutamate concentrations). Hypothermia may suppress apoptosis (pro­ grammed cell death) by blocking caspases, a family of cellu­ lar proteases that normally mediate this process. 12 3 Finally, hypothermia reduces the inflammatory response, which is a feature of the post-cardiac arrest period . Inflammatory mediators are thought to exacerbate delayed neurologic 111Jury. Two randomized clinical trials and a meta-analysis showed improved outcome in adults who remained coma­ tose after initial resuscitation from out-of-hospital ventricu­ lar fibrillation (VF) cardiac arrest and were cooled within minutes to hours after ROSC.3•4• 12 5 Patients in these studies were cooled to 3 3 °C or to the range of 3 2 °C to 3 4°C for 1 2 t o 2 4 hours . The Hypothermia After Cardiac Arrest (HACA) study included a small subset of patients with in­ hospital cardiac arrest.3 Four studies with historical control groups showed benefit after therapeutic hypothermia in comatose survivors of out-of-hospital cardiac arrest after non-VF arrest1 2 6 and all rhythm arrests/·6•8 1 respectively. Other observational studies also indicate its possible benefit following cardiac arrest from other initial rhythms and in other settings. 12 7• 128 Mild hypothermia is the only therapy given in the post-cardiac arrest setting that has been shown to increase survival, and it should be part of a standardized treatment strategy for comatose survivors of cardiac arrest.6• 12 9• 1 30 The precise patients that may benefit from this treatment, the ideal induction technique (alone or in combi­ nation), target temperature, duration, and rewarming rate have yet to be established. Animal studies demonstrate a benefit of very early cool­ ing either during CPR or within 1 5 minutes of ROSC when cooling is maintained only for a short time ( 1 -2 hours). m , m However, when prolonged cooling is used (>24 hours), less is known about the therapeutic window. The median time to

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achieve target temperature in the HACA trial was 8 hours (interquartile range [IQR] 6-2 6) , 3 while in the B ernard study, average core temperature was reported to be 3 3 . 5 °C within 2 hours of ROSC.4 Clearly, additional clinical studies are needed to optimize this effective therapeutic strategy. At this time, each center should use a strategy that best suits its infrastructure, logistics, and treatment plan.

·�····································································································· S e e W e b s i t e f o r I LCO R S c i e n t i f i c St a te m e n t

"V'

o n Hyp o t h e r m i a

Practical Application of Therapeutic Hypothermia The practical application of therapeutic hypothermia is divided into three phases: induction, maintenance, and rewarming. Induction can be achieved easily and inexpen­ sively with intravenous ice-cold fluids (3 0 mL/kg of saline 0.9% or Ringer's lactate) 1 3 3-1 3 7 or traditional ice packs placed in the groins, armpits , and around the neck and head. Infusion of 30 mL/kg of 4aC crystalloid will reduce the core temperature by approximately 1 . 5°C. In most cases, it is easy to cool patients initially after ROSC because the tempera­ ture normally decreases within this first hour. 8·5 1 Initial cool­ ing is facilitated by concomitant neuromuscular blockade and sedation, which will prevent shivering. 1 3 8 Magnesium sulphate, a naturally occurring NMDA receptor antagonist that reduces the shivering threshold slightly, can also be given. 1 3 9 Other potential benefits of magnesium are that it is a vasodilator, which will increase the cooling rate; 1 40 it is antiarrhythmic, and there are some animal data indicating that it offers additional neuroprotection in combination with hypothermia. 141 Magnesium sulphate 5 g can be infused over 5 hours, which will cover the period of induction of hypothermia. The shivering threshold can also be reduced by warming the skin; the shivering threshold is reduced by 1 °C for every 4°C increase in skin temperature . 1 42 Application of a forced-air warming blanket will reduce shivering during intravascular cooling. 1 43 If indicated, the patient can be transferred to the angiography laboratory with ongoing cooling using these methods.6•7 Surface or internal cooling devices (described below) can also be used alone. 128· 1 44 In the maintenance phase, a cooling method with effec­ tive temperature monitoring that avoids temperature fluctu­ ations is preferred. This is best achieved with external or internal cooling devices that include continuous temperature feedback to achieve a set target temperature. The tempera­ ture is typically monitored from a thermistor placed in the bladder and/or esophagus. Typical external devices are cool­ ing blankets or pads with water-filled circulating systems or more advanced systems that include cooling tents (witl1 cold air) . 1 2 8• 1 44-1 49 Typical internal cooling devices include intravascular cooling catheters, placed usually in the femoral or subclavian veins. 128 However, less sophisticated methods such as cold wet blankets on the torso and around the extremities or ice packs combined with ice cold fluids can also be effective; however, these methods may be more time-con-

suming for nursing staff, may result in greater temperature fluctuations, and do not enable controlled rewarming. Ice­ cold fluids alone cannot be used to maintain hypothermia. 1 50 As yet, there are no data indicating that any specific cooling technique increases survival when compared with any other cooling technique; however, internal devices enable more precise temperature control compared with external tech­ niques. 1 45 Overcooling and rebound hyperthermia are more likely to occur with external cooling techniques 1 5 2 because of the inevitable lag time between a change in the temperature setting of the external device and the core temperature. The rewarming phase can be achieved with either exter­ nal or internal cooling devices (if these are used) or with other heating systems. The optimal rate of rewarming is not !mown, but the consensus is currently about 0.2 5°C to 0. 5°C of warm­ ing per hour. 1 2 7 Particular care should be taken during the cool­ ing and rewarming phases because metabolic rate, plasma elec­ trolyte concentrations, and hemodynamics may change rapidly. Therapeutic hypothermia is associated with several complications in addition to the shivering, which has been discussed. 1 5 2 Mild hypothermia increases systemic vascular resistance, which reduces cardiac output. A variety of arrhythmias can be induced by hypothermia, but bradycardia is the most common to be documented in therapeutic hypothermia studies. 12 8 Hypothermia induces a diuresis, and any associated hypovolemia will compound hemodynamic instability. Hypothermia also causes electrolyte abnormalities such as hypophosphatemia, hypokalemia, hypomagnesemia, and hypocalcemia; these, in turn, can cause arrhythmias. 1 5 2 ·153 Hypothermia decreases insulin sensitivity and insulin secre­ tion, which results in hyperglycemia.4 This should be treated with insulin (see below). As a consequence of its effect on platelet and clotting function, mild hypothermia impairs coagulation and increases bleeding. Hypothermia can impair the immune system and increase infection rates. 1 54 In the HACA study, pneumonia was more common in the cooled group, but this did not reach statistical significance. 3 The serum amylase concentration is almost always increased dur­ ing hypothermia, but the significance of this unclear. The clearance of sedative drugs and neuromuscular blockers is reduced by up to 3 0 % at a temperature of 3 4°C. 155 Relative contraindications to hypothermia include severe systemic infection, cardiogenic shock (systolic blood pres­ sure < 9 0 mm Hg despite inotropic drugs), established multiple organ failure, and preexisting medical coagulopa­ thy. Although thrombolytic therapy is not considered a con­ traindication to therapeutic hypothermia, the interaction of these therapies when simultaneously administered has not been formally studied in post-cardiac arrest patients. In summary, both preclinical and clinical evidence indi­ cates that mild therapeutic hypothermia is an effective therapy for PCAS. Unconscious adult patients with spontaneous circu­ lation after out-of-hospital VF cardiac arrest should be cooled to 3 2 °C to 3 4°C for at least 12 to 24 hours. 12 9 Most experts rec­ ommend cooling for at least 24 hours. While data support cooling to 3 2 °C to 3 4°C, the optimal temperature has not been determined. Induced hypothermia might also benefit uncon­ scious adult patients with spontaneous circulation after out-of­ hospital cardiac arrest from a nonshockable rhythnl or cardiac arrest in hospital. 12 9 Although the optimal time to start cooling

CHAPTER 28

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POST-CARDIAC ARREST SYNDROME AND MANAGEMENT

has not been defined clinically, it is reasonable to induce hypothermia as soon as possible. The therapeutic window, or time after ROS C at which therapeutic hypothermia is no longer beneficial, has also not been clinically defined. Rapid infusion of ice-cold fluid at 30 mL/kg is a very effective, simple method for initiating cooling. Shivering should be treated by ensuring adequate sedation and/or giving neuromuscular blocking drugs. Bolus doses of neuromuscular blockers are usually adequate, but infusions are occasionally necessary. Slow rewarming is recommended (0.25°C-0.5°Cihr), although the optimal rate for rewarming has not been clinically defined. If therapeutic hypothermia is not undertaken, any pyrexia occur­ ring in the first 72 hours after cardiac arrest should be aggres­ sively treated with antipyretics or active cooling.

Seizure Control and Prevention S eizures and/or myoclonus occur in 5 % to 1 5 % of adult patients who achieve ROSC and in 1 0% to 40% of those who remain comatose. 22 •30•1;6• 1 ;7 Seizures increase cerebral metab­ olism by up to threefold. 1 ;8 There are no studies that directly address the use of prophylactic anticonvulsant drugs after car­ diac arrest in adults. Anticonvulsants such as thiopental, and especially phenytoin, have been shown to be neuroprotective in experimental studies, 1 ;9-161 but a clinical trial of thiopental after cardiac arrest showed no benefit. 162 Myoclonus can be particularly difficult to treat; phenytoin is often ineffective. Clonazepam is the most effective antimyoclonic drug, but sodium valproate and levetiracetam may also be effective. 2 9 Effective treatment of myoclonus with propofol has been described. 1 63 With therapeutic hypothermia, survivors with good neurologic function have been reported, despite initially displaying severe postarrest status epilepticus. 164•165

Glucose Control Tight control of blood glucose (4.4-6. 1 mmol/L or 80-1 1 0 mg/dL) using insulin reduced hospital mortality in critically ill adults in a surgical ICU 1 66 and appeared to protect the central and peripheral nervous system. 1 67 When the same group repeated this study in a medical ICU, the overall mor­ tality was similar in the intensive insulin and control groups. 1 68 Among the patients with an ICU stay of 3 days or longer, intensive insulin therapy reduced the mortality from 5 2 . 5 % (control group) to 43 % (P 0.009). Of the 1 ,2 00 patients in the medical ICU study, 6 1 had neurologic dis­ ease; the mortality among these patients was the same in the control and treatment groups (2 9 % versus 3 0 %). 1 68 In the United Kingdom, the median length of ICU stay for ICU survivors after admission following cardiac arrest is 3 .4 days, 1 2 which is the same as that in Norway.6 In a study from Finland, 90 unconscious survivors of out-of-hospital VF cardiac arrest were cooled and random­ ized into two treatment groups: a strict glucose control group (SGC), with a blood glucose target of 4 to 6 mmol!L (2 7-1 08 mg/dL) , and a moderate glucose control group (MGC), with a blood glucose target of 6 to 8 mmoi!L ( 1 0 8- 1 44 mg/dL) . 1 69 B oth groups were treated with an =

435

insulin infusion for 48 hours. Episodes of moderate hypo­ glycemia (< 3 .0 mmol/L or 54 mg/dL) occurred in 1 8 % of the SGC group and 2 % of the MGC group (P 0.008); however, there were no episodes of severe hypoglycemia ( 2 ng/mL in conjunction with clinical signs of toxicity. In the acute setting, the patient will have more dramatic clinical and laboratory findings than in the chronic setting. Patients with chronic toxicity will be more symptomatic, with lower corresponding digoxin serum levels. Key prognostic factors indicating increased risk for death are age > 5 5 , atrioventricular block, and potassium >4.5 mEq/L. 1 45

453

Management Patients with possible digoxin toxicity should be managed aggressively owing to the potential for morbidity and mor­ tality. 1 44 All patients should have IV access, frequent assess­ ment of vital signs, and continuous cardiac monitoring. If the patient's mental status is adequate, activated charcoal can be administered as a single dose. Multiple doses of charcoal have been reported to be of value for digitoxin or digoxin preparations and may be useful if antidotal therapy is not available. 1 46· 147 Digoxin immune Fab fragments are specific antidigoxin antibodies raised in sheep. Only the Fab fragment is used in order to decrease the risk of immunogenicity. This antidote has been used successfully in adults since the 1 9 70s. Administration of the Fab fragments is indicated in cases of severe digitalis intoxication that is suspected by history, by a high level, or in those manifesting significant signs and symp­ toms of toxicity. Specific indications are based on absolute level, amount ingested, potassium level, and symptoms, as generated from case series and observational studies. 1 48-1 53 In general, those with potentially life-threatening dysrhythmias, significant GI symptoms, altered mental status, or a potas­ sium >5 mEq/L in the setting of elevated digoxin levels are candidates for antidote administration. Markedly elevated 6hour levels even in the absence of symptoms should also prompt consideration of antidotal therapy. Most patients who respond to Fab fragment therapy do so within 1 hour and have a complete response by 4 hours. 149 Similarly, the effect on potassium concentration is delayed, which prompts the need for standard interventions for hyperkalemia in addition to Fab fragments. Glucose, insulin, and bicarbonate are appropriate. Calcium salts should be avoided because of the risk of exacerbating cardiotoxicity and precipitating cardiac arrest, although this risk has recently been disputed. 1 54· 1 55 Dosage of Fab fragments is based either on the acute ingestion of a known amount or on the steady-state serum concentration. Guidelines are available in the package insert or at http://us.gsk.com/products/assets/us_digibind.pdf. It is

important to note that following treatment with Fab total digoxin levels will be markedly elevated. Free digoxin levels may be obtained that will correlate with the amount ofdrug that is biologically active. Fab fragments are the cornerstone of therapy for the digoxin-toxic patient. However, the time to onset of Fab fragments mandates use of adjunctive therapies in the unsta­ ble patient. Atropine is appropriate for symptomatic brady­ cardia. The class Ib antiarrhythmics phenytoin and lidocaine may be effective. Phenytoin was first proposed as therapy for digoxin toxicity in the 1 950s and was widely used until the advent of Fab fragments . 1 56· 1 57 Both suppress ventricular automaticity without affecting conduction, and phenytoin improves AV conduction. 1 58 Hypokalemia should be corrected with careful attention to avoiding overcorrection. Magnesium therapy has been reported as efficacious in refractory ventricular arrhyth­ mias. 159·1 60 It should be repleted in deficient states, as hypo­ magnesemia may lead to refractory hypokalemia; but care should be taken in cases of renal insufficiency to avoid toxicity.

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Cardiac pacing has not been shown to decrease mortal­ ity when compared with maximal medical therapy that includes Fab fragments, and it carries a high rate of compli­ cations. 1 5 2· 1 6 1 Cardiac pacing should only be used as a ther­ apy once other interventions have proven futile or are not available. Hemodialysis, hemofiltration, and hemoperfusion do not aid in the management of digoxin toxicity. Patients who are asymptomatic, without dysrhythmias, or with minor ingestions or undetectable to therapeutic lev­ els 6 hours after ingestion may be medically cleared. Any patient that has signs and symptoms of digoxin toxicity should be admitted to a monitored bed. All patients with sig­ nificant signs and symptoms and in whom the use of Fab fragments is being considered should be admitted to an ICU. Consultation with the poison control center, toxicolo­ gist, or cardiologist familiar with the treatment of these cases is recommended.

Plants Containing Cardiac Glycosides Foxglove (Digitalis purpurea), lily of the valley (Convallaria majalis), common oleander (Nerium oleander), and yellow oleander (Thevetia peruviana) all contain digitalis-like glyco­ sides. Ingestion of yellow oleander results in the most sig­ nificant degree of toxicity. Of all varieties of oleander, yellow oleander has been responsible for the greatest number of fatal poisonings worldwide. All parts of the plant contain several cardiac glycosides and can produce a syndrome sim­ ilar to digoxin poisoning when ingested. The patient may manifest abdominal pain, nausea, vom­ iting, and diarrhea as well as weakness, bradycardia, and AV block. Because some of the plant glycosides are structurally similar but not identical to digoxin, a serum digoxin level may not be accurate. Treatment with digoxin immune Fab fragments is safe and effective for toxicity caused by yellow oleander. 162 The exact dose required is unknown, but a recent randomized con­ trolled trial suggests that much higher doses may be needed than those used to treat digoxin overdose. 162 As with many modern therapeutic agents, a lack of availability in the devel­ oping world has resulted in increased morbidity from this treatable illness. 1 63 Fortunately, as an alternative, multiple­ dose activated charcoal can be efficacious in this setting. 1 64

Anticholinergic Agents Toxicology Acetylcholine is the neurotransmitter involved in the activa­ tion of both nicotinic and muscarinic cholinergic receptors. Nicotinic receptors are ligand-gated sodium and calcium channels. Muscarinic receptors are G protein-coupled. 1 65 Three of these muscarinic receptors are stimulatory, increas­ ing cAMP and intracellular calcium; two are inhibitory, reducing cAMP and intracellular calcium. The anticholinergic toxidrome results from competitive inhibition of acetylcholine at muscarinic receptors . Muscarinic receptors are found throughout the CNS and in sympathetic and parasympathetic ganglia. This toxidrome is

quite common and may result from both pharmaceutical preparations and various plant species. Anticholinergic or antimuscarinic toxicity may be divided into central and peripheral effects. Central effects include alteration in mental status including delirium, hallu­ cinations, agitation, and seizures. Peripheral effects include mydriasis, tachycardia, flushing, dry skin and mucous mem­ branes, urinary retention, and decreased GI motility. The onset of anticholinergic toxicity varies depending on the particular toxin but usually occurs within several hours . Although central and peripheral anticholinergic effects are commonly seen simultaneously, the central effects may occasionally persist after the peripheral effects have resolved. An often-used mnemonic to remember the clinical manifestations of anticholinergic toxicity is "Hot as a hare, Blind as a bat, Dry as a bone, Red as a beet, Mad as a hatter. " The more significant components of anticholinergic toxicity is blockade of muscarinic receptors in the brain. The excessive CNS excitation that results clinically manifests as agitation, anxiety, delirium, lethargy, drowsiness, coma, and occasionally seizures. Peripheral blockade of muscarinic receptors also leads to cardiovascular effects such as tachy­ cardia from antagonism of vagal tone, mydriasis with the inability to accommodate, decreased activity of sweat glands, hyperthermia, urinary retention, and reduced gut motility. Drugs that may cause anticholinergic symptoms include antihistamines, antipsychotics, tricyclic antidepressants, and atropine. The antihistamine diphenhydramine is a common cause. In addition to its anticholinergic properties, it has type IA antidysrhythmic effects. A prolonged QRS interval with a subsequent prolonged QT may result, and severe car­ diac dysrhythmias can occur. 1 66-1 68 Cases of torsades de pointes have also been reported. 1 69 Tricyclic antidepressants, which are discussed in a later section, behave similarly, although their cardiotoxic effects are more severe. Serum drug concentrations are neither readily available nor helpful in the clinical setting. In overdoses, a screening acetaminophen level is indicated because products contain­ ing a combination of acetaminophen and antihistamine are common. Patients with severe psychomotor agitation and seizures should have a serum creatine kinase assessed because of the possibility of rhabdomyolysis. Patients who ingest the antihistamine doxylamine are particularly at risk for rhabdomyolysis. 1 70-17 2 Injury is likely due to direct drug injury to striated muscle. m Although most anticholinergic toxicity will result from ingestion, systemic anticholinergic toxicity has been reported from cutaneous absorption and from ocular exposure. 1 74· 1 75

Management In most cases of anticholinergic toxicity, supportive care (i. e. , benzodiazepines to treat agitation or seizures; cooling for hyperthermia) will be adequate therapy. Activated char­ coal should be considered. Other associated complications, such as rhabdomyolysis from doxylamine, are also treated supportively with good outcome. However, cases of doxy­ lamine-related renal failure requiring hemodialysis are reported. 1 73 Wide-complex cardiac dysrhythmias from

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severe diphenhydramine toxicity should be treated with boluses ( 1 -2 mEq/kg) of IV sodium bicarbonate to reverse the sodium channel effects. 1 68• 1 76•1 77 For patients demonstrating profound central anti­ cholinergic toxicity (delirium, hallucinations, tachydys­ rhythmias, or seizures) unresponsive to traditional doses of benzodiazepines, physostigmine may be used as antidotal therapy. Physostigmine is an anticholinesterase agent that antagonizes the effects of anticholinergic agents. It is suffi­ ciently lipophilic to cross the blood-brain barrier and can counteract both peripheral and central effects. The onset of action is within several minutes, and the half-life of the drug is approximately 1 5 minutes. For agents that have a pro­ longed anticholinergic effect on the CNS , such as scopo­ lamine, redosing may b e necessary. Physostigmine has demonstrated efficacy for severe anticholinergic syndromes and has proven to be more effective than benzodi­ azepines. 1 78-1 8 1 Physostigmine was a first-line agent for anticholinergic poisoning in the 1 970s, even in cases of cyclic antidepres­ sant ingestions. 1 82 In 1 980, Pentel and Peterson published two cases of asystolic cardiac arrest following physostig­ mine use in the setting of tricyclic overdose; as a result, it became a rarely used drug. 1 83 Currently, physostigmine is considered appropriate therapy only in patients wim anti­ cholinergic syndromes who meet strict criteria: normal QRS and QTc intervals, clear historical evidence that tri­ cyclic antidepressants have not been ingested, and absence of mechanical bowel and/or urogenital tract obstruction. Relative contraindications are reactive airways disease, seizure, cardiac conduction abnormalities, and peripheral vascular disease. 1 84 Adverse effects of physostigmine include cholinergic crisis with increased bronchial secretions, bradycardia, and seizures. Although s eizures have been reported with physostigmine, they are also a complication of severe anti­ cholinergic syndrome. The association between physostig­ mine, tricyclic antidepressants , and seizures is well reported in the literature . 1 85-1 87 Controversy often results, as this is one of me CNS manifestations that physostig­ mine may resolve . S eizures occur more commonly in patients with QRS durations > 1 00 ms, which may indicate more significant intoxication. 1 87 Rapid administration of physostigmine may induce seizure; therefore, it is impera­ tive to use small doses, titrating upward to desired effect. 1 88 The patient should be closely monitored and the practi­ tioner should be prepared for cholinergic toxicity with oral and laryngeal suction, endotracheal intubation, and atropine, as needed. Patients who have significant anticholinergic toxicity and those treated with physostigmine should be admitted to an intensive care setting. Patients exposed to anticholinergic agents with additional toxicity (e. g . , tricyclic antidepres­ sants, phenomiazines) should also be closely observed for a minimum of 6 hours regardless of resolution of symptoms. Those with minimal anticholinergic toxicity from an inges­ tion without additional toxicity can be observed in the emer­ gency department until symptoms resolve. Once symptoms resolve, they may be medically cleared.

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Tricyclic Antidepressants Toxicology Antidepressants continue to represent a large portion of poi­ son center referrals and poisoning fatalities in the United States. Historically, tricyclic antidepressants (TCAs) were the leading cause of poisoning fatalities. Owing to their superior efficacy, lower adverse-effects profile, and a reduced incidence of serious toxicity, selective serotonin reuptake inhibitors (SSRis) and atypical antidepressants are currently prescribed more frequently than TCAs. TCAs have a small therapeutic index, such that 1 0 to 2 0 mg/kg of most TCAs will cause significant toxicity. In infants or toddlers, this correlates to only one or two 1 00mg tablets. Life-threatening exposures in adults are associ­ ated with ingestions > 1 ,000 mg. TCAs are rapidly and eas­ ily absorbed in the intestine, although in overdose the anticholinergic effects may decrease gut motility, resulting in delayed absorption with prolonged or cyclic symptoms. TCAs and their metabolites are highly lipophilic and exten­ sively protein-bound. Despite this, they have a large volume of distribution, resulting in a high tissue-to-plasma ratio. In overdose, TCAs affect the cardiovascular system, the autonomic nervous system, and the CNS . This manifests as cardiac conduction delays , dysrhythmias, hypotension, altered mental status, and seizures. There are four main mechanisms by which TCAs manifest their toxic effects . Inhibition o f norepinephrine and serotonin reuptake occurs at central presynaptic terminals and may result in early tachycardia and hypertension. 1 89 Peripheral and central antagonism of muscarinic acetylcholine receptors results in anticholinergic symptoms and tachycardia. 1 90 Sodium chan­ nel blockade causes a quinidine-like effect, prolonging the QRS interval, provoking atrial and ventricular arrhythmias, and perhaps ultimately resulting in bradycardia and hypotension. 1 9 1-1 93 Antagonism of peripheral alpha -adren­ 1 ergic receptors may also cause hypotension. 1 89 TCAs can also prolong the QT interval due to potassium channel effects , and cases of torsades de pointes have been reported. 1 94-1 96 Altered mental status and CNS depression are due to central anticholinergic effects, but the patho­ physiology of lowered seizure threshold is not fully under­ stood. Possible explanations include an increased level of monoamines, antidopaminergic properties, inhibition of neuronal sodium channels, or interaction with CNS GABA receptors. Clinical presentations consistent witl1 TCA poisoning include lethargy, coma, seizures, cardiac dysrhythmias, and conduction delays. Clinical deterioration can be sudden and unpredictable, but patients with significant ingestions will typically demonstrate symptoms within 6 hours of presenta­ tion. 1 97 , 198 Cardiovascular toxicity manifests as tachycardia, brady­ cardia, conduction delays, dysrhythmias, and hypotension. With the exception of sinus tachycardia and infrequent pre­ ventricular contractions (PVCs), ECG abnormalities are often associated with neurologic dysfunction. 1 99 QRS pro­ longation is a marker for serious toxicity, although absence of this finding does not rule it out. 200-2 02 In comparison to QRS

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prolongation, an R wave in AVR measuring > 3 mm may be a more sensitive marker. 203-2 05 Physiologic consequences of tricyclic antidepressant overdose are dynamic, and the accompanying ECG changes may not manifest early in the clinical course. Therefore, serial ECGs and continuous car­ diac monitoring are essential in the first 6 to 8 hours. 2 06 CNS toxicity manifests as altered mental status, agita­ tion, coma, and seizures . S eizures are more common in patients with ECG abnormalities. 1 87 They are usually gener­ alized, brief, and tend to occur within the first few hours after presentation. 197•198 Other anticholinergic effects that are fre­ quently seen are urinary retention, dry flushed skin, dry mouth, dilated pupils, and hyperthermia. Compared with the classic tricyclic antidepressants, the atypical agents amoxap­ ine and maprotiline are associated with a higher incidence of seizures, but the argument that they have less cardiovascular toxicity is not supported in the literature. 187•196•207

Management Aggressive supportive care, GI decontamination when appropriate, and close observation are essential to the man­ agement of patients with TCA overdose. There is no role for enhanced elimination with hemodialysis, hemofiltration, or hemoperfusion because of the high volume of distribution and extensive protein binding of these agents . 1 01 Physostigmine should be avoided for reasons outlined in the prior section on anticholinergic toxicity. Cardiovascular toxicity is treated with sodium bicar­ bonate, administered by IV bolus, as a first-line agent. The beneficial effects of sodium bicarbonate are clear, as indi­ cated by numerous case reports and case series, although there are no randomized controlled trials. 2 08 Alkalinization has been shown to decrease heart rate, narrow QRS inter­ vals, and increase blood pressure. 2 09• 2 10 Sodium bicarbonate bolus has been demonstrated to reverse TCA-induced ven­ tricular tachycardia despite preexisting alkalosis. 2 1 1 The exact mechanism is unclear, but is likely related to both sodium loading and reversal of acidosis. The exact QRS interval at which to initiate sodium bicarbonate therapy is debated, with both > 1 00 ms being documented. Other indi­ cations for sodium bicarbonate include hypotension and compromising dysrhythmias . There is no evidence for prophylactic sodium bicarbonate use or with regard to utilizing a bicarbonate infusion following the bolus . However, acidosis should be avoided and the pH should be maintained below 7 . 5 5 . Repeat boluses should be adminis­ tered for recurrence of symptoms or ECG abnormalities. Hypotension is treated by volume expansion with isotonic saline. Vasopressors are utilized in cases refractory to volume expansion. Dopamine may be effective; however, owing to the depletion of endogenous norepinephrine seen in TCA overdose, norepinephrine infusion is preferred. 2 12 It offers the advantages of beta agonism for myocardial depression and alpha agonism for vasoconstriction. Refractory dysrhythmias or hypotension despite alka­ linization require additional therapy. Lidocaine, a class Ib antiarrhythmic, is considered second-line therapy for ven­ tricular dysrhythmias in TCA poisoning; however, its use is

poorly supported by the literature. 1 93 Lidocaine was found to be ineffective in a rat model of amitriptyline toxicity and transiently effective in a canine model; however, it also resulted in hypotension. 2 1 3 • 2 1 4 Lidocaine has minimal effects on phase 0 of the action potential, which is likely the reason adverse effects have not been reported. Likewise, concerns that its sodium channel-blocking properties may be deleterious are not sup­ ported by the literature. Class Ia and Ic antiarrhythmics are contraindicated due to blockade of fast sodium channels. Class III antiarrhythmics have potassium channel-blocking effects and are, therefore, contraindicated owing to risk of prolong­ ing the QT interval. Phenytoin, another class Ib antiarrhyth­ mic and antiepileptic, has been considered as an agent to reverse TCA-induced dysrhythmias. It was generally ineffec­ tive in rabbits and found to be proarrhythmic in dogs. 2 15•2 1 6 Therefore, the use of phenytoin cannot be recommended. There are conflicting animal data regarding the efficacy of magnesium sulfate for TCA toxicity. 2 1 3 • 2 17•2 1 8 Despite this, there are three case reports demonstrating efficacy in per­ sistent ventricular dysrhythmias. Amitriptyline ingestions in two pediatric patients resulted in ventricular tachycardia that was refractory to standard measures. Following magne­ sium sulfate infusions, the patients converted to sinus rhythm. 2 1 9• 22 0 Amitriptyline ingestion in an adult patient caused ventricular fibrillation refractory to standard meas­ ures. The patient converted to "stable regular heart rhythm" after magnesium sulfate infusion followed by "electrocon­ version" therapy. 22 1 Seizures are usually brief and self-limited, but pro­ longed seizures can lead to acidosis, hyperthermia, rhab­ domyolysis, and hypoxia, all of which can exacerbate cardio­ vascular toxicity. Benzodiazepines are first-line treatment, followed by barbiturates or propofol. 222 Phenytoin should be avoided out of concern for arrhythmogenicity and because it is generally ineffective for toxin-induced seizures. 2 16 Patients who at presentation have signs of maj or toxic­ ity, such as seizures, coma, dysrhythmia, hypotension, respi­ ratory depression, or a QRS interval > 1 00 ms, require admission to a monitored setting. Patients who have received appropriate GI decontamination, have no signs of maj or toxicity, have a QRS interval < 1 00 ms, and are observed for 6 hours without change in clinical course or serial ECGs are unlikely to manifest symptoms. 1 97• 198 These patients may be medically cleared.

Serotonin .. Specifi.c Reuptake Inhibitors and Atypical Antidepressants Toxicology The pharmacologic mechanism of SSRI medications, as the name suggests, is to inhibit serotonin reuptake. In overdose, the typical clinical manifestations are nausea, vomiting, sedation, and tachycardia; but QT prolongation and seizures also have been reported. SSRis are better tolerated in over­ dose than tricyclic antidepressants and have far less cardiotoxicity. 22 3 In direct comparison to venlafaxine and

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tricyclic antidepressants, SSRis were found to be less epilep­ togenic and cardiotoxic but to result in more serotonin tox­ icity. 22 4 This, however, did not translate into less ICU time or mortality. The more significant symptoms of QT prolon­ gation and seizure are most often related to ingestions of citalopram and escitalopram. 225•22 6 Citalopram is a racemic formulation of inactive R and active S enantiomers, whereas escitalopram contains solely the S enantiomer. 22 7 The R and S enantiomers undergo hepatic metabolism to their respective desmethylcitalo­ pram products . 22 8 D esmethylcitalopram retains some of the pharmacologic activity of the parent compound. It also has affinity for alpha- adrenergic, dopamine, histamine, an d muscarinic receptors . 2 2 9 This m a y explain the antimuscarinic effects that can be seen with citalopram in overdose. D esmethylcitalopram is further metabolized to didesmethylcitalopram, which may be responsible for the cardiotoxic effects of the drug. 2 30· 2 3 1 However, this con­ tention is based on limited animal work and remains con­ troversial. 2 3 2 Regardless of mechanism, QT prolongation related to citalopram overdose has been demonstrated in two case series. 22 5•2 3 3 These studies also showed an association with seizures in overdose. One case series documented an increased frequency of QRS prolongation and seizure with ingestions of >600 mg in comparison with smaller inges­ tions. 2 3 4 In this report, QT prolongation was not com­ mented on. Additional publications of citalopram ingestions document delayed seizure, delayed QT prolongation, and torsades de pointes. 22 6 , 2 J I , 23 5-2 3 7 Atypical antidepressants are neither tricyclics, MAOis, or SSRis; however, they tend to be derivatives of the SSRI class . They include mirtazapine, bupropion, venlafaxine, duloxetine, and trazodone. With the exception of mirtazap­ ine, they have significantly more toxicity in overdose than the SSRis, although they are less toxic than tricyclics. 2 3 8 Bupropion is a unicyclic antidepressant that inhibits dopamine uptake, with a less significant effect on reuptake of serotonin and norepinephrine . Patients may exhibit tachycardia, hypertension, nausea, vomiting, drowsiness, and agitation. Seizure is common, occurring in over 1 0 % of cases in one series. 2 3 9 Although rare, cardiotoxicity with pro­ longed QT, QRS, cardiogenic shock, and cardiac arrest has been reported with larger ingestions. 2 40-2 42 Venlafaxine and duloxetine both block serotonin and norepinephrine reuptake and can be expected to have simi­ lar effects in overdose, although duloxetine is a more effec­ tive reuptake inhibitor. 2 43 An analysis of 2 3 5 consecutive venlafaxine overdoses demonstrated a significant occurrence of sympathomimetic syndrome, QTc prolongation, seizure, and rhabdomyolysis. 2 44· 2 45 Venlafaxine has been shown to be more epileptogenic than tricyclics, to prolong the QRS in comparison to SSRis, and to result in serotonin toxicity. 22 4 Trazodone is an antidepressant with anxiolytic and hyp­ notic properties. It inhibits serotonin reuptake but differs from other atypical antidepressants by having antagonist activity at the 5-HT2A postsynaptic serotonin receptor. It has a high therapeutic index, being associated with few deaths as reported in the literature. 2 46 Sedation and ortho-

45 7

static hypotension are the main findings in overdose. 2 47 Seizures are rare and where reported are related to marked hyponatremia. 2 48 There are several reports of QT prolonga­ tion; however, they are likely related to coingestants. 2 49-2 5 1 Mirtazapine is a relatively new agent that increases neu­ ronal serotonin and norepinephrine through inhibition of presynaptic alpharadrenergic receptors and postsynaptic serotonin receptors. It appears to have less toxicity in over­ dose than other atypical antidepressants. 22 5 A retrospective review of 1 5 3 mirtazapine overdoses demonstrated mild clinical symptoms and no significant cardiotoxicity other than tachycardia. 2 5 2 Altered mental status and CNS depres­ sion may be effects of mirtazapine overdose; however, it is difficult to distinguish a true effect from that of coingestant based on the available literature. There are no documented cases of significant cardiotoxicity.

Management The clinical presentation of an acute SSRI overdose with the most commonly used agents is that of nausea, vomiting, dizziness, blurred vision, CNS depression, tremor, sinus tachycardia, and mydriasis. S erotonin syndrome only rarely follows isolated SSRI overdose but should be monitored for closely in the symptomatic patient. SSRI poisoning should be suspected in any patient with lethargy, coma or seizures, and no significant cardiotoxicity. No readily available laboratory tests or clinical parame­ ters identify and predict the course of SSRI and atypical antidepressant exposures. A decision tool has been devel­ oped to assist in management of citalopram-related QT pro­ longation, but it has not been adequately validated and its clinical utility is undetermined. 2 3 3 Qualitative and quantita­ tive testing will not help in the acute setting. An early ECG is essential owing to the risk of coingested medicines and to evaluate for QT prolongation, but sinus tachycardia is often the only ECG finding. SSRis and atypical antidepressants rarely manifest the severe toxicity common with tricyclics. Treatment includes appropriate use of activated char­ coal, supportive care, and close observation. Charcoal may be effective in reducing citalopram-related QT prolonga­ tion. 2 53 In cases of serotonin syndrome, aggressive cooling and benzodiazepines are essential, and cyproheptadine may be effective. There is no role for extracorporeal therapies. Seizures, hypotension, and conduction disturbances can be managed as for TCA overdose and are guided by ECG find­ ings . Cases with prolonged QT intervals should prompt optimization of potassium, magnesium, and calcium levels. In tl1e case of torsades de pointes, a 2 - to 5 -g IV magnesium bolus is indicated. Intralipid infusion has been utilized in a case of severe bupropion and lamotrigine overdose refrac­ tory to standard measures. 2 54 Serotonin syndrome should be treated with cessation of the offending agent, supportive care, and measures to decrease muscle rigidity and control hyperthermia. No disposition algorithm for SSRI and atypical antide­ pressant exposure has been studied or established. In general, admission is not required in the absence of symptoms or an abnormal ECG after an adequate observation period extending

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through the peak absorption and distribution period. Exceptions to this rule are in the case of citalopram, escitalo­ pram, bupropion, venlafaxine, duloxetine, or extended-release preparations, where admission is warranted because of the potential for delayed onset of QT prolongation or seizure.

Antipsychotics Toxicology Antipsychotic drugs are effective and widely utilized. It is con­ venient to classify them as either typical or atypical agents. Typical agents are useful in ameliorating positive symptoms such as aggression, hallucinations, delusions, and paranoia. Atypical agents have the additional benefit of combating such negative symptoms as social withdrawal and flat affect. In overdose, antipsychotics may cause CNS depression, antimuscarinic symptoms, acute dystonia, akathisia, and hypotension mediated through alpha -adrenergic blockade. 1 Lower-potency drugs such as thioridazine and chlorpro­ mazine result in more sedation and cardiotoxic effects. 2 55•256 Seizures may occur, are dose-dependent, and occur more commonly with clozapine and chlorpromazine . 2 57 Cardiotoxicity with QRS prolongation is discussed for typi­ cal agents, although there is limited support for this effect. QT prolongation is more common with typical antipsy­ chotics; however, a significant effect is also seen with ziprasi­ done. Neuroleptic malignant syndrome, while rare, is life­ threatening. Symptoms consistent with this syndrome are altered mental status, hyperthermia, autonomic instability, and "lead pipe" rigidity. 2 58 The cardiotoxicity of antipsychotics is related to their effect on fast sodium channels and delayed rectifier potas­ sium channels. In psychiatric patients on therapeutic doses of antipsychotics, thioridazine-followed by ziprasidone, haloperidol, quetiapine, and risperidone-was found to have the greatest effect on QT prolongation. 2 59 The effect on QT prolongation may be exacerbated by concurrent therapy with antidepressants, other drugs known to prolong the QT interval, inhibitors of select p45 0 enzymes, hypokalemia, hypomagnesemia, hypocalcemia, female gender, and comor­ bid disease. 260-2 62 Prolonged QT intervals may trigger torsades de pointes. Blockade of the delayed rectifier potassium channel shifts phase 3 of the cardiac action potential, delaying recov­ ery of phase 4, and creating a circumstance where a prema­ ture action potential could result in this dysrhythmia. 2 63 There are numerous case reports of torsades de points related to the use of antipsychotic medications. 2 64-2 68 Many are complicated by coingestants or comorbidities, making a clear causal relationship difficult to establish. However, this fact reinforces the importance of concurrent risk factors as a cause of this malignant rhythm. Typical antipsychotics have effects on fast sodium chan­ nels, which manifest as prolongation of the QRS interval. In vitro work has shown the ability of haloperidol to block sodium channels in guinea pig myocytes. 2 69 A retrospective study demonstrated increased risk of prolonged QT dura­ tion, QRS duration, and ventricular arrhythmias with thior-

idazine overdose. 2 55 Case reports identify instances of wide­ complex arrhythmias related to mesoridazine and risperi­ done; however, there are also cases related to ziprasidone/ bupropion and meperidine/promethazine/chlorpromazine combinations in overdose. 270-2 74 Asystolic cardiac arrest has been reported with haloperidol. 2 75• 2 76

Management Aggressive supportive care, GI decontamination where appropriate, and close observation are indicated. Patients with underlying depression, bipolar disease, or schizophre­ nia are often on multiple psychotropic medications, so atten­ tion to possible coingestants is essential. There is no role for enhanced elimination with hemodialysis, hemofiltration, or hemoperfusion. Antipsychotic cardiovascular toxicity is treated as it is for S S Ris and TCAs . Following initial resuscitation, an ECG should be obtained early in the clinical course to guide therapy. IV magnesium, sodium bicarbonate, or both may be indicated in addition to standard ACLS interventions. Hypotension is managed with crystalloid infusion, and vasopressors are utilized if the hypotension is refractory. Agents with direct alpha effects, such as norepinephrine, are preferred over dopamine. As with S S Ris and tricyclics, seizures are usually brief and self-limited but may require intervention to avoid exacerbating cardiovascular toxicity. B enzodiazepines constitute the first-line treatment, fol­ lowed by barbiturates or diprivan. 222 Phenytoin should be avoided out of concern for arrhythmogenicity and because it is generally ineffective for toxin-induced seizures. 2 1 6 Patients with signs of major toxicity, such as seizures, coma, dysrhythmia, hypotension, respiratory depression, or ECG abnormalities, require admission to a monitored set­ ting. Patients who have received appropriate GI decontam­ ination, have no signs of major toxicity, have a normal ECG, and are observed beyond the peak absorption and distribu­ tion times of the ingested drug are unlikely to develop symp­ toms. These patients may be medically cleared.

D rugs of Abuse Commonly Causing Toxicity in Overdose Amphetamines and Amphetamine Derivatives Toxicology In 20 0 5, there were 1 0,92 1 exposures to amphetamine and 3 ,456 exposures to methamphetamine reported to poison conrol centers nationwide. 69 These resulted in 16 and 3 7 deaths , respectively. In 2 004, some 1 .4 million people reported methamphetamine use in the preceding year, and 5 8 3 ,000 reported use within the prior month. These statis­ tics make methamphetamine the most abused amphetamine in the United States. 277

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Methamphetamine is also known as "speed," "meth," "chalk, " "crystal, " "crank, " and "ice. " The ice preparation is precipitated in a purified crystalline form that is less likely to be adulterated. It can be smoked, injected, or nasally insuf­ flated. Effects persist up to 2 4 hours. Auditory hallucina­ tions, paranoid reactions, delirium, and violent behavior are reported to be more frequent with ice than with other forms of amphetamine. The pharmacologic properties of amphetamines paral­ lel those of endogenous catecholamines. However, depend­ ing on substitution, amphetamines may be sympath­ omimetic, anorectic, or hallucinogenic. Pharmacologic activity is classically described as being indirect and occur­ ring by three distinct mechanisms: triggering neurotrans­ mitter release at the cell membrane by exchange diffusion, diffusing across the cell membrane and interacting with the neurotransmitter storage vesicle membrane, and diffusing through the cell and vesicle membrane and inducing neuro­ transmitter release via alkalinization. 2 78 Abuse of the substi­ tuted varieties of amphetamine is a significant problem, as these drugs can cause both neurotoxicity and cardiotoxicity that may not be reversibleY9-28 1 Methamphetamine is a substituted amphetamine that has numerous central and peripheral effects resulting in mood elevation, psychomotor activation, and with chronic use or overdose, psychotic and violent behavior. The car­ diovascular effects result from alpha-adrenergic agonist properties resulting in stimulation of vascular smooth mus­ cle and vasoconstriction. Methamphetamine stimulates both cortical and medullary centers in the CNS to increase sympathomimetic outflow. Peripherally, methampheta­ mine causes release of norepinephrine, stimulating both alpha- and beta-adrenergic receptors . B eta- adrenergic activity increases cardiac contractility and heart rate. Methamphetamines may also inhibit endogenous cate­ cholamine breakdown via inhibition of monoamine oxi­ dase. With intoxicated patients , these sympathomimetic effects are exaggerated. It is common for abusers to use the drug several times within a short period, which may exac­ erbate the cardiotoxic effects Y9 The substituted amphetamine 3 , 3 -methylene dioxymethamphetamine (MDMA, or " ecstasy") has simi­ lar characteristics; however, it also has affinity for sero­ tonergic neurons. This may explain the hallucinations seen in both recreational use and in toxicity. Ecstasy intox­ ication will, therefore, result in both sympathomimetic and serotonergic syndromes . The clinical syndrome asso­ ciated with amphetamine toxicity consists of vasoconstric­ tion, tachycardia, and hypertension, which are associated with agitation and CNS excitation. In acute toxicity, car­ diovascular and CNS complications require immediate intervention. Cardiovascular complications of amphetamine use include chest pain and acute coronary syndrome (ACS), aor­ tic dissection, and sudden death. 282 · 2 83 Ischemic and hemor­ rhagic stroke are both reported and often occur in associa­ tion with marked hypertension. 2 84 Carotid artery dissection may present with neurologic deficits with or without neck pain. 2 8;

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The respiratory tract is vulnerable following either nasal insufflation or smoking of amphetamines. Comp­ lications include nasal septal perforation, barotrauma, pul­ monary edema, pneumothorax, pneumomediastinum, and pneumonia. 2 86· 2 87 Long-term use may result in pulmonary hypertension. 288 Mild amphetamine-induced hyperthermia is common in overdose and likely relates to agitation. Hypertonicity due to dehydration may be present. However, acute nontrau­ matic cerebral edema associated with hyponatremia is reported as a complication of the use of MDMA. 2 89· 2 90 Severe hyperthermia (40.C) is of multifactorial origin, with dopamine and serotonin dysregulation, increased metabolic demands , and psychomotor agitation all being involved. 2 91-2 93 It is associated with hepatic necrosis, rhab­ domyolysis, and shock. Amphetamine toxicity should be suspected in any patients who exhibit signs and symptoms consistent with sympathomimetic toxidrome. They will present with CNS excitation, mydriasis, tachycardia, hypertension, and hyper­ thermia. This must be distinguished from anticholinergic toxidrome, which will have the characteristic features of dry skin and mucous membranes, hypoactive bowel sounds, and urinary retention.

Management Less severe cases of intoxication with amphetamines or amphetamine derivatives will present with agitation, mild tachycardia, and hypertension. B enzodiazepine sedation, often with large doses, may be all that is required to resolve these clinical manifestations. In patients with marked hypertension that requires intervention, vasodilators such as nitroprusside or nitroglyc­ erin are appropriate . Phentolamine, an alpha-adrenergic antagonist, may also be utilized. If rate control is required, diltiazem is preferred. Beta-blockers, including labetalol, should be avoided while the patient is in the hyperadrener­ gic state, as unopposed alpha stimulation may cause or exac­ erbate a hypertensive crisis. There is little information guid­ ing therapy for amphetamine-related chest pain and ACS . Given the similarities between cocaine and methampheta­ mine toxicity, these complications should be treated simi­ larly. 2 94 Seizures should be controlled with benzodiazepines; second-line agents are propofol and phenobarbital . Phenytoin is not useful for drug-induced seizures. Severely intoxicated patients witl1 hyperthermia or seizures should have hepatic enzymes, bilirubin, coagulation parameters, creatinine kinase, and urine myoglobin assayed . Marked hyperpyrexia may lead to acute hepatic failure, disseminated intravascular coagulopathy, and rhabdomyolysis, similar to that seen in environmental heat stroke. Rhabdomyolysis is treated with volume diuresis. Alkalinization of the urine may also be required. Variable protein binding and large volumes of distribu­ tion hinder hemodialysis or other means of extracorporeal elimination. Asymptomatic or mild cases of amphetamine toxicity can adequately be observed for 4 to 6 hours in the

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emergency department until sympathomimetic signs and symptoms normalize. Patients with moderate to severe symptoms are admitted to a monitored setting.

Cocaine Toxicology Cocaine, also known as benzoylmethylecgonine, is a natu­ rally occurring anesthetic and sympathomimetic. The drug can be purified into crystalline cocaine hydrochloride, pro­ ducing a concentrated formulation that is rapidly absorbed from mucous membranes, lung tissue, and, somewhat less rapidly, the GI tract. Cocaine hydrochloride is heat-labile and undergoes pyrolytic degradation. Conversely, cocaine that has been precipitated from an alkaline medium crystal­ lizes as the alkaloid "free base," which is heat-stable when smoked. The physiologic effects of cocaine are both sympath­ omimetic and membrane-stabilizing. 2 95 Presynaptic reup­ take of biogenic amines such as norepinephrine, serotonin, and dopamine is inhibited, resulting in CNS stimulation and heightened adrenergic tone. 2 8 1 •296·297 The membrane-stabi­ lizing effects exacerbate cardiotoxicity and may result in QRS prolongation; QT prolongation is seen and may be related to potassium channel blockade. 2 98 Cocaine-induced myocardial infarction is well docu­ mented. 2 99 Cocaine causes coronary vasoconstriction, is thrombogenic, and increases myocardial work. 3 00-3 04 It occurs in young patients, in those without preexisting coro­ nary artery disease, and with an incidence as high as 6% in those presenting with cocaine-related chest pain.305-308 The epileptogenic property of cocaine is multifactorial; it is related to the sympathomimetic toxidrome, increases in neuroexcitatory chemicals, and reduction in GABAergic tone. 3 09-3 1 1 Cocaine's membrane-stabilizing effects may compound the probability of seizures. Coadministration of cocaine with lidocaine, another membrane-stabilizing drug, has been shown to lower the seizure threshold in ani­ mals. 3 12·3 1 3 The primary target organs are the CNS , cardio­ vascular system, lungs, GI tract, skin, and thermoregulatory center, although all physiologic systems are at risk. The clinical manifestations of acute cocaine toxicity may be mild, with transient anxiety, tachycardia, and hyper­ tension. With more significant ingestions, marked cardio­ vascular and neurologic abnormalities will be observed. Chest pain is common, and select cases may be related to an acute coronary event, aortic dissection, or pulmonary complication. Pulmonary complications include cardiogenic and noncardiogenic pulmonary edema, pulmonary hemor­ rhage , pneumothorax, pneumomediastinum, and pneu­ mopericardium. 286·287 Vascular complications in the GI and genitourinary tracts are less common but include mesenteric ischemia and renal infarction . 3 1 4·3 1 5 Orally ingested cocaine can cause ischemic complications in the GI tract, including acute abdominal pain, hemorrhagic diarrhea, and shock from mesenteric ischemia. However, ingestions of large amounts

of cocaine, as in the case of "body stuffers" or "body pack­ ers," is more likely to result in marked systemic cocaine tox­ icity than focal abdominal complaints. Hyperthermia related to cocaine intoxication may be severe. Peripheral vasoconstriction and lack of heat percep­ tion limit heat loss, while psychomotor agitation increases heat production.3 1 6 Increased ambient temperatures exacer­ bate these phenomena and increase mortality from cocaine overdose.3 1 7 Complications include disseminated intravascu­ lar coagulation and fulminant hepatic necrosis. S evere hyperthermia (40'C) correlates with mortality and should be treated aggressively. 3 1 8• 3 1 9 Rhabdomyolysis occurs both in the presence and absence of hyperthermia. Cocaine toxicity is likely in patients who exhibit signs and symptoms consistent with sympathomimetic stimula­ tion. They often present with CNS excitation, mydriasis, tachycardia, hypertension, and hyperthermia . As with amphetamines, this must be distinguished from an anti­ cholinergic toxidrome, which will have the characteristic features of dry skin and mucous membranes, hypoactive bowel sounds, and urinary retention.

Management Less severe cases of cocaine intoxication will present with agitation, mild tachycardia, and hyp ertension. Benzodiazepine sedation, often with large doses, may be all that is required to resolve these clinical findings . In patients with marked hypertension requiring intervention, vasodilators such as nitroprusside or nitroglycerin are appropriate . Phentolamine, an alpha-adrenergic antago­ nist, may also be utilized. If rate control is required, dilti­ azem is preferre d . B eta-blockers, including labetalol, should be avoided while the patient is in the hyperadren­ ergic state. They have been found to be detrimental in an animal model and may induce unopposed alpha stimula­ tion, causing or exacerbating a hypertensive crisis . 3 2 0 All patients with significant toxicity should have an ECG early in the evaluation. Activated charcoal adsorbs unpackaged or poorly pack­ aged orally ingested cocaine and is useful for gastric decon­ tamination. The majority of cocaine intoxications involve IV inj ection, insuffiations, or inhalation, limiting the utility of activated charcoal. Variable protein binding and large vol­ umes of distribution hinder hemodialysis or other means of extracorporeal elimination. Cocaine-associated ACS in the hyperadrenergic patient should be managed as with noncocaine-associated ACS , with several caveats. Benzodiazepines should be utilized as first-line sympatholytic agents . Nitroglycerin is indicated for hypertension and coronary vasodilation in the setting of chest pain and may be more effective when used in combi­ nation with benzodiazepines . 3 2 1•322 Calcium channel block­ ers may be useful for alleviating coronary vasospasm, hyper­ tension, and tachycardia. 2 94 B eta-blockers, including labetalol, do not reduce coronary vasospasm and may actu­ ally exacerbate it. 304·3 2 3· 3 2 4 For this reason in conjunction with the reasons outlined above, this class of medications should be avoided.

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The cardiovascular toxicity of cocaine is not limited to ACS . Severe intoxications may result in QT prolongation, QRS prolongation, or more malignant rhythms . These aberrancies are in part rate- and pH-dependent. They are exacerbated by seizures and the resultant acidosis, tachycar­ dia, and hypoxia. Prolonged QRS duration related to fast sodium channel blockade is ominous. It should be aggres­ sively treated with sodium bicarbonate, administered by IV bolus. Animal studies have demonstrated a clear beneficial effect by reversing QRS prolongation in acute cocaine­ induced dysrhythmias.3 25- 3 2 7 Case reports confirm the salu­ tary effect in human cases. 3 28 •3 2 9 The benefit of a sodium bicarbonate infusion following bolus therapy is not clear; however, it may be useful to avoid recurrent acidosis. Marked alkalosis should be avoided, with a pH goal below 7 . 5 5 . Repeat boluses should be administered for recurrence of symptoms or ECG abnormalities. In the setting of refractory ventricular arrhythmias poorly responsive to sodium bicarbonate, lidocaine is con­ sidered the second-line antiarrhythmic. However, its utility is not clear. In vitro work indicates that it may be effective in treating wide-complex dysrhythmias, although it may also prolong QT intervals . 3 3 0-3 3 2 Animal work demonstrates a clear increased rate of seizures and a mixed effect on mor­ tality. 3 12 , 3 1 3 , 3 3 3 Prolonged Q T intervals leading t o torsades d e pointes are related to potassium channel blockade. Prolonged QT intervals should prompt optimization of potassium, magne­ sium, and calcium levels. In the case of torsades de pointes, a 2- to 5-g IV magnesium bolus is indicated. Refractory cocaine toxicity that results in hypotension should be treated with volume expansion using isotonic saline. Vasopressors are utilized as second-line agents. Seizures should be controlled with benzodiazepines; second-line agents are propofol or phenobarbital. Phenytoin is not useful for toxin-induced seizures. Severely intoxicated patients with hyperthermia or seizures should have hepatic enzymes , bilirubin, coagulation parameters, creatinine kinase, and urinary myoglobin assayed. Marked hyper­ pyrexia may lead to acute hepatic failure, and disseminated intravascular coagulopathy, and rhabdomyolysis, similar to that seen in environmental heat stroke. Rhabdomyolysis is treated with volume diuresis and urinary alkalinization as indicated. Body stuffers may swallow cocaine in an attempt to avoid prosecution when confronted by the police. Body packers intentionally swallow or pack body orifices with drug in an attempt to conceal and illegally transport the product. Body packing often entails very elaborate methods of packaging so as to make rupture less likely. 334 Conversely, body stuffing implies poorly wrapped cocaine, which is likely to become bioavailable . 3 3 5 Even carefully packaged packets can rupture, and this setting typically involves potentially lethal doses of cocaine. Types of packages most likely to rup­ ture are paper, aluminum foil, or poorly secured plastic bags. The physician may be able to gather enough informa­ tion regarding the amount of cocaine ingested and the type of packaging to assess the potential for toxicity. Abdominal radiographs are generally not useful for body stuffers but

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may be more helpful with body packers . A Gastrografin swallow or CT scan of the abdomen with contrast may reveal ingested packets in cases where plain radiographs are negative but suspicion of ingestion is high. In body stuffers and packers, gastric lavage is con­ traindicated, as it may cause rupture of the packets . Conservative therapy utilizing polyethylene glycol whole­ bowel irrigation is recommended in asymptomatic patients.45•336 It is important to ensure that all ingested pack­ ets pass before the patient is discharged, which may require repeat imaging. Body packers who are symptomatic or have a bowel obstruction should have a surgical consultation. Laparotomy may be a necessary lifesaving intervention to remove leaking packets . 3 3 7 Asymptomatic o r mild cases o f cocaine toxicity should be observed for 4 to 6 hours in the emergency department until sympathomimetic signs and symptoms normalize. Patients with moderate to severe symptoms are admitted to a monitored setting.

Inhalants Toxicology Inhalant abuse includes the practices of sniffing, huffing, and bagging. Sniffing entails the inhalation of a volatile sub­ stance directly from a container, as occurs with airplane glue or rubber cement. Huffing involves pouring a volatile liquid onto fabric (e.g., a rag or sock) and placing it over the mouth and nose while inhaling. Huffing is the method used by over half of those who abuse volatile substances. "Bagging" refers to spraying a solvent into a plastic or paper bag and rebreathing from the bag several times; spray paint is among the agents commonly used. A multitude of inhalational substances are abused, most being volatile hydrocarbons. Commonly inhaled hydrocar­ bons include gasoline, spray paints, lighter fluid, and glue. In many cases, the class of the substance is identified rather than the specific chemical. Since exact components may vary between products, this method is often inaccurate and imprecise. The volatile hydrocarbons can be further divided into aliphatic hydrocarbons, aromatic hydrocarbons, halo­ genated hydrocarbons, and alkyl nitrites. The alkyl nitrites include amyl, butyl, and isobutyl nitrite and are sold in shops dealing in sex and drug paraphernalia. Amyl nitrite is con­ tained in small glass capsules known as "poppers. " When covered in gauze and crushed, the capsules release the nitrite and make a characteristic sound. Amyl, butyl, and isobutyl nitrites are sold as room deodorizers or liquid incense in small vials typically containing 1 0 to 3 0 mL. The most commonly used nonhydrocarbon inhalant is nitrous oxide. Nitrous oxide, or "laughing gas," is used ther­ apeutically as an inhalational anesthetic. Cartridges of the compressed gas, known as "whippets," are sold for commer­ cial use in whipped cream dispensers. These battery-sized metal containers of compressed gas are punctured using a "cracker" and the escaping gas is either inhaled directly or collected in a balloon and then inhaled.

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Inhalants are highly lipophilic agents that readily gain entrance into the CNS . Early CNS effects include euphoria, visual and auditory hallucinations, as well as headache and dizziness. As intoxication progresses, CNS depression wors­ ens and patients may develop slurred speech, confusion, tremor, and weakness. Further CNS depression is marked by ataxia, lethargy, seizures, coma, respiratory depression, and death. The mechanism of inhalant effects on the CNS is poorly studied, although some generalizations can be made. Volatile alkyl nitrites likely mediate their effects through cGMP-mediated vasodilation, although it is unclear if they have direct CNS effects. 3 3 8•3 3 9 Nitrous oxide may inhibit excitatory NMDA receptors and affect dopaminergic activity.340·34 1 Volatile solvents and fuels such as toluene and trichloroethane produce effects similar to those of CNS depressants such as ethanol and barbiturates, likely mediated through GABA receptors . 3 3 9 Toluene is also thought to have NMDA antagonist activity.342·343 Cardiotoxicity, in its most abrupt form, results in the "sudden sniffing death." History surrounding these events indicates that the user, while intoxicated, was startled imme­ diately prior to death. Although mechanism is not clear, these findings implicate catecholamine surge in the setting of inhalant-induced cardiac channelopathy as a mechanism. This effect has been studied in children undergoing halothane (a halogenated hydrocarbon) anesthesia for den­ tal procedures.344 During dental extraction or emergence, the children were noted to have an increased rate of ven­ tricular arrhythmias in comparison to those on sevoflurane anesthesia. The effective use of halothane-epinephrine for generating animal models of ventricular arrhythmias sup­ ports this concept. 345 Potassium channel blockade is sus­ pected, as this correlates with the QT prolongation that has been documented following volatile anesthetic administra­ tion.3 46 The rapid delayed rectifier potassium channel is often implicated in drug-induced myocardial sensitization; it is particularly sensitive to the effects of hydrophobic (aro­ matic or halogenated) hydrocarbons.347 An animal model of toluene toxicity demonstrated loss of R-wave height, broad­ ening of the R wave, inverted T waves, and ST-segment depression, an effect that may have been related to hypoxia, or toluene intoxication . 3 48 Sodium channel blockade by toluene has been demonstrated in vitro, although this mech­ anism is less substantiated.349 Pulmonary toxicity associated with volatile hydrocar­ bons is often due to aspiration following attempted ingestion of a liquid hydrocarbon. Asphyxiation may be ascribed to the inhalant or to suffocation from a plastic bag utilized for inhalant delivery. 3 50 Volatile hydrocarbons are pulmonary irritants that may induce coughing, dyspnea, bronchospasm, and pneumonitis. Hydrocarbon pneumonitis is character­ ized by rales or rhonchi on lung auscultation, tachypnea, fever, leukocytosis, and radiographic abnormalities. 3 5 1 Cardiac and pulmonary toxicities are effects of volatile hydrocarbons, and toxicity to other organ systems is unique to the specific chemical. Hepatoxicity has been associated with carbon tetrachloride and other halogenated hydrocar­ bons, including chloroform, trichloroethane, trichloroethyl­ ene, and toluene.

Inhalation of toluene, which is often found in spray paints and glues, may cause a distal renal tubule acidosis (RTA) and hypokalemia. Although distal RTAs are associ­ ated with a hyperchloremic metabolic acidosis and a normal anion gap, some patients have been found to have an increased anion gap following toluene inhalation. Methylene chloride, most commonly found in paint removers and degreasers, differs from other halogenated hydrocarbons in that it is metabolized by cytochrome P450 to carbon monoxide. Carboxyhemoglobin levels may be sig­ nificantly elevated and may not rise for several hours after exposure because of the time required for metabolism. Inhalation of amyl, butyl, and isobutyl nitrites may induce methemoglobinemia. These agents also cause peripheral vasodilatation and can result in orthostatic hypotension and syncope. The clinical presentation of inhalant use varies widely among individuals. In general, symptoms will resolve within 2 hours of exposure. Following acute exposure, there may be a distinct odor of the abused substance on the patient's breath or clothing. Depending on the agent used and the method, there may be discoloration of the skin around the nose and mouth. Mucous membrane irritation may cause sneezing, coughing, and tearing. Patients may complain of dyspnea and palpitations . GI complaints include nausea, vomiting, and abdominal pain. After an initial period of euphoria, patients may have headache and dizziness. Syncope is one of the more serious clinical events that may occur with inhalant abuse. Patients may present with a persistent altered level of consciousness or in cardiac arrest. The most common causes of such events are hypoxia from simple asphyxiation, profound respiratory depression, and malignant dysrhythmia. Determining the exact cause of syn­ cope or death is difficult, as most events are unwitnessed. Clinical testing and autopsy generally reveal little confirma­ tory information.

Management In the vast maj ority of patients , symptoms will resolve quickly and hospitalization will not be required. Agitation, either from acute effects of the inhalant or from withdrawal, is safely managed witl1 benzodiazepines. Regardless of sever­ ity, consultation with a regional poison control center is appropriate to assist with identification of the toxin and spe­ cific management issues. Mild pulmonary symptoms such as wheezing are ade­ quately treated with oxygen and nebulized albuterol. Respiratory distress prompts consideration of chemical pneumonitis and the addition of continuous cardiorespira­ tory monitoring, ECG, chest radiography, screening for electrolyte abnormalities, and, in severe cases, intubation and mechanical ventilation. Neither prophylactic antibiotics nor steroids have proven beneficial. Symptomatic patients with a history of alkyl nitrite use should be screened for methemoglobinemia. Methylene chloride induces carboxyhemoglobinemia, which may be delayed. Initial screening for this complication is warranted, and should be repeated in several hours if the patient

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remains symptomatic or worsens. Treatment with high-flow oxygen is generally sufficient. Cardiac dysrhythmias associated with inhalant abuse carry a poor prognosis. There appears to be no premonitory signal to the user, and the effect of the inhalant on the myocardium lingers after inhalation has stopped. There are no evidence-based treatment guidelines for the management of inhalant-induced cardiac dysrhythmias; standard ACLS protocols should be followed. Animal work and studies of dysrhythmias under halo­ genated hydrocarbon anesthesia indicate increased morbid­ ity with elevated sympathomimetic tone.344•345 It is recom­ mended that use of sympathomimetic agents be minimized, although it is understood that this may not be possible in cases of respiratory distress, shock, or cardiac arrest. Agents with beta-blocking activity may be cardioprotective in the hydrocarbon-sensitized myocardium. Esmolol has been shown to both prevent and suppress halothane-epinephrine induced ventricular arrhythmias in an animal model. 35 2 In a similar model, propranolol was shown to abolish ventricular arrhythmias. 3 5 3 There are case reports of both esmolol and propranolol resolving trichloroethylene-induced ventricular arrhythmias. 3 54•355 Considering this evidence, beta-blockers should be considered in the setting of hydrocarbon-induced ventricular arrhythmias.

Opioid-induced pulmonary edema occurs in 1 % to 3 % of patients with heroin overdose. 1 4•356•357 The etiology is unclear but may involve opioid-induced capillary leak and sympa­ thetic surge in the setting of profound hypoxia. Seizure in the setting of opioid overdose is often related to hypoxia. However, some opioids are proconvulsant. The meperidine metabolite normeperidine has a longer half-life than its parent compound. In patients receiving large doses or in those with renal insufficiency, it may accumulate and result in seizure activity.358 Tramadol is a weak agonist at the mu opioid receptor and an inhibitor of monoamine uptake. Supratherapeutic doses have been shown to induce seizures in animal models, an effect that is well described in humans.3 59•360 Seizures have been reported with pentazocine (Talwin)/tripelennamine, although this seems to be less commonly abused than in past years.69•36 1 Propoxyphene is a weak opioid agonist that is metabo­ lized to nordextropropox:yphene. It may cause CNS depres­ sion, seizures , and cardiotoxicity among other adverse effects, even at therapeutic doses. 3 6 2 In a case series of 2 2 2 patients, 1 0% had seizures, 45 % had respiratory failure, and 48 % had cardiotoxicity.363 Overall mortality was 8 % . Cardiotoxicity resulting from propoxyphene i s complex and may be mediated through both sodium and potassium channels .364•365 Significant toxicity is associated with pro­ longed QRS complexes.364•366•367

Opioids

Management

Toxicology Opioid agonists bind to a family of inhibitory G protein-coupled receptors, namely the mu, kappa, and delta receptors. They inhibit adenylate cyclase, which reduces the formation of cAMP, close calcium chmmels decreasing neu­ rotransmitter release, and open potassium cha1mels inducing cell hyperpolarization. The physiologic effects depend on which receptor subtype is involved and the location of the receptor. The important clinical effects from a toxicological perspective are a result of activity at the f.1 receptor. J.L 1 Receptors mediate sedation, analgesia, and euphoria. J.L2 Receptors mediate respiratory depression and bradycardia, among other effects. The etiology of miosis is unclear. The clinical presentation of opioid intoxication is pri­ marily that of depressed mental status and respiratory insuf­ ficiency. Miosis will likely be present, but may be absent in patients ingesting meperidine, pentazocine, propox:yphene, tramadol, heroin mixed with adulterants or cocaine, or diphenoxylate/atropine. CNS depression ranges from mild sedation to stupor and coma. Patients may be hypotensive, hypothermic, bradycardic, and hyporeflexic. Vomiting may occur, and when coupled with respiratory depression and a diminished gag reflex, places the patient at risk for aspiration. Additional pulmonary effects may include bronchospasm due to histamine release or pulmonary irritation induced by insufflating or inhaling opioids cut with impurities or adul­ terants. In massive overdoses, the pulmonary toxicity can also cause severe hypoxia, hypercarbia, and acute lung injury.

In a patient with a clinically significant opioid overdose, the practice of routine intubation before naloxone administra­ tion is not recommended.4 When opioid overdose patients have respiratory insufficiency with a detectable pulse, an attempt at opioid reversal before tracheal intubation is war­ ranted provided that adequate ventilatory support can be given with bag-valve-mask. Patients with opioid-induced cardiac arrest or impend­ ing cardiac arrest should have aggressive airway manage­ ment, including intubation, prior to consideration of nalox­ one. The endpoint obj ectives for opioid reversal are adequate airway reflexes and ventilation, not complete arousal. Acute, abrupt opioid withdrawal may increase the likelihood of severe complications, such as aspiration pneu­ monitis, pulmonary edema, ventricular arrhythmias, and severe agitation and hostility.8 Compared with longer-acting opioid antagonists, nalox­ one is preferred, despite having a shorter duration of effect (45-60 minutes) than most opioids. Repeat doses may be required, particularly in dealing with opioids with longer durations of action, such as oxycodone, methadone, and diphenoxylate-atropine (Lomotil). A continuous IV infusion of naloxone can be instituted. The drip rate can be calculated by using two-thirds of the initial dose required to reverse the patient's respiratory depression and administering this amount hourly. There is debate over which route of admin­ istration is preferred; however, if IV access is possible, it should be established and utilized. Alternate routes include endotracheal, SQ, or IM administration and administration by nebulizer with a comparably rapid onset of action.

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Seizures resulting from meperidine, tramadol, penta­ zocine, or propoxyphene should be managed as are other toxin-induced seizures. B enzodiazepines are the drug of choice, with second-line agents being propofol and pheno­ barbital. Phenytoin is not useful for drug-induced seizures. Similarities between the cardiotoxicity of propoxyphene and TCAs indicate that propoxyphene dysrhythmias should respond to the same therapy. Case reports have demon­ strated efficacy of both IV sodium bicarbonate and lidocaine for QRS prolongation in this setting. 366•367 Patients who present as body packers or stuffers of heroin or opioid-containing drugs may require GI deconta­ mination with whole-bowel irrigation using polyethylene glycol solution to enhance the elimination of drug packets. Contraindications to whole-bowel irrigation include unsta­ ble vital signs, respiratory compromise, and lack of bowel sounds or gut motility. Activated charcoal should be given prior to whole-bowel irrigation to adsorb any leaking drug from the packets. Charcoal noted in the rectal effluent indi­ cates successful whole-bowel irrigation. In contrast to cases involving cocaine, a less aggressive approach to surgical intervention is warranted with heroin. Supportive care and antidotal therapy with naloxone should be effective in the case of leaking packets. In the case of bowel obstruction, sur­ gical consultation is indicated. Patients presenting with CNS depression from opioid overdose who respond to naloxone administration can be medically cleared after 4 to 6 hours of observation. Patients who continue to demonstrate respiratory compromise or require repeated doses of naloxone should be observed for a longer period of time. Agents with a prolonged half-life, such as methadone, are much more likely to cause recurrence of CNS and res­ piratory depression. The toxicity of diphenoxylate-atropine (Lomotil) may be delayed or prolonged due to anticholiner­ gic effects. 368 Therefore, these patients should be observed in a monitored setting for at least 24 hours.

Environmental, Occupational, and Iatrogenic Toxins Carbon Monoxide and Carboxyhemoglobin Toxicology Carbon monoxide is among the most common environmen­ tal toxins and a leading cause of death by poisoning. It is col­ orless, tasteless, odorless, and nonirritating yet highly toxic. The diagnosis may be obvious when there is a history of fire, combustion appliances, or automobiles utilized in an enclosed space; however, the diagnosis may be unrecog­ nized. Symptoms are typically vague or present like other common disorders. A high index of suspicion and careful attention to historical clues, such as multiple symptomatic patients or animals from the same dwelling, is essential.

Readily absorbed upon inhalation, carbon monoxide binds avidly to hemoglobin with an affinity > 2 00 times greater than that of oxygen.369 Carbon monoxide binding to hemoglobin has the effect of increasing the affinity of the remaining binding sites for oxygen, thus shifting the oxyhe­ moglobin dissociation curve to the left. 3 70•3 7 1 Carbon monoxide also binds to myoglobin and cytochrome oxidase, resulting in cytotoxicity and cardiotoxicity. 3 7 2 •373 In a series of 2 3 0 patients with moderate to severe car­ bon monoxide poisoning, ischemic ECG changes were found in 3 0 % , and 3 5 % had elevated cardiac biomarkers. 3 74 Echocardiographic evidence of myocardial dysfunction has been documented.375 CNS dysfunction is multifactorial, with hypotension, hypoxia, cytotoxicity, and lipid peroxidation all likely involved. Certain brain regions are more sensitive to carbon monoxide toxicity, such as the cortical rather than subcorti­ cal areas, basal ganglia, and Purkinje cells in the cerebel­ lum.373 Carbon monoxide poisoning may be associated with delayed neurologic sequelae, which is the basis of the argu­ ment for hyperbaric oxygen therapy. The clinical presentation of carbon monoxide toxicity is widely varied. Signs and symptoms range from headache, nau­ sea, vomiting, weakness, and decreased mental status to syn­ cope, seizures, coma, myocardial dysfunction, and arrhyth­ mias. Severe cases can present in shock and cardiac arrest. Elevated carboxyhemoglobin levels document expo­ sure, although a normal level does not exclude the possibil­ ity that exposure has occurred. Carbon monoxide levels are usually measured using arterial blood, although venous blood levels are comparable. S tandard oximeters cannot quantify carboxyhemoglobin percentage and typically give normal readings in carbon monoxide poisoning. Cooximeters are able to make the distinction between these species and quantify the percentage of carboxyhemoglobin. In mild to moderate toxicity, laboratory testing other than a carboxyhemoglobin level is rarely helpful. A mild metabolic (lactic) acidosis may be present; however, this is very non­ specific and does not guide therapy. A markedly elevated lactate and significant symptoms in house fire victims is suggestive of concomitant cyanide poisoning.

Management The initial resuscitation of patients with carbon monoxide toxicity is similar to that for other critically ill patients . Careful assessment of the airway for burns should occur in the patient presenting from a fire. First, 1 00 % oxygen by face mask or endotracheal intubation if required is essential. Carboxyhemoglobin half-life, as measured in volunteers, averages 5 hours. 376•377 This drops to approximately 90 min­ utes in those receiving 1 00 % oxygen therapy. 3 78•3 79 Oxygen therapy should be continued for 4 to 6 hours to ensure the elimination of carbon monoxide. In the pregnant patient, oxygen therapy should be administered approximately five times longer once the mother has normalized so as to ensure adequate carbon monoxide clearance from the fetus. Considerable controversy exists regarding the utility of hyperbaric oxygen in carbon monoxide toxicity. A number of

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large trials have attempted to evaluate the efficacy of this therapy; however, the results are conflicting and not without criticism. 3 80-3 83 D espite a lack of clear, evidence-based guidelines, hyperbaric therapy is generally felt to be indi­ cated for patients with altered mental status, syncope, coma, seizure, focal neurologic deficit, or an absolute carboxyhe­ moglobin level >2 5 % ( 1 5 % in pregnancy, or with signs of fetal distress). More recent work has identified patients > 3 6 years o f age and those with exposure intervals 2: 2 4 hours as being at risk of delayed neurologic sequelae and likely to benefit from hyperbaric oxygen therapy. 3 84 Critically ill patients present an additional complication in that they must be stable enough to withstand the duration of therapy in an isolating hyperbaric chamber. If a local chamber is not avail­ able, patients should be stabilized prior to transfer. Patients exposed to carbon monoxide who have low documented levels, are asymptomatic, and are without evi­ dence of subtle neuropsychiatric dysfunction may be med­ ically cleared. Carbon monoxide-poisoned patients whose symptoms resolve with normobaric oxygen may be med­ ically cleared but should be seen in follow-up as outpatients to assess for delayed neuropsychiatric sequelae. Any patient requiring hyperbaric therapy, with coma, altered mental sta­ tus, or other evidence of end-organ involvement should be admitted to the ICU. W'hen the fetus is viable following treatment with hyperbaric oxygen, obstetric consultation with fetal monitoring is warranted for carbon monoxide poi­ sonmg m pregnancy. The oxidation of reduced hemo­ globin (Fe2 +) transforms the iron moiety from a ferrous to a ferric state. Methemoglobin (Fe3+) results, and this oxidized molecule is unable to bind and transport oxygen. Typically, methemoglobinemia is induced by oxidizing medications or toxins. The list of inducers is extensive as indicated in Table 2 9- 1 . The more commonly reported methemoglobin induc­ ers include nitrates and nitrites. The source may be food, well water contaminated with nitrogenous waste, or medica­ tions, which have a more pronounced effect. Topical anes­ thetics are often implicated, as are dapsone and phenazopy­ ridine. Of 1 98 benzocaine-related adverse events reported to the U.S. Food and Drug Administration between 1 997 and 2 002 , a total of 1 3 2 were attributed to methemoglobine­ mia. 3 86 Of these, 1 07 were considered serious and there were two deaths. In a retrospective review of 1 3 8 cases at two teaching hospitals, dapsone was the most common offending agent. 385 Under normal physiologic conditions, NADH derived from the glycolytic pathway relieves this oxidant stress. The reaction is catalyzed by NADH methemoglobin reductase, which converts methemoglobin (Fe3 +) to hemoglobin (Fe2 +). Patients with hereditary methemoglobinemia are at risk for additional toxicity due to a preexisting deficiency of this enzyme. 387 Alternatively, methemoglobin is reduced via NADPH generated by the hexose monophosphate shunt. This reaction predominantly occurs in the presence of methylene blue and is catalyzed by NADPH methemoglo­ bin reductase. Patients with G6PD deficiency are at risk for hemolysis when treated with methylene blue as it competes Methemoglobinemia

TA B LE 2 9 - 1

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Methemoglobin Inducers

A myl n i trite A n i l i n e dyes B u tyl n i tr i te Benzocaine Ceta c a i n e Ch l o r o q u i n e Dapsone E M LA F l u ta m i d e Herbicides I s o b u tyl n i tr i te Isoso rbide d i n itrate Li d o c a i n e Metoclopramide Naphthalene N itrates Nitric o x i d e Nitrous oxide Nitrobenzene N i t r o e th a n e P e s ti c i d e s P e tr o l o c ta n e b o o s t e r P h e n a z o pyri d i n e Prilocaine Primiquine Pyr i d i u m Riluzole S u l fo n a m i d e s Si lve r n i t r a t e So d i u m n i t a t e T r i n i t r o to l u e n e S o u r c e : A s h - B e r n a l R , W1se R , Wr � g h t S M . A c q u 1 r e d m e th e m o g l o b 1 n e m 1 a : a r e t r o ­ s p e ctive s e r 1 e s o f 1 3 B c a s e s a t 2 t e a c h m g h o s p 1 t a l s . Med1c1ne (B altim ore) 2 0 0 4 , B 3 (5)· 2 6 5-2 7 3 .

for a n already limited supply of NADPH. These risks aside, methylene blue is the first-line therapy for methemoglo­ binemia and has proven efficacy. The clinical presentation of methemoglobinemia varies. Witl1 levels of up to 1 5 % , patients may be asymptomatic, although mild cyanosis and abnormal pulse oximetry are likely. Above 1 5 % , cyanosis will be readily apparent and the blood may appear chocolate-brown. At levels of 2 0 % , patients will develop symptoms such as headache, dyspnea, fatigue, and light-headedness. As the metl1emoglobin level approaches 5 0 % , patients will appear critically ill, with tachypnea, CNS depression, seizures, metabolic acidosis, and dysrhythmias. 388 Those with underlying comorbidities

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such as coronary and pulmonary disease will be symptomatic at lower levels and are more likely to become critically ill. Pulse oximetry decreases with rising methemoglobin levels. In dogs, oxygen saturation measured by pulse oxime­ ter was found to drop steadily with rising methemoglobin levels until it reached a plateau of 8 5 % , corresponding to a methemoglobin level of 3 0 % to 3 5 % . 3 89 Prior to reaching this plateau, the pulse oximeter overestimated oxygen satu­ ration; at higher methemoglobin levels, the relationship was nonlinear. The recent development of cooximeters that have the ability to measure both methemoglobin and carboxyhe­ moglobin will likely aid in diagnosis, although experience is limited at this time.390

Management The initial resuscitation of patients with methemoglobine­ mia should proceed as with other critically ill patients . Careful attention to airway management is essential. Supplemental oxygen by face mask or endotracheal intuba­ tion if required should be provided. Physical exam findings and pulse oximetry findings may clarify the diagnosis, as will a history of methemoglobin-inducing drug ingestion. An arterial or venous blood gas level should be ordered early to assess for methemoglobin and carboxyhemoglobin levels. Mild symptoms with levels < 2 5 % may be treated with sup­ plemental oxygen. 3 85 Those with moderate to severe symp­ toms, or levels > 2 5 % (regardless of symptoms) should receive IV methylene blue 1 mg/kg.3 85 The dose should be repeated for recurrence of symptoms. Dapsone-induced methemoglobinemia is unique in that this agent has a half-life of approximately 3 0 hours and is more likely to cause recurrence. 101 Refractory patients who are markedly symptomatic may respond to exchange trans­ fusion or hyperbaric therapy. Asymptomatic patients and those with levels that drop to < 1 5 % without therapy may be medically cleared. Persistently symptomatic patients and those who require methylene blue should be admitted to an intensive care setting.

Cyanide Toxicology Cyanide poisoning is unusual in the United States, although its contribution to toxicity and death may be underestimated in victims of smoke inhalation. Cyanide exposure by this route is known to be a major cause of toxicity among fire vic­ tims; however, it is often not considered in the critically ill fire victim. 3 91 Combustion of wool, silk, synthetic fabrics, and building materials may form hydrogen cyanide. The increasing use of synthetic building materials compounds the risk of cyanide toxicity resulting from building fires. Underscoring this risk is work by Baud et a1.392 Of 1 09 res­ idential fire victims, the 43 who died had a mean cyanide concentration of 3 . 1 4 mg!L. 3 92 This was sixfold higher than cyanide levels in the 66 survivors, although there was con­ siderable variability within both groups.

Workplace exposures to hydrogen cyanide gas are rare but do occur. 393 Risk factors are industrial settings where chemicals are stored or used, as in electroplating or precious metal extraction . 3 94•395 Hydrogen cyanide gas is rapidly absorbed in the lungs and may cause profound toxicity within seconds. Intentional ingestions of cyanide salts, such as sodium cyanide and potassium cyanide, are more likely in knowledgeable health care or laboratory workers who have access to such chemicals. 396 They are rapidly absorbed across the gastric mucosa and may result in toxicity within minutes. There are a number of other sources of cyanide toxicity. Acetonitrile is a component of nail glue remover. It is used to remove artificial nails and should not be confused with nail polish remover, which typically contains acetone. Acetonitrile undergoes microsomal oxidation to liberate cyanide; the rate and severity of toxicity are dependent on this conversion.397 The clinical implication of this in vivo liberation of cyanide is that toxicity may be delayed for several hours. Clinically sig­ nificant cyanide levels have been documented as far out as 1 2 to 7 2 hours postingestion and may recur following treatment due to the prolonged half-life of acetonitrile.398 Laetrile, or vitamin B , was developed in the 1 950s and 17 promoted as an antineoplastic agent, although it has no effi­ cacy against malignancies.399 It is similar to the naturally occurring cyanogenic molecule amygdalin with the excep­ tion of one less sugar moiety. When ingested, intestinal beta glucosidase converts it to glucose, aldehyde, and cyanide. It is available on the Internet, making it readily available to the public. 400-402 Cyanogenic plants include cassava, and those of the Prunus species among others. Linamarin is the predominant naturally occurring cyanogen found in cassava. It is com­ monly ingested in the tropics and is safe if prepared prop­ erly. Prunus species include choke cherries, black cherries, plums, bitter almonds, peaches, and apricots. Exposures to cyanogenic plants are fairly common and outcomes are less severe, although significant toxicity is reported.403 •404 Finally, the antihypertensive agent sodium nitroprusside may result in cyanide toxicity. In general, it occurs in patients on pro­ longed infusions and those with renal failure.405 The mechanism of cyanide toxicity is disruption of the cytochrome oxidase system, resulting in cellular hypoxia. Cyanide has a high affinity for the ferric iron (FeH) moiety of cytochrome a3 . When it binds, it disrupts the mitochon­ drial respiration, reduces ATP production, and results in lac­ tic acidosis. The critical targets of cyanide are those organs most dependent on oxidative phosphorylation, namely the brain and heart. The body has endogenous detoxification mechanisms for cyanide. Approximately 80% is detoxified by sulfurtrans­ ferase which, in the presence of thiosulfate, converts cyanide to nontoxic thiocyanate. Thiocyanate is renally excreted. Thiosulfate is rapidly depleted in cyanide poisoning, thus limiting this endogenous mechanism. Alternatively, a lim­ ited amount of cyanide is converted to nontoxic cyanocobal­ amin in the presence of hydroxocobalamin. The reported elimination half-life in humans is highly variable, and treat­ ment should be guided by clinical condition rather than pre­ dicted toxicokinetics.

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The clinical presentation depends on the route and dose of exposure. Inhalation of cyanide gas causes loss of con­ sciousness witl1in seconds, whereas symptoms from an oral exposure develop anywhere from 3 0 minutes to several hours from the time of ingestion. Toxicity will initially man­ ifest in the central nervous and the cardiovascular systems. Initial symptoms in victims not experiencing rapid loss of consciousness include headache, anxiety, confusion, blurred vision, palpitations, nausea, and vomiting. With progression of toxicity, patients may experience a feeling of neck con­ striction, suffocation, and unsteadiness. Early clinical signs of cyanide poisoning are CNS stim­ ulation or depression, tachycardia or bradycardia, hyperten­ sion, and dilated pupils. Funduscopy may reveal bright red retinal veins. Late signs of poisoning are seizures, coma, apnea, cardiac arrhythmias, and cardiovascular collapse. The characteristic musty smell of "bitter almonds" may b e detected i n some cases. Although cyanide poisoning causes cellular hypoxia, the presence of cyanosis is a relatively late finding. The absence of cyanosis in the presence of clinical evidence of severe hypoxia should prompt the examiner to consider the diagnosis of cyanide poisoning. Whole blood cyanide levels < 0 . 5 J.Lg/mL are consid­ ered nontoxic; those > 3 J.Lg/mL are lethal without treat­ ment. Arterial blood gas measurements indicate metabolic acidosis with chemistry results reflecting an anion-gap meta­ bolic acidosis, both secondary to lactate accumulation. When venous blood gas results are available, comparison with the arterial specimen may reveal a reduced arterial-venous oxygen difference due to reduced oxygen extraction. The ECG may demonstrate tachycardia, brady­ cardia, conduction defects, or ischemic changes, all depend­ ent on the degree of cellular hypoxia and underlying comor­ bidities.

Management The management of cyanide poisoning requires immediate supportive care as well as specific antidotal therapy. Oxygen is immediately administered and rapid sequence intubation may be necessary. Fluid resuscitation is initiated in patients with hypotension. Sodium bicarbonate should be considered in profound acidosis. Standard decontamination procedures should be followed in order to limit any further absorption by the patient and any absorption by health care personnel, although contamination of health care providers away from the scene is unlikely. Gastric decontamination with activated charcoal may be considered only in a patient who arrives with minimal symptoms soon after an oral exposure. The traditional antidote available in the United States for cyanide poisoning is a kit containing amyl nitrite, sodium nitrite, and sodium thiosulfate. The nitrite components are oxidizing agents, converting hemoglobin to methemoglobin (FeH). Cyanide has a higher affinity for methemoglobin than cytochrome a 3 , such that they bind and form the relatively nontoxic cyanomethemoglobin. Cyanomethemoglobin pro­ duction displaces cyanide from cytochrome a3 and allows resumption of oxidative phosphorylation and aerobic metab­ olism.

467

Clinical improvement following nitrite administration occurs within minutes, yet nitrite-induced methemoglo­ binemia is known to be a relatively slow process. This has prompted alternative theories regarding nitrite reversal of cyanide toxicity, with the focus on the effects of nitrite­ induced nitric oxide. Nitrite is a potent vasodilator, which is likely related to its reduction to nitric oxide by deoxyhemoglobin.406 This may partially ameliorate cyanide-induced circulatory dys­ function and contribute to the rapid antidotal efficacy of sodium nitrite. More likely, the effect is at the mitochondrial level. Endogenous nitric oxide has been found to augment cyanide binding to cytochrome a3 , whereas high exogenous levels, such as that induced by IV sodium nitrite, paradoxi­ cally inhibit cyanide binding.407 This would explain the rapid effect of sodium nitrite in the absence of significant methe­ moglobinemia. Hydroxocobalamin is an effective cyanide antidote, infusions of which are associated with transient but clinically significant hypertension. The proposed mechanism under­ lying this hypertension is nitric oxide scavenging.408 This complicates the previously mentioned theories regarding early efficacy of nitrites being mediated through nitric oxide. Nevertheless, cyanide binding to methemoglobin or hydroxocobalamin is the key mechanism, with the effects of nitric oxide being variable and likely less significant. When the traditional cyanide antidote kit is used, amyl nitrite is administered first. The ampules are crushed in gauze and held near the nose and mouth for 3 0 seconds, which should produce a methemoglobin level of 3 % to 7 % . Once an IV line is established and sodium nitrite adminis­ tered, amyl nitrite may be discontinued. In critically ill or comatose patients, amyl nitrite will have little utility. Sodium nitrite is administered as 3 00 mg ( 1 0 mL of a 3 % solution) at a rate of 2 . 5 to 5 mL/min. In an unstable hypotensive patient, the dose may be given over 3 0 minutes. WJth the slower rate of infusion, the methemoglobin level peaks in 3 5 to 7 0 minutes and rises to roughly 1 0 % to 1 5 % . Side effects of nitrite administration include headache, blurred vision, nausea, vomiting, and hypotension. High methemoglobin levels result in similar symptoms and impair oxygen delivery. Therefore, methemoglobin levels should be monitored closely. Following sodium nitrite, 1 2 . 5 g of sodium thiosulfate should always be administered. It provides a sulfur donor for the sulfurtransferase-mediated conversion of cyanide to thiocyanate, augmenting the nitrate-induced effect. Thiosulfate has minimal side effects; however, thiocyanate levels > 1 0 mg/dL may be associated with nausea, vomiting, arthralgias, and confusion. Thiocyanate is renally excreted, so these symptoms may be exacerbated in the setting of renal failure. Typically, symptoms and signs of cyanide poisoning begin to respond within minutes of the administration of nitrites. When symptoms recur following antidote adminis­ tration, both the sodium nitrite and sodium thiosulfate may be given again at half the original doses. In a situation in which cyanide poisoning is being considered but the diag-

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nosis is uncertain, the use of sodium thiosulfate alone may be considered. This has particular utility in fire victims . These patients may have cyanide toxicity; however, inducing methemoglobinemia in a critically ill, hypoxic, potentially carbon monoxide-poisoned patient prior to documenting a clear need is controversial. Hydroxocobalamin was recently approved by the U. S . Food and Drug Administration for treatment o f known or suspected cyanide poisoning. Hydroxocobalamin complexes with cyanide to form nontoxic cyanocobalamin, which is excreted in the urine. It is an attractive alternative to the tra­ ditional cyanide antidote kit, as it is not associated with hypotension or methemoglobinemia. It has a mild side­ effect profile, although chromaturia and skin redness are common.409 Clinically significant increases in systolic and diastolic blood pressure are seen, as well as mild decreases in heart rate correlating with the hypertension.409 Hydroxocobalamin has been used in France for over 3 0 years in both the hospital and prehospital settings and has been evaluated as an antidote for cyanide poisoning related to smoke inhalation in two observational studies.4 1 0•4 1 1 Case series and retrospective chart reviews document efficacy in cyanide poisoning unrelated to smoke inhalation.402 •4 12-414 A lack of controlled trials establishing clear superiority of hydroxocobalamin is the remaining criticism. D espite this , there is strong evidence in support of its use. Hydroxocobalamin is a safe and effective first-line therapy for cyanide toxicity and should be carefully considered as empiric therapy for victims of smoke inhalation when cyanide toxicity is likely. Patients who are asymptomatic and whose exposure has apparently been minimal are observed for several hours . Those who have ingested cyanogenic glycosides are observed for at least 6 hours for evidence of toxicity. Those ingesting acetonitrile-containing compounds are observed for 1 2 to 24 hours. Patients requiring antidotal treatment are admitted to an ICU, where vital signs, mental status, arterial blood gases, methemoglobin, and carboxyhemoglobin levels can be checked frequently. Following recovery, patients are observed for 24 to 48 hours.

Organophosphates and Carbamates Toxicology Unintentional pesticide poisonings, including those attrib­ uted to organophosphates and carbamates, have declined significantly over the past decade.41 5 Despite this fact, these agents remain a significant source of toxicity, with almost 1 0,000 combined cases reported to U. S . poison centers in 2005 .69 The cholinergic toxidrome is identical to that of the chemical weapons sarin, soman, tabun, and VX, although these agents are markedly more potent in comparison. Organophosphates are well absorbed in the lungs and GI system as well as through mucous membranes and skin. They inhibit acetylcholinesterase, resulting in accumulation of acetylcholine in nicotinic and cholinergic nerve terminals. The central and autonomic nervous system as well as neu­ romuscular junctions in skeletal muscle are affected.

Under normal conditions, acetylcholinesterase cleaves acetylcholine into acetic acid and choline, with choline undergoing reuptake into the presynaptic nerve terminal. Organophosphates phosphorylate the active hydroxyl group of acetylcholinesterase, rendering it inactive. During this period the inactivated enzyme undergoes slow hydrolysis. The addition of pralidoxime enhances this reaction. "Aging" occurs after a delay of 24 to 72 hours; one of the aromatic or aliphatic groups bound to the central phosphorus leaves and the enzyme is permanently inactivated. The initial process is similar for carbamates; however, aging does not occur. Enzymes that have undergone carbamylation slowly hydrolyze and the enzyme is reactivated. The clinical presentation of the cholinergic toxidrome is classically described as defecation, urination, miosis, bron­ chospasm, bronchorrhea, emesis, lacrimation, and salivation (DUMBBELS). This acronym reflects the muscarinic com­ ponent of toxicity, which may not be uniformly present. Nicotinic stimulation results in muscle fasciculations, twitching, and weakness. Significant CNS and cardiac complications are com­ mon with severe poisonings. CNS manifestations include anxiety, confusion, seizure, and coma.416 Cardiac manifesta­ tions are less prominent than with other direct cardiotoxins; however, hypertension, hypotension, PR and QT prolonga­ tion, ST-segment and T-wave abnormalities, atrial fibrilla­ tion, ventricular tachycardia, and ventricular fibrillation have been observed.417 Onset of symptoms may be acute and usually occurs within < 1 2 hours.416 Longer delays are seen with compounds that require in vivo activation and those that are very lipid-soluble.

Management Aggressive supportive care and thorough decontamination with appropriate protection for health-care workers is essen­ tial to the management of cholinergic toxins. Attention to life­ threatening manifestations takes precedence. Respiratory fail­ ure from bronchorrhea and respiratory muscle weakness should be managed with early endotracheal intubation. Seizures are treated with benzodiazepines and phenobar­ bital unless they are brief and self-limited. Vasopressors are indicated for hypotension that does not respond to atropine. Following the initial resuscitation, attention is turned to man­ aging muscarinic symptoms. Atropine competitively antago­ nizes acetylcholine at muscarinic receptors and is the treat­ ment of choice. Unlike standard ACLS-recommended doses of atropine, the initial dose is 1 to 5 mg, with subsequent doses doubled and administered every 2 to 3 minutes as needed.4 1 8 The endpoint of treatment is improvement of pulmonary symptoms, which may require large doses. Pralidoxime is effective in regenerating acetyl­ cholinesterase that has been inactivated by an organophos­ phate. It should be considered even in late presentations. Bound enzyme that has not undergone the aging process is liberated when the nucleophilic oxime attacks the phospho­ rus atom of the bound organophosphate. The increase in acetylcholinesterase should ameliorate both muscarinic and nicotinic symptoms, whereas atropine is effective only for

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muscarinic symptoms. It is not considered useful for carba­ mates; however, it is generally not contraindicated and should be utilized when it is unclear whether an organophosphate or carbamate is involved. Patients who are asymptomatic or who have mild symp­ toms that resolve without treatment may be discharged home. Patients with persistent symptoms should be admit­ ted. Those requiring treatment should be closely observed for recurrence and have red blood cell cholinesterase levels assayed. They may be medically cleared once they have been asymptomatic for 24 to 48 hours and their red blood cell cholinesterase levels are stable.

Conclusion Utilizing a methodical approach that focuses on aggressive supportive care and the principles of ACLS optimizes care of the critically ill poisoned patient. Consideration must be given to nonstandard absorption, distribution, and elimina­ tion when drugs are taken in overdose. Attention to clinical clues and laboratory findings can narrow the differential diagnosis. The focus can then turn to advanced decontami­ nation, enhanced elimination, and antidotal therapy. Synthesis of basic science and clinical research is essen­ tial for continued optimal advanced care of the poisoned patient. Examples of such advances are hydroxocobalamin for cyanide toxicity, HIE therapy for poisoning with a cal­ cium channel antagonist, and the emerging utility of intralipid. This work has expanded therapeutic options and is important for the management of these common yet potentially complicated cardiotoxic patients.

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whole bowel irrigation succimer therapy and endoscopic removal of ingested lead pellets. Pediat1' Ernerg Can 2 002 ; 1 8(3):2 00-2 0 2 . Kaczorowski JM, Wax PM. Five days o f whole-bowel irrigation in a case of pediatric iron ingestion. Ann Emerg Med 1 996;2 7(2):2 5 8-2 6 3 . Roberge RJ, Martin TG. Whole bowel irrigation i n a n acute oral lead intoxication. Am J Eme1'g Med 1 992 ; 1 0(6) : 5 77-5 8 3 . Hoffman RS, Smilkstein MJ, Goldfrank LR. Whole bowel irriga­ tion and the cocaine body-packer: a new approach to a common problem. Am J Enze1·g Med 1 990;8(6) : 5 2 3-52 7 . Burkhart KK , Kulig KW, Rumack B. Whole-bowel irrigation as treatment for zinc sulfate overdose. Ann Enze1'g Med 1 990; 1 9( 1 0):

1 1 67-1 1 70. 47. Vale JA. Position statement and practice guidelines on the use of

multi-dose activated charcoal in the treatment of acute poisoning. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists . ] Toxicol Clin Toxicol 1 999;3 7(6): 7 3 1-75 1 . 48. Bradberry SM, Vale JA. Multiple-dose activated charcoal: a review of relevant clinical studies. J Toxicol Clin Toxicol 1 995 ; 3 3 (5):407-4 1 6. 49. Ilkhanipour K, Yealy DM, Krenzelok EP. The comparative effi­ cacy of various multiple-dose activated charcoal regimens. Am J Enze1'g Med 1 992 ; 1 0(4):2 98-3 00. 50. Proudfoot AT, Krenzelok EP, Vale JA. Position paper on urine alkalinization. J Toxicol Clin Toxico/ 2 004;42 ( 1 ) : 1 -2 6 . 5 1 . Proudfoot AT, e t a ! . Does urine alkalinization increase salicylate elimination? If so why? Toxicol Rev 2 003 ; 2 2 (3 ) : 1 2 9- 1 3 6. 5 2 . Macpherson CR, Milne MD, Evans BM. The excretion of salicy­ late. B1' J Pbamtacol Cbernotbe1' 1 9 5 5 ; 1 0(4):484-489. 5 3 . Flomenbaum NE. Salicylates. In Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, eds. Goldfmnk's Toxicologic Enze1·gencies, 8th ed. New York: McGraw-Hill, 2 0 0 7 . 54. Temple AR. Acute and chronic effects of aspirin toxicity and their treatment. Anb Intem Med 1 9 8 1 ; 1 4 1 (3 Spec No) : 3 64-3 69. 5 5 . Yip L, Dart RC, Gabow PA. Concepts and controversies in sali­ cylate toxicity. Emerg Med Clin Nonb Am 1 994; 1 2 (2 ) : 3 5 1 -3 64. 56. Tapolyai M, et a!. Hemodialysis is as effective as hemoperfusion for drug removal in carbamazepine poisoning. Nepbron 2002 ;90(2):2 1 3-2 1 5 . 5 7 . Schuerer DJ, et a!. High-efficiency dialysis for carbamazepine overdose. ] Toxicol Clin Toxico/ 2000;3 8(3) : 3 2 1 -3 2 3 . 5 8 . Kielstein JT, et a!. High-flux hemodialysis-an effective alterna­

tive to hemoperfusion in the treatment of carbamazepine intoxi­ cation. Clin Nepb1·ol 2 002 ; 5 7 (6):484-486. 59. Kielstein JT, et a!. Efficiency of high-flux hemodialysis in the treatment of valproic acid intoxication. J Toxicol Clin Toxicol 2003 ;41 (6) : 8 7 3-876. 60. Kay TD Playford HR, Johnson DW. Hemodialysis versus con­

tinuous veno-venous hemodiafiltration in the management of severe valproate overdose. Clin Nepbro/ 2 0 0 3 ; 5 9 ( 1 ) : 5 6-5 8 . 6 1 . Hicks LK, McFarlane PA. Valproic acid overdose and haemodial­ ysis. Nepb1'ol Dial 1i'ansplant 2 00 1 ; 1 6(7) : 1 48 3 - 1 486. 62 . Kane SL, et a!. High-flux hemodialysis without hemoperfusion is effective in acute valproic acid overdose. Ann Pbarrnacotber· 2000;34( 1 0): 1 1 46-1 1 5 1 . 6 3 . Shalkham AS , et a!. The availability and use o f charcoal bema­ perfusion in the treatment of poisoned patients. Am J Kidney Dis 2 006;48(2):2 3 9-2 4 1 . 64. AJ Aly Z, Yalamanchili P, Gonzalez E. Extracorporeal manage­

ment of valproic acid toxicity: a case report and review of the lit­ erature. Se7nin Dia/ 2 005 ; 1 8 ( 1 ) : 62-66. 65. Meyer RJ, et a!. Hemodialysis followed by continuous hemofil­ tration for treatment of lithium intoxication in children. Am J Kidney Dis 2 00 1 ; 3 7(5) : 1 044- 1 047 . 66. van Bommel EF, Kalmeijer MD, Ponssen HH. Treatment of life­

threatening lithium toxicity with high-volume continuous ven­ ovenous hemofiltration. Am J Nepb1·ol 2 000;2 0(5) :408-4 1 1 . 67. Rosenberg J , et a!. Hyperthermia associated with drug intoxica­ tion. Cht Care Med 1 986: 1 4( 1 1 ) :964-969. 68. Martinez M, et a!. Drug-associated heat stroke. Soutb Med J 2002 ;95 (8): 799-802 . 69. Lai MW, et a!. 2005 Annual Report of the American Association

of Poison Control Centers' national poisoning and exposure data­ base. Clin Toxicol (Pbila) 2 006;44(6-7) :803-9 3 2 .

70. Frishman WH Clinical differences between beta-adrenergic blocking agents : implications for therapeutic substitution. Am Heart J 1 98 7; 1 1 3 (5): 1 1 90-1 1 9 8 . 7 1 . Katz AM. Selectivity and toxicity of antiarrhythmic drugs: molec­ ular interactions with ion channels. Anz J Med 1 99 8 ; 1 04(2 ) : 1 79-1 9 5 . 7 2 . Frishman WH Clinical significance o f beta ! -selectivity and .

.

intrinsic sympathomimetic activity in a beta-adrenergic blocking drug. Am J Cardiol l 98 7 ; 5 9( 1 3 ) : 3 3 F-3 7F. 7 3 . Henry JA, Cassidy SL. Membrane stabilising activity: a major cause of fatal poisoning. Lancet 1 986; 1 (8495): 1 4 1 4-1 4 1 7 . 74. Love JN, e t a ! . Electrocardiographic changes associated with beta-blocker toxicity. Ann Emerg Med 2 002 :40(6): 603-6 1 0. 7 5 . Frishman W, et a!. Clinical pharmacology of the new beta-adren­ ergic blocking drugs: Part 8. Self-poisoning with beta-adrenocep­ tor blocking agents: recognition and management. Am Hem?: J 1 979;98( 6): 798-8 1 1 . 7 6 . Love JN, et a!. Acute beta blocker overdose: factors associated with the development of cardiovascular morbidity. J Toxicol Clin Toxico/ 2 000; 3 8(3):2 7 5-2 8 1 . 7 7 . Weinstein RS. Recognition and management o f poisoning with beta-adrenergic blocking agents Ann Enze1·g Med 1 984; 1 3 ( 1 2 ) : 1 1 2 3 -1 1 3 1 . 7 8 . Brubacher ] . Beta-adrenergic agonists . In Flomenbaum NE, Howland M, Goldfrank LR, et a!, eds. Goldfrank 's Toxicologic Emergencies, 8th ed. New York: McGraw-Hill, 2007. 79. Hohnloser SH, Woosley RL. Sotalol. N Eng/ J Med 1 994; 3 3 1 ( 1 ) : 3 1 -3 8. 80. Reith DM, et a!. Relative toxicity of beta blockers in overdose. J Toxicol Clin Toxico/ 1 996;34(3) : 2 7 3 -2 7 8 . 8 1 . Delk C, Holstege CP, Brady WJ. Electrocardiographic abnor­ malities associated with poisoning. Am J Erne1'g Med 2 007;2 5 (6) : 672-6 8 7 . 82 . Pollack CV Jr. Utility of glucagon in the emergency department. J Emerg Med 1 993 ; 1 1 (2): 1 95-2 0 5 . 8 3 . Taboulet P, et a!. Pathophysiology and management of self-poi­ soning with beta blockers . J Toxicol Clin Toxicol 1 99 3 ; 3 1 (4) : 5 3 1 -5 5 1 . 84. Yagami T. Differential coupling o f glucagon and beta-adrenergic

receptors with the small and large forms of the stimulatory G pro­ tein. Mol Pbamtaco/ 1 99 5 ;48(5) : 849-8 54. 85. Rochais F, et a!. A specific pattern of phosphodiesterases controls the cAMP signals generated by different Gs-coupled receptors in adult rat ventricular myocytes. Circ Res 2 006;98(8): 1 08 1 - 1 0 8 8 . 86. Donovan KD, Gerace RV, Dreyer J F. Acebutolol-induced ven­ tricular tachycardia reversed with sodium bicarbonate. J Toxicol Clin Toxico/ 1 999; 3 7 (4):48 1 -484. 87. Kerns W II. Management of beta-adrenergic blocker and calcium channel antagonist toxicity. Eme1•g Med Clin N011b Ant 2 007;2 5 (2): 3 09-3 3 1 ; abstract viii. 8 8 . Kerns W, et a!. Insulin improves survival in a canine model of acute beta-blocker toxicity. Ann Emerg Med 1 997 ;2 9( 6): 7 48-7 5 7 . 8 9 . Holger JS, e t a!. Insulin versus vasopressin and epinephrine to treat beta-blocker toxicity. Clin Toxicol (Phi/a) 2 0 0 7 ; 4 5 (4) : 3 96-40 1 . 90. Yuan TH, et a!. Insulin-glucose a s adjunctive therapy for severe calcium channel antagonist poisoning. J Toxicol Clin Toxico/ 1 999; 3 7 (4) :463-474. 9 1 . Kenyon CJ, et a!. Successful resuscitation using external cardiac

pacing in beta adrenergic antagonist-induced bradyasystolic arrest. Ann Emerg Med 1 9 8 8 ; 1 7 (7) : 7 1 1 -7 1 3 . 92 . Lane AS , Woodward AC, Goldman MR. Massive propranolol overdose poorly responsive to pharmacologic therapy: use of the intra-aortic balloon pump . Ann Emerg Med 1 98 7 ; 1 6( 1 2 ) : 1 3 8 1-1 3 8 3 . 93 . Rooney M , et a!. Acebutolol overdose treated with hemodialysis and extracorporeal membrane oxygenation. J Clin Pharnzacol 1 996;3 6(8): 760-763 . 94. Saitz R, Williams BW, Farber HW Atenolol-induced cardiovas­ cular collapse treated with hemodialysis. Crit Cm·e Med 1 99 1 ; 1 9( 1 ) : 1 1 6- 1 1 8 . 9 5 . Salhanick S D , Wax PM.Treatment of atenolol overdose in a

patient with renal failure using serial hemodialysis and hemoper­ fusion and associated echocardiographic findings. Vet Hum Toxicol 2 000;42 (4) : 2 2 4-2 2 5 .

CHAPTER 29

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T O X I C O L O G Y I N E M E R G E N C Y C A R D I O VA S C U L A R C A R E

47 1

ulated receptor mechanism of action of sodium and calcium chan­ nel-blocking drugs. Annu Rev Pbarnzacol Toxico/ 1 984;24: 3 8 7-42 3 . 1 0 1 . Leikin JB, Palouchek FP, eds. Poisoning and Toxicology Handbook, 3 rd ed. Hudson, OH: Lexi-Comp, 2 002 . 1 0 2 . Levine M, et al. Assessment of hyperglycemia after calcium chan­ nel blocker overdoses involving diltiazem or verapamil. Crit CmT

1 2 5 . Hendren WG, S chieber RS, Garrettson LK. Extracorporeal bypass for the treatment of verapamil poisoning. Ann Enzerg Med 1 989; 1 8(9):984-9 8 7 . 1 2 6 . Gheorghiade M, Adams KF ]r, Colucci WS .Digoxin in the man­ agement of cardiovascular disorders. Circulation 2 004; 1 09(24) : 2 9 5 9-2 964. 1 2 7 . Hauptman P], Garg R, Kelly RA. Cardiac glycosides in the next millennium. P1·og Cardiovnsc Dis 1 999;4 1 (4):247-2 54. 1 2 8 . Levi AJ, Boyett MR, Lee CO. The cellular actions of digitalis gly­ cosides on the heart. P1•og Biophys Mol Biol 1 994;62 ( 1 ) : 1-54. 129. Dvela M, et a!. Diverse biological responses to different car­ diotonic steroids. Pntbopbysiology 2007; 1 4(3-4) : 1 5 9- 1 66. 1 3 0. Antman EM, Smith TW Digitalis toxicity. Annu Rev Med 1 9 8 5 ; 3 6 : 3 5 7-3 6 7 . 1 3 1 . Quan KJ, et a!. Endocardial stimulation of efferent parasympa­

Med 2 007 ;3 5 (9): 2 0 7 1 -2 0 7 5 . 1 0 3 . Caulfield MP, Birdsall NJ. International Union of Pharmacology

thetic nerves to the atrioventricular node in humans: optimal stimulation sites and the effects of digoxin. J Intel'Vent Cm·diol

XVII Classification of muscarinic acetylcholine receptors.

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Pbarmacol Rev 1 998;5 0(2):2 79-2 90. 1 04. Wolf LR, Spadafora MP, Otten EJ. Use of amrinone and glucagon in a case of calcium channel blocker overdose. Ann Enzerg Med 1 99 3 ; 2 2 (7): 1 2 2 5- 1 2 2 8 . 1 0 5 . Haddad LM. Resuscitation after nifedipine overdose exclusively with intravenous calcium chloride. Anz J Emerg Med 1 996; 1 4(6): 602-603 .

1 06. Lam YM, Tse HF, Lau CP. Continuous calcium chloride infusion for massive nifedipine overdose. Chest 2 00 1 ; 1 1 9(4): 1 2 80- 1 2 8 2 . 1 0 7 . Luscher TF, e t al. Calcium gluconate i n severe verapamil intoxi­ cation. N Eng! J Med 1 994;3 3 0 ( 1 0) : 7 1 8-720. 1 0 8 . Spiller HA, et a!. Delayed onset of cardiac arrhythmias from sus­ tained-release verapamil. Ann Enzerg Med 1 9 9 1 ;2 0(2) : 2 0 1 -2 0 3 . 1 09. Perkins CM. Serious verapamil poisoning: treatment with intra­ venous calcium gluconate. B1· Med J 1 9 7 8 ;2 (61 45): 1 1 2 7 . 1 1 0. Crump BJ, Holt D W, Vale JA. Lack o f response t o intravenous cal­ cium in severe verapamil poisoning. Lancet 1 982;2(83 04): 93 9-940. 1 1 1 . Horowitz BZ, Rhee KJ. Massive verapamil ingestion: a report of two cases and a review of the literature. Am J Enzerg Med 1 989; 7(6):624-63 1 . 1 1 2 . Kline ]A, Leonova E , Raymond RM . Beneficial myocardial meta­ bolic effects of insulin during verapamil toxicity in the anes­ thetized canine. Crit Cm·e Med 1 995;2 3 (7): 1 2 5 1 - 1 2 6 3 . 1 1 3 . Kline ]A, et al. Myocardial metabolism during graded intraportal verapamil infusion in awake dogs. J Cm•diovasc Pharmacol 1 996; 2 7(5): 7 1 9-72 6 . 1 1 4. Kline JA, et al. The diabetogenic effects of acute verapamil poi­ soning. Toxico! Appl Pbarnzaco/ 1 997 ; 1 45 (2): 3 5 7-3 62 . 1 1 5 . Kline ]A, et al. Insulin improves heart function and metabolism

during non-ischemic cardiogenic shock in awake canines. Cardiovasc Res 1 99 7 ; 3 4(2):2 89-2 9 8 . 1 1 6. Boyer EW, Shannon M. Treatment of calcium-channel-blocker intoxication with insulin infusion. N Eng! J Med 2 00 1 ;3 44(22):

1 72 1 - 1 72 2 . 1 1 7 . Boyer E W, Duic PA, Evans A . Hyperinsulinemia/euglycemia therapy for calcium channel blocker poisoning. Pediatr Enzerg Care 2 002 ; 1 8 ( 1 ) : 3 6-3 7 . 1 1 8 . Rasmussen L, Husted SE, Johnsen SP. Severe intoxication after an intentional overdose of amlodipine. Acta Anaesthesiol Scand 2 0 0 3 ; 4 7(8): 1 0 3 8-1 040. 1 1 9. Marques ME, et al. Treatment of calcium channel blocker intoxi­

cation with insulin infusion: case report and literature review. Rmtscitation 2 003 ; 5 7(2):2 1 1-2 1 3 .

1 2 0 . Harris NS. Case records o f the Massachusetts General Hospital Case 24-2 006. A 40-year-old woman with hypotension after an overdose of amlodipine. N Eng! J Med 2 006;3 5 5(6): 602-6 1 1 . 1 2 1 . Ortiz-Munoz L , Rodriguez-Ospina LF, Figueroa-Gonzalez M. Hyperinsulinemic-euglycemic therapy for intoxication with cal­ cium channel blockers. Bo!Asoc Med P R 2 005 ;97(3 Pt 2): 1 82-1 89. 1 2 2 . Lheureux PE, et a!. Bench-to-bedside review: hyperinsuli­ naemia/euglycaemia therapy in the management of overdose of calcium-channel blockers. C1·it Can 2 006; 1 0(3):2 1 2 . 1 2 3 . Holzer M , e t al. Successful resuscitation o f a verapamil-intoxi­ cated patient with percutaneous cardiopulmonary bypass. Crit Care Med 1 999;2 7 ( 1 2) :2 8 1 8-2 82 3 .

124. Frierson ], et a!. Refractory cardiogenic shock and complete heart block after unsuspected verapamil-SR and atenolol overdose. Clin Cardio/ 1 99 1 ; 1 4( 1 1):93 3 -93 5 .

1 34. 135. 1 3 6. 137. 1 3 8.

1 3 9.

glycosides in heart failure patients. Direct evidence from sympa­ thetic neural recordings. Circulation 1 989;80(1):65-7 7 . Kelly RA, Smith TW Recognition and management o f digitalis tox­ icity. Am J Cardio/ 1 992 ;69(1 8): 1 08G-1 1 8G; discussion 1 1 8G-1 1 9G. Clausen T. Clinical and therapeutic significance of the Na + K + pump. Clin Sci (Lond) 1 998;95 ( 1 ) : 3- 1 7 . Bigger J T Jr, Sahar DI. Clinical types o f proarrhythmic response to antiarrhythmic drugs. Ant J Cardio/ 1 98 7 ; 5 9 ( 1 1 ) :2 E-9E. Smith TW, et al. Digitalis glycosides: mechanisms and manifesta­ tions of toxicity: Part I. PTog Cardiovasc Dis 1 984;26(5) :41 3-45 8 . Hack JB, Lewin NA. Cardioactive steroids. I n Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, eds. Goldfran k 's Toxicologic Enze1·gencies, 8th ed. New York: McGraw-Hill, 2 006. Wofford JL, Ettinger WH . Risk factors and manifestations of digoxin toxicity in the elderly. Am J Emerg Med 1 9 9 1 ;9(2 Suppl 1):

1 1- 1 5 . 1 4 0 . Mahdyoon H, et a!. The evolving pattern of digoxin intoxication: observations at a large urban hospital from 1 980 to 1 9 8 8 . Anz Hean J 1 990; 1 2 0(5): 1 1 89- 1 1 94. 1 4 1 . Lely AH, van Enter CH. Large-scale digitoxin intoxication. B1· Med J 1 97 0 ; 3 ( 5 7 2 5 ) : 7 3 7-740. 1 42 . Irons GV Jr, Orgain ES. Digitalis-induced arrhythmias and their management. Prog Cm·diovnsc Dis 1 966;8(6) : 5 3 9-569. 1 4 3. Smith SW, et al. Bidirectional ventricular tachycardia resulting from herbal aconite poisoning. Ann Enze1·g Med 2005;45(1): 1 00-1 0 1 . 1 44. Ordog GJ, e t al. S erum digoxin levels and mortality i n 5 1 00 patients. Ann Enze1·g Med 1 9 8 7 ; 1 6( 1 ) : 3 2-9. 1 4 5 . Dally S , et a!. [Prognostic factors in acute digitalis poisoning (author's trans!)] . Nouv Pmse Med 1 98 1 ; 1 0(2 7):2 2 5 7-2 2 60. 146. Critchley JA, Critchley LA. Digoxin toxicity in chronic renal fail­

ure: treatment by multiple dose activated charcoal intestinal dial­ ysis. Hunz Exp Toxicol 1 997 ; 1 6( 1 2 ) : 7 3 3 -7 3 5 . 147. Lalonde RL, e t al. Acceleration o f digoxin clearance by activated charcoal. Clin Pbarmacol Tbe1• 1 9 8 5 ; 3 7 (4): 3 67-3 7 1 . 148. Hickey AR, et al. Digoxin Immune Fab therapy in the manage­ ment of digitalis intoxication: safety and efficacy results of an observational surveillance study. J Am Colt Cardiol 1 99 1 ; 1 7 ( 3 ) : 590-598. 149. Antman EM, et a!. Treatment of 1 50 cases of life-threatening dig­

italis intoxication with digoxin-specific Fab antibody fragments. Final report of a multicenter study. Ci1•culation 1 990; 8 1 (6): 1 744- 1 7 5 2 . 1 50. Smith TW, et a!. Tream1ent o f life-threatening digitalis intoxica­

tion with digoxin-specific Fab antibody fragn1ents: experience in 26 cases. N Eng! J Med 1 9 8 2 ; 3 07(22) : 1 3 5 7- 1 3 62 . 1 5 1 . Smolarz A , e t al. Digoxin specific antibody (Fab) fragments in 3 4 cases of severe digitalis intoxication. J Toxicol Clin Toxicol 1 9 8 5 ; 2 3 (4-6) : 3 2 7-3 40. 1 5 2 . Taboulet P, et a!. Acute digitalis intoxication--is pacing still appropriate? J Toxicol Clin Toxico/ 1 993 ; 3 1 (2):2 6 1 -2 7 3 . 1 5 3 . Smith TW, et a!. Reversal o f advanced digoxin intoxication with Fab fragments of digoxin-specific antibodies. N Eng! J Med 1 976;294( 1 5):797-800.

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ERICKSON

1 54. V.·m Deusen SK, Birkhahn RH, Gaeta TJ. Treatment of hyper­ kalemia in a patient with unrecognized digitalis toxicity. J Toxicol Clin Toxico/ 2 003 ;4 1 (4) : 3 7 3 -3 76. 1 5 5 . Hack JB, et al. The effect of calcium chloride in treating hyper­ kalemia due to acute digoxin toxicity in a porcine model. J Toxicol Clin Toxico/ 2 004;42 (4) : 3 3 7-3 42 . 1 5 6. Rumack BH, Wolfe RR, Gilfrich H. Phenytoin (diphenylhydan­ toin) tream1ent of massive digoxin overdose. B1� Hem-t J 1 974;3 6(4): 405-408. 1 5 7 . Harris AS, Kokernot RH. Effects of diphenylhydantoin sodium

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ing in a wide-complex tachycardia: successful treatment with sodium bicarbonate. Ann Emerg Med 1 992;2 1 (3 ): 3 1 8-3 2 1 . 1 69. Pratt CM, et al. Risk o f developing life-threatening ventricular arrhythmia associated with tefenadine in comparison with over­ the-counter antihistamines ibuprofen and clemastine. Am J Cardio/ 1 994; 7 3 (5 ) : 3 46-3 5 2 . 1 70. Soto LF, Miller CH, Ognibere AJ. Severe rhabdomyolysis after doxylamine overdose. Postgrad Med 1 993 ;93 (8) : 2 2 7-2 3 2 . 1 7 1 . Frankel D, Dolgin J, Murray BM. Non-traumatic rhabdomyoly­ sis complicating antihistamine overdose. J Toxicol Clin Toxicol 1 993 ; 3 1 (3):493-496 . 1 7 2 . Leybishkis B, Fasseas P, Ryan KF. Doxylamine overdose as a poten­ tial cause of rhabdomyolysis. Am J Med Sci 2 00 1 ; 3 2 2 ( 1 ) : 48-49. 1 7 3 . Koppel C, Ibe K, Oberdisse U. Rhabdomyolysis in doxylamine overdose. Lancet 1 9 8 7 ; 1 (8 5 3 0):442-443 . 1 74. Reilly JF Jr, Weisse ME. Topically induced diphenhydramine tox­ icity. J Eme1�g Med 1 990; 8 ( 1 ) : 59-6 1 . 1 7 5 . Reilly Ki\1 , e t al. Systemic toxicity from ocular homatropine. A cad Eme1�g Med 1 99 6 ; 3 (9): 8 68-8 7 1 . 1 76. Sharma AN, et al. Diphenhydramine-induced wide complex dys­ rhythmia responds to treatment with sodium bicarbonate. Am J Eme1�g Med 2 003 ;2 1 (3):2 1 2 -2 1 5 . 1 7 7 . Farrell M, Heinrichs M, Tilelli JA. Response of life threatening

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dopaminergic systems by nitrous oxide in rats: a possible neuro-

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convulsant effects of tramadol its enantiomers and its Ml metabo­ lite in the rat kindling model of epilepsy. Bz· J Pharmacal 2 000; 1 3 1 (2):203-2 1 2 . 3 60. Jovanovic-Cupic V, Martinovic Z , Nesic N . Seizures associated with intoxication and abuse of tramadol. Clin Toxicol (Phi/a) 2 006; 44(2) : 14 3 - 1 46. 3 6 1 . Pok:lis A. Pentazocine/tripelennamine (T's and blues) abuse: a five-year survey of St Louis, Missouri. Dz7zg Alcohol Depend 1 9 8 2 ; 1 0(2-3):2 5 7-2 67. 3 6 2 . Barkin RL, Barkin SJ, Barkin OS. Propoxyphene (dextro­

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3 69. Douglas CG, Haldane JS, Haldane JB. The laws of combination of haemoglobin with carbon monoxide and oxygen. J Physiol 1 9 1 2 ;44(4) : 2 7 5-3 04. 3 70. Roughton FJW, Darling RC. The effect of carbon monoxide on the oxyhemoglobin dissociation curve. Am J Physio/ 1 944; 1 4 1 ( 1 ) : 1 7-3 1 . 3 7 1 . Okada Y, et al. Effect o f carbon monoxide on equilibrium between oxygen and hemoglobin. Am J Physio/ 1 976;2 3 0(2):47 1-47 5 . 3 7 2 . Ball EG, Strittmatter C F, Cooper 0 . The reaction o f cytochrome oxidase with carbon monoxide. J Bioi Chenz 1 9 5 1 ; 1 9 3 (2):63 5-647. 3 7 3 . Prockop LD, Chichkova Rl. Carbon monoxide intoxication: an updated review. ] Neural Sci 2007;262(1-2) : 1 22-1 3 0 . 3 7 4 . Satran D, et a l . Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Colt Cm�dio/ 2 005 ;45 (9) : 1 5 1 3- 1 5 1 6. 3 7 5 . Kalay N, et al. Cardiovascular effects of carbon monoxide poi­ soning. Am J Ctwdio/ 2007;99(3 ) : 3 2 2-3 24. 3 76. Pace N, Strajman E, Walker EL. Acceleration of carbon monox­ ide elimination in man by high pressure oxygen. Science 1 9 5 0 ; 1 1 1 (2 894):652-654. 3 77. Peterson JE, Stewart RD . Absorption and elimination of carbon monoxide by inactive young men. Arch Envi7�on Health 1 970;2 1 (2): 1 65-1 7 1 . 3 7 8 . Jay GD, et al. Portable hyperbaric oxygen therapy in the emer­ gency deparm1ent with the modified Gamow bag. Ann Emerg Med 1 995;2 6(6) : 707-7 1 1 . 3 79. Weaver LK, et al. Carboxyhemoglobin half-life in carbon monox­ ide-poisoned patients treated with l 00% oxygen at atmospheric pressure. Chest 2 000; 1 1 7(3): 8 0 1 -808. 3 80. Raphael JC, et al. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 1 98 9 ; 2 (8660): 4 1 4-4 1 9 . 3 8 1 . Thom S R , e t a l . Delayed neuropsychologic sequelae after carbon

3 82 .

383. 3 84. 3 85 .

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cytochrome b5 reductase in erythrocytes of normal and methe­ moglobinemic individuals measured with a quantitative radioim­ munoblotting assay. J Clin Invest 1 9 8 7 ; 80(5): 1 2 96- 1 3 02 . 3 8 8 . Price D . Menthemoglobin inducers. In Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, eds. Goldfrank 's Toxicologic Eme1xencies, 8th ed. New York: McGraw-Hill, 2 006. 3 89. Barker SJ, Tremper KK, Hyatt ]. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 1 989;70( 1 ) : 1 1 2-1 1 7 . 3 90. Barker SJ, e t al. Measurement o f carboxyhemoglobin and methe­

moglobin by pulse oximetry: a human volunteer study. Anesthesiology 2 006; 1 0 5 (5):892-8 9 7 . 3 9 1 . Eckstein M, Maniscalco PM. Focus on smoke inhalation-the most common cause of acute cyanide poisoning. P1·ehosp Disaste1· Med 2 006;2 1 (2 Suppl 2):s49-s 5 5 . 3 9 2 . Baud FJ, e t al. Elevated blood cyanide concentrations i n victims of smoke inhalation. N Eng! J Med 1 99 1 ; 3 2 5 (2 5): 1 7 6 1 - 1 766.

393. Lam KK, Lau FL. An incident of hydrogen cyanide poisoning. Am J Emerg Med 2 000; 1 8(2): 1 72-1 7 5 . 3 94. Piccinini N , e t al. Risk o f hydrocyanic acid release i n the electro­ plating industry. J Hazm·d Mater 2 000; 7 1 ( 1 -3 ) : 3 95-40 7 . 3 9 5 . Blanc P, et al. Cyanide intoxication among silver-reclaiming workers. JAMA 1 98 5 ;2 5 3 (3 ) : 3 67-3 7 1 . 396. Binder L , Fredrickson L . Poisonings in laboratory personnel and health care professionals. Am ] Enmx Med 1 9 9 1 ;9(1): 1 1-1 5 . 3 9 7 . Tanii H, Hashimoto K . Studies o n the mechanism o f acute toxic­ ity of nitriles in mice. Anh Toxico/ 1 984; 5 5 ( 1 ):47-54. 3 9 8 . Michaelis HC, et al. Acetonitrile serum concentrations and

cyanide blood levels in a case of suicidal oral acetonitrile ingestion. J Toxicol Clin Toxico/ 1 99 1 ;2 9(4):447-3 5 8 . 3 99. Unproven methods o f cancer management. Laetrile. CA Cancer J Clin 1 99 1 ;4 1 (3): 1 8 7- 1 9 2 . 400. Beamer WC, Shealy RM , Prough D S . Acute cyanide poisoning from laetrile ingestion. Ann Enzerg Med 1 9 8 3 ; 1 2 (7):449-45 1 . 40 1 . O 'Brien B , Quigg C , Leong T. S evere cyanide toxicity from "vitamin supplements. " Exw J Enze1�g Med 2 005 ; 1 2 (5):2 5 7-2 5 8 . 402 . Bromley J, e t al. Life-threatening interaction between comple­

mentary medicines: cyanide toxicity following ingestion of amyg­ dalin and vitamin C. Ann Pharmacother 2 0 0 5 ; 3 9(9) : 1 5 66- 1 5 69. 403 . Hall AH, Rumack BH. Clinical toxicology of cyanide. Ann Etm1·g Med 1 986; 1 5 (9) : 1 067-1 074. 404. Suchard JR, Wallace KL, Gerkin RD . Acute cyanide toxicity caused by apricot kernel ingestion. Ann Enm·g Med 1 99 8 ; 3 2 (6) : 742 -744. 405 . Hollenberg SM. Vasodilators in acute heart failure. Heart Fail Rev 2007; 1 2 (2): 1 43 - 1 4 7 . 4 0 6 . Cosby K, et al. Nitrite reduction to nitric oxide by deoxyhemo­ globin vasodilates the human circulation. Nat Med 2 0 0 3 ; 9 ( 1 2 ) : 1 498-1 5 0 5 . 407 . Leavesley H B , e t a l . Interaction of cyanide and nitric oxide with

cytochrome c oxidase: implications for acute cyanide toxicity. Toxicol Sci 2 008; 1 0 1 ( 1 ) : 1 0 1 -1 1 1 . 408 . Gerth K, et al. Nitric oxide scavenging by hydroxocobalamin may account for its hemodynamic profile. Clin Toxicol (Phi/a) 2 006;44(Suppl 1 ) : 2 9-36. 409. Uhl W, et a!. Safety of hydroxocobalamin in healthy volunteers in a randomized placebo-controlled study. Clin Toxicol (Phi/a) 2 006;44(Suppl 1 ) : 1 7-2 8 . 4 1 0 . Fortin J L , e t a l . Prehospital administration of hydroxocobalamin for smoke inhalation-associated cyanide poisoning: 8 years of experience in the Paris Fire Brigade. Clin Toxicol (Phi/a) 2 006;44(Suppl 1 ) : 3 7-44. 4 1 1 . Borron SW, et al. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med 2 007;49(6): 794-80 1 . 4 1 2 . Weng TI, et al. Elevated plasma cyanide level after hydroxo­ cobalamin infusion for cyanide poisoning. Ant J Eme1·g Med 2 004;22 (6):492-49 3 . 4 1 3 . Fortin JL, e t al. Hydroxocobalamin for poisoning b y ingestion of potassium cyanide: A case study. Clin Toxico/ 2 005 ;43 (6): 7 3 1 . 4 1 4. Borron S W, et al. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Anz J Eme7'g Med 2 007;2 5 (5 ) : 5 5 1 -5 5 8 . 4 1 5 . Blondell JM. Decline i n pesticide poisonings i n the United States from 1 995 to 2 004. Clin Toxicol (Phi/a) 2007 ;45 (5): 5 89-5 92 . 4 1 6. Namba T, et al. Poisoning due to organophosphate insecticides. Acute and chronic manifestations. Ant J Med 1 97 1 ;5 0(4):47 5-492 . 4 1 7 . Saadeh AM , Farsakh NA, al-Ali MK. Cardiac manifestations of acute carbamate and organophosphate poisoning. Hem·t 1 99 7 ; 7 7 (5) :46 1 -464. 4 1 8 . Clark RF. Insecticides: organic phosphorus compounds and car­

bamates. In Flomenbaum NE, Gold frank LR, Hoffman RS, et a!, eds. Goldfrank :, Toxicologic Eme,�gencies, 8th ed. New York: McGraw-Hill, 2 006.

David Szpilman , Anthony ] . Handley , Joost Bierens , Linda Quan , and Rafael Vasconcellos Drowning is an injury whose treatment may involve many layers of personnel from laypersons , lifeguards , and prehospital care providers to highly specialized hospital staff. Care of the drowning victim is unique in that bystanders or rescuers need specific skills that allow them to help the victim without becoming victims themselves . However, prevention , not resuscitation , is the primary objective with regard to drowning and adequate supervision of children is the most important preventative goal . • • •

•

•

Updated definition- Drowning i s progressive respiratory impairment from submersion in a liquid The maj ority of drownings while accidental are due to negligence and failure of supervision The most effective intervention for drowning is prevention Additional medications may include antihistamines, corticosteroids, and glucagon. Use a drowning algorithm for triage, treatment and prognosis

On a sunny weekend day, a family was invited to a barbecue at a friends swimming pool. Suddenly, the mother noticed that her 4-year-old boy was missing. After about 7 minutes, he was found at the bottom of the pool brough< up "' 3 2 °C to 3 4°C. If core temperature exceeds 3 4°C, hypothermia (3 2 °C-3 4aC) should be achieved as soon as possible and sustained for 12 to 2 4 hours. Hyperthermia should be prevented at all times in the acute recovery period. Unfortunately, studies that have evaluated the results of cerebral resuscitation measures in drowning victims have failed to demonstrate that therapies directed at controlling intracranial hypertension and maintaining cerebral perfu­ sion pressure (CPP) improve outcome. These studies have shown poor outcomes (i. e . , death or moderate to profound neurologic sequelae) when the intracranial pressure was :::: 2 0 m m H g and the CPP was ::::; 60 mm H g despite therapies directed at controlling and improving these pressures. More research is needed to evaluate the specific efficacy of neu­ roresuscitative therapies in drowning victims. 3 1 New therapeutic interventions for drowning victims, such as extracorporeal membrane oxygenation, artificial sur­ factant, nitric oxide, liquid lung ventilation, and early initia­ tion of mild hypothermia, are still at the investigational stage.

Pulmonary Assessment and Interventions Grade 4 to 6 patients who have received prehospital ALS care usually arrive in the ED with mechanical ventilation and acceptable oxygenation. If not, PEEP should be insti­ tuted. Once the desired oxygenation is achieved at a given level of positive airway pressure, that level of PEEP should be maintained unchanged for 48 hours before attempting to decrease it, in order to allow adequate surfactant regenera­ tion. During that time, if the patient begins to breathe ade­ quately on his or her own, extubation may proceed, but with continuous positive airway pressure (CPAP) plus ventilatory pressure support mode (PSV). In selected cases, CPAP may be provided initially by mask or nasal cannula (in infants who are obligate nasal breathers), but usually this is not tolerated by older patients, and pulmonary edema generally necessi­ tates intubation. After the airway is secured, nasogastric tube placement reduces gastric distention and prevents further aspiration. A clinical picture very similar to ARD S is common after significant drowning (grades 3 -6). The difference is that the acute respiratory distress seen with drowning has a much faster time to recovery and usually no pulmonary sequelae. Management is similar to that of other patients with ARD S , including efforts t o minimize volutrauma and barotrauma. However, lung salvage involving permissive hyp ercapnia probably is not suitable for grade 6 drowning victims with significant hypoxic-ischemic brain injury. Instead, mild to moderate hyperventilation, aiming for a Paco in the range 2 of 3 0 to 3 5 mm Hg, is probably indicated, together with other therapeutic measures to control cerebral edema.

•

VA S C O N C E L L O S

B arotrauma The clinician must be aware of and con­ stantly vigilant for potential complications of therapy and underlying pulmonary injury, namely, volutrauma and baro­ trauma. 3 2 Spontaneous pneumothoraces are common ( 1 0%) secondary to positive-pressure ventilation and local areas of hyperinflation. Any sudden change in hemody­ namic stability during mechanical ventilation should be considered a pneumothorax or other barotrauma until proven otherwise.

Cardiovascular Assessment and Interventions In patients who are hemodynamically unstable or have severe pulmonary dysfunction (grades 4-6), pulmonary artery catheterization or noninvasive techniques may improve the ability to assess and treat the victim. Colloid solutions are controversial and should be used only for refractory hypovolemia when replacement with crystalloid was not enough to restore blood pressure promptly. No evi­ dence exists to support the routine administration of hyper­ tonic solutions and blood transfusions for freshwater drowning or the use of hypotonic solutions in saltwater drowning. 1 5· 2 3 Pulmonary artery catheterization or other less invasive techniques also enable the clinician to monitor car­ diac function, pulmonary function, and adequacy of tissue oxygenation and perfusion as well as to assess the response of these parameters to various therapies. Echocardiography to assess cardiac function and ej ection fraction can help guide the clinician in deciding on inotropic agents, vasa­ pressors , or both if crystalloid volume replacement has failed. Some studies have shown that early cardiac dysfunc­ tion with low cardiac output is common following severe drowning (grades 4-6). 1 5 Important supportive measures include Foley catheter placement to monitor urine output. Low cardiac output is associated with high pulmonary cap­ illary occlusion pressure, high central venous pressure, and high pulmonary vascular resistance; it can persist for days after reoxygenation and reperfusion. The result is the addi­ tion of cardiogenic pulmonary edema to the noncardiogenic pulmonary edema. Despite a depressed cardiac output, furosemide therapy is not a good idea. One study has even suggested that volume infusion benefits drowning victims . Other studies suggest that dobutamine infusion to improve cardiac output is the most logical and potentially beneficial therapy. 1 9 Metabolic acidosis occurs in 70% of patients arriving at the hospital. 1 7 Correction should be considered only when pH is 93.2"F) M i ld hypotherm i a • •

_____.

Pulse

• •

• •

Passive rewarming Active external rewarming

• • •

•

I

I f unknown, use 200 J - AED. dev ice specific - M ono phas i c : 360 J Resume CPR immediately Attempt, confirm , secure airway Ve nti late with warm, humid oxygen Establish IV access I nfuse warm NS (42"C to 44"C

_____.

• •

f+

•

•

Act ive i n tern a l rewa rm ing2 • Warm IV fluids (43"C [1 09" F]) • Warm , humid oxygen (42"C to 46"C [1 08"F to 1 1 5" F)) • • •

Peritoneal lavag e (KCI -free flu id) Extracorporeal rewarm ing Esophageal rewarming t u bes•

(42"C to 46"C [1 08"F to 1 1 5"F])'

[1 08"F to 1 1 1 .2"F]2

�

5 0 % of fatal asthma may not be recognized as such because the deaths occur at home or during transport to the hospital. Most acute episodes result­ ing in death are related to severe underlying disease, inade­ quate baseline management, and acute exacerbations of inflammation.

LATEST GUIDELINES

Several consensus groups have developed excellent practice guidelines for the diagnosis and treatment of asthma. These groups include the National Asthma Education and Prevention Program of the National Institutes of Health, 10 • 12 the Global Initiative for Asthma, 1 1 and the Canadian Association of Emergency Physicians and the Canadian Thoracic Society. 1 3 • 14 •

• •

National Asthma Education and Prevention Program: http://www. nhlbi.nih.gov/about/naepp/ Global Initiative for Asthma: http://www. ginasthma.com/ CAEP: http://www. caep.ca/

L ife ..Threatening and Fatal Asthma Pathophysiology Asthma represents a spectrum of disease characterized by a cascade of inflammatory mediators. The pathophysiology of asthma consists of three key abnormalities:

• • •

•

S E V E R E , L I F E - T H R E AT E N I N G A S T H M A

5 13

Bronchoconstriction Airway inflammation Mucous impaction

Severe exacerbations of asthma can rapidly lead to death. Cardiac arrest in patients with asthma has been linked to a vari­ ety of pathophysiologic mechanisms that complicate exacerba­ tions of asthma, but the most likely cause is thought to be bron­ chospasm with subsequent plugging of the narrowed airways by mucus.9 Marked airway thickening and rapid infiltration of neut::rophils into the airways are consistent findings in acute, severe asthma and may differentiate these patients from those with milder disease. In fatal cases, a 2 5 - to 3 0-fold greater degree of thickening of the airways has been noted.4 At autopsy, these patients display marked mucous plugging, airway edema, exudation of plasma proteins, hypertrophy of airway smooth muscle, and cellular activation, with increased production and activation of inflammatory mediators. 15-1 7 Some patients expe­ rience a sudden, severe onset of bronchospasm that responds rapidly to inhaled beta agonists. 1 8 This observation suggests 2 that marked bronchiolar smooth muscle spasm is the major component in at least some cases of fatal asthma. Acute, severe asthma results in hypoxemia secondary to the processes of hyperinflation and regional ventilation/per­ fusion mismatch. Carbon dioxide retention does not typi­ cally occur until FEV falls below 2 5 % of predicted.4 Airway 1 occlusion due to smooth muscle bronchoconstriction, air­ way edema, inflammation, and formation of mucous plugs forms the pathologic basis of the gas-exchange abnormali­ ties observed in acute, severe asthma, and leads to the devel­ opment of extensive intrapulmonary shunting. Metabolic lactic acidosis may also coexist at later stages of the disease. 7 Bronchoconstriction and airway obstruction from mucous plugging cause hyperinflation and increased airway resistance (Fig. 3 3 - 1 ). As a consequence, the work of breath-

• A s t h m a o c c u rs in t h e setti n g o f u n d e r lyi n g i n f l a m m a t i o n . D i ff u s e b r o n c h o s p a s m o c c u r s , c a u s i n g a i r p a s s a g e s to c o n st r i c t . Hyp e r s e c r e ti o n o f m u c o u s l e a d s to p l u g s , w h i c h b l o c k o xyg e n a t i o n a n d v e n t i l a t i o n . A . N o r m a l h e a l t h y b r o n c h u s B. B r o n c h i o l e d u r i n g a s t h m a a tt a c k .

FIGURE 3 3 -1

5 14 1

BAREN

ing increases dramatically. For example, at an FEV of 50 % 1 of predicted, the work o f breathing increases t o 1 0 times nor­ mal. At an FEV of 2 4 hours that is attributable to a focal vascular cause and results in an inter­ ruption of the blood supply to a region of the brain. The sud­ den onset offocal brain dysfunction is the hallmark of stroke. 1 9 Experts and clinicians most often classify strokes as either hemorrhagic or ischemic. Hemorrhagic stroke occurs when a blood vessel within the brain ruptures. Ischemic stroke occurs when a blood vessel becomes blocked, typically by plaque and/or clot, interrupting flow to a region of the brain. If blood flow is interrupted long enough, irreversible infarc­ tion of brain tissue often ensues. Although the causes of stroke are numerous, the distinction between ischemic and hemorrhagic types is important, since therapy differs signif­ icantly based on stroke type (Fig. 3 6-2).

Ischemic Stroke

ization of the vascular lesion. 2 0 Strokes are generally subdi­ vided into the following categories: 2 0 •

Thrombotic

stroke

(large

artery

atherosclerotic

stroke): An acute thrombus that occludes

•

an artery is super­ imposed on chronic arterial narrowing, acutely altered endothelial lining, or both. This pathophysiology parallels that for acute coronary syndromes (ACS), where a ruptured or eroded plaque is the proximate cause of most episodes of ACS . The artery may be extracranial or intracranial. Embolic stroke : Intravascular material, most often a blood clot, separates from a proximal source and flows through an artery until it occludes a distal site. Many of these events are cardioembolic-originating from the heart-in patients with atrial fibrillation, valvular heart disease, acute MI, or rarely endocarditis. Cardiogenic

• I s c h e m i c Stroke

H e m orrhag i c Stroke

• I ntracerebral

• S u barach n o i d

Definition and Categories of Ischemic Stroke In an ischemic stroke (87 % of all strokes 1), interruption in the blood supply is caused by occlusion of an artery to a region of the brain. Ischemic strokes can be defined on the basis of etiology and duration of symptoms. With the more widespread use of modern brain imaging, many patients with symptoms lasting ::::; 2 4 hours are found to have an infarction. The most recent definition of stroke for clinical trials has required either symptoms lasting > 2 4 hours or imaging of an acute, clinically relevant brain lesion in patients with rapidly vanishing symptoms. Ischemic stroke is classified into categories based upon the presumed mechanism of stroke and the type and local-

FIGURE 3 6- 2 • Typ e o f s tr o k e . S o m e 87% o f s tr o k e s a r e i s c h e m i c a n d p o t e n ti a l ly e l i g i b l e f o r fi b r i n o lyti c t h e r a py i f p a t i e n ts o t h e rwise q u a l i fy ; 1 3 % o f str o k e s a r e h e m o r r h a g i c , a n d t h e m aj o r i ty o f t h e s e a r e i n t r a c e r e b r a l . M e n h ave 1 . 2 5 t i m e s t h e n u m b e r o f s tr o k e s a s wo m e n , a n d b l a c k s h ave a l m ost twi c e t h e r i s k o f f i r s t - ev e r str o k e c o m p a r e d w i t h w h i t es . 1 1

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cerebral embolism is responsible for about 2 0 % of ischemic strokes. There is a history of nonvalvular atrial fibrillation (AF) in about half of these patients, valvular heart disease in one fourth, and left ventricular (LV) thrombus in almost one third.2 1 Other causes: These include small-vessel disease and other causes such as sickle cell disease, hypercoagulable states, and arterial dissection, resulting in a more global pattern of brain infarction. This is typically due to periods of signifi­ cant systemic hypotension and inadequate cerebral perfu­ sion that cannot support the metabolic demands of the brain tissue. Hypoperfusion stroke often occurs in patients who recover cardiac function after sudden cardiac arrest.

By conventional clinical definitions, if the neurologic symp­ toms continue for 2 4 hours, a person is diagnosed with stroke; otherwise a focal neurologic deficit lasting :s 2 4 hours is defined as a TIA. However, approximately one third of all TIAs would be classified as stroke based on diffusion­ weighted magnetic resonance imaging, 22 and new diagnostic techniques have shown that up to 60% of patients with a TIA have definite radiographic evidence of brain infarc­ tion. 2 3 A proposed new definition of TIA is a "brief episode of neurologic dysfunction caused by a focal disturbance of brain or retinal ischemia, with clinical symptoms typically lasting < 1 hour, and without evidence of infarction. " 2 4 The distinction between TIA and ischemic stroke has become less important in recent years because many of the preventive approaches are applicable to both groups. TIA and stroke share pathogenetic mechanisms; prognosis may vary, depending on their severity and cause; and definitions are dependent on the timing and degree of the diagnostic evaluation. TIAs, however, are an important determinant of stroke, with 90-day risks of stroke reported as high as 1 0 . 5 % and the greatest stroke risk apparent in the first week. 25•2 6 Risk scores have been developed and validated to allow risk stratification of patients with TIA, including duration of symptoms. 25•27-2 9

Classification by Vascular Supply Strokes are also classified by vascular supply and anatomic location: Anterior circulation (carotid artery territory) stroke:

Stroke that results from occlusion of branches of the

carotid artery. Such strokes usually involve the cerebral hemispheres. •

•

Undetermined

Transient Ischemic Attack

•

rhage into the surrounding tissue. Damage typically results from direct trauma to brain cells; expanding hematoma effects leading to elevated intracranial pressure; release of damaging neurotoxic mediators; local vascular spasm; and loss of blood supply to brain tissue downstream from the ruptured vessel. There are two types of hemorrhagic stroke, based on the location of the arterial rupture: 3 0

Posterior circulation (vertebrobasilar artery territory) stroke:

Stroke that follows occlusion of branches of the

vertebral or basilar arteries. These strokes usually involve the brainstem or cerebellum.

Hemorrhagic Stroke Hemorrhagic strokes ( 1 3 % of all strokes) occur when a blood vessel in the brain suddenly ruptures, with hemor-

•

(10%): Occurs when blood ruptures directly into the brain parenchyma, usu­ ally from small intracerebral arterioles pathologically altered by chronic hypertension. • Hypertension is the most common cause of intracere­ bral hemorrhage. 3 1 • Among the elderly, amyloid angiopathy appears to play a major role in intracerebral hemorrhage. Subarachnoid hemorrhagic stroke (3 %): Occurs when blood leaks from a cerebral vessel into the subarachnoid space. If the rupture occurs in a cerebral artery, the blood is released at systemic arterial pressure, causing sudden, painful, and dramatic neurologic symptoms. • Aneurysms cause most subarachnoid hemorrhages. • Arteriovenous malformations cause approximately 5 % o f subarachnoid hemorrhages.

Intracerebral hemorrhagic stroke

Pathophysiology

Concept of the Evolving "Ruptured Plaque" The "ruptured plaque" pathophysiologic concept of ACS is also applicable to many ischemic strokes (see Chapter 1 , Figures 1 - 1 and 1 - 5).3 2-34 An ulcerated ruptured plaque is the key mechanism of most thrombotic and embolic strokes in patients without valvular heart disease or atrial fibrillation. In thrombotic stroke, complete occlusion typically develops at an atherosclerotic plaque.35•36 In embolic stroke, the developing thrombus breaks off and floats downstream, ultimately lodging in and obstructing a smaller arterial vessel. A thrombotically active carotid plaque associated with high inflammatory infil­ trate was observed in about 7 5 % of patients with ipsilateral major stroke. In addition, ruptured plaques of these patients affected by stroke were characterized by the presence of a more severe inflammatory infiltrate-comprising monocytes, macrophages, and T lymphocytes-compared with those observed in the TIA and asymptomatic groups.37 Ruptured plaques may occur not only in the intracranial branches of the carotid and vertebrobasilar arteries but also in the extracranial portions of the carotid arteries and in the aorta. Vessel occlusion results from the interaction between blood vessels, activated coagulation components of blood, inflammatory cells, and chemical mediators of inflammation. The pathology of recently symptomatic carotid plaques is sim­ ilar to that of culprit coronary plaques, with strong correlations between macrophage infiltration and plaque instability.34 •

The most common cause of acute ischemic stroke is ath­ erosclerosis of the carotid or vertebrobasilar artery.

CHAPTER 3 6

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STR0KE

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FIGURE 3 6-3 • O c c l u s i o n in a a r t e ry d u e to c e r e b r a l e m b o l i s m a t t h e a rt e r i a l b i f u r c a ti o n . A . A r e a o f i n f a r c ­ tion surro u n d i n g immed iate site a n d distal portion of b r a i n t i ss u e a ft e r o c c l u s i o n . B . A r e a o f i s c h e m i c p e n u m ­ b r a [ i s c h e m i c b u t n o t yet i n fa r c t e d (d e a d) b r a i n t i ss u e ] s u r r o u n d i n g a r e a s o f i n f a r c ti o n . T h i s i s c h e m i c p e n u m b r a tiss u e i s a l ive b u t dysfu n c ti o n a l b e c a u s e o f a l te r e d m e m b r a n e p o t e n t i a l s . T h e dysfu n c t i o n i s p o t e n ti a l ly reversi b l e . C u r r e n t s t r o k e t r e a t m e n t a tte m p ts to k e e p the area of permanent brain infarction as small as pos­ s i b l e b y p r eve n t i n g t h e a r e a s o f r eve r s i b l e b r a i n i s c h e m i a i n t h e p e n u m b r a f r o m t r a n s fo r m i n g i n t o l a r g e r a r e a s o f i r r ev e rs i b l e b r a i n i n f a r c t i o n . [ R e p r i n t e d w i t h p e r m i ssi o n o f G e n e n t e c h , I n c , f r o m t h e I n te r n e t Stro k e Ce n t e r (www. str o k e c e n te r . o r g ) . C o pyr i g h t G e n e n t e c h , I n c . ]

•

•

Varying degrees of inflammation in vulnerable atheroscle­ rotic plaques predispose these arteries to endothelial ero­ sion, plaque rupture, and platelet activation as well as aggregation. The ensuing development of a thrombus-composed of platelets, fibrin, and other elements of coagulation-can completely occlude an artery already narrowed by ather­ osclerosis. This occlusion of blood flow first leads to ischemia and ultimately to infarction of downstream brain tissue, producing a thrombotic stroke. The thrombus, either before or immediately after it becomes completely occlusive, may dislodge and travel to more distal cerebral arteries, producing an embolic stroke (Fig. 3 6- 3 ).

Postocclusion Dynamics Downstream from the thrombotic or embolic obstruction, brain cells begin to die and necrosis occurs. With persistent occlusion, an area of irreversible brain damage (infarction or necrosis) develops. •

•

Surrounding the central area of necrosis or infarction is an area of ischemia called the ischemic penumbra. This area of "threatened" but still viable brain tissue is an area of potentially reversible brain injury.38-4°

"TIME IS BRAIN"

The recently coined term "brain attack" and the phrase "time is brain" convey the sense of urgency in stroke care. Once restriction of blood flow occurs as a result of occlusion, an ever-increasing amount of brain tissue becomes irreversibly inj ured over time. There is only a limited amount of time available to recognize and treat reversible brain ischemia. 41 -43

Other Pathophysiologic Processes Atrial Fibrillation Atrial fibrillation remains the most frequent cause of car­ dioembolic stroke. 44 •

•

The noncontracting walls of the fibrillating left atrium and left atrial appendage serve as both a stimulus and a reservoir for small emboli. The risk of stroke in patients with nonvalvular atrial fib­ rillation averages 5% per year, two to seven times that of people without atrial fibrillation.45-47

Hypertension Hypertension causes a thickening of the walls of small cere­ bral arteries, leading to reduced flow and a predisposition to thrombosis. •

•

Lacunar infarcts exemplify the type of thrombotic stroke caused by chronic hypertension. They are thought to result from occlusion of a small perforating artery to the subcortical areas of the brain. The maj or cerebrovascular burden imposed by chronic hypertension is hemorrhagic stroke.

Stroke Risk Factors Risk factors can be identified in most stroke patients .48 Primary and secondary stroke prevention requires identifi­ cation of a patient's risk factors, followed by elimination, control, or treatment of as many factors as possible: • • •

Elimination (e.g., smoking) Control (e.g., hypertension, diabetes mellitus) Treatment (e.g., antiplatelet therapy, carotid endarterec­ tomy when indicated)

Table 3 6-2 lists the major modifiable stroke risk factors.

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Str o k e R i s k : F a c t o r s T h a t Ca n B e M o d i f i e d

Risk Fa ctor

Co m m e n ts • • • •

•

Tr a n s i e n t I s c h e m i c

• • • •

• • •

• •

O n e o f t h e m o st i m p o r t a n t m o d i f i a b l e r i s k f a c t o r s f o r i s c h e m i c a n d s p o n ta n e o u s h e m o r r h a g i c str o k e 2 6 • 27 R i s k of h e m o r r h a g i c str o k e i n c r e a s e s m a r k e d ly with e l ev a ti o n s i n sys to l i c p r e s s u r e Co n t r o l o f hyp e rt e n s i o n s i g n i f i c a n tly d e c r e a s e s t h e r i s k o f str o k e 2 6 • 2 8 • 2 9 A l l o f t h e fo l l owi n g s m o k i n g e f f e c ts h ave b e e n l i n k e d to str o k e : - Accelerated atherosclerosis - Tr a n s i e n t e l ev a ti o n s i n b l o o d p r e s s u r e - R e l e a s e o f to x i c e n zy m e s (l i n k e d to fo r m a t i o n o f a n e u rys m s) - A l t e r e d p l a t e l e t f u n c ti o n a n d r e d u c e d p l a t e l e t s u rviva 1 3 0 • 3 1 Cessa ti o n o f c i g a r ette s m o k i n g r e d u c e s t h e r i s k o f str o k e 3 2 • 3 3 H i g h ly s i g n i fi c a n t i n d i c a t o r o f a p e r s o n a t i n c r e a s e d r i s k f o r str o k e 5 • 3• 2 5 % of str o k e p a t i e n ts h ave h a d a p r evi o u s T I A 3 5 1 0 % o f p a t i e n ts p r e s e n t i n g to a n E D with T I A wi l l h ave a c o m p l e t e d str o k e with i n 9 0 d ays ; h a l f o f t h e s e with i n t h e f i r s t 2 d ays36 A n ti p l a te l e t a g e n ts (e . g . , a s p i r i n , ti c l a p i d i n e) c a n r e d u c e the r i s k of str o k e i n p a t i e n ts with T I A Co r o n ry a r t e ry d i s e a s e a n d h e a r t fa i l u r e d o u b l e t h e r i s k o f s t r o k e 3 7 A t r i a l fi b r i l l a t i o n i n c r e a s e s t h e r i s k o f e m b o l i c str o k e P r o p hyl a c t i c wa r fa r i n , g iven to p a t i e n ts w i t h a tr i a l fi b r i l l a ti o n , r e d u c e s t h e r i s k o f e m b o l i c str o k e 3a-.o H i g h ly a s s o c i a t e d with a c c e l e r a t e d a t h e r o s c l e r o s i s C a r e fu l m o n i t o r i n g a n d c o n t r o l o f hyp e r g lyc e m i a r e d u c e t h e r i s k o f m i c rovas c u l a r c o m p l i c a t i o n s d u e t o d i a b e t e s , a n d r e d u c t i o n o f m i c rovas c u l a r c o m p l i c a t i o n s r e d u c e s str o k e r i s k

•

A ny hyp e r c o a g u l a tive s t a t e (e . g . , p r o t e i n S o r C d e f i c i e n cy, c a n c e r , p r e g n a n cy) i n creases the risk of stro k e

•

A m o d e r a t e i n c r e a s e i n R B C c o u n t i n c r e a s e s t h e r i s k o f str o k e I n c r e a s e s i n R B C c o u n t c a n b e t r e a t e d b y r e m ovi n g b l o o d a n d r e p l a c i n g i t with IV fl u i d o r by a d m i n i s te r i n g an a n ti c o a g u l a n t Si c k l e c e l l a n e m i a i n c r e a s e s t h e r i s k o f str o k e b e c a u s e " s i c k l e d " r e d b l o o d c e l l s c a n c l u m p , c a u s i n g a r t e r i a l o c c l u s i o n . Str o k e r i s k f r o m s i c k l e c e l l a n e m i a m ay b e r e d u c e d b y m a i n ta i n i n g a d e q u a t e o xyg e n a ti o n a n d hyd r a t i o n a n d b y p r ovi d i n g e x c h a n g e t r a n s fu s i o n s

• •

• • •

C a r o t i d b r u i ts o f t e n i n d i c a t e p a r t i a l o b s t r u c ti o n ( a th e r o s c l e r o s i s) o f a n a r te ry i n d i c a ti n g vas c u l a r d i s e a s e a n d a s s o c i a t e d str o k e r i s k T h i s r i s k i s r e d u c e d by s u r g i c a l e n d a r t e r e c t o my b u t o n ly i n sym p t o m a t i c p a t i e n ts with > 7 0 % s t e n o s i s 4 1 So m e evi d e n c e s u g g ests t h a t c a r o t i d e n d a r t e r e c t o my i s b e n e f i c i a l i n s e l e c t e d a sym p t o m a t i c p a t i e nts w i t h h i g h - g r a d e ste n o s i s• 2

' A b s e n c e o f a b r u 1 t d o e s n o t p r e c l u d e v a sc u l a r d 1 s e a s e . R B C , r e d b l o o d c e l l ; T I A , tr a n s 1 e n t 1 s c h e m 1 c atta c k

PHYSICAL ACTIVITY REDUCES THE RISK OF STROKE • •

A meta-analysis of reports of 3 1 observational studies conducted mainly in the United S tates and Europe found that moderate and high levels of leisure-time and occupational physical activity

protected against total stroke, hemorrhagic stroke, and ischemic stroke Y Physical activity reduces stroke risk. Results from the Physicians' Health Study showed a lower stroke risk associated with vigorous exercise among men. 2 4• 2 5 The Harvard Alumni Study also showed a decrease in total stroke risk in men who were highly physically active.

CHAPTER 3 6

Stroke Management Stroke treatment begins with the recognition of the symp­ toms of stroke. An important component in this initial step is education-of the patient, family, community, 9 1 1 dispatcher, prehospital care provider, and health care provider. Once recognition of potential stroke symptoms occurs, manage­ ment involves expeditious transfer of the patient to an appro­ priate facility for further assessment and care. Stroke centers are important because they focus on the integration of multi­ disciplinary care helping ensure appropriate hemodynamic management, optimal glucose control, prevention of aspira­ tion, and rehabilitation. Figure 3 6-4 is the suspected stroke algorithm, which identifies treatment goals for these patients.

Signs and Symptoms of Ischemic Stroke The warning signs of an ischemic stroke or TIA may be var­ ied, subtle, and transient, but they represent a potentially life-threatening neurologic illness (Fig. 3 6-4, Box 1). Like the symptoms of an ACS, symptoms of ischemic stroke can be misinterpreted and denied by patients. Emergency health care providers should recognize the importance of these symptoms and respond quickly with effective interventions in stroke management. The signs and symptoms of a stroke may be subtle and include: •

•

• •

•

Sudden numbness or weakness of the face, arm, or leg, especially on one side of the body Sudden confusion, trouble speaking or understanding speech Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance or coordination Sudden severe headache with no known cause

Out.. of..Hospital Management: The Important Role of the Community EMS System in Stroke Care (Fig. 3 6 .. 4, Box 2 )

•

STROKE

55 1

1 4 % to 3 2 % of them arrive within 2 hours of symptom onset. 5 2 ·5 3 EMS use is strongly associated with decreased time to initial physician assessment, computed tomogra­ phy (CT) imaging for stroke , and neurologic evalua­ tion.54 , 5 5 TIME T O STROKE TREATMENT

EMS use is strongly associated with decreased time to • • •

II'

Initial physician assessment CT imaging for stroke Neurologic evaluation

Detection: Early Recognition of Stroke Signs and Symptoms

Early treatment of stroke depends on the patient, family members, or other bystanders recognizing the event. Patients often ignore the initial signs and symptoms of a stroke and delay access to care for several hours after the onset of symp­ toms. Because of these time delays, many patients with ischemic stroke may not benefit from time-dependent thera­ pies such as intravenous fibrinolytic treatment, which must be started within 3 hours of symptom onset. In one study of 1 00 stroke patients, only 8 % had received information about the signs of stroke, yet nearly half had previously had a prior TIA or stroke.48 Unlike many acute myocardial infarctions in which chest pain can be a dramatic and unrelenting symptom, a stroke may have a sub­ tle presentation with only mild facial paralysis or speech dif­ ficulty. Mild signs or symptoms may go unnoticed or be denied by the patient or bystander. Strokes that occur while the patient is asleep or when he or she is alone further ham­ per prompt recognition and action. II'

Dispatch: Call 91 1 and Priority EMS Dispatch

Stroke patients and their families must understand the need to call 9 1 1 and activate the EMS system as soon as they suspect stroke signs or symptoms. The EMS system pro­ vides the safest and most efficient method for transporting the patient to the hospital. 56

EMS Assessments and Actions EMS assessments and actions for patients with suspected stroke include the following steps: •

Three of the four links in the stroke chain of survival and the first three of the seven Ds of stroke care (detection, dispatch, and delivery) require effective operation of the EMS system. For this reason the 2005 AHA Guidelines for

Cardiopulmonary Resuscitation and Emergency Cardiovascular Care and the 2 00 7 AHA/ ASA guidelines for the early management of adults with ischemic stroke strongly emphasize the important role of these personnel and serv­ ices. 8 Recent data show that 2 9 % to 6 5 % of patients with signs and symptoms of stroke contact local EMS , but only

• • •

•

Rapid identification of patients with signs and symptoms of acute stroke (through the performance of a prehospital stroke assessment tool) Support of vital functions Prearrival notification of the receiving facility Rapid transport of the patient to the most appropriate receiving facility (often a primary stroke center) Whenever possible, EMS should bring a witness with the patient to the receiving facility.

Emergency medical dispatchers play a critical role in the timely treatment of potential stroke patients. Data show that dispatchers correctly identify stroke symptoms on the basis

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1 Identify signs of possible stroke

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2

Critical EMS assessments and actions • • •

N I N DS TIME GOALS

•

•

•

ED Arrival

Support ABCs; give oxygen if needed Perform prehospital stroke assessment (Tables 1 and 2) Establi sh time when patient last known normal (Note: therapies m ay be available beyo n d 3 hours from onset) Transport ; consider triage to a center with a stroke unit if appropriate; consider bring ing a witness, famil y member, or caregiver Alert hospital Check glucose if possible 3 I m m ed iate general assessment and stabil ization

Assess ABCs, vital signs

•

Provide oxygen if hypoxem i c

•

Obtain

•

ac ces s and blood samples

Perform neurologic screen ing assessment

•

Activate stroke team

•

Order emergent CT scan of brain

•

O btai n 1 2-lead ECG

•

ED Arrival

IV

Check g lu co se ; treat if indicated

•

4 I mmediate neuro logic assessment by stroke team • •

min

•

Review patient history

or

d es i g nee

Establish sym ptom onset

Perform n e urolog i c examination (N I H Stroke Scale or Canadian Neurologic Scale)

ED Arrival

5

(

Does CT scan show any hemorrhage?

)

No Hemorrhage

Hemorrhage

6

7

C o nsul t n e u rolog i st

Probable acute ischemic stroke; consider fibrinolytic therapy • •

exclusions (Table 36-9) Repeat neurologic ex a m : are deficits rapidl y i m p rovi n g to normal?

8 ED Arrival 60 m i n

10

Patient remains candidate for

fibrinolytic therapy?

t

Candi date

) J

Not

Review risks/benefits with p atient and family: If acceptable •

•

Give tPA No anticoagulants or antiplatelet treatment for 24 hours

a

Candidate 11 •

• • •

• •

C 2005 American Heart Assoc i ation FIGURE 3 6-4

•

A l g o r i t h m for suspe cted stro k e .

or

neurosurgeon;

consid e r transfer if not available

Check for fibrinolytic

{

9 Administer asp irin

)

Begin stroke pathway Admit to stroke unit if available Monitor BP; treat if indicated (Table 36-8) Monitor neurologic status; emergent CT if deterioration Monitor blood glucose; treat if needed I nitiate supportive therapy ; treat comorbidities

CHAPTER 3 6

T A B LE 3 6 - 3

•

Key Co m p o n e n ts of a F o c u s e d Str o k e P a t i e n t H i story

O n s e t of sym p t o m s R e c e n t eve n ts Str o k e Myo c a r d i a l i n fa r c ti o n

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STROKE

553

The history must include this information. The provider may need to obtain this and other details of the patient's history from family or the appropriate bystander. Preferably this per­ son should be transported with the patient. Prehospital providers can help establish the precise time of stroke onset or the last time the patient was noted to be neurologically normal. This time point is viewed as "time zero," a starting point that is critical for time-dependent treatments.

Tra u m a

Out,of,Hospital Stroke Scales for Early Detection and Delivery

S u r g e ry Bleeding

The assessment includes a brief and focused examination for stroke. Providers can conduct a rapid neurologic assessment using validated prehospital stroke assessment tools such as the Cincinnati Prehospital S troke Scale58•59 or the Los Angeles Prehospital Stroke Screen.60•61 Studies have con­ firmed the sensitivity and specificity of these two scales for prehospital identification of patients with ischemic stroke.

Co m o r b i d d i s e a s e s Hyp e r t e n s i o n Dia betes m e l l itus Use of medications A n t i c o a g u l a nts Insulin

Cincinnati Prehospital Stroke Scale (CPSS) The CPSS (Table 3 6-4) is based on physical examination only, and it can be completed in 3 0 to 60 seconds.58 The EMS responder checks for three physical findings:

A n t i hy p e r t e n sives S o u r c e : A H A/ A S A I s c h e m 1 c Str o k e G u i d e l i n e s .

•

of just the initial phone description in more than half of all stroke cases.5 2 •57 Dispatchers can triage emergencies over the telephone and prioritize calls to ensure a rapid response by the EMS system. Specific dispatch educational efforts about stroke are encouraged, and stroke dispatch should be given a priority, like that for acute myocardial infarction and trauma. V Delivery: Prompt Transport and Prearrival Notification to Hospital

Leaders in EMS and emergency medicine must develop training programs and patient care protocols to guide the actions of prehospital care providers. After the basic life sup­ port (BLS) primary and ACLS secondary surveys and appro­ priate actions have been performed for airway, breathing, and circulation, EMS providers should immediately obtain a focused history and patient assessment (Table 3 6-3). A key component o f the patient's history i s the time of

symptom onset or when the patient was last known to be normal. I TA B LE 3 6 - 4

•

• •

Facial droop (Fig. 3 6-5) Arm weakness Speech abnormalities

The LAPSS (Table 3 6-5) requires the examiner to rule out other causes of altered level of consciousness (e . g . , history of seizures, severe hyperglycemia or hypoglycemia) and then identify asymmetry (right versus left) in any of three exam categories: Los Angeles Prehospital Stroke Screen (LAPSS)

• • •

Facial smile or grimace Grip Arm strength (Fig. 3 6-6)

The LAPSS builds on the physical findings of the CPSS, adding criteria for age, history of seizures, symptom duration, blood glucose level, and ambulation. A person with positive findings for all six criteria has a 97% probability of stroke.

T h e Ci n c i n n a t i P r e h o s p i t a l Str o k e S c a l e

Test

Findings

Facial Droop: H ave t h e p a t i e n t s h ow t e e t h o r s m i l e (F i g u r e 3 6 - 5)

•

Arm Drift: P a t i e n t c l o s e s eye s a n d e x te n d s b o t h a r m s stra i g h t o u t . with p a l m s u p , f o r 10 s e c o n d s (F i g u r e 3 6 - 6)

• •

Abnormal Speech: H ave t h e p a t i e n t say "yo u c a n ' t t e a c h an o l d d o g n ew tr i c k s "

•

•

•

Normal- b o t h s i d e s of f a c e m ove e q u a l ly Abnormal-o n e s i d e o f f a c e d o e s n o t m ove a s we l l a s t h e o t h e r s i d e Normal-b o t h a r m s m ove t h e s a m e o r b o t h a r m s d o n o t m ove a t a l l (oth e r fi n d i n g s , s u c h a s p r o n a t o r d r i f t , m ay b e h e l p f u l ) Abnormal-o n e a r m d o e s n o t m ove o r o n e a r m d r i fts d own c o m p a r e d w i t h the other Normal-p a t i e n t u s e s c o r r e c t wo r d s with n o s l u r r i n g Abnormal-p a t i e n t s l u r s w o r d s , u s e s t h e wr o n g wo r d s , o r i s u n a b l e to s p e a k

S o u r c e : K o t h a r i R , H a l l K , B r o tt T , e t o l . E a rly str o k e r e c o g n 1 t 1 o n : deve l o p m g o n o u t - o f h o s p 1 t o l N I H str o k e s c a l e Acad Emerg Med 1 9 97 ; 4 : 9 8 6-9 9 0 .

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FIGURE 3 6-5

Out-of-hospital stroke scales provide objective, validated methods for early detection of stroke and enable appropriate triage and prearrival notification to the receiving hospital. When EMS personnel discover findings consistent with stroke on either the CPSS or the LAPSS, they should notify the receiving hospital that they have a patient with possible I TA B LE 3 6 - 5

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Facial droop.

acute stroke. This information allows the hospital to activate stroke protocols before the patient arrives to ensure rapid patient evaluation and therapy. Advanced planning and col­ laboration allow medical control physicians to direct EMS providers to transport the patient to a hospital designated and organized to provide the full range of acute stroke care.

Los A n g e l e s P r e h o s p i t o l Str o k e S c r e e n

F o r evalu a t i o n o f a c u t e , n o n c o m a t o s e , n o n tr a u m a tic n e urlogic c o m p lain t. If i t e m s 1 t h r o u g h 6 a r e all cheeked "Yes" ( o r " U n k n own ") , p r ovi d e p r e a r r ivo l n o ti f i c a ti o n to h o s p i t a l o f p o t e n ti a l s tr o k e p a t i e n t . I f a ny i t e m i s c h e c k e d " N o , " r e t u r n to a p p r o p r i a te t r e a t m e n t p r o to c o l . In terpre t a tio n : 93% o f p a t i e n ts with str o k e wi l l h ave a p o s i tive LAPSS s c o r e (s e n s i tivi ty 9 3 %) , a n d 9 7 % o f t h o s e with a p o s i tive LA PSS s c o r e wi l l h ave a str o k e (s p e c i f i c i ty = 9 7 %) . N o te t h a t t h e p a t i e n t m ay sti l l b e e x p e r i e n c i n g a str o k e i f LAPSS c r i t e r i a a r e n o t m e t. =

Crite r i a

Yes

U n k n own

No

1 . A g e > 4 5 ye a r s

0

0

0

2 . H i s t o ry o f s e i z u r e s o f e p i l e p sy a b s e n t

0

0

0

3 . Sym p t o m d u r a t i o n < 2 4 h o u rs

0

0

0

4 . A t b a s e l i n e , p a t i e n t i s n o t wh e e l c h a i r b o u n d o r b e d r i d d e n

0

0

0

5 . B l o o d g l u c o s e b e twe e n 6 0 a n d 4 0 0

0

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0

6 . O bvi o u s a sym m e try (r i g h t v s l e ft) i n a ny o f t h e fo l l owi n g 3 e x a m c a t e g o r i e s (must b e unilateral):

0

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0

Equal

R We a k

L We a k

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0 Droop

0 Droop

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0 We a k g r i p 0 No grip

0 We a k g r i p 0 No grip

0

0 D r i fts d own 0 F a l l s r a p i d ly

0 D r i fts d own 0 F a l l s r a p i d ly

I

.

S o u r c e s : K 1 dw e l l CS, Sover J l , S c h u b ert G B , et o l . D e s 1 g n o n d r e t r o s p e ctive o n o lys1 s of t h e los A n g e l e s p r e h o s p 1 t o l str o k e s c r e e n (lAPSS) Preh osp Emerg Care 1 9 9 B , 2 2 6 7-2 7 3 . K 1 dw e l l CS , Sta r k m a n S, E c k s t e 1 n M , et al I d e n t 1 fy1 n g str o k e 1n t h e f 1 e l d p r o s p e ct1ve vo l 1 d a t 1 o n o f t h e los A n g e l e s P r e h o s p 1 t a l S t r o k e S c r e e n (lA PSS) Stroke 2 0 0 0 , 3 1 7 1-7 6

CHAPTER 3 6

FIGURE 3 6-6

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STROKE

555

O n e - s i d e d m o t o r we a k n e ss

(r i g h t a r m) .

Destination Hospital Protocols

Prehospital Initial Studies

Once a patient with probable stroke is identified, EMS per­ sonnel should transport him or her to the nearest most appro­ priate facility. Prearrival notification of the facility is key and allows for decreasing time to examination by a physician, CT imaging, and reperfusion therapy. An ambulance may bypass a hospital that does not have the resources or the institutional commitment to treat patients with stroke if a more appropriate hospital is available within a reasonable transport interval. Air medical transport appears to be beneficial, but stud­ ies are limited. Helicopters' ability to rapidly transport patients to appropriate facilities may improve the opportunity for reperfusion therapy in more rural areas.62-66 Helicopter transfer of patients has been shown to be cost-effective.65

Prehospital care and assessment beyond initial management should be completed during patient transport and should not delay transport to the hospital. Prehospital intervention in potential stroke patients includes establishing intravenous (IV) access with normal saline, ensuring adequate oxygena­ tion and ventilation, hemodynamic support if necessary, avoiding glucose-containing fluids unless hypoglycemia is strongly suspected or present (hyperglycemia [blood glucose > 2 00] is associated with worse outcomes in stroke patients67-7 1), checking and treating abnormal blood glucose levels, and initiating cardiac monitoring. Obtain a 1 2 -lead electrocardiogram (ECG) if the patient has symptoms con­ cerning for ACS .

HOSPITAL BYPASS

In .. Hospital Management

An ambulance may bypass a hospital if The facility does not have the resources for acute stroke care. The facility lacks an institutional commitment to treat patients with stroke. A more appropriate hospital is available within a reasonable transport interval.

Collaborative stroke protocols should be employed in the ED to minimize delay to definitive diagnosis and therapy.7 2 Diagnostic studies ordered in the ED are aimed at:

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See Web site for A H A/ASA reco m m e n d ations f o r c o m p r e h e n s ive st r o k e c e n t e r s .

V

Excluding other nonstroke causes of the patient's symptoms (hypoglycemia, etc.) Establishing stroke as the cause of the patient's symptoms Differentiating ischemic from hemorrhagic stroke Rapidly providing stroke therapy to appropriate patients with ischemic stroke, which may include intravenous tPA if no contraindications are present

Door: Immediate ED Triage

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Immediate General Assessment and Stabilization (Fig. 3 6�4, Box 3 ) As

a goal, ED personnel should assess the patient with suspected stroke within 1 0 minutes o f arrival in the ED . The ED physician, typically the first member of the stroke team to evaluate the patient, should min ensure respiratory and hemodynamic stabil­ ity, perform a neurologic screening assess­ ment, order an emergent CT scan of the brain if stroke is believed possible, coordinate with the other members of the stroke team, or arrange consultation with a stroke expert if available. General care includes assessment and support of airway, breathing, and circulation and evaluation of baseline vital signs. Oxygen should be administered to hypoxemic patients or those with unknown oxygen saturation. Clinicians may consider giving oxygen to patients who are not hypox­ emic. High-flow oxygen therapy in a small clinical trial of patients without hypoxia was associated with transient improvement in clinical deficits and abnormalities on mag­ netic resonance imaging (MRI), but large scale clinical trials are not available.73 •74 Oxygen saturation should be monitored and maintained at 2: 92 % . Establish (or confirm) IV access and obtain blood samples for baseline studies (blood connt, coagulation studies, blood glucose, electrolytes, etc.). Hypoglycemia should be treated immediately if present. A 1 2 -lead ECG and other ancillary studies do not rou­ tinely take priority over the CT scan of the brain. However, the ECG may ultimately identify a recent acute myocardial infarction or arrhythmia (e . g . , atrial fibrillation) as the cause of a cardioembolic stroke and is recommended early in the evaluation of patients with stroke.75 If the patient is hemodynamically stable, immediate treatment of arrhyth­ mias prior to CT scan-including bradycardia, premature atrial or ventricular contractions, or abnormal atrioventric­ ular conduction-may be unnecessary. 76 ED

Arrival

� 10 � -

V

Data: ED Evaluation, Prompt Laboratory Studies, CT Imaging

Immediately initiate diagnostic studies in all patients to assess for conditions that may mimic stroke and comorbid problems that can complicate management. Consider the need for additional studies and perform them in selected patients. See Table 3 6-6. Establish Time of Onset ( < 3 Hours Required for

Protocols for EMS personnel should direct them to ask the patient and family about when they

Intravenous tPA)

DO NOT DELAY CT IMAGING OR FIBRINOLYTIC THERAPY

Ancillary diagnostic studies should not delay CT imaging or time­ dependent stroke therapies such as fibrinolysis when indicated unless contraindications to such therapies exist: 1. There is clinical suspicion of a bleeding disorder. 2 . The patient has recently received heparin or warfarin. 3 . Hypertension requires control.

I TA B LE 3 6 - 6

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ED Eva l u a t i o n a n d D i a g n o s t i c Stu d i e s

A l l P a t i e n ts

S e l e c t e d P a t i e n ts

•

•

• • • • • • •

N o n c o n t r a s t b r a i n CT o r M R I Blood g l ucose S e r u m e l e c t r o lytes R e n a l fu n c ti o n CBC and platelet count Co a g u l a ti o n s tu d i e s (PIT , P T , I N R) O xyg e n s a t u r a t i o n ECG

• • • • • •

C h e s t x - r ay H e p a t i c f u n c ti o n Blood alcohol and t o x i c o l o gy s c r e e n A r te r i a l b l o o d g a s lu m b a r p u n c t u r e EEG P r e g n a n cy t e s t

C B C , c o m p l e te b l o o d c o u n t , CT . c o m p u t e d t o m o g r a p hy: E C G , e l e c t r o c a r d i o ­ g r a m , E E G , e l e c t r o e n c e p h a l o g r a m : I N R , m t e r n a t1 o n a l n o r m a l n e d r at 1 o , M R I , m a g n e t i c r e s o n a n c e 1 m a g 1 n g : P T . p r o t h r o m b i n t 1 m e : PTT, p a r t 1 o l t h r o m b o p l a s ­ tin t1me.

first noted any stroke symptoms. Neither the patient nor family members may recall the exact hour and minute, but they may be able to relate the onset of symptoms to other events, such as a television or radio program that was play­ ing, a telephone call, or someone's arrival or departure. B e aware that time of onset is difficult t o establish for patients who are discovered unconscious, are unable to communi­ cate, or awaken from sleep with neurologic abnormalities. In these cases the time of onset is considered the last time the patient was seen normal. Inability to establish the time ofsymptom onset with accuracy is a contraindication to tPA therapy! Ifprehospital care personnel cannot reliably determine a specific time, ED personnel should continue the inquiries. Call or speak directly to a family member, coworker, or bystander. Immediate Neurologic S creening Assessment The clinical status of stroke patients often fluctuates. Health care providers should perform serial focused neurologic exami­ nations to detect any deterioration or improvement.

Immediate Neurologic Assessment by Stroke Team or Designee The patient's history and physical examination findings should be reviewed by a physician who is part of the stroke team, or, in the absence of a formal stroke team, a physician with expertise in the evaluation and management of acute stroke patients. Remote stroke expertise may also be helpful to the evaluation and care of such 25 patients. (Fig. 3 6-4, Box 4). This may require min interviewing out-of-hospital providers, wit­ nesses, and family members to establish the time that the patient was last known to be normal. Neurologic assessment is performed incorporating either the National Institutes of Health (NIH) Stroke Scale or Canadian Neurologic Scale (see the ASA Web site: www.strokeassociation.org). ED

Arrival

0

Determine Severity of Stroke (NIH Stroke Scale) The NIH Stroke Scale (NIHS S) is a validated measure of stroke

CHAPTER 3 6

severity based on a detailed neurologic physical examina­ tion.4 1 The NIH Stroke Scale allows nurses, midlevel providers, nursing staff, and physicians to perform standard­ ized neurologic evaluations of a patient.4 1 ·77 The score cor­ relates with long-term outcome in patients with ischemic stroke77-79 and is designed to provide a reliable,80 valid, and easy-to-perform alternative to the standard neurologic examination. The NIH Stroke Scale can be performed in < 7 minutes. This instrument received further validation during the National Institute of Neurological Disorders and Stroke (NIND S) trial of tPA for acute ischemic stroke .4 The NIHSS is associated with final size of infarct volume, prog­ nosis, and hemorrhagic risk and potential response to fibri­ nolytic therapy.8 1 The total score ranges from 0 (normal) to 42 points. The scale covers the following major areas :8 2 •

•

• •

• •

Level of consciousness: alert, drowsy; knows month, age; performs tasks correctly Visual assessment: follows finger with or without gaze palsy, forced deviation; hemianopsia (none, partial, com­ plete, bilateral) Motor function: face, arm, leg strength Sensation: pinprick to face, arm, trunk, leg; compare side after side; neglect (extinction and inattention). Cerebellar function: finger to nose, heel to shin Language: aphasia (name items, describe a picture, read sentences); dysarthria (evaluate speech clarity by having patient repeat listed words)

An NIH Su·oke Scale score of 1 8 5 m m H g o r d i a s to l i c > 1 1 0 m m H g La b e ta l o l 1 0 to 2 0 m g I V ove r 1 t o 2 m i n u t e s , m ay r e p e a t x 1 ; or N i t r o p a s t e 1 to 2 i n c h e s ; or N i c a r d i p i n e i n fu s i o n , 5 m g / h r , t i t r a t e u p b y 2 . 5 m g / h r a t 5 - to 1 5 - m i n u t e i n terva l s , m a x i m u m d o s e 1 5 m g / h r ; wh e n d e s i r e d b l o o d p r e s s u r e a t ta i n e d , r e d u c e to 3 m g / h r If b l o o d pressure does n o t decline a n d r e m a i n s > 1 85/1 1 0 m m Hg, d o n o t a d m i n ister rtPA

D u r i n g o r A f t e r Tr e a t m e n t • •

•

M o n i t o r b l o o d p r e s s u r e eve ry 1 5 m i n u t e s d u r i n g t r e a t m e n t a n d t h e n f o r a n o t h e r 2 h o u r s , t h e n every 3 0 m i n u t e s f o r 6 h o u r s , a n d t h e n eve ry h o u r f o r 1 6 h o u r s B l o o d p r e s s u r e l eve l : Systo l i c 1 8 0 to 2 3 0 m m H g o r d i a sto l i c 1 0 5 t o 1 2 0 m m H g La b e t a l o l 1 0 m g I V ove r 1 to 2 m i n u t e s , m ay r e p e a t every 1 0 to 2 0 m i n u t e s , m a x i m u m d o s e o f 3 0 0 m g ; or La b e ta l o l 1 0 m g IV fo l l ow e d b y a n i n fu s i o n a t 2 to 8 m g / m i n Systo l i c > 2 3 0 m m H g o r d i a s to l i c 1 2 1 to 1 4 0 m m H g La b e t a l o l 1 0 m g I V ove r 1 to 2 m i n u t e s , m ay r e p e a t eve ry 1 0 to 2 0 m i n u t e s , m a x i m u m d o s e o f 3 0 0 m g ; or La b e t a l o l 1 0 m g I V fo l l owed b y a n i n fu s i o n a t 2 to 8 m g / m i n ; or N i c a r d i p i n e i n f u s i o n , 5 m g / h r , t i t r a t e u p to d e s i r e d e f f e c t b y i n c r e a s i n g 2 . 5 m g / h r eve ry 5 m i n u t e s to m a x i m u m o f 1 5 m g / h r I f b l o o d p r e s s u r e n o t c o n tr o l l e d , c o n s i d e r s o d i u m n i t r o p r u s s i d e

S o u r c e : R H R/RSR g u 1 d e l 1 n e s f o r e a r l y m a n a g e m e n t o f a d u l ts w1th 1 s c h e m 1 c str o k e Stro ke 2 0 0 7 ; 3 8 : 1 6 7 1 .

The C T scan i s central t o the triage and treatment of the stroke patient. If the CT scan shows no evidence of hem­ orrhage, the patient may be a candidate for fibrinolytic ther­ apy (Fig. 3 6-4, Boxes 6 and 8). A NORMAL CT

=

CANDIDATE FOR

FIBRINOLYTIC THERAPY

An important point to remember is that a completely normal CT scan-no sign of hemorrhage, and no hypodense areas-is supportive of tPA administration in a stroke patient who otherwise meets the criteria for fibrinolytic therapy.

!>chemic Stroke During the first few hours of a throm­ botic or embolic stroke, the noncontrast CT scan will gen­ erally appear normal. Brain structures without normal blood flow appear initially the same as structures with good blood flow on the CT scan. For this reason the CT scan will con­ tinue to appear "normal" for a few hours after blood flow is obstructed or reduced to an area of the brain. A well-defined area of hypodensity, purported to be caused by lack of blood flow past an occlusion, will rarely develop within the first

3 hours of a stroke. If the brain tissue downstream of an occlusion is indeed ischemic, it soon begins to swell with edema and inflammation. After 6 to 12 hours, the edema and swelling are suffi­ cient to produce a hypo dense area that is usually visible on a CT scan. This well-defined hypodensity rarely develops within the 3 -hour limit required for administration of tPA. In fact, the time since stroke onset is likely to be > 3 hours if a well-defined hypodensity is present on the CT scan. For this reason a large hypodense area on the CT scan generally excludes a patient from fibrinolytic therapy. Changes of early ischemia and infarction from ischemic stroke may cause CT changes, but these changes are often subtle, such as obscur­ ing of the gray-white matter junction, loss of the insular rib­ bon, sulcal effacement, or early hypodensity.

Hemorrhagic Stroke If the initial non contrast CT scan shows intracerebral or subarachnoid hemorrhage , the treating physician should immediately consult a neurosur­ geon or neurointerventionalist to initiate appropriate actions for acute hemorrhage (see below and Fig. 3 6-4, Boxes 7 and 1 1 ) . V Decision:

Diagnosis and Decision: Appropriate Therapy

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F i b r i n o lyti c Ch e c k l i s t

U s e o f t P A i n P a t i e nts With A c u t e I s c h e r n i c Str o k e All b o x e s m us t b e ch e c k e d b e fo r e tPA c a n b e give n . N o t e : T h e fo l l owi n g c h e c k l i s t i n c l u d e s F D A - a p p roved i n d i c a t i o n s a n d c o n tr a i n d i c ti o n s f o r t P A a d m i n i s t r a t i o n f o r a c u t e i s c h e m i c

str o k e . A p hys i c i a n with e x p e r t i s e i n a c u te str o k e c a r e m ay m o d i fy t h i s l i st. In clusio n Cri teria (all YES b o x e s i n t h i s s e c ti o n m us t b e c h e c k e d) :

Yes 0 A g e 1 8 ye a r s o r o l d e r ? 0 Cl i n i c a l d i a g n o s i s o f i s c h e m i c str o k e with a m e a s u r a b l e n e u r o l o g i c d e f i c i t ? 0 Ti m e o f sym p t o m o n s e t (wh e n p a t i e n t was l a st s e e n n o r m a l) we l l e s ta b l i s h e d a s < 1 8 0 m i n u t e s (3 h o u rs) b e f o r e t r e a t m e n t wo u l d b e g i n ? Exclusion Cri teria (all N o b o xes i n "Con train dic a ti o n s " s e c ti o n m us t b e ch e c k e d) :

Contra indications: No 0 Evi d e n c e of i n tr a c r a n i a l h e m o r r h a g e on p r e t r e a t m e n t n o n c o n t r a s t h e a d CT ? 0 Cl i n i c a l p r e s e n t a t i o n s u g g estive of s u b a r a c h n o i d h e m o r r h a g e eve n with n o r m a l CT? 0 CT s h ows m u l ti l o b a r i n fa r cti o n (hyp o d e n s i ty g r e a t e r th a n o n e t h i r d c e r e b r a l h e m i s p h e r e)? 0 H i s t o ry o f i n tr a c r a n i a l h e m o r r h a g e ? 0 U n c o n t r o l l e d hyp e rt e n s i o n : A t t h e ti m e t r e a t m e n t s h o u l d b e g i n . systo l i c p r e s s u r e r e m a i n s > 1 8 5 m m H g o r d i a s to l i c p r e s s u r e r e m a i n s > 1 1 0 m m H g d e s p i t e r e p e a t e d m e a s u r e m e n ts ? 0 K n own a r t e r i ove n o u s m a l fo r m a ti o n , n e o p l a s m , o r a n e u rys m ? 0 A c tive i n t e r n a l b l e e d i n g o r a c u t e tr a u m a (fr a c t u r e ) ? b 0 A c u t e b l e e d i n g d i a t h e s i s , i n c l u d i n g b u t n o t l i m i t e d to • Plalet count < 1 00 OOO/mm3? • H e p a r i n r e c e ived wi t h i n 4 8 h o u r s , r e s u l t i n g i n a n a c tiva t e d p a rti a l th r o m b o p l a sti n t i m e (a PTT) t h a t i s g r e a t e r th a n u p p e r l i m i o f n o r m a l f o r l a b o r a t o ry? • Cu r r e n t use o f a n t i c o a g u l a n t ( e . g . , wa r fa r i n s o d i u m) t h a t h a s p r o d u c e d an e l ev a t e d i n t e r n a ti o n a l n o r m a l i z e d r a t i o (I N R) > 1 . o r p r o th o m b i n ti m e (PT) > 1 5 s e c o n d s ? • 0 With i n 3 m o n t h s o f i n tr a c r a n i a l o r i n t r a s p i n a l s u r g e ry , s e r i o u s h e a d tr a u m a , o r p r evi o u s str o k e ? 0 A r te r i a l p u n c t u r e a t a n o n c o m p r e s s i b l e s i t e with i n p a s t 7 d ays ? Relative Contraindications/Precautions: R e c e n t e x p e r i e n c e s u g g ests t h a t u n d e r s o m e c i r c u m s t a n c e s-wi t h c a r e f u l c o n s i d e r a t i o n a n d we i g h i n g o f r i s k - to - b e n e f i t r a t i o­ p a t i e n ts m ay r e c e ive fi b r i n o lyti c t h e r a py d e s p i t e o n e o r m o r e r e l a tive c o n tr a i n d i c a ti o n s . Co n s i d e r t h e p r o s a n d c o n s o f t P A a d m i n i s t r a t i o n c a r e fu l ly i f a ny o f t h e s e r e l a tive c o n tr a i n d i c a t i o n s i s p r e s e n t: • O n ly m i n o r o r r a p i d ly i m p r ovi n g str o k e sym p t o m s (c l e a r i n g s p o n ta n e o u sly) • With i n 1 4 d ays o f m aj o r s u r g e ry o r s e r i o u s tr a u m a • R e c e n t g a st r o i n testi n a l o r u r i n a ry t r a c t h e m o r r h a g e (wi th i n p r evi o u s 2 1 d ays) • R e c e n t a c u t e myo c a r d i a l i n fa r c ti o n (wi t h i n p r evi o u s 3 m o n t h s) • P o stmyo c a r d i a l i n fa r cti o n p e r i c a r d i ti s • A b n o r m a l b l o o d g l u c o s e l eve l (< 5 0 o r > 4 0 0 m g / d l [ < 2 . 8 o r > 2 2 . 2 m m o i / L]) ' I n p a t 1 e nts With o u t recent u s e of oral a n t 1 c o o g u l a n t s o r h e p a nn , treatment w1th t P A c a n b e 1 n 1 t 1 a t e d b e f o r e ava i l a b i l i ty o f c o a g u l a t i o n s t u d y r e s u lts b u t s h o u l d b e d 1 s c o n t 1 n u e d 1 f t h e 1 n t e r n a t1 o n a l n o r m a l i z e d r a t 1 o ( I N R) I S > 1 7 o r t h e p a r t 1 a l t h r o m b o p l a s t i n t 1 m e I S e l eva t e d by l o c a l l a b o r a t o ry sto n d a r d s . ' N o t e : A H A/ A S A 2 0 0 7 I s c h e m i c S t r o k e U p d a t e · S e 1 z u re s a t o n s e t I S n ow a relative contraindication.

ED Arrival

60 m i n

Risk Assessment and Administration of IV tPA (Fig. 3 6,4, Boxes 6, 8, and 1 0 )

When the CT scan shows no hemorrhage, the stroke team or physician expert should review the inclusion and exclusion criteria for IV fibrinolytic therapy (Table 3 6-9)

and perform a repeat the neurologic examination (incorpo­ rating the NIH S troke Scale or Canadian Neurological Scale) . If the patient's neurologic signs are spontaneously improving (i. e. , function is rapidly improving toward nor­ mal) and are near baseline, fibrinolytic administration is not recommended (Fig. 3 6-4, Box 6).

CHAPTER 3 6

Risk-Benefit of tPA Therapy The administration of IV tPA has been controversial since its initial approval by the FDA in 1 996 but is now generally accepted in carefully selected patients with ischemic stroke. 88 In the Canadian Stroke Registry, only 8 . 9 % of patients received tPA.89 This treatment rate is due to several factors, most importantly treatment time from symptom onset. Of all stroke patients, only 1 0 % to 2 0 % are eligible within the 3 -hour time win­ dow and half of these are not treated for other reasons.89·90 New imaging techniques such as MRI may identify a sub­ group of patients eligible beyond the 3 -hour window.9 1 Triage to a stroke center may also allow additional patients to be treated up to 6 hours with intra-arterial fibrinolysis, although this is not yet approved by the FDA, or mechani­ cal reperfusion modalities.

Benefit-Improved Neurologic Outcome Without Increased Mortality Several studies have documented a higher likeli­ hood of good to excellent functional outcome when intra­ venous tPA is administered to adults with acute ischemic stroke within 3 hours of symptom onset.4·92•93 Such results are obtained when intravenous tPA is administered by physi­ cians in hospitals with a stroke protocol that rigorously adheres to the eligibility criteria and therapeutic regimen of the NIND S study protocol. These results have been sup­ ported by a subsequent 1 -year follow-up study,94 reanalysis of the NIND S data,95 and a meta-analysis.96 Evidence from prospective, randomized studies in adults also documents a greater likelihood of benefit the earlier treatment is begun. Many physicians have emphasized imbalances in the NIND S trials.97·98 However additional analyses of the orig­ inal NIND S data by an independent group of investigators95 confirmed the validity of the results, verifying that improved outcomes in the IV tPA treatment arm persist even after imbalances in baseline stroke severity among treatment groups were corrected.99

Major Risk-Intracranial Hemorrhage and Death Like all medications, fibrinolytics have potential adverse effects. The physician must verify that there are no exclusion crite­ ria, consider the risks and benefits to the patient, and be pre­ pared to monitor and treat any potential complications. The maj or complication of IV tPA for stroke is symptomatic intracranial hemorrhage. This complication occurred in 6.4% of the 3 1 2 patients treated in the NIND S trial4 and 4.6% of the 1 , 1 3 5 patients treated in 60 Canadian centers. 100 A meta-analysis of 1 5 published case series on the open-label use of tPA for acute ischemic stroke in general clinical prac­ tice shows a symptomatic hemorrhage rate of 5 . 2 % among 2 , 6 3 9 patients treated. 1 01 Other complications include orolingual angioedema (occurs in about 1 . 5 % of patients), acute hypotension, and systemic bleeding. In one large prospective registry, major systemic bleeding was uncom­ mon (0.4%) and usually occurred at the site of femoral groin puncture for acute angiography. 1 00· 102 D espite these risks, when administered in accordance with the NIND S study protocol, tPA is both safe and effective. The American College of Emergency Physicians (ACEP) has a developed policy statement on use of tPA in

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ischemic stroke. This document provides additional insight and guidance on risk stratification and selection of patients for tPA administration.

·�····································································································· S e e W e b s i t e f o r A C E P p o l i cy s t a t e m e n t a n d "V'

p o l i cy r e s o u r c e a n d e d u c a t i o n p a p e r o n i n t r a ve n o u s t P A f o r t h e m a n a g e m e n t o f a c u t e s t r o k e i n t h e e m e r g e n cy d e p a r t m e n t .

How t o Minimize Risks and Maximize B enefits of

In the NIND S trial, fatal intracranial hemorrhage occurred in approximately 3 of every 1 00 patients treated with intravenous tPA (3 %) but only 3 of every 1 ,000 (0. 3 %) receiving placebo. This means that the risk of fatal bleeding into the brain was 10 times greater in the tPA-treated patients. But it is important to note that overall mortality was not increased in the tPA­ treated group ( 1 7 % versus 2 1 % for the placebo group). For a perspective on this risk, consider that the rate of fatal hem­ orrhagic stroke in patients given tPA within 1 2 hours of acute coronary artery occlusion averages < 1 % . To minimize the risks and maximize the benefits, responsible clinicians must adhere strictly to the inclusion and exclusion criteria (Table 3 6-9). Intravenous tPA therapy is acceptable only with strict adherence to these criteria. Intravenous tPA for Acute Stroke

Strategies for Success

Administration of IV tPA to patients with acute ischemic stroke who meet the NINDS eligibility criteria is recom­ mended if tPA is administered by physicians in the setting of a clearly defined protocol, a knowledgeable team, institu­ tional commitment, and the patient's informed consent. It is important to note that the superior outcomes reported in both community and tertiary care hospitals in the NIND S trials have been difficult to replicate in hospitals with less experience in and institutional commitment to acute stroke care. 1 03• 1 04 Failure to adhere to protocol is associated with an increased rate of complications, particularly the risk of symptomatic intracranial hemorrhage . 1 05· 106 There is also strong evidence to avoid all delays and treat patients as soon as possible. Community hospitals have reported outcomes compa­ rable to the results of the NIND S trials after implementing a stroke program with a focus on quality improve­ ment. 1 00· 1 07·108 The experience of the Cleveland Clinic sys­ tem is instructive . 1 04· 1 08 A quality improvement program increased compliance with the tPA treatment protocol in nine community hospitals, and the rate of symptomatic intracerebral hemorrhage fell from 1 3 .4% to 6.4% . 108 There is a relationship between violations of the NINDS treatment protocol and increased risk of symptomatic intra­ cerebral hemorrhage and death. 101 In Germany there was an increased risk of death after administration of tPA for acute ischemic stroke in hospitals that treated five or fewer patients per year, which suggests that clinical experience is an important

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factor in ensuring adherence to protocol. 102 The addition of a dedicated stroke team to a community hospital can increase the number of patients with acute stroke treated with fibrinolytic therapy and produce excellent clinical outcomes. 1 09 These findings show that it is important to have an institutional com­ mitment to ensure optimal patient outcomes. To provide standardized and comprehensive stroke care, the Brain Attack Coalition published criteria for pri­ mary stroke centers (PSC) and comprehensive stroke cen­ ters (CSC). A PSC has resources to care for many of the patients with uncomplicated stroke. A CSC provides com­ prehensive and specialized care for patients with a compli­ cated stroke and those requiring specialized care, such as surgery or stroke intensive care. 1 10

has passed since the onset of the stroke must be docu­ mented. IV infusion of the fibrinolytic agent must begin within 1 80 minutes of the beginning of stroke symptoms.

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ANTICOAGULANTS AND ANTIPLATELET THERAPY

Neither anticoagulants nor antiplatelet treatment should be administered for 2 4 hours after administration of tPA, typically until a follow-up CT scan at 24 hours shows no hemorrhage (Fig. 3 6 -4, B ox 1 0). If the patient has brain hemorrhage, D O NOT GIVE ASPIRIN (Fig. 3 6-4, B ox 7).

•

If the patient has ischemic stroke but is not a candidate for tPA, consider aspirin.

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STROKE GUIDELINES UPDATE

New recommendations for stroke care include: •

• •

Transport to closest facility with resources to care for stroke patients (i.e., hospital bypass) D evelopment of primary stroke centers-strongly recommended Certification of stroke centers by external agency-strongly encouraged

V

Drug: Administration of tPA When Indicated and Other Therapies

Additional Actions Before Fibrinolytic Therapy Review for CT Exclusions: Are Any Observed? •

•

Hemorrhage, either intracerebral or subarachnoid, must be excluded. Failure to identify a small area of hemor­ rhage could be a fatal error. Large areas of well-defined hypodensity are generally CT exclusions because they indicate either that > 3 hours have passed since the infarction or that a large area of the brain is threatened. Larger brain infarctions are prone to undergo hemorrhagic transformation, exposing a patient receiving a fibrinolytic agent to the risk of fatal intracere­ bral hemorrhage. A knowledgeable stroke expert must carefully weigh risk-benefit ratios in consultation with the patient.

•

DO NOT administer heparin (unfractionated or low molecular weight). Heparin is associated with an increased risk of bleeding within the first 24 hours.

V

Drug: Administration and Monitoring of tPA Infusion

IV fibrinolytic therapy is a class I recommendation for a highly selected, well-defined subset of ischemic stroke patients. Treatment with IV tPA within 3 hours of the onset of ischemic stroke improved clinical outcome at 3 months. ED- or hospital-based stroke specialists should aim to start the initial bolus within 60 minutes of arrival in the ED. Ten percent of a total dose of 0.9 mg/kg (maximum 90 mg) is given by bolus administration and the remainder infused over 60 minutes. During tPA infusion: •

•

•

•

Monitor neurologic status; if any signs of deterioration develop, stop the IV tPA and obtain an emergent CT scan. Monitor blood pressure, which may increase during fibri­ nolytic treatment. Initiate antihypertensive treatment with any increase over 1 80 mm Hg systolic or over 1 05 mm Hg diastolic (see above and Table 3 6-8). Admit patient to the critical care unit, stroke unit, or other skilled facility capable of careful observation, frequent neurologic assessments , and cardiovascular monitoring. Avoid anticoagulant or antiplatelet treatment for the next 24 hours.

Review Fibrinolytic Exclusions: Are Any Observed? •

Table 3 6-9 lists the major exclusions for the use of fibri­ nolytics. Such a checklist, in a form suitable for inclusion in a patient's medical record, should be available wherever stroke patients might be treated with fibrinolytics.

Review Patient Data: Is Time Since Symptom Onset Now •

;:::: 3

Hours?

This step reminds the clinician to make one last review of all the information gathered during the patient assess­ ments . In particular, the estimated length of time that

lntra�arterial tPA For patients with acute ischemic stroke who are not candi­ dates for standard IV fibrinolysis, administration of intra­ arterial fibrinolysis within 6 hours from symptom onset (class I, level of evidence B) or mechanical embolectomy (class lib , level of evidence B) in centers that have the resources and expertise available may be considered within the first few hours after the onset of symptoms J Intra­ arterial administration of tPA has not yet been approved by the FDA.

CHAPTER 3 6

T ransition to Critical Care

General Stroke Care

Additional stroke care includes support of the airway, oxy­ genation and ventilation, and nutritional support. Normal saline is administered at approximately 7 5 to 1 00 mL/hr to maintain euvolemia if needed. The reported frequency of seizures during the first days of stroke ranges from 2 % to . . ;o . 1 1 1-1 1 4 M ost seiZures 2 3 o/ occur d unng th e fi rst day and can recur. Seizure prophylaxis is not recommended. Treatment of acute seizures followed by administration of anticonvul­ sants to prevent further seizures is recommended, consistent with the established management of seizures.7 Monitor the patient for signs of increased intracranial pressure . Continued control of blood pressure is required to reduce the risk of bleeding in patients who have received tPA.

Hyperglycemia Hyperglycemia is present in about one third of patients admitted with stroke . Hyperglycemia is associated with worse clinical outcome in patients with acute ischemic stroke than is normoglycemia, but there is no direct evi­ dence that active glucose control improves clinical out­ come . 1 1 5 ' 1 1 6 There is evidence that insulin treatment of hyperglycemia in other critically ill patients improves sur­ vival rates. For this reason administration of IV or subcuta­ neous insulin may be considered to lower blood glucose in patients with acute ischemic stroke when the serum glucose level is > 1 0 mmol/L (> � 2 00 mg/dL). I t 7 , 1 1 8

Temperature Control Increased temperature in stroke is associated with poor neu­ rologic outcome. No data have demonstrated that lowering temperature improves outcome, but fever > 3 7 . 5 °C (99. 5°F) should be treated and the source of fever identified and treated if possible. Induced hypothermia may exert neuroprotective effects after a stroke . 1 1 9- 1 2 3 Hypothermia has been shown to improve survival and functional outcome in patients follow­ ing resuscitation from ventricular fibrillation sudden cardiac arrest, but it has not been shown in controlled human trials to be effective for acute ischemic stroke . In some small human pilot studies and in animal models, hypothermia (3 3 °C to 3 6°C [9 1 .4°F to 96. 8°F]) for acute ischemic stroke has been shown to be relatively safe and feasible. 1 22• 124, l 2 5 Although effects of hypothermia on both global and focal cerebral ischemia in animals have been promising, cooling to ::s; 3 rC (9 1 .4°F) appears to be associated with increased complications, including hypotension, cardiac arrhythmias, cardiac failure, pneumonia, thrombocytopenia, and a rebound increase in intracranial pressure during rewarm. . msu . . . fi c ing . 12 0 , 12 1 , 12 3 , 12 6 , 12 7 At present th ere IS ffictent sCient! evidence to recommend for or against the use of hypother­ mia in the treatment of acute ischemic stroke.7

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Stroke Units Patients should be admitted to a stroke unit (if available) for careful observation, including monitoring of blood pressure and neurologic status and treatment of hypertension if indi­ cated. If the patient's neurologic status deteriorates, order an emergent CT scan to determine if cerebral edema or hemor­ rhage is responsible for the deterioration and treat if possible. All patients with stroke should be screened for dyspha­ . before anything is given by mouth. A simple bedside gia screening evaluation involves asking the patient to sip water from a cup. If the patient can sip and swallow without diffi­ culty, he or she is asked to take a large gulp of water and swallow. If there are no signs of coughing or aspiration after 3 0 seconds, it is safe for the patient to have a thickened diet until he or she is formally assessed by a speech pathologist.7 Medications may be given in applesauce or jam. Any patient who fails a swallow test may be given medications such as aspirin rectally or, if appropriate, via the rv; intramuscular, or subcutaneous route.

Summary As in the management of the patient with an ACS, the patient with ischemic stroke requires a time-dependent therapy and a c? ordinated interdisciplinary system of care. Rapid recog­ . muon of stroke symptoms and activation of EMS speeds patient assessment and management and may result in earlier reperfusion, stroke volume reduction, and improved short­ and long-term prognosis. Stroke centers provide many of the hospital-based ele­ ments of this system of care, including stroke units, written care protocols for stroke health care professional interdisci­ plinary teams, neurologic expertise, and coordinated com­ prehensive consultation and support. When properly inte­ grated, these centers and systems are associated with improved outcomes for stroke patients. 1 1 0· 128 Stroke center certification is progressing, and the Joint Commission on Accreditation of Healthcare Organizations QCAHO) began a formal process for certification of Primary Stroke Centers (PSC) in 2 004. At present, > 2 00 hospitals have been certi­ fied as stroke centers. Use of destination hospital protocols routing acute stroke patients to a PSC has increased the number of patients receiving tPA. 12 9 Although initial reper­ fusion of ischemic stroke patients has focused on the use of IV fibrinolytic therapy (tPA), stroke centers are now evalu­ ating the use of other reperfusion methods including intra­ arterial tPA and mechanical reperfusion methods for patients ineligible for pharmacologic agents. It is possible that these evolving methods combined with neuroprotection will, in the future, extend the time window for salvage of ischemic brain in stroke patients.

References 1. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke sta­ tistics-2 008 update: a report from the American Heart Association

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community practice and patient care. The National Institute of Neurological Disorders and Stroke (NINDS) rt-PA Stroke Study Group. St1'oke 1 997;2 8(8): 1 5 3 0-1 540. Singhal AB, Benner T, Roccatagliata L, et a!. A pilot study of nor­ mobaric oxygen therapy in acute ischemic stroke. St1'oke 2 0 0 5 ; 3 6(4) : 797-802 . Singhal AB, Ratai E, Benner T, et a!. Magnetic resonance spec­ troscopy study of oxygen therapy in ischemic stroke. St1'oke 2007 ; 3 8 ( 1 0):2 8 5 1 -2 8 54. Adams HJ, Brott T, Crowell R, et a!. Guidelines for the manage­ ment of patients with acute ischemic stroke: a statement for health­ care professionals from a special writing group of the Stroke Council, American Heart Association. St1'oke 1 994;2 5 : 1 90 1 - 1 9 1 4. Oppenheimer SM, Cechetto DF, Hachinski VC. Cerebrogenic cardiac arrhythmias: cerebral electrocardiographic influences and their role in sudden death. Anh Neurol 1 990;47(5):5 1 3-5 1 9 . Lyden P, Rapp K , Babcock T, et a!. Ultra-rapid identification, triage, and enrollment of stroke patients into clinical trials. J StrokeCe1·eb1·ovasc Dis 1 994;2 : 1 06-1 1 3 . Brott T. Utility o f the NIH stroke scale. Cerelrrovasc Dis 1 992 ; 2 : 241-2 42 . Lyden P, Lu M, Jackson C , et al. Underlying structure o f the National Institutes of Health Stroke Scale: results of a factor analysis. NINDS tPA Stroke Trial Investigators. Stroke 1 999;3 0(1 1): 2 3 47-2 3 54. Goldstein LB, Bertels C, Davis JN. lnterrater reliability of the NIH stroke scale. Anh Nezu'o/ 1 989;46(6):660-662 . Spilker J, Kongable GL. The NIH Stroke Scale: its importance and practical application in the clinical setting. Stroke Intervent 2000;2 : 7 - 1 4 (for further information refer to Web site http://www.stroke-site.org). Spilker ], Kongable GL. The NIH Stroke Scale: its importance and practical application in the clinical setting. Su·oke Intervent 2000; 2 : 7-14. (For further information refer to http://www.stroke-site.oz-g). Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. The NINDS t-PA Stroke Study Group. Su·oke 1 997;2 8(1 1 ):2 1 09-2 1 1 8 . Adams H, Adams R , Del Zoppo G , e t a!. Guidelines for the early management of patients with ischemic stroke: 2 005 guidelines update a scientific statement from the Stroke Council of the An1erican Heart Association/American Stroke Association. Su·oke 2005 ;3 6(4) : 91 6-92 3 . Adams HP Jr, Adams RJ, Brott T, et a!. Guidelines for the early management of patients with ischemic stroke: A scientific state­ ment from the Stroke Council of the American Stroke Association. Su·oke 2 003 ; 3 4(4): 1 05 6- 1 0 8 3 . Connors JJ III, Sacks D, Furlan AJ, et al. Training, competency, and credentialing standards for diagnostic cervicocerebral angiog­ raphy, carotid stenting, and cerebrovascular intervention: a joint statement from the An1erican Academy of Neurology, American Association of Neurological Surgeons, American Society of lnterventional and Therapeutic Radiology, An1erican Society of Neuroradiology, Congress of Neurological Surgeons, AANS/CNS Cerebrovascular Section, and Society of lnterventional Radiology. Radiology 2005;2 3 4(1):26-34. Schriger DL, Kalafut M, Starkman S , et al. Cranial computed tomography interpretation in acute stroke : physician accuracy in determining eligibility for thrombolytic therapy. JAlviA 1 998; 2 79(1 6): 1 2 93 - 1 2 9 7 . Lyden P. Th1'ombolytic Therapy fo r Acute St1'oke, 2 n d e d . Totowa N]: Humana Press, 2005. Nadeau ]0, Shi S, Fang J, et a!. TPA use for stroke in me Registry of the Canadian Stroke Network. Can J Neural Sci 2005 ; 3 2 (4) : 43 3-439. Hills NK, ] ohnston SC. Why are eligible thrombolysis candidates left untreated? Am J Prev Med 2 006;3 1 (6 Suppl 2):S2 1 0-S2 1 6 . Albers G W Expanding the window for thrombolytic therapy in acute stroke. The potential role of acute MRI for patient selection. Stroke 1 999;3 0 ( 1 0):2 2 3 0-2 2 3 7 . Hacke W, Dorman G , Fieschi C, et a!. Association o f outcome wim early stroke treatment: pooled analysis of ATLANTIS, ECASS, and NINDS rt-PA stroke trials. Lancet 2 004; 3 6 3 (94 1 1): 768-774. Hill MD, Buchan Al\1.. Thrombolysis for acute ischemic stroke: results of the Canadian Alteplase for Stroke Effectiveness Study. Canadian Alteplase for Stroke Effectiveness Study (CASES) Investigators. CMAJ 2005; 1 72(1 0)(1 0): 1 3 07 .

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94. Kwiatkowski TG, Libman RB, Frankel M, et al. Effects of tissue plasminogen activator for acute ischemic stroke at one year. National Instimte of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study Group. N Engl J Med 1 999; 340(2 3): 1 7 8 1 - 1 7 8 7 . 9 5 . Ingall TJ, O'Fallon WM, Asplund K , e t al. Findings from the reanalysis of the NINDS tissue plasminogen activator for acute ischemic stroke treatment trial. Stroke 2 004; 3 5 ( 1 0):241 8-2424. 96. Wardlaw JM, Zappa G, Yamaguchi T, et al. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev 2 0 0 3 (3 ) : CD0002 1 3 . 97. Mann ] . Truths about the NIND S study: setting the record straight. West ] Med 2 002 ; 1 76(3): 1 92-1 94. 98. Lindley RI. Further randomized controlled trials of tissue plas­ minogen activator within 3 hours are required. St7'oke 2 00 1 ; 3 2 ( 1 1):2 708-2 709. 99. Kwiatkowski T, Libman R, Tilley BC, et al. The impact of imbal­ ances in baseline stroke severity on outcome in the National Institute of Neurological Disorders and Stroke Recombinant Tissue Plasminogen Activator Stroke Study. Ann Emn'g Med 2 005 ;45 (4): 3 7 7-3 84. 100. Hill MD, Buchan AM Thrombolysis for acute ischemic stroke: results of the Canadian Alteplase for Stroke Effectiveness Study. Canadian Alteplase for Stroke Effectiveness Study (CASES) Investigators. CMAJ 2005 ; 1 72 ( 1 0): 1 3 07-1 3 1 2 . 1 0 1 . Graham GD . Tissue plasminogen activator for acute ischemic stroke in clinical practice: a meta-analysis of safety data. Stroke 2 003 ; 3 4(1 2):2 847-2 850. 1 0 2 . Heuschmann PU, Berger K, Misselwitz B, et al. Frequency of thrombolytic therapy in patients with acute ischemic stroke and the risk of in-hospital mortality: the German Stroke Registers Study Group. Stroke 2003 ; 3 4(5): 1 1 06-1 1 1 3 . 1 0 3 . Bravata DM, Kim N , Concato ], e t al. Thrombolysis for acute stroke in routine clinical practice. Anh Inte17Z Med 2 002 ; 1 62 ( 1 7): 1 994-2 00 1 . 1 04. Katzan IL, Furlan AJ, Lloyd LE, e t al. Use o f tissue-type plas­ minogen activator for acute ischemic stroke: the Cleveland area experience. JAMA 2 000;2 8 3 (9): 1 1 5 1 -1 1 5 8 . 1 0 5 . Katzan IL, Hammer MD, Hixson ED, e t al. Utilization o f intra­ venous tissue plasminogen activator for acute ischemic stroke. A1'cb Neuro/ 2 004; 6 1 (3 ) : 3 46-3 50. 1 06. Lopez-Yunez AM Bruno A, Williams LS, et al. Protocol viola­ tions in community-based rTPA stroke treatment are associated with symptomatic intracerebral hemorrhage. St1'oke 2 00 1 ; 3 2 ( 1): 12-16. 1 0 7 . Asimos AW, Norton H], Price MF, e t a l . Therapeutic yield and outcomes of a community teaching hospital code stroke protocol. Acad Enzerg Med 2 004; 1 1 (4) : 3 6 1-3 70. 108. Katzan IL, Hammer MD, Furlan A], et al. Quality improvement and tissue-type plasminogen activator for acute ischemic stroke: a Cleveland update. Stroke 2 003 ; 3 4(3): 799-800. 1 09. Lattimore SU, Chalela ], Davis L, et al. Impact of establishing a primary stroke center at a community hospital on the use of thrombolytic therapy: the NIND S Suburban Hospital Stroke Center experience. Su·oke 2 003 ; 3 4(6):e5 5-e 5 7 . 1 1 0 . Alberts MJ, H a de menos G , Latchaw RE, e t a l . Recommendations for the establishment of primary stroke centers. Brain Attack Coalition. JAMA 2 000;2 8 3 (2 3 ): 3 1 02-3 1 09. 1 1 1 . Kilincer C, Asil T, Utku U, et al. Factors affecting the outcome of decompressive craniectomy for large hemispheric infarctions : .

1 12. 1 13. 1 1 4. 1 15.

1 1 6. 1 1 7. 1 1 8. 1 1 9. 120. 121. 122. 123. 1 24.

,

125.

126. 127.

128. 129.

a prospective cohort study. Acta Neurochir (Wien) 2005; 147(6): 5 8 7-594; discussion 5 94. Burn ], Dennis M, Bamford ], et al. Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Proj ect. BMJ 1 997;3 1 5 (7 1 2 2): 1 5 82-1 5 8 7 . Davalos A , Cendra E, Genis D, e t a l . The frequency, characteris­ tics and prognosis of epileptic seizures at the onset of stroke. J Nezwol New'om rg Psychiauy 1 9 8 8; 5 1 ( 1 1): 1 464. Kilpatrick CJ, Davis SM, Hopper JL, et al. Early seizures after acute stroke. Risk of late seizures. Arch Nezwol 1 992 ;49(5): 5 09-5 1 1 . Scott ]F, Robinson GM, French JM, et al. Glucose potassium insulin infusions in the treatment of acute stroke patients with mild to moderate hyperglycemia: the Glucose Insulin in Stroke Trial (GIST). Su,oke 1 999;3 0(4):793-799. Gray CS, Hildreth A], Alberti GK, et al. Poststroke hyper­ glycemia: natural history and immediate management. Su,oke 2 004;3 5(1): 1 22-126. Van den Berghe G, Wouters P], Bouillon R, et al. Outcome ben­ efit of intensive insulin therapy in the critically ill: insulin dose versus glycemic control. O'it Cm'e Med 2 003 ;3 1 (2): 3 5 9-366. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001 ;345(19): 1 3 5 9-1 3 67 . De Georgia MA Krieger D W, Abou-Chebl A , e t al. Cooling for Acute Ischemic Brain Damage (COOL AID): a feasibility trial of endovascular cooling. Neurology 2 004;63 (2): 3 1 2-3 1 7 . Georgiadis D, Schwarz S, Aschoff A , e t al. Hemicraniectomy and moderate hypothermia in patients with severe ischemic stroke. Su,oke 2 002 ; 3 3 (6): 1 5 84-1 5 8 8 . Georgiadis D, Schwarz S, Kollmar R , e t a l . Endovascular cooling for moderate hypothermia in patients with acute stroke : first results of a novel approach. Su,oke 2 00 1 ; 3 2 ( 1 1):2 5 50-2 5 5 3 . Wang H , Olivero W, Lanzino G , e t al. Rapid and selective cere­ bral hypothermia achieved using a cooling helmet. J New'oszt 1'g 2 004; 1 00(2):2 72-2 7 7 . Schwab S, Schwarz S, Spranger M, e t a l . Moderate hypothermia in the treatment of patients with severe middle cerebral artety infarction. Stroke 1 998;29(12):246 1 -2466. Kammersgaard LP, Rasmussen BH, Jorgensen HS, et al. Feasibility and safety of inducing modest hypothermia in awake patients with acute stroke through surface cooling: A case-control study: the Copenhagen Stroke Study. Su,oke 2 000;3 1 (9):2 2 5 1 -2256. Knoll T, Wimmer ML, Gumpinger F, et al. The low normother­ mia concept-maintaining a core body temperature between 36 and 3 7 degrees C in acute stroke unit patients. J Neurosurg Anesthesio/ 2002 ; 1 4(4) : 3 04-3 08. Schwab S , Georgiadis D , Berrouschot ], et al. Feasibility and safety of moderate hypothermia after massive hemispheric infarc­ tion. Stroke 2 0 0 1 ; 3 2 (9):203 3-203 5 . Krieger D W, De Georgia MA Abou-Chebl A , e t al. Cooling for acute ischemic brain damage (cool aid): an open pilot study of induced hypothermia in acute ischemic stroke. Su,oke 2 00 1 ; 3 2 (8): 1 847- 1 8 54. Alberts M], Latchaw RE, Selman WR, et al. Recommendations for comprehensive stroke centers: a consensus statement from the Brain Attack Coalition. Stroke 2005;3 6(7): 1 5 97-1 6 1 6. Wojner-Alexandrov AW, Alexandrov AV, Rodriguez D , et al. Houston paramedic and emergency stroke treatment and out­ comes study (HoPSTO). Su,oke 2005;3 6(7): 1 5 12-1 5 1 8 . ,

,

Ethics Chapter 3 7 Ethics in Emergency Cardiovascular Care Kenneth V. Iserson While the idea of applying ethics to and during cardiopulmonary resuscitation (CPR) may seem daunting, the basic principle is quite easy to understand: the patient's value system is paramount . •

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Patient values should guide resuscitation decisions. In emergency care, adequate information about the patient and the prognosis is required if treatment is to be withheld. Advance directives and surrogate decision makers are used if the patient lacks decisionmaking capacity. A patient's decision-making capacity is a clinical determination made at the bedside. Family members may be allowed to observe resuscitation attempts. Trained personnel must be provided to notify and care for survivors.

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Three ethical issues surround emergency cardiovascular care: • • •

Who makes treatment decisions? On what basis are these decisions made? How should clinicians interact with families during and after cardiac resuscitations?

While the idea of applying ethics to cardiopulmonary resuscitation issues may seem daunting, the basic principle is quite easy to understand: the patient's value system is para­ mount. It determines his or her goals of therapy and willingness to assume treatment bur­ dens to achieve a certain outcome. The only exceptions are when the patient lacks the capacity to make a decision or when it is not possible to honor his or her treatment requests or when they are not consistent with the possible goals of medicine.

Patient and Societal Values The patient's values, which are sometimes expressed through surrogate decision makers or advance directives, incorporate many personal factors, such as religious and cultural beliefs, social relationships, learned behaviors, and self-image. Even though patients may not be able to verbalize the factors they consider in making their health care decisions, 567

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the decisions themselves express their values. In pluralistic societies, clinicians treat multiple individuals with many dif­ ferent value systems, so they must be sensitive to others' beliefs and traditions. People learn their values from the culture in which they live, through observation, and through secular (including professional) and religious education. One common source of personal values is organized religion, which helps to mold and maintain societal values. Although various religions may appear dissimilar, most teach the Golden Rule: "Do unto others as you would have them do unto you." This meshes with, and was probably the source of, commonly accepted secular principles, such as beneficence and nonmaleficence. Problems surface in trying to apply religion-based rules to specific bioethical situations. For example, although the eth­ ical proscription "Do not kill" is generally accepted, inter­ pretations vary on which activities constitute "killing: " active or passive euthanasia, terminal sedation, or other end-of-life palliative medical care. 1 Although each individual is entitled to have a personal system of values, certain values have become generally accepted by the medical community, courts, legislatures, and society at large (Table 3 7 - 1 ). Although some groups disagree about each of the generally accepted values, this dissension has not affected their application to medical care in many western countries. 2

Principle of Autonomy ( Self�Determination ) Patient autonomy, or self-determination, has long been the overarching professional and societal bioethical value (as well as the key value in health care law). Autonomy recog­ nizes an adult individual's right to accept or rej ect recom­ mendations for medical care, even to the extent of refusing all care, if that individual has appropriate decision-making capacity. 3 This is the counterweight to the medical profes­ sion's long-practiced paternalism (or parentalism), wherein

TA B LE 3 7 - 1

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medical care was based o n whatever the practitioner deter­ mined was "good" for the patient regardless of whether the patient agreed. Coercion to influence behavior or choice through the force of authority is often coupled with pater­ nalism. The j oining of the august figure in white with implied or explicit threats has been and still is a potent force for counteracting any potential patient autonomy. However, the thrust of modern bioethics is to respect patients by hon­ oring their autonomy. 2

Health Care Professionals' Values CPR and other resuscitation measures should be used only when they may benefit the patient. They should never be used when they merely prolong the dying process. In emergency situations, when information about patients, their wishes, and their medical conditions are unknown, clinicians must assume that resuscitation is warranted until clinical signs demonstrate thatfurther intervention will not be effective.

Health care workers, both in the prehospital arena and in health care facilities, have specific goals for their interven­ tions. Most entered the healing professions to help others, a principle termed beneficence; they dislike intervening when it will not benefit the patient. Some practitioners have a conflict with specific profes­ sional or societal values on a religious, philosophic, or prac­ tical basis.4 When such a conflict exists in a practitioner's mind, it is deemed morally and legally acceptable, within certain constraints, for the individual to follow a course of action based on a personal value system. When conflicts between the practitioner's and the patient's values exist, how­ ever, it is essential for the practitioner to recognize the patient's identity, dignity, and autonomy and to avoid the

Co m m o n ly A c c e p t e d S o c i e t a l a n d B i o e t h i c a l Va l u e s

D o i n g g o o d . A d u ty to c o n fe r b e n e f i t s . P r o d u c t i o n of b e n e f i t . I '

T h e p r e s u m p t i o n t h a t w h a t t h e p a t i e n t t e l l s t h e p hys i c i a n wi l l n o t b e reve a l e d to a ny o t h e r p e rs o n o r i n st i t u ti o n w i th o u t t h e p a t i e n t ' s p e r m i ss i o n .

D i s tr i b u tive j u sti c e

F a i r n e ss i n t h e a l l o c a t i o n o f r e s o u r c e s a n d o b l i g a t i o n s . T h i s va l u e i s t h e b a s i s o f a n d i s i n c o r p o r a t e d i n to s o c i e tywi d e h e a l t h c a r e p o l i c i e s .

Nonmaleficence

N o t d o i n g h a r m , p r eve n t i o n o f h a r m , a n d r e m ova l o f h a r m f u l c o n d i t i o n s .

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A d h e r i n g to o n e ' s o w n r e a s o n e d a n d d e f e n s i b l e s e t o f va l u e s a n d m o r a l sta n d a r d s . C o n t r o l l i n g t h e e x t e n t , ti m i n g , a n d c i r c u m s t a n c e s o f s h a r i n g o n e s e l f (p hys i c a l ly , b e h avi o r a l ly , o r i n t e l l e c tu a l ly) w i t h o t h e r s .

S o u r c e : A d o p t e d f r o m : I s e r s o n KY. B 1 o et h 1 c s . I n M o r x J A , H o c k b e r g e r R S , Wa l l s R M , et a l . e d s . Rosen 's Emergency Med1c1n e : Con c ep ts a n d Cl1mca/ Pract1 c e . 6 t h e d . P h i l a d e l p h 1 o : M osby. 2 0 0 6 3 1 27-3 1 3 9 , w1th p e r m 1 s s 1 o n

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error of blindly imposing one's own values on another. Even when the physician plans to follow a treatment course con­ sistent with accepted societal values, it is desirable to review the case's specific circumstances and the hierarchical impor­ tance of the values involved. In each case, the ethical analy­ sis must recognize all practicable courses of action and the benefits and detriments of each, while at the same time respecting the patient's values.5 For emergency cardiovascular care , the key to this analysis is to recognize that the goals are to preserve life, restore health, relieve suffering, limit disability, and reverse clinical death .6 CPR and other resuscitation measures should be used only when they may benefit the patient. They should never be used when they merely prolong the dying process. "B enefit" means attempting to meet the patient's goals of therapy. In emergency situations, when information about patients, their wishes, and their medical conditions are unknown, clinicians must assume that resus­ citation is warranted until clinical signs demonstrate that further intervention will not be effective. Patient self-determination may not apply when insuffi­ cient resources exist to provide the desired intervention. This often occurs in disasters and in less developed nations. In these situations, the ethical principle of comparative, or distributive, justice comes into play. Health care policy based on this principle requires that individuals and groups with similar problems should receive similar (generally an equi­ table, not necessarily an equal) distribution of available resources. Such a public health policy should be triggered by specific events; it should not be applied ad hoc by individual clinicians at the bedside. 2 •7 Clinicians often attempt to use legal justifications for their actions or inactions in end-of-life care, including car­ diac resuscitation. In general, physicians' legal knowledge is often incorrect, only partially true, or applied incorrectly.8 Patients and health care providers are best served if the patient's values and goals of therapy guide the physician's course of action.

·�····· ······························································································· S e e W e b s i t e f o r A CE P p o l i cy s t a te m e n t o n V' e t h i c a l i s s u e s f o r r e s u s c i t a t i o n .

Withholding and Withdrawing CPR

Prehospital Considerations Resuscitative efforts should not be withheld or withdrawn on the basis of DNAR (do not attempt resuscitation) tattoos or other nonstandard requests that do not involve discussions with patients or their legal surrogate decision makers.

Bystander CPR In the prehospital setting, what is known about patients in cardiopulmonary arrest can vary greatly depending upon the setting and the nature of bystanders' knowledge. Given the general paucity of facts and the wide range of skill levels among those who may be in a position to initiate CPR, the standard for withholding life-sustaining treatments in the prehospital setting is much higher and more specific than that for other settings. Based on the assumption that most people in cardiopulmonary arrest would want resuscitation, lay-rescuers and bystanders normally should initiate CPR. There are only three exceptions to this rule: (1) when a per­ son has obvious clinical signs of irreversible death (e.g., rigor mortis, dependent lividity, injuries incompatible with life, decomposition, or burned beyond recognition), (2) when performing CPR would place the rescuer at risk, and (3) when an available and interpretable advance directive speci­ fies that the individual does not desire resuscitation. 6 Advance directives may not apply in cases of a failed suicide attempt.9-1 1

INDICATIONS FOR WITHHOLDING PREHOSPITAL BASIC LIFE SUPPORT 1 . Clinical signs of irreversible death

2 . Risk of injury or death to rescuer 3. Available and interpretable advance directive

Resuscitative efforts should not be withheld or with­ drawn on the basis of DNAR (do not attempt resuscitation) tattoos or other nonstandard requests that do not involve discussions with patients or their legal surrogate decision makers. 1 2• 1 3 They should also not be withheld or withdrawn based on the patient's age, socioeconomic status, insurance coverage, cultural background, or relationship to the crimi­ nal justice system. Having begun, those performing CPR should continue until one of the following occurs: •

Differing levels of knowledge about patients, their medical conditions, and their desire for resuscitation require the use of separate approaches to withholding and withdrawing CPR in the prehospital, emergency department, and inpa­ tient settings. Inpatients may also have ongoing u·eatments withdrawn.

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Effective , spontaneous circulation and ventilation are restored. Care is transferred to a more senior-level emergency medical professional. Reliable criteria indicating irreversible death are present. The rescuer is unable to continue due to exhaustion or the presence of dangerous environmental hazards or because

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continuation of resuscitative efforts places other lives in jeopardy. A valid and interpretable DNAR order is presented to res­ cuers. 6•14

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Emergency Medical Services Emergency medical services (EMS) providers have a higher level of training and more experience than lay-people, resulting in a greater awareness of when to refrain from resuscitative efforts. EMS providers may also have the emo­ tional distance and clinical expertise to know when to stop CPR. The ability to provide advanced cardiac life support (ACLS) interventions, do electrocardiograms, and contact a base station for medical direction helps them make these decisions. However, neither lay-rescuers nor EMS person­ nel should make judgments about the present or future qual­ ity of life of a cardiac arrest victim on the basis of current or anticipated neurologic status. Such snap judgments are often inaccurate. Quality of life should never be used by EMS per­ sonnel as a criterion to withhold CPR, because conditions such as irreversible brain damage or brain death cannot reli­ ably be assessed or predicted. 1 5-20

while being transported to the hospital will survive to hos­ pital discharge, but EMS personnel in the United States continue to transport them, usually "Code 3 , " posing an unnecessary risk to themselves and others .6• 22 • 2 4• 2 8-3 0 This may be due to rules within the EMS system or to their dis­ comfort with having to stop efforts in a victim's home, which they may see as publicly acknowledging "failure. "3 1 In addi­ tion, both family and EMS personnel are often uncomfort­ able in leaving a body at the scene.

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issues.

To end these unnecessary, wasteful, and potentially dan­ gerous transports, it is vital that EMS systems establish pro­ tocols for death pronouncement in out-of-hospital settings in a manner consistent with state and national regulations. The AHA, American College of Emergency Physicians (ACEP), and National Association of EMS Physicians sup­ port this.3 1 Even where a death pronouncement protocol exists, there may be significant variability among base hos­ pitals in the rate with which they pronounce deaths using online medical controP0 Additionally, even with protocols in place, paramedics may be reluctant to terminate resusci­ tation efforts in children in the prehospital setting.3 2

EMS Termination of Resuscitation Efforts

The most poweiful discriminatory criterion on the appropriateness of CPR is knowledge of the time of onset of CPR (i. e., witnessed cardiac arrest).

· .. �··································································································· S e e W e b s i t e f o r A C E P p o l i cy s t a t e m e n t o n

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When, then, should EMS personnel cease resuscitative efforts? Although there are no scientifically valid clinical cri­ teria that accurately predict the futility of CPR, the most powerful discriminatory criterion on whether CPR is appro­ priate are whether the cardiac arrest was witnessed and whether the rescuer knows the time of onset of the arrest. 2 1-2 5 Most commonly, patients with an unwitnessed cardiac arrest are persons who died and were later discovered. 2 6 Another useful criterion to cease CPR is the absence of a "shockable" rhythm on the defibrillator after an adequate trial of CPR, even if ACLS providers are not available. 6 The American Heart Association (AHA) has affirmed that "emergency transportation of patients requiring con­ tinuing CPR after ACLS-level care in the field is rarely indi­ cated or successful. Any such transportation for reasons other than to benefit the patient is unethical . " 2 6 Unless patients are suffering from rare, specific pathologic condi­ tions (e.g., hypothermia or drug overdose), there are no in­ hospital interventions that will successfully resuscitate those who fail out-of-hospital efforts. 2 7 Studies have consistently shown that < 1 % of patients who continue to receive CPR

Emergency Department In emergency medicine, a significant difference rightfully persists between the withholding and the withdrawal of life­ sustaining medical treatment. The justification for this stems in part from the nature of emergency medical practice and the unique manner in which clinicians apply many ethical principles. Because emergency physicians often lack vital information about their patients' identities, medical condi­ tions, and goals for medical treatment, withholding emer­ gency medical treatment is more problematic than is later withdrawing unwanted or useless interventions. Owing to the nature of emergency medicine, both in the prehospital and the emergency department settings, higher standards are required to withhold than to withdraw medical treatment.33 Physicians should begin or continue resuscitation of those patients who arrive at the emergency department without sufficient evidence to determine that the resuscita-

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tion effort will b e unsuccessful. The only reason to withhold CPR is when the physician has clear evidence (e.g., a stan­ dard advance directive) indicating that the patient did not wish this done. Without this information, the presumption must be to intervene. The only reason to withhold CPR is clear evidence (e.g., a standard advance directive) indicating that the patient did not wish resuscitation to be initiated.

Once the emergency physician obtains information confirming a patient's wish not to be resuscitated or about a medical condition not amenable to resuscitation, resuscita­ tive efforts and other medical treatment may appropriately be withdrawn. This information may be obtained from an advance directive, patient surrogate, recent documentation in the medical chart, or medics detailing the failed results of the ongoing resuscitative effort. With rare exceptions, such as after failed suicide attempts, resuscitative efforts should be withdrawn when information is provided either that the patients did not want such efforts or that their medical con­ dition precludes success. 1 1• 1 4 Many factors influence the potential success of resusci­ tative efforts, including time to CPR; time to defibrillation, IV line, and first epinephrine dose; time to insertion of first advanced airway device; comorbid disease; prearrest state; and initial arrest rhythm. No combination of these factors, though, clearly predicts the outcome. 2 6•34 The most impor­ tant factor associated with poor outcome is the duration of unsuccessful resuscitative efforts. The possibility of a successful resuscitation becomes clearer as time progresses: a patient's chance of b eing dis­ charged from the hospital alive and neurologically intact diminishes if spontaneous circulation does not return after 1 0 minutes of intensive resuscitative efforts . 2 0 •3 5-3 7 Malpractice concerns have led some physicians to prolong all resuscitation attempts until they reach the point at which there have been no survivors. 2 6 In reality, cardiac resuscita­ tion with properly executed ACLS interventions and docu­ mented asystole should not last > 30 minutes and should usually end much sooner except in unusual circumstances, as with prearrest hypothermia, after some drug-induced events, following lightning or electrical shocks, or in infants or children with refractory ventricular fibrillation (VF) or ventricular tachycardia (VT) . 2 6•3 7-4° Indeed, without these mitigating factors , prolonged resuscitative efforts are unlikely to be successfulY Cardiac resuscitation with properly executed A CLS interventions and documented asystole should not last > 30 minutes and should usually end much sooner except in unusual circumstances, as with prearrest hypothermia, after some drug-induced events, following lightning or electrical shocks, or in infants or children with refractory VF or VT.

Three special situations should be noted. ( 1 ) Cardiac arrest from blunt trauma is nearly uniformly fatal, so there is

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little benefit from doing chest compressions for any extended length of time after the airway is secured.42 (2) When health care resources are limited, as during disasters, avail­ able resources (i. e . , time, personnel, and equipment) should be devoted to those patients with the greatest chance of benefiting. This may lead to withholding or more rapid discontinuation of resuscitative efforts than is standard in normal practice. (3) It is unethical to prolong resuscitative efforts to practice or teach procedures or to complete research protocols . 1 4

In the Hospital In health care institutions, staff generally know or have medical records showing their patients' medical condition, prognosis, wishes regarding resuscitation, and goals for medical treatment. Resuscitation attempts should be con­ sistent with these goals and medical conditions . As the AHA notes, "It is inappropriate to start CPR when survival is not expected or the patient is expected to survive with­ out the capacity for meaningful human communication . " 2 6 Therefore, CPR should not be instituted when the patient's vital functions have already deteriorated despite maximal therapy (e .g., as in progressive septic or cardia­ genic shock). CPR should not be instituted when the patient's vitalfunctions have already deteriorated despite maximal therapy (e.g., as in progressive septic or cardiogenic shock).

In neonates, withholding resuscitation attempts in the delivery room is appropriate when gestation, birth weight, or congenital anomalies are associated with almost certain early death and when unacceptably high morbidity is likely among the rare survivors.6 This includes not initiating or discontinuing resuscitation in the delivery room of preterm newborns of < 2 4 weeks' gestation or weighing < 5 00 g, infants whose Apgar score remains zero at 10 minutes,43 and newborns with confirmed or overt lethal malformations and/or chromosomal abnormalities.44

In the Hospital: Withdrawal of Ongoing Life Support The decision to withdraw life support may be made minutes or even decades after the initial resuscitation. Usually it is the result of obtaining additional information from the patient, the discovery of advance directives, or a decision by the surrogate. Often the patient or surrogate requests that interventions be stopped because he or she believes that the "successful" resuscitation has not met the goal of an accept­ able result or that the burden to the patient of continued treatment would exceed any benefits. Other reasons to with­ draw support include the clinicians' determination that the interventions cannot ultimately be successful or that the patient is dead by brain criteria, in which case it is no longer technically "life support."

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Goals of Therapy While withdrawing life-support treat­ ment may be an emotionally difficult decision for family and staff, it is ethically permissible under the circumstances described above. The goal is to avoid prolonging the dying process without degrading the quality of the patient's remaining life . This practice has widespread ethical and legal support.45 Nevertheless, decisions about the with­ drawal of artificially provided nutrition and hydration and, less commonly, about other modalities continue to be suf­ fused with religiocultural polemics. If disagreement exists about the course of action, the institution's bioethics com­ mittee or consultant should be called in and, when necessary, asked to mediate between physicians, family, and staf£.46 In some circumstances, chaplains can effectively intervene, especially when families refuse t o allow discontinuation o f machines in "brain dead" patients because "a miracle" may occur. In determining how to limit or withdraw treatments, clinicians and surrogates should carefully consider the patient's goals for therapy. For example, if a goal is to main­ tain the patient until loved ones arrive, it may be appropri­ ate to continue mechanical ventilation. In general, interven­ tions that do not contribute to achieving the patient's goals should be discontinued. Throughout this process, care must continue; comfort measures, including needed analgesics, must never be withdrawn. Since the initial recommendations for discontinuing ventilator support were published in 1 9 8 3 , withdrawal of ventilators, dialysis, vasopressors, and other life-sustaining treatments has become more common.47-49 The frequency with which treatments are withdrawn from intensive care unit (ICU) patients before death varies among institutions, with some never withdrawing treatments and others doing so in nearly all eligible patients. 5 1 It is unclear whether these differences reflect physician or institutional values regarding respecting patient preferences. 5 2

Critically ill patients often have multiple types of life-sustaining treat­ ments. Withdrawing or foregoing these treatments may be done sequentially or simultaneously. The normal sequence in critical care units is to first withdraw dialysis, then to forego further diagnostic workups and discontinue vasa­ pressors. Next, clinicians generally stop intravenous fluids, hemodynamic and electrocardiographic monitoring, and antibiotic treatment. The last interventions to be with­ drawn usually are artificial nutrition and mechanical venti­ lation. 5 2 The rationale for this "stepwise retreat" may not reflect optimal patient care. Rather, the order of withdrawal may relate to the intervention's symbolic importance, such as artificial feeding, or to how immediately its withdrawal will lead to death, as with a ventilator. Physicians appear reluc­ tant to withdraw interventions that treat iatrogenic prob­ lems and are more comfortable withdrawing therapies related to their own subspecialty.53 •54 Surrogates are often more willing to eschew new interventions, such as antibi­ otics or dialysis, because the link between these decisions and death is not as obvious. 5 1

Methods of Withdrawing Tre atments

After a decision to withdraw treatment is made, staff should continue to maintain the patient's comfort and dig­ nity. Varying symptoms accompany the withdrawal of each life-support intervention. Appropriate therapies should be provided to minimize suffering associated with pain, dysp­ nea, delirium, convulsions, and other terminal complica­ tions. To accomplish this, it is ethically acceptable to gradu­ ally increase the dosage of narcotics and sedatives to relieve pain and other symptoms, even to levels that might con­ comitantly shorten the patient's life. 7 For example, methods of withdrawing mechanical ven­ tilation vary considerably among physicians and specialties. With any method, the goal is to keep the patient comfort­ able using appropriate medications, usually titrated opioids and benzodiazepines. Neuromuscular blocking agents should not be used and, if already in use, should be reversed. To achieve comfort, opioid-tolerant patients may need doses one order of magnitude higher than normal (e .g., 5 0 0- 1 ,000 mg/hr) . D o cumentation in the patient chart must specify that this medication is being used for com­ fort. 5 1 If a patient has an implanted pacemaker or defibrillator ICD, this should normally be inactivated; although the residual rhythm that will persist is unpredictable, this may prevent automatic and uncomfortable defibrillations from the device at the end of life. 55 Most modern devices can be made ineffective by noninvasive reprogramming. 56 Before removing or inactivating such a device, the clinician should inform the patient or surrogate that such action could result in sudden death. 57 Occasionally, in the process of withdrawing life support, clinicians may need to use terminal sedation (i. e. , high doses of sedatives to relieve extremes of physical distress). This is a last-resort clinical response to extreme, unrelieved physi­ cal suffering. The purpose of the medications is to relieve suffering, not to intentionally end the patient's life. While it is an extraordinary measure, withholding such treatment in certain circumstances has been deemed "inhumane . " 58 Terminal sedation is commonly used in critical care units to treat symptoms of suffocation when mechanical ventilation is withdrawn in dying patients. 59•60

D ecision ..Making Capacity, Advance Directives, and Surrogate Decision Makers Advance directives-such as living wills, durable powers of attorney for health care, and prehospital advance directives­ are used to guide a patient's health care decisions only when they are unable to do so themselves (i. e . , when they lack decision-making capacity). When a patient lacking decision­ making capacity does not have an advance directive, a sur­ rogate list may be used. The first step for clinicians, how­ ever, is to determine a patient's decision-making capacity at the bedside.

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Decision.-Making Capacity In much of western culture, patient autonomy, also called self­ determination, is a bedrock principle of modern biomedical ethics as well as law. Justice Benjamin Cardozo codified the principle in 1 9 1 4 when he wrote that "Every human being of adult years and sound mind has a right to determine what shall be done with his own body. . . . "3 This means that adult patients with decision-making capacity may autonomously make their own health care decisions, including choosing ? etween treatment options, refusing treatment, and designat­ mg someone else to make their health care decisions even if �ey are able to do so themselves. Exercising one's autonomy . IS the way to Implement one's own values. In clinical practice, the word "competence" is often used to mean capacity. "Competence" is a legal term and can be determined only by the court. The capacity to make one's own health care decisions may vary with the complexity of the decision, such as deciding between invasive or pharmacologic treatment of an arrhythmia or the seriousness of a decision's outcome as with a heart transplant. D ecision-making capacity ca � also vary over time . Elderly patients who "sundown" and patients p artially incapacitated by drugs or physiologic events such as post-cardiac arrest or transient ischemic attack may not immediately b e able to make their own health care d e cisions, although they may regain this capacity. Clinicians must often decide whether patients cur­ rently have the capacity to make specific health care deci­ sions . It is the treating physician's responsibility to deter­ mine the patient's decision-making capacity. The process of making this determination should be standardized and the results documented in the patient's medical record. Simply refusing a physician's recommendation for a commonly accepted treatment option such as thrombolytics or coro­ nary angiography during an acute myocardial infarction does not, in itself, indicate that the person lacks decision­ making capacity. To h ave adequate decision-making capacity in any par­ . . ticular circumstance, an individual must understand the options, the consequences of acting on the various options, and the costs and benefits of these consequences, by relating them to a relatively stable framework of personal values and priorities.6 1 One simple method, outlined below, for deter­ mining decision-making capacity at the bedside is to assess the patient's responses to three questions.62 If any of them cannot adequately be answered, the capacity to make that decision is lacking.

Determining Decision�Making Capacity at the Bedside After providing a patient with sufficient information to make an informed choice, information about the given condition and prognosis, the nature of the proposed intervention, alternatives, and risks and benefits, the patient is asked: 1. What options did the clinician present? (e.g., to be hos­ pitalized or not.)

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2. What are the risks and benefits to you for each option? 3 . Why did you select the option you did? To have decision-making capacity, the patient must pro­ vide coherent, appropriate answers to all three questions. Assessing the last response requires weighing the patient's answer against what is known about his or her value system. The choice should be accepted if it seems to con­ form to the patient's values, even if it is not the choice most people would select (e.g., "I don't want any more medical treatment" or "I'm not sick enough to go into the hospital"). However, the answer may be bizarre and not consistent with reality (e.g., "They'll poison me like they do everyone else" or "The voices are telling me not to do it"). Such answers indicate a lack of decision-making capacity. Often, those accompanying the patient may be able to help determine how close the answer is to the patient's normal value sys­ tem. 2 .6 1 It may be especially difficult to evaluate decision-making capacity for patients in the prehospital system via telephone or radio. In these cases, medics can ask the questions and transmit the answers, or the patient can be put on the tele­ phone or radio while the physician asks the questions. Unconscious patients, such as those in cardiopulmonary arrest, clearly lack decision-making capacity. Unless contra­ dictory information is immediately available, such as a stan­ dard prehospital advance directive, consent for resuscitation procedures is presumed. 2 Patients who retain decision-making capacity may still prefer to have a health care decision made by someone else. Many cultures, including some within western countries, rely on traditional decision-making models other than patient autonomy; usually this is family- or community­ based decision making.63 In those cases, the surrogates must be identified and given the same information the patient would need to make a decision. When a patient lacks decision-making capacity, an advance directive or surrogate decision maker must be used. A significant number of patients in the hospital and in the acute setting have neither a directive nor an identifiable sur­ rogate. In those cases, the clinician acts as surrogate.64

Advance Directives The term "advance directives" includes several types of legal and quasi-legal documents. Advance directives indicate what medical interventions should be done for a patient in extremis who is no longer able to give or withhold permis­ sion for treatment. These forms, signed by the patient or surrogate , are usually written to avoid prolonging an mevitable, often painful or nonsentient dying process. Advance directives are usually variations of a living will, durable power of attorney for health care, or prehospital advance directive. Forms are specific to individual states; forms from other states have legal weight only if state statutes specifically permit it (e.g., Arizona). However, even if they carry no legal weight, these documents can provide caregivers and surrogates with valuable information about

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the person's wishes. State-specific statutes and forms can be obtained from the American Hospital Association, American Medical Association, American Bar Association, and American Association of Retired Persons or their state affil­ iates, and state governments. Most can be downloaded at no cost from the Internet. Unfortunately, < 5 0 % of all patients needing others to make their health care decisions have advance directives.65-7 2 People from some cultures may be less willing to discuss resuscitation status or to forego life-sustaining treatment and so may be less likely to complete advance directives.73•74 Whites and individuals who are better educated are more likely to have advance directives .75·76 The federal Patient Self-Determination Act of 1 9 9 1 was designed to increase the use of advance directives.77 It requires health care institu­ tions and managed care organizations to ask newly admitted patients if they have advance directives and to facilitate the completion of these forms if they do not. Copies of any directives must be put in a patient chart if the patient desires it. However, there is little evidence that the act has increased the use of advance directives. In general, ignoring advance directives has no clear legal repercussions. Advance directives are patient- or surrogate-initiated. These differ from physicians' orders regarding end-of-life treatment, which are discussed below.

Living Will The living will is a relatively standardized form adopted in most states and the District of Columbia. Michigan and Massachusetts do not have statutes. This document usually requests that health care workers not perform resuscitative measures, but on occasion it requests the opposite-that all measures be taken to keep the patient alive . It goes into effect only if the individual lacks decision-making capacity; until that point, the patient continues to determine the med­ ical course, despite anything said in the living will. Living wills normally require both that a physician certify an indi­ vidual as terminally ill and that the patient has the mental capacity to understand its provisions at the time it is signed. Arizona, in a break with tradition, does not use "terminally ill," since all extant definitions are unclear. No ill effects have resulted.78 States allow varying levels of specificity in the document, including, in some cases, the ability to refuse arti­ ficial nutrition and hydration. Most living wills specify that the patient's physician must have seen and accepted the document's provisions in advance. This requirement establishes a physician who will act on the patient's behalf. For physicians, it protects those whose value systems will not allow them to abide by the doc­ uments' provisions. It also encourages families and physi­ cians to discuss the circumstances surrounding the time of death and the actions they can take. 2 The limitation of living wills is that they list specific actions-either to take or to eschew-in a limited set of cir­ cumstances. This reduces their usefulness and has led to a more flexible and powerful advance directive that names a trusted surrogate decision maker: the durable power of attorney for health care.

Durable Power of Attorney for Health Care (DPAH) A more commonly used advance directive that specifies a surrogate decision maker is the durable power of attorney for health care. It goes by many names, including "durable power of attorney with medical provisions" and "medical directive . " All states and the District of Columbia have statutes authorizing such directives. In its usual form, a durable power of attorney other than for health care takes effect immediately. However, a DPAH takes effect only when the individual no longer has the capacity to make his or her own medical decisions. Typically, a relative or close friend is named as a surro­ gate, since he or she should know something about the indi­ vidual's values related to medical treatment. More than one surrogate may be named; they are generally listed in prefer­ ential order, with the first one who is able to be contacted and is willing and able to act as surrogate making the deci­ sions. 2 The DPAH allows more flexibility than the living will because the surrogate is able to make any health care deci­ sions that the patient would ordinarily make, including gath­ ering new information and choosing among multiple treat­ ment options as the medical situation changes. Optimally, the surrogate's decisions are guided by other written or oral directions the patient has left, including those in a living will. In reality, surrogates often consider many factors when mak­ ing decisions. 79

Prehospital Directives Ambulances are often inappropriately called for patients in cardiopulmonary arrest who had previously expressed the desire not to be resuscitated. Many of these patients are chronically ill or have a terminal illness . 80-82 To avoid unwanted resuscitative efforts, prehospital directives were developed-first as local EMS protocols and then through legislation.83 As of 2 0 0 3 , 43 U. S . jurisdictions had enacted methods whereby patients outside of health care facilities could avoid unwanted resuscitation attempts . These usually take the form of either a prehospital DNAR order or a prehospital advance directive. 83 Often confused, the two forms differ greatly in their philosophies. The prehospital DNAR order is a physician-originated document. 84 The prehospital advance directive is generated by a patient or legal surrogate, with little or no involvement by health care personnel. Both instruct EMS personnel who have been inappropriately called at the time of deatl1 not to attempt to resuscitate the patient or to stop resuscitation efforts if they have already begun when such a form is found. Both types of form have proved effective. 83-86 The most common reason for having physician-initiated forms is the fear that murders and sui­ cides could be aided by patient-initiated documents. In prac­ tice, this has not occurred. In EMS systems, prehospital DNAR policies provide direction and guidance for these sit­ uations. ACEP has provided general guidelines addressing the integration of public, EMS , and physician directives on a community-wide basis.

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how their "directive" might be interpreted or whether it was still what was desired. In general, emergency physicians should not rely on these indicators to make critical deci­ sionsY·1 3

Surrogate Decision Makers Of the existing protocols, 3 4 were specifically authorized by statute, usually supplemented by regulation or guidelines. Eight states implemented protocols solely through regula­ tions or guidelines, without a change in their legal code. Eight states have no statewide protocol in place. In an affront to patient autonomy, 3 9 are physician orders requiring a physician's signature; 7 states require only a physician's sig­ nature; and 3 3 states require signatures of both a physician and the patient. 84 Three protocols are patient-initiated advance directives that are valid with a witnessed patient sig­ nature, with no physician involvement required. 87 These instruments are of varying complexity; some include liability protection for EMS personnel and base-station providers and some may be usable for pediatric patients.18·83 Table 3 7-2 contains a list of the elements ideally included in a prehospi­ tal advance directive/DNAR policy. There is evidence that out-of-hospital health care providers can interpret and are willing to implement DNAR orders and other documents limiting treatment. Studies indicate that while emergency medical technicians (EMTs) and paramedics are willing to honor patient preferences, they need written, uniform directives or physician orders to do so. 1 7 , 88-90 Prehospital DNAR orders or directives must be under­ standable to all involved (e.g., EMS persmmel, physicians, patients, family members, and police, who may also respond to 9 1 1 calls). These documents can take many forms (e.g., uniform system or state forms, physician orders, standard wal­ let identification cards or identification bracelets, and other mechanisms approved by the local EMS system). As noted below (Table 3 7 -2), the ideal prehospital directive should con­ tinue to be effective, at least in the emergency department, if the patient is transferred to a health care institution.83

Nonstandard Advance Directives Clinicians occasionally encounter medallions, tattoos, or other information that purport to be advance directives. These may cause consternation, since they fall outside soci­ ety's bounds for indicating life-determining decisions. What should clinicians do if these indicators are found during resuscitations? To be useful, advance directives must be available to the treating clinicians when they are needed, be a product of the patient's or sometimes the surrogate's deliberations, b e understandable, and be applicable i n the patient's current medical situation. Nonstandard directives are usually abbre­ viated or abstract, such as a tattooed symbol for "do not defibrillate; " thus they fail to meet these requirements. One problem is that the nature of such indicators may make it unclear whether the patient or surrogate either understood

When patients do not have the capacity to make medical decisions for themselves and lack advance directives con­ taining specific instructions or naming a surrogate, someone must make the decision for them. This works far better in the United States than it does in Europe, where physicians are reluctant to accept surrogate decision makers.9 1 Surrogates ideally make decisions based on two distinct standards : substituted judgment and best interests . Substituted judgment is used by surrogates who believe they know enough about the patient's values to make a decision similar to that which the patient would make. It is not clear that anyone can know that much about a person.92 Surrogates use the best interest standard when they do not know what the patient would want done in a particular sit­ uation but, as in the case of Karen Ann Quinlan, the patient once had the capacity to make such decisions.93 In that case, a 2 2 -year-old woman, after two apneic episodes a year previ­ ously, lay in a persistent vegetative state. Her parents requested that life support be removed. The court allowed her parents to use the patient's prior statements and behavior to attempt to extrapolate her values, making a decision as close as possible to what the she would have wanted. Some states may require explicit written directives for surrogates to fol­ low.94·95 The best-interest standard also applies, as in the Saikewicz case, when the patient has never had adequate deci­ sion-making capacity.96 In that case, a 67-year-old profom1dly retarded man with an IQ of 1 0 was diagnosed with leukemia. Painful and disabling chemotherapy offered only a 3 0 % to 50% probability of producing a short remission. The court ruled that most people would not want such treatment and that decision could be made not to institute treatment. Refusal of such treatment, they said, should not be denied simply because the patient lacked decision-making capacity. Although ethicists and clinicians expect surrogates to use substituted judgment or patients' best interests when making decisions, studies show that many surrogates rely on other factors, such as their own best interests or mutual interests of themselves and the patient. 79 In many cases, sur­ rogates opt for far more medical treatment than the patient would have wanted, perhaps owing to a lack of understand­ ing about end-of-life issues and options.97-99 There are five major classes of decision makers : family, statutory surrogates, bioethics committees, physicians, and the courts. 2 Family Traditionally and usually in practice, a family member-especially a spouse-acts as the surrogate decision maker for a patient who lacks the capacity to make his or her own medical decisions. It should be understood, however, that even when there is a strong family tie, emotional or fis­ cal costs may sway the surrogate decision maker from cer­ tain courses of action the patient would wish taken.

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TA B LE 3 7 - 2

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G u i d e l i n e s f o r D eve l o p i n g a P o l i cy f o r O u t - o f- H o s p i t a l A dva n c e D i r e ctives

To e n s u r e m a x i m u m c o h e r e n c e and c o m p l i a n c e , a c o m p r e h e n s ive o u t - o f- h o s p i t a l D N A R p o l i cy s h o u l d b e e n d o rs e d by the w i d e s t p o ss i b l e j u r i s d i c ti o n ( i . e . , l o c a l , r e g i o n a l , s t a t e , a n d t h e m e d i c a l c o m m u n i ty , i n c l u d i n g t h e E M S g ove r n i n g b o dy) . Wh e n ever f e a s i b l e , l e g i s l a tive s u p p o r t f o r such a p o l i cy s h o u l d b e s o u g h t . T h e o u t- o f - h o s p i t a l D N A R p o l i cy s h o u l d : 1 . N o t e t h e e s ta b l i s h e d f a c t t h a t c u r r e n t b a s i c a n d a dva n c e d l i fe s u p p o r t i n t e rve n t i o n s m ay n o t b e a p p r o p r i a t e o r b e n e f i c i a l i n c e r t a i n c l i n i c a l setti n g s . •

D eve l o p a m e a n s to e d u c a t e t h e p u b l i c a b o u t t h e a p p r o p r i a t e u s e o f 9 1 1 a f t e r e x p e c t e d d e a th s .

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E s ta b l i s h t h e f a c t t h a t c o m fo r t c a r e a n d p a l l i a tive c a r e a r e a f fi r m a tive a c t i o n s f o r p a t i e n ts w i t h D N A R o r d e r s . T h e s e a p p r o p r i a te i n t e rve n t i o n s (e . g . , h o s p i c e o r r e s p i t e c a r e) d o n o t r e q u i r e E M S a c tiva t i o n a n d c a n o ft e n b e a r r a n g e d b y c a l l ­ i n g t h e p a t i e n t ' s p hysi c i a n i n a n ti c i p a t i o n o f d e a t h .

•

D eve l o p a m e a n s to e d u c a t e h e a l t h c a r e w o r k e r s o n t o p i c s o f a dva n c e d i r e c tive s , i n c l u d i n g i n fo r m a t i o n o n l o c a l o u t - o fh o s p i t a l D N A R s , c o m m u n i ty h o s p i c e a l t e r n a tive s , a n d b e r e ave m e n t s e rvi c e s .

2 . E s ta b l i s h c o n s e n s u s o n t h e i d e a l i d e n t i fi c a t i o n d evi c e f o r D N A R d i r e ctives to a s s u r e c o n ti n u i ty o f c a r e a c r o s s s e tti n g s . 3 . R e i t e r a t e t h a t i n i t i a l r e s u s c i t a tive a t te m p ts a r e u s u a l ly i n d i c a t e d wh e n t h e p a t i e n t ' s wi s h e s a r e n o t k n own . 4 . D e f i n e t h e c o n d i t i o n s u n d e r wh i c h a n o u t- o f - h o s p i t a l D N A R o r d e r c a n b e c o n s i d e r e d , i n c l u d i n g its u s e i n l o n g - te r m - c a r e s e t ­ ti n g s a n d i n t h e e m e r g e n cy d e p a r t m e n t .

5 . D e fi n e wh i c h p a t i e n ts h ave t h e d e c i s i o n a l c a p a c i ty to a g r e e to a D N A R o r d e r a n d wh e t h e r s u r r o g a t e s c a n s i g n s u c h o r d e r s . 6 . E s ta b l i s h a m e c h a n i s m f o r d e t e r m i n i n g t h e p r e c e d e n c e o f va r i o u s d i r e ctives [ e . g . , l ivi n g wi l l , d u r a b l e p ow e r o f a t to r n ey f o r h e a l t h c a r e , p r e h o s p i t a l a d va n c e d i r e ctive (D N A R) ] . 7 . D eve l o p a s t a t u t o ry p r i o r i t i z e d l i s t o f s u r r o g a t e s t o u s e wh e n t h e r e a r e n o a dva n c e d i r e ctives a n d t h e p a t i e n t ' s d e c i s i o n a l c a p a c i ty i s i m p a i r e d . 8 . Co n s i d e r l a n g u a g e a c k n owl e d g i n g t h e g r owi n g h o m e h o s p i c e m ove m e n t a s i t c o n c e r n s c h i l d r e n a n d i n c o r p o r a te p r ovi s i o n s f o r document use in m i nors. 9 . E s ta b l i s h t h a t t h e d e c i s i o n n o t to a t te m p t r e s u s c i ta t i o n m u s t b e a n i n fo r m e d d e c i s i o n m a d e b y t h e p a t i e n t o r s u r r o g a t e . 1 0 . I d e n t i fy t h e i n fo r m a t i o n t h a t s h o u l d b e c o n ta i n e d i n t h e D N A R o r d e r a n d t h e a u th o r i ty t h a t wi l l b e r e s p o n s i b l e f o r d eve l o p i n g such a mechanism. 1 1 . I d e n t i fy t h e c l i n i c a l p r o c e d u r e s t h a t a r e to b e p r ovi d e d a n d t h o s e with h e l d i n t h e a d h e r e n c e with t h e D N A R o r d e r , o r s p e c i fy

wh i c h a u th o r i ty wi l l ve r i fy a d h e r e n c e . 1 2 . D e fi n e t h e e x a ct m a n n e r i n wh i c h t h e D N A R o r d e r i s to b e fo l l owe d , i n c l u d i n g t h e r o l e o f o n l i n e m e d i c a l d i r e c ti o n . E a c h sys t e m s h o u l d e n s u r e t h a t a c o m m u n i c a t i o n p a th to a c c e s s o n l i n e m e d i c a l d i r e c t i o n is i m m e d i a t e l y ava i l a b l e wh e n n e c e s s a ry. 1 3 . E s ta b l i s h l e g a l i m m u n i ty p r ovi s i o n s for t h o s e who i m p l e m e n t D N A R o r d e rs in g o o d fa i t h .

1 4 . E s ta b l i s h d a ta c o l l e c ti o n a n d p r o t o c o l eva l u a t i o n to p e rf o r m p e r i o d i c o p e r a ti o n a l a s s e ss m e n t s . 1 5 . I d e n t i fy p e r m i ss i b l e e x c e p ti o n s to c o m p l i a n c e with D N A R o u t - o f - h o s p i ta l d i r e ctives. F o r e x a m p l e : •

T h e p a t i e n t i s a b l e to revo k e a wri tte n d i r e c tive a t a ny ti m e .

•

T h e E M S p e r s o n n e l c a n c a n c e l t h e o u t - o f- h o s p i t a l D N A R o r d e r i f th e r e a r e d o u bts a b o u t t h e d o c u m e n t ' s va l i d i ty.

S o u r c e : F r o m S c h e o rs RM, Morco C A , Jserson KV. " D o - n o t - atte m p t - r e s u s c r t a t i O n " ( D N A R) p o l i cy r n t h e o u t - o f - h o s p r t a l s e tt r n g . Ann Emerg Med 2 0 0 4 ; 4 4 ( 1) : 6 8-7 0 , wrth p e r m r ssr o n .

Children represent a special situation. Individuals younger than the age of majority or who are unemancipated are usually deemed incapable of making their own medical decisions. Nevertheless, in most cases the same rules that apply to adult capacity apply to children. As the seriousness of the consequences increases, the child must have more understanding of the options , consequences, and values involved in order to make a decision. Even if a parent is pres-

ent, it is not always clear that the adult is acting in the best interest of the child. In such cases, child protective services may become involved. Disagreements between parents are also possible. In some cases, this results in the involvement of bioethics committees or the courts. 100 Statutory Surrogate Lists If an adult patient lacks deci­ sion-making capacity and has no advance directive, many

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states allow individuals to automatically become the per­ son's surrogate. In practice, this almost always means that the patient's spouse may act in that capacity. Some states have a statutory surrogate list, which simplifies the process. The most extensive list specifies, in order, spouse not divorced or legally separated, a majority of adult children who can be reasonably contacted, parents of an adult, domestic partner, sibling, close friend, and the attending physician in consultation with a bioethics committee.78 For children, the parents are nearly always their health care decision makers . Multidisciplinary bioethics committees now exist in most large hospitals to help solve bioethical dilemmas. These cases often involve surrogate decision making or patients who lack both advance directives and an identifiable surrogate. Bioethics committees also recon­ firm prognoses and mediate between dissenting parties. Some smaller hospitals have bioethics consultants, rather than com­ mittees, to perform many of the same functions. These com­ mittees, composed of medical and nonmedical members, pre­ sumably help make decisions based on the best-interest standard.

Bioethics Committees and Consultants

In the past, physicians often made unilateral decisions for their patients , whether or not the patients had the capacity to decide for themselves. This still occurs of course-especially in stressful situations, such as with acute and unexpected illnesses and injuries or in the rela­ tively large p atient p opulation lacking b oth decision­ making capacity and surrogates . 1 01 It may fall to the clini­ cian both to determine decision-making capacity and, if it is absent, to make a medical treatment decision for the patient. These decisions are often made without judicial or institutional review.64 Although physicians often try to discern their patients ' best interests, patients' preferences are hard to predict. Assumptions based on quality of life, age, or functional status may b e inaccurate, and physi­ cians' choices may reflect their own preferences more than those of their patients . 1 02 In identical situations, dif­ ferent physicians may choose wid ely varying levels o f care. 1 03 Rarely considered is that physicians should con­ sider their conflicts of interest when making these deci­ sions . 1 04 When making unilateral decisions, physicians should recognize that they are not omniscient. Prognoses are often incorrect and medical knowledge is finite. In these situa­ tions, "buying time" with a bioethics consultation may be worthwhile. Physicians

The courts often act as the final adjudicators of disagreements over medical care. They appoint legal guardians and, in a select few cases, set precedent that is fol­ lowed as health law. The courts, though, are usually neither expeditious nor necessarily cognizant of bioethical princi­ ples. They can only follow the societal values that are codi­ fied in the law. Many courts have suggested that, whenever possible, health care decisions should remain at the bedside rather than in legal chambers.93-95 Courts

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D o ..Not..Attempt Resuscitation (DNAR), Limitation .. of.. Treatment, and Do ..Not..Hospitalize (DNH) Orders Often lumped with advance directives, these documents are physician orders that dictate what is to be done for patients in the case of a cardiopulmonary arrest or other deteriora­ tion in the patient's condition. Physicians must write specific orders so that staff will not perform unwanted or nonbene­ ficial CPR and other resuscitation activities or to avoid inap­ propriately sending patients to the hospital from nursing homes . These orders can take several forms, including DNAR, DNH, Prehospital DNAR (PHDNAR), and limita­ tion-of-treatment orders. The orders are normally written in hospitals, nursing homes, and hospices and for home-hos­ pice patients.

Do .. Not.-Attempt.-Resuscitation (DNAR) Orders Unlike other medical interventions, CPR is expected to be initiated without a physician's order, based on presumed consent for emergency treatment. Therefore, a physician's order is necessary to withhold CPR. A DNAR order, some­ times called do-not-initiate-resuscitation (DNIR) or, less realistically, a do-not-resuscitate (DNR) order, is a physi­ cian's order in the hospital chart informing other medical personnel that they should not institute CPR in the event of cardiopulmonary arrest and explaining the rationale for the order. Ideally, this order is put on charts only after con­ sultation with the patient poss essing decision-making capacity and the family and is usually written for chroni­ cally ill patients with a poor prognosis for long-term sur­ vival. These orders usually work well within a specific institu­ tion. But if patients are transferred, as from a nursing facil­ ity or home to a hospital, the act of transfer or the activation of the EMS system negates the order. This can be directly contrary to a patient's wishes for terminal care. However, if a patient arriving at the hospital still has the capacity to make a decision concerning resuscitation, it is the admitting physi­ cian's duty to document such a decision in the patient's chart, including the specific actions to be limited, the circum­ stances of the discussion, and the individuals present during the discussion. 2 • 105· 1 06 When DNAR orders are written after consultation with the patient or, if the patient lacks decision-making capacity, the surrogate decision maker, physicians should document their discussions and follow institutional guidelines on how to document the order in the patient's medical record. Oral DNAR orders are not acceptable, although if the attending

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physician is not physically present, nursing staff may accept a DNAR order by telephone with the understanding that the physician will sign the order promptly.6 Some institutions require telephonic orders to be done with at least two nurses on the line with the attending physician. DNAR orders should be reviewed periodically, particularly if the patient's condition changes. Rather than automatically canceling them before surgery, as is done in some institutions, DNAR orders should be reviewed by the anesthesiologist, attending sur­ geon, and patient or surrogate to determine their applicabil­ ity in the operating room and postoperative recovery room. I 07- I 09 Physicians must also make certain that the proper steps are taken to notify the rest of the patient's care team, includ­ ing anyone who may be in a position to "call a code" or respond on a code team. This includes the nurses, consult­ ants, other attending physicians, and house staff. A grievous error in modern health care has often been to equate a DNAR order with decreasing the level of care provided to the patient. Unfortunately, orders to not attempt resuscitation can lead to near abandonment of patients or to denial of appropriate and necessary medical and nursing care. DNAR orders should never convey a sense of "giving up" to the patient, family, or health care providers at the patient's bedside. 2 6 Basic nursing and comfort care (i.e., oral hygiene, skin care, patient positioning, and meas­ ures to relieve pain and symptoms) must always be contin­ ued. DNAR orders withhold only resuscitative efforts and do not imply that other forms of treatment should be dimin­ ished.6 When the intent is for specific other medical treat­ ments to be withheld, these orders should be written sepa­ rate from the DNAR order, preferably on a "limitation of medical treatment" form, after discussions with the patient or surrogate. See discussion below. A DNAR order should not prohibit a patient from receiving appropriate diagnostic procedures or treatment interventions, including admission to intensive care or crit­ ical care units. If admitted to an intensive or critical care unit, routine orders for resuscitation should be modified on an individual basis.

Limitation.-of .. Treatment Orders Many institutions have now recognized that simple DNAR forms may be inadequate to describe the limitations of med­ ical treatment requested for some patients. A DNAR order does not automatically preclude interventions other than CPR. For clarity, some institutions have adopted limitation­ of-treatment orders to specify exactly what treatments are to be withheld in addition to CPR. These may include car­ dioversion, intubation, mechanical ventilation, the adminis­ tration of parenteral fluids or nutrition, oxygen, antibiotics, blood products, sedation, antiarrhythmics, or vasopressors. As an ethical matter, appropriate analgesia should never be with­ held. Problems can arise when these orders become incon­ sistent with rational medical treatment. Some patients, for example, may choose to accept defibrillation and chest

compressions but not intubation and artificial ventilations . Such conflicts arise when patients or surrogates have not been fully briefed on the nature of the proposed medical treatments . It is the responsibility of the attending physi­ cian to ascertain that the order set is rational and that the patient or surrogate understands why it is being written as it is.

Do.-Not.-Hospitalize (DNH) Orders One type of physician order that has been used success­ fully in many locales is the "do not hospitalize" order. Normally written for hospice and nursing home patients, it prevents many unwanted in-hospital resuscitation attempts and procedure-laden hospitalizations. Do-not­ hospitalize physician orders instruct nurses not to send patients to the hospital when further medical interven­ tions are not desired by either the patient or their surro­ gate decision maker. This allows people to die peacefully, rather than having the "last rites of CPR" performed when they are futile or unwanted. The only caveat to applying DNH orders is that staff must know that patients should still be sent to the hospital if they need palliative care not available in the nursing facility. 1 1 0 Barriers to using DNH orders include unrealistic fam­ ily expectations, fear of litigation, and staff discomfort with managing patients experiencing clinical decline. 1 1 1 Large variations in the use of DNH orders occur throughout the United States. Nursing home residents most likely to have a DNH order are those in independent facilities, in an urban location, who are white, with total functional dependence (usually advanced dementia), and having a living will or durable power of attorney for health care. 1 12• 1 1 3 EMS and extended or terminal care facilities should establish protocols that allow patients who decline resuscita­ tive efforts, including transport and hospitalization, to still receive the full range of comfort care, emergency medical treatment, and ambulance transport. 2 6

Issues Related to Out.-of.. Hospital Resuscitation In situations in which the EMS personnel cannot obtain clear information about the patient's wishes, resuscitative measures should be initiated.

About 3 2 5 ,000 cardiac disease-related deaths occur in the prehospital setting and emergency departments in the United States annually. 1 1 4 About 60% of unexpected cardiac deaths are treated by EMS personnel. 1 1 5 A basic principle for prehospital providers is that when in doubt, attempt to resuscitate. The key is knowing when not to start resuscitation: when patients have rigor mortis, livor mor­ tis, injuries incompatible with life, or are burned beyond

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recognition. Bystanders doing CPR should call 9 1 1 , and if EMS personnel have questions about whether to continue resuscitation, they can contact their base station for medical direction. Many patients for whom 9 1 1 is called because of cardiac arrest have been chronically ill, have a terminal illness, or have a written advance directive. States and other jurisdic­ tions have varying laws about prehospital DNAR orders and advance directives. 1 1 6 In some cases in which a DNAR order exists, especially where there are differing opinions among family members, it may be difficult to determine whether resuscitation should be initiated. In situations in which the EMS personnel cannot obtain clear information about the patient's wishes, resuscitative measures should be initiated.

INITIATION OF CPR IN PRESENCE OF DNAR ORDER OR DIRECTIVE

EMS professionals should initiate CPR and ACLS if they believe that: 1 . There is reasonable doubt about the validity of a DNAR order or advance directive.

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withdrawn if more information surfaces. Not initiating resus­ citative procedures and discontinuing life-sustaining treat­ ment are ethically equivalent. In situations in which the prog­ nosis is uncertain, a trial of treatment should be considered while further information is gathered to help determine the likelihood of survival and the expected clinical course.6

Iatrogenic Cardiac Arrest Should patients be resuscitated if the cardiopulmonary arrest or instability was directly due to a health care worker's actions or inactions (i . e . , an iatrogenic cardiopulmonary arrest)? Many physicians seem to believe that DNAR orders do not apply in cases involving their error or another iatro­ genic cause . Even when they believe the DNAR orders remain valid, health care personnel may still attempt resus­ citation to assuage their feelings of guilt or responsibility for the event. 1 1 8 This abnegates patient self-determination. It also perpetuates the common misconception that errors are avoidable evils of medicine rather than expected results in modern practice. 1 19 There is now general agreement that these patients' DNAR orders should be respected.

2 . The patient may have changed his or her mind. 3. The best interests of the patient are in question.

DNAR Orders and the Operating Room

CPR decisions are often made in seconds by rescuers who may not know the patient or if an advance directive exists. As a result, administration of CPR may sometimes conflict with a patient's desires or best interests. Neither bystanders nor EMS personnel should attempt to interpret unique, lawyer or personally written, or other non-standard advance directives. They should adhere only to standard, EMS system-approved forms. 2 •83 • 1 1 7 Mter starting a resuscitation attempt, relatives or other medical personnel may arrive and confirm that the patient had clearly expressed a wish that resuscitation not b e attempted. I f these instructions appear t o be clear, CPR or other life-support measures may be discontinued. If possi­ ble, EMS should also confirm this with their base hospital.6

Should DNAR orders automatically be suspended during surgery? This may also apply to patients with prehospital advance directives undergoing outpatient surgery. Some anesthetic procedures-such as intubation, ventilation, and the use of vasopressors-are identical to those used during resuscitation. This has led many institutions to automati­ cally discontinue DNAR orders for patients going to the operating room and during the perioperative period. There is now widespread agreement that, while some modifications may need to be made in the DNAR orders, these should be discussed and clarified with the patient or sur­ rogate and the surgeon and anesthesiologist. Automatically discontinuing a DNAR order preoperatively or reinstituting it postoperatively deprives patients of their right to self­ determination. 107-109 As the American College of Surgeons stated some years ago,

Issues Related to In ..Hospital Resuscitation CPR is the only medical intervention that requires an order to not do it. Given that, some unique issues arise. Since many patients have DNAR orders, it is incumbent on those discovering a patient in cardiac arrest or responding with a "code team" to quickly obtain accurate information about the patient's DNAR status. It is tragic to prolong a patient's dying by providing inappropriate resuscitative meas­ ures. Even so, if there is any doubt about whether a patient should be resuscitated, begin CPR. Life support can always be

The best approach is a policy of 'required reconsideration ' of previous advance directives. The patient and the physicians who will be responsible for the patient's care should discuss the new risks and the approach to potentia/ life-threatening problems during the perioperative period. The results of such discussions should be documented in the record. The operative and anesthetic permit should indicate that the patient or the duly authorized patient's representative has had the opportunity to discuss and reconsider any advance directive.

The American Society of Anesthesiologists has sug­ gested that the operative permit specify one of thre e options based o n discussions with the patient or surrogate :

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( 1 ) full attempt at resuscitation, with revocation of the DNAR order during the perioperative period; (2) limited attempt at resuscitation defined with regard to specific pro­ cedures after the patient or surrogate is informed about which procedures (a) are essential to the success of the anesthesia and the proposed procedure, and (b) are not essential and may be refused; or ( 3 ) limited attempt at resuscitation defined with regard to the patient's goals and values, allowing the surgical team to determine whether the burden and outcome of resuscitation meets the patient's goals of therapy. 1 2 1

F amily Attendance at "Codes" While prehospital resuscitation attempts often occur i n the home with family present and the EMS team communicat­ ing with them during the process, family members and other survivors are often barred from witnessing these procedures in health care institutions. This may be owing to institu­ tional tradition, to fear that family members may become disruptive or interfere with resuscitation procedures, to con­ cern that they may faint and injure themselves, or to fears that their naive interpretation of events may increase the cli­ nicians' exposure to legal liability. Health care providers' opinions vary widely about whether family should be pres­ ent during resuscitation attempts. In general, nurses, EMS providers, pediatricians, and, most recently, emergency physicians have been more amenable to family presence dur­ ing resuscitations than have other health care profession­ als. ' 22-1 3 0 Many studies have shown that family members want to be offered the opportunity to be present for critical care pro­ cedures and during resuscitation, especially for a child. 1 3 1-1 3 7 Parents' presence during pediatric resuscitations has become relatively common and has been endorsed by the American Academy of Pediatrics and the Ambulatory Pediatric Association. 6· 2 6 The American Heart Association endorses giving fam­ ily members the opportunity to be present as long as the patient has not previously raised obj ections. This position stems from the benefit families can derive from their pres­ ence during resuscitation attempts, the lack of harmful effects on them from viewing these resuscitations, and their quasi-right to be there based on the nature of their relation­ ship to the patient.6· 2 6 ACEP endorses end-of-life measures directed at the patient and family.

·�····································································································· S e e We b s i t e f o r A CE P p o l i cy s t a te m e n t o n e n d � o f - l i f e i s s u e s i n t h e e m e r g e n cy d e p a rt m e n t .

Benefits Both the survivors and the health care team benefit from family presence during the resuscitation process. Most of those viewing resuscitations indicate that they would not be hesitant to do so again, saying that they felt that they had both helped their loved one and had eased their own grieving. 1 J J , I 40-143 This has been confirmed by standard psychological questionnaires showing that family members present during resuscitative efforts demonstrate less anxiety and depression and more constructive grief behavior than family members absent from the resuscitation attempt. 1 3 5 Most spouses and family members who have not witnessed a resuscitation effort say they would want to be present. Family members who witness resuscitation attempts rec­ ognize the enormous effort that goes into resuscitation and the skill and compassion that the health care team exhibits. Rather than being cloistered in a back room, awaiting news, they see for themselves the struggle to save their loved one's life. Afterward they rarely ask the question that so often accompanies an unsuccessful resuscitation attempt: Was everything done? They may also thank the resuscitation team for their efforts, something that rarely occurs otherwise .m

Procedure EMS agencies and health care institutions should develop protocols to guide family member presence during resusci­ tations. These protocols will, by necessity, vary with the set­ ting. In the prehospital setting, EMS providers must be aware of stresses on family members who may not have wished to view the resuscitation. When possible, such fam­ ily members should be removed to another area using the help of other bystanders. This may be especially important for children. When it will not compromise the resuscitative effort, it is vital that EMS personnel describe their activities in lay terms and communicate additional information to those survivors who remain to watch. l J J Family members seldom ask i f they can be present for resuscitations unless encouraged to do so by health care providers. But if encouraged, a surprisingly large number will speak up . Health care providers should extend the opportunity to family members whenever possible . 1 44 Resuscitation team members should be made aware that family members are present and be sensitive to their feel­ ings. This, however, should never compromise the resusci­ tative effort. A calm, experienced, and knowledgeable staff member not involved in tl1e resuscitation (e.g., chaplain, social worker, or charge nurse) should be assigned to the family members and remain with them during the resuscita­ tion to see to their needs and to answer any questions they may have. 1 3 3 •1 43 -1 45 Being present during the resuscitation attempt demonstrates to the survivor that everything possi­ ble is being done-a question that is often asked if they are not present-and provides them with a sense of closure that they otherwise cannot achieve. 1 3 3 •145

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If the resuscitation attempts fail, survivors wimessing the process should never be asked if the team should stop; that is a medical decision based on the clinical situation. Rather, they should be informed that the team will stop. 1 3 3 , I 45 An increasing number of institutions are developing these types of protocols. 1 3 3 · 1 46-1 54

Providing Emotional Support to the Family: Death Notification Despite our best efforts, most resuscitations fail. Notifying family members of a loved one's death is an important aspect of a resuscitation attempt. It should be done compassion­ ately and in a manner that accommodates the family's cul­ tural and religious beliefs and practices. 141 · 145 Facing someone whose loved one has just died is one of the most difficult and stressful tasks health care profession­ als must do. Notifiers primarily fear the survivors' loss of control once they tell them that their loved one has died. Reactions are unpredictable and professionals must be pre­ pared to respond appropriately. Notifiers also fear their own reactions, their interactions with survivors, their ability to communicate this news, and the questions survivors may ask. Additional fears involve being blamed by survivors for the death as well as fear of their own death or disabilities. 1 3 3 · 1 45

45 Notifications 1 33 • 1 The physician usually delivers the news, often accompanied by a chaplain, nurse, or social worker. If the physician is involved with another critical task, most survivors have no obj ection if a nurse, chaplain, or social worker gives them the news immediately as long as they have subsequent con­ tact with the physician. 1 56 Notification, however, should never be relegated to the unit assistant, medical or nursing student, or other untrained or partially trained person unless that individual is in the process of being educated and is accompanied by an experienced, supervising mentor. Directness, truth, consistency, and clarity are the key factors when delivering information about a sudden, unex­ pected death. Perceptive survivors can easily tell which noti­ fiers care and which are only "going through the motions. " A key psychological response that often diminishes notifiers' effectiveness is identifying too closely with survivors, pro­ ducing a sense of awkwardness or inadequacy and causing notifiers to rush through the process to hide their own emo­ tions. Consequently, their presentation may seem callous or insensitive and the exact opposite of what they desired. Using a "D" word is one of the hardest parts of the process. "D" words are "Died, " "Death, " or "Dead," includ­ ing " D ead by brain criteria. " Notifiers often find euphemisms such as "passed away, " "left us, " " didn't make

58 1

it, " "lost him , " " gone, " or " expired" easier to say, even though they should not be used, because these do not regis­ ter with some people at this stressful time. If survivors don't seem to understand, another 'D' word should be used in a different context. 1 3 3 · 1 45 Notifiers should also use "helpful," rather than the all too common "harmful, " phrases to interact with survivors (Table 3 7-3). Helpful phrases allow the individual to emote and to begin to deal with their loss in a constructive manner. Harmful phrases often provoke anger, imply blame, and may raise unnecessary issues. 1 3 3 · 1 45

TA B LE 3 7 - 3 S u rvivo rs

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H e l p f u l a n d H a r m f u l P h r a s e s in S p e a k i n g With

Helpful Phrases •

I c a n ' t i m a g i n e h o w d i ffi c u l t t h i s i s f o r yo u .

•

I k n ow t h i s i s ve ry p a i n f u l f o r yo u .

•

I ' m s o s o r ry f o r yo u r l o s s (I n c l u s ive r a t h e r th a n p i tyi n g ) .

•

I t ' s h a r d e r th a n m o s t p e o p l e th i n k .

•

I t ' s o k ay to b e a n g ry with G o d .

•

I t m u st b e h a r d to a c c e p t.

•

Te l l m e h ow yo u ' r e f e e l i n g .

•

I k n ow yo u a r e fe e l i n g t o t a l ly overwh e l m e d r i g h t n ow.

•

Te l l me a b o u t (d e c e d e n t ' s n a m e) a n d yo u r l i fe t o g e t h e r .

•

M ay I j u st s i t h e r e w i t h yo u ?

•

I s t h e r e a nyo n e I c a n c a l l f o r yo u ?

Harmful Phrases •

I t was a c tu a l ly a b l e ssi n g b e c a u s e . . . . (G o d c l i c h e)

•

O n ly t h e g o o d d i e yo u n g . (G o d c l i c h e)

•

G o d n ever g ives u s m o r e th a n we c a n h a n d l e . (G o d c l i c h e)

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A r e n ' t yo u l u c ky t h a t a t l e a st. . . . (U n h e a l t h y e x p e c t a ti o n)

•

Yo u m u st b e s tr o n g f o r yo u r (oth e r) c h i l d r e n , s p o u s e , e t c . (U n h e a l t h y e x p e ct a t i o n)

•

Yo u ' l l g e t ove r t h i s . (U n h e a l t hy e x p e ct a t i o n)

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Yo u ' r e yo u n g . . . yo u ' l l f i n d s o m e o n e e l s e . (U n h e a l t h y e x p e c t a ti o n)

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I t m u st h ave b e e n h i s o r h e r ti m e to g o . (I g n o r a n ce)

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Everyth i n g i s g o i n g to b e o k ay. ( B a s i c i n s e n s i tivi ty)

•

D i d h e o r s h e m a k e p e a c e with G o d b e f o r e t h e e n d ? ( B a s i c i n s e n s i tivi ty)

S o u r c e F r o m I s e r s o n KV Grave Words. Nottfymg Survtvors A b o u t Sudden, Unexp e c t e d D e a ths. T u cs o n , AZ· G a l e n P r e s s , 1 9 9 9 · 4 9-5 1 , w1th p e r m 1 ss1 o n .

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Notification After an Unsuccessful Resuscitation Attempt133 • 145 Death notifications after attempted resuscitations are com­ mon occurrences in emergency departments and ICUs. If a family arrives at the hospital while resuscitation attempts are ongoing, a chaplain, social worker, or nurse may be delegated to inform the family of the patient's status. Families may be grateful that these individuals may be more inclined to use nonmedical words to explain what is occurring than would a physician. To avoid miscommunication, health care workers who act as notifiers should use "heart attack" rather than "MI , " "breathing machine" rather than "ventilator, " and "heart stopped" rather than "cardiac arrest. " These noti­ fiers-the same person or at least one person from the group who initially spoke with the family-should continually update the family. Progressive notification that things are not looking good alerts survivors to the grave situation and gives them at least a little time to prepare for bad news. When the family speaks another language, either use a non-family member interpreter or a telephone interpreting service. If the resuscitation attempts fail, any survivors who have not observed the resuscitation attempt should be asked if they want to view the body. Parents may be encouraged to hold their child and, in some cases, even get into the bed with the body. Most hospitals find it useful to have information pack­ ets about transportation of the body from a home or hospi­ tal, death certification, and autopsy and medical examiner requirements. Information on body, organ, and tissue dona­ tion should be included.

Education It is essential that those who deal with resuscitations and death notification on a regular basis pass their knowledge of how to care for survivors, the newest patients, on to the next generation of health care professionals. Professionals whose job includes delivering news about sudden unexpected deaths need to learn how to perform this difficult task before doing it. Unfortunately, most medical "short courses" deal­ ing with resuscitation have not incorporated death notifica­ tion into their training programs or manuals. 1 3 3 Occasionally, physicians give the job o f death notifica­ tion to residents, medical students, or nurses. Although all three groups should be present to learn the techniques involved, they should not be left to deliver death notifica­ tions on their own. That is a form of professional abandon­ ment and, in a teaching hospital, the worst form of student abuse. 2 • 1 3 3

References 1. McCormick RA. Theology and bioethics. Hastings Cent Rep 1 989; 1 9(2): 5 - 1 0 . 2 . Iserson KV. Bioethics. In MarxJA, Hockberger R S , Walls RM et al, eds. Rosen 's Enm-gency Medicine: Concepts and Clinical Practice, 6th ed. Philadelphia: Mosby, 2006: 3 1 2 7-3 1 3 9. 3 . Schloendorff v Society ofNew Yiwk Hospital, 1 0 5 NE 92 , 9 3 , 1 9 14. ,

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54. Christakis NA, Asch DA. Biases in how physicians choose to withdraw life support. Lancet 1 99 3 ; 3 42 :642-646. 5 5 . Quill TE, Barold SS, Sussman BL. Discontinuing an implantable cardioverter defibrillator as a life-sustaining treatment. Anz J Cardio/ 1 994;74:205-207. 56. Braun TC, Hagen NA, Hatfield RE, et al. Cardiac pacemakers and implantable defibrillators in terminal care. J Pain Symptom Manage 1 999; 1 8 : 1 2 6-1 3 1 . 5 7 . Mueller PS, Hook CC, Hayes DL. Ethical analysis of withdrawal of pacemaker or implantable cardioverter-defibrillator support at the end of life. Mayo Clin Proc 2 003 ;78 :959-96 3 . 5 8 . Quill TE, Dresser R , Brock DW. The rule o f double effect: a cri­ tique of its role in end-of-life decision making. N Eng! J Med 1 997;3 3 7 : 1 768-1 7 7 1 . 5 9 . Brody H, Campbell ML, Faber-Langendoen K , e t al. Withdrawing intensive life-sustaining treatment-recommenda­ tions for compassionate clinical management. N Eng! J Med 1 997 ; 3 3 6:652-6 5 7 . 6 0 . Quill TE, Byock IR. Responding t o intractable terminal suffer­ ing: the role of terminal sedation and voluntary refusal of food and fluids. Ann Intem Med 2 000; 1 3 2 :408-414. 61. Buchanan AE. The question of competence. In Iserson KV et al, eds. Ethics in Enze1'gency Medicine, 2nd ed. Tucson, AZ: Galen Press, 1 99 5 . 62 . Iserson KV, Sanders AB, Mathieu D R , eds. Ethics i n Eme1'gency Medicine, 2nd ed. Tucson, AZ: Galen Press, 1 99 5 . 6 3 . MartinezJM, L6pez JS, Martin A, e t a l . Organ donation and fam­ ily decision-making within the Spanish donation system. Soc Sci Med 2 00 1 ;5 3 (4) :405-42 1 . 64. White DB, Curtis JR, Lo B, e t al. Decisions to limit life-sustain­ ing treatment for critically ill patients who lack both decision­ making capacity and surrogate decision-makers. Cl'it Care Med 2 006; 3�205 3-2059. 65. Wenger NS, Oye RK, Desbiens NA, et al. The stability of DNR orders on hospital readmission. The SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. J Clin Ethics 1 996;7 :48-54. 66. Teno JM, Murphy D , Lynn J , et al. Prognosis-based futility guidelines: does anyone win? SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatment. J Am Grxiatr Soc 1 994;42 : 1 2 02- 1 2 0 7 . 67. Teno JM, Licks S, Lynn J, et a!. Do advance directives provide instructions that direct care? SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatment. ] Am Geriatr Soc 1 997;45 : 5 08-5 1 2 . 6 8 . Terra JM, Hakim RB, Knaus WA, e t al. Preferences for car­ diopulmonary resuscitation: physician-patient agreement and hospital resource use, The SUPPORT Investigators. J Gen lntem Med 1 99 5 ; 1 0 : 1 79-1 86. 69. Phillips RS, Wenger NS, Teno ], et a!. Choices of seriously ill patients about cardiopulmonary resuscitation: correlates and out­ comes. SUPPORT Investigators . Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. Am J Med 1 996; 1 00: 1 2 8-1 3 7. 70. Hofmann JC, Wenger NS, Davis RB, et a!. Patient preferences for communication with physicians about end-of-life decisions. SUPPORT Investigators. Study to Understand Prognoses and Preference for Outcomes and Risks of Treatment. Ann Intern Med 1 997; 1 2 7 : 1 - 1 2 . 7 1 . Lynn }, Teno JM, Phillips R S , et a!. Perceptions b y family mem­ bers of the dying experience of older and seriously ill patients. SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. Ann Intem Med 1 997 ; 1 2 6:97-106. 72. The SUPPORT Principal Investigators. A controlled trial to improve care for seriously ill hospitalized patients: the Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments (SUPPORT) . JAMA 1 99 5 ; 2 7 4 : 1 5 9 1 1 598. 7 3 . Blackball LJ, Murphy ST, Frank G , et a!. Ethnicity and attitudes toward patient autonomy. JAMA 1 995;274:820-82 5 . 74. Garrett JM, Harris RP, Norburn JK, et a!. Life-sustaining treat­ ments during terminal illness: who wants what? J Gen lntem Med 1 993 ; 8 : 3 6 1-3 68.

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7 5 . Kiely DK, Mitchell S, Marlow A, et al. Racial and state differ­ ences in the designation of advance directives in nursing home residents. J Am Geriatr Soc 2 0 0 1 ;49(10): 1 3 46-1 3 5 2 . 7 6 . Lahn M , Friedman B, Bijur P, e t al. Advance directives i n skilled nursing facility residents transferred to emergency departments. Acad Eme1�g Med 2 0 0 1 ;8(12): 1 1 5 8-1 1 62 . 7 7 . Federal Patient Self Determination Act 1 990. 42 U.S.C. 1 3 95 cc (a). 7 8 . Arizona Living \Vilis and Health Care Directives Act, Ariz Rev Stat Ann ss3 6-3 2 0 1 to 3 6 - 3 2 8 7 , 2000. 79. Vig EK, Taylor JS, Starks H, et al. Beyond substituted judgment: how surrogates navigate end-of-life decision-making. J Am Geriau� Soc 2006;54: 1 68 8-1 693 . 80. Becker LJ, Yeargin K, Rea TD , et al. Resuscitation of residents with do-not-resuscitate orders in long-term care facilities. Prehosp Emerg Care 2 003 ; 7 : 3 03-306. 8 1 . Dull SM, Graves J , Larsen MP, et al. Expected death and unwanted resuscitation in the prehospital setting. Ann Emerg Med 1 994;2 3 (5):997- 1 002 . 8 2 . Guru V, Veerbeck VP, Morrison LJ. Response of paramedics to terminally ill patients with cardiac arrest: an ethical dilemma. CMAJ 1 999; 1 6 1 ( 1 0): 1 2 5 1 - 1 2 54. 8 3 . Iserson KV. A simplified prehospital advance directive law: Arizona's approach. Ann Emerg Med 1 993 ;2 2 : 1 1 : 1 703-1 7 1 0. 84. Iserson Kv. If we don't learn from history . . . ethical failings in a new prehospital directive. Am J Emerg Med 1 995 ; 1 3 :241 . 8 5 . Crimmins TJ. Prehospital do-not-resuscitate orders. In Iserson KV et al, eds. Ethics in Eme1�gency Medicine, 2nd ed. Tucson, AZ: Galen Press, 1 99 5 . 86. Iserson Kv. Foregoing prehospital care: should ambulance staff always resuscitate? J Med Ethics 1 9 9 1 ; 1 7 : 1 9 . 8 7 . Schears RM , Marco CA, Iserson Kv. Do not attempt resuscita­ tion" (DNAR) in the out-of-hospital setting. Ann Erne1�g Med 2 004;44(1):68-70. 8 8 . Schmidt TA, Hickman S, Tolle SW, et al. The Physician Orders for Life-Sustaining Treatment (POLST) program: Oregon emer­ gency medical technicians' practical experiences and attitudes. J Am Ge,�iau� Soc 2 004; 5 2 : 1-7. 89. Naess AC, Steen E, Steen PA. Ethics in treatment decisions during out-of-hospital resuscitation. Resuscitation 1 997; 3 5 :2452 5 6. 90. American College of Emergency Physicians. Ethical Issues fo7� Resuscitation. Policy #400 1 3 3 ; approved 1 992 ; reaffirmed 1 997 and 2 00 1 . 9 1 . Moselli NM, Debernardi F, Piovano F. Forgoing life sustaining treatments: differences and similarities between North America and Europe. Acta Anaesthesia! Scand 2 006;50: 1 1 7 7-1 1 86. 92 . Sonnenblick M, Friedlander Y, Steinberg A. Dissociation between the wishes of terminally ill patients and decisions by their offspring, ] Am Ge1�iatr Soc 1 993 ;4 1 : 5 99-604. 93 . In 1�e Quinlan, 70 NJ 1 0 , 3 5 5 A2 d 647, 1 976, cert denied, 42 9 US 92 2 , 1 976. 94. C1'7tzan v Dinctm; Missozn�i Depm7ment ofHealth, US 5 8 LW 49 1 6 , 1 990. 95. Rasmussen v Fleming, 1 54 Ariz 207, 741 P2d 674, 1 9 8 7 . 9 6 . Superintendent of Belchertown v SaikrUJicz, 3 7 3 Mass 7 2 8 , 3 70 NE 2d 4 1 7 , 1 9 7 7 . 97. L i LLM, Cheong KYP, Yaw LK, et a!. The accuracy of surrogate decisions in intensive care scenarios. Anaesth Intens Care 2 007;3 5 :46-5 1 . 98. Silveira MJ, DiPiero A, Gerrity MS, et al. Patients' knowledge of options at the end of life-ignorance in the face of death. JAMA 2 000;284:2483-2488. 99. Doig C, Murray H, Bellomo R, et al. Ethics roundtable debate: patients and surrogates want " everything done"-what does "everything" mean? Crit Care 2006; 1 0 : 2 3 1 -2 3 8 . 1 00. Meisel A . Rights o f minors. In Iserson KV, Sanders AB, Mathieu D, eds. Ethics in Eme1-gency Medicine, 2nd ed. Tucson, AZ: Galen Press, 1 9 9 5 : 72-76. 1 0 1 . Siegel M. Alone at life's end: trying to protect the autonomy of patients without surrogates or decision-making capacity. c,�it Care Med 2006;34(8):22 3 8-2 2 3 9 . 1 0 2 . Danis M , Patrick D L , Southerland LI, e t al. Patients' and fami­ lies' preferences for medical intensive care. JAMA 1 9 8 8 ; 2 6 0 : 797-802 .

1 0 3 . Cook DJ, Guyatt GH, Jaeschke R, et al. Determinants in Canadian health care workers of the decision to withdraw life support from the critically ill. JAMA 1 99 5 ;2 7 3 :703-708. 1 04. Veatch Ri\tl . Assault or homicide: treating and letting die without consent. C1�it Care Med 2002 ; 3 0 : 9 3 7-93 8 . 1 0 5 . Iserson KV. Getting advance directives to the public: a role for emergen(.y medicine. Ann Eme1�g Med 1 99 1 ;2 0 : 692 . 1 06. Iserson KV. Federal advance directives legislation: potential effects on emergency medicine. J Enterg Med 1 9 9 1 ;9:67. 107. Lo B . DNR in the OR and afterwards. AHR Q WebM&M. S eptember 2 006. Available at: http ://www. webmm . ahrq.gov/ case.aspx? caseiD = 1 3 5 . Accessed July 7, 2 00 7 . 1 0 8 . Veterans Health Administration. May do-not-resuscitate (DNR) orders be suspended for surgery? EthicsRX. January 2 0 0 5 . Available a t : www. ethics .va. gov/ETHIC S/docs/rx/EthicsRx_ 2 0 0 5 0 1 0 1 _ S u s p e n d i n g_D NR_O r d ers_For_ S u r g e ry. p d f. Accessed July 7, 2007. 1 09. Craig DB. Do-not-resuscitate orders in the operating room. Can J Anaesth 1 996;4 3 :(8): 840-8 5 1 . 1 1 0. Iserson KV. Ethical considerations in emergency care. Israeli J Ernerg Med 2 004;4(2):8- 1 5 . 1 1 1 . Culberson J, Levy C, Lawhorne L. Do-not-hospitalize orders in nursing homes : a pilot study. J Ant Med Di1� Assoc 2 0 0 5 ; 6 ( 1 ) : 22-26. 1 1 2 . Mitchell SL, Teno JM, Intrator 0 , et al. Decisions to forgo hos­ pitalization in advanced dementia: a nationwide study. J Am Geriatr Soc 2 007 ; 5 5 :432--43 8 . 1 1 3 . Levy CR, Fish R , Kramer A . Do-not-resuscitate and do-not-hospi­ talize directives of persons admitted to skilled nursing facilities under the Medicare benefit. J Am Geriatr Soc 2005 ; 5 3 ( 1 2): 2060-2068. 1 1 4. Vital Statistics of the U. S., Data Wtwehouse, NCHS. http://www. cdc.gov/nchs/datawh.htm Accessed July 7, 2 007. 1 1 5 . Chugh SS, Jui J, Gw1son K, Stecker EC, et a!. Current burden of sudden cardiac death: multiple source surveillance versus retro­ spective death certificate-based review in a large U.S. commu­ nity. J Ant Colt Cardia/ 2 004;44: 1 2 68-1 2 7 5 . 1 1 6 . Tolle S W, Tilden VP, Nelson CA, e t al. A prospective study o f the efficacy of the physician order form for life-sustaining treatment. J Am Geriau� Soc 1 998;46: 1 097-1 1 0 2 . 1 1 7 . Bossaert L. European Resuscitation Council guidelines for resus­ citation. In The Ethics of Resuscitation in Clinical Practice. Amsterdam: Elsevier; 1 998:2 06-2 1 7 . 1 1 8 Casarett DJ, Stocking CB, Siegler M. Would physicians override a do-not-resuscitate order when a cardiac arrest is iatrogenic? J Gen inta·n Med 1 999; 14:3 5-3 8 . 1 1 9. Casarett DJ, Ross L F. Overriding a patient's refusal o f treatment after an iatrogenic complication. N Eng! J Med 1 997; 3 3 6(2 6) : 1 908-1 909. 1 2 0. American College of Surgeons. [ST- 1 9] Statement on advance directives by patients : "do-not-resuscitate" in the operating room. But Am Colt Sw�g 1 994;79(9):29. 1 2 1 . American Society of Anesthesiologists. Ethical Guidelines for the Anesthesia Cm�e ofPatients with Do-Not-Resuscitate Orde1�s. Available at: http :1/www. asahq. org/publica tionsAndS ervices/standards/ 09. html. Accessed July 7, 2 007. 1 2 2 . Engel KG, Desmond JS, Brandt M, et a!. Provider experience and attitudes towards family presence during resuscitation proce­ dures. Acad Emerg Med 2 005 ; 1 2 (5 Suppl. 2):8 1 . 1 2 3 . Emergency Nurses Association. Position statement. Family P1�esence at the Bedside Du1�ing Invasive P1�ocedures and Resuscita­ tion. 2 00 1 . Available at: http ://ena. org/about/position/PDFs/ 4E6C2 56B2 6994E3 1 9F66C65 748BFBDBF.pdf Accessed July 7 , 2007. 1 24. Ellison S . Nurses' attitudes toward family presence during resus­ citative efforts and invasive procedures. J Eme1�g Nurs 2003 ;29: 5 1 5-52 1 . 1 2 5 . Sacchetti A, Paston C , Carraccio C . Family members do not dis­ rupt care when present during invasive procedures. Acad Enterg Med 2 005 ; 1 2 :477--479. 1 2 6. Heckendorn JT, Chakel S S , Ubel PA, et al. Family presence during critical resuscitation in the emergency department: do patients and family members agree? Acad Eme1�g Med 2 0 05 ; 1 2 (5 Suppl 2) : 8 1 .

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1 2 7 . Eichhorn DJ, Meyers TA, Guzzett CE, et al. Family presence during invasive procedures and resuscitation: hearing the voice of the patient. Am J Nurs 2 00 1 ; 1 0 1 (5):48-5 5 . 1 2 8 . Fein JA, Ganesh J, Alpern ER. Medical staff attitudes toward family presence during pediatric procedures. Pediatr Emerg Cm'e 2 004;20(4):224--2 2 7 . 1 2 9 . Marrone L, Fogg C. Family presence during resuscitation: are policies allowing family into the trauma room humane and nec­ essary-or just asking for trouble? Nursing 2005 ; 3 5 (8 ED Insider Suppl):2 1-2 2 . 1 3 0. Merlevede E, Spooren D, Henderick H, e t al. Perceptions, needs and mourning reactions of bereaved relatives confronted with a sudden unexpected death. Resuscitation 2 004;6 1 : 3 4 1-348. 1 3 1 . Boie ET, Moore GO, Brummett C, et a!. Do parents want to be present during invasive procedures performed on their children in the emergency department? A survey of 400 parents. Ann Emerg Med 1 999;34:70-74. 1 3 2 . Boyd R. Witnessed resuscitation by relatives. Resuscitation 2 000;43 : 1 7 1-1 76. 1 3 3 . Iserson KV. Gmve Wo1'ds: Notifying Survivors About Sudden, Unexpected Deaths. Tucson, AZ: Galen Press, 1 999. 1 34. Beckman AW, Sloan BK, Moore GP, et al. Should parents be pres­ ent during emergency department procedures on children, and who should make that decision? A survey of emergency physician and nurse artitudes. Acad Enu:rg Med 2 002 ;9: 1 54--1 58. 1 3 5 . Robinson SM, Mackenzie Ross S, et al. Psychological effect of witnessed resuscitation on bereaved relatives. Lancet 1 998 ; 3 5 2 : 6 1 4--6 1 7 . 1 3 6. Barratt F, Wallis DN. Relatives in the resuscitation room: their point of view. J Accid Eme1x Med 1 998; 1 5 : 1 09-1 1 1 . 1 3 7 . Piira T, Sugiura T, Champion GD , et al. The role of parental presence in the context of children's medical procedures: A sys­ tematic review. Child Cm·e Healtb Dev 2005;3 1 : 2 3 3-243 . 1 3 8 . Gold KJ, Gorenflo DW, Schwenk TL, et a!. Physician experience with family presence during cardiopulmonary resuscitation in children. Pediatr O·it Cm'e Med 2 006;7(5): 42 8-43 3 . 1 3 9. Henderson D P, Knapp JF. Report o f the national consensus confer­ ence on family presence during pediatric cardiopulmonary resusci­ tation and procedures. ] Emerg Nurs 2006;32(1):23-29. 140. Doyle C], Post H, Burney RE, et al. Family participation during resuscitation: an option. Ann Emerg Med 1 9 8 7 ; 1 6:673-67 5 . 1 4 1 . U K Resuscitation Council. Bereavement. In: Resuscitation Council UK Advanced Life Suppm't Coune Manual. 1 99 8 : London : Resuscitation Council.

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1 42 . Adams S, Whitlock M, Higgs R, et al. Should relatives be allowed to watch resuscitation? BMJ 1 994; 3 0 8 : 1 687-1 692 . 143 . Eichhorn DJ, Meyers TA, Mitchell TG, et al. Opening the doors: family presence during resuscitation. J Cm,diovasc Nurs 1 996; 1 0 : 5 9-70. 1 44. Cobb LA, Eliastam M, Kerber RE, et a!. Report of the American Heart Association Task Force on the Future of Cardiopulmonary Resuscitation. Circulation 1 992 ; 8 5 : 2 3 46-2 3 5 5 . 145. Iserson KV. Gravest words : notifying survivors about sudden, unexpected deaths. Res Staff Physician 2 0 0 1 ;47(7):66-68;7 1-7 2 . 1 4 6 . MacLean S L , Guzzetta C E , White C, e t al. Family presence dur­ ing cardiopulmonary resuscitation and invasive procedures: prac­ tices of critical care and emergency nurses. Ant J Crit Care 2 003 ; 1 2 :246-2 5 7 . 1 4 7 . Meyers TA, Eichhorn OJ, Guzzetta CE, et a!. Family presence dur­ ing invasive procedures and resuscitation: the experiences of family members, nurses, and physicians. Am J Nun 2000; 1 00:3 2-42 . 148. McClenathan BM, Torrington KG, Uyehara CF. Family member presence during cardiopulmonary resuscitation: a survey of US and international critical care professionals. Chest 2002 ; 1 2 2 :2204--2 2 1 1 . 149. Emergency Nurses Association. Presenting the Option for Family Pnsence. 2nd ed. Des Plaines, Ill: Emergency Nurses Association; 2 00 1 . 1 50. Eichhorn DJ, Meyers TA, Guzzetta CE, et a!. Family presence during invasive procedures and CPR: when pigs fly. In Mason OJ, Leavitt JK, Chaffee MW, eds. Policy and Politics in Nuning and Health Care, 4th ed. Philadelphia: Saunders, 2 002 : 3 45-3 6 1 . 1 5 1 . Mason D]. Family presence: evidence versus tradition. A nt J Crit Care 2003 ; 1 2 : 1 90-1 9 2 . 1 5 2 . McGahey PR. Family presence during pediatric resuscitation: a focus on staff. C1'it Cm'e Nzme 2002 ;22(6) :29-34. 1 5 3 . Sacchetti A, Carraccio C, Leva E, et a!. Acceptance of family member presence during pediatric resuscitation in the emergency department: effects of personal experience. Pediatr Erne1'g Care 2 000; 1 6 : 85-8 7 . 1 54. Helmer SD, Smith R S , Dort JM, et a!. Family presence during trauma resuscitation: a survey of AAST and ENA members . American Association for the Surgery of Trauma. Emergency Nurses Association. ] Ii'aunza 2 000;48 : 1 0 1 5-1 024. 1 5 5 . Iserson KV. Notifying survivors about sudden, unexpected deaths. West J Med 2 000; 1 7 3 : 2 6 1 -2 6 5 . 1 5 6. Silverman P R . Services t o the widowed: first steps i n a program of preventive intervention. Conmz Mental Health J 1 9 67 ; 3 : 3 8-44.

. . Eleven. .

Education and Research

Benjamin S . Abella and Lance B . Becker A wide variety of individuals are interested in saving lives following sudden cardiac death and cardiac arrest. There are exciting options for career paths , funding, and collaborative models that make resuscitation science a rich and intriguing arena in which to contribute . Translational medical research provides a bridge to more directly connect basic research and patient care . Resuscitation science centers have been established, empowering translational science to provide models for collaborative interdisciplinary teams . Rich and rewarding careers are possible . •

Translational and resuscitation science provide an interdisciplinary foundation for basic and clinical investigation. • Bench-to-bedside training is available for those interested in careers in resuscitation science. A wide range of interdisciplinary portals and funding is available and emerging. • Collaboration between academic investigators and industry partners has proven to be fruitful in advancing resuscitation science .

.lntr.oduc.ti.o.n. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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THe daunting challenge of improving survival from cardiac arrest will require the collec­ tive energies of a wide variety of clinical investigators, basic scientists, public health experts, educators, paramedics, nurses, and physicians. In addition, given the importance of mechanical and electronic devices in emergency cardiovascular care (defibrillators, mechanical chest compression devices, biosensors, etc.), there is an enormous opportu­ nity for contribution from the bioengineering industry as well. Collaboration between academic investigators and industry partners has proven to be particularly fruitful in advancing resuscitation science, and such interaction will provide wide opportunities in coming years.

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T ranslational Science and Resuscitation Care Resuscitation science, with its wide-ranging areas of inquiry and involvement from the laboratory to the community, is in many ways the ideal model for translational investigation. As the National Institutes of Health (NIH) and other funding organizations focus their interest on projects with a transla­ tional scope, resuscitation scientists, emergency cardiovas­ cular care (ECC) community educators, bioengineers, and others have an opportunity to collaborate in teams that can truly move science into the clinical arena and bring clinical phenomena back to the laboratory. A recent body of work exemplifies this notion: the investigation of chest compres­ sion only cardiopulmonary resuscitation (CPR). Work by a variety of research teams has studied CPR physiology in the animal laboratory and others have furthered this work in clinical observational trials . 1-4 This will require further translation into educational, training, and community assessment work in coming years . Further iterations will require a return to the laboratory to better understand the role of respiration and oxygenation in more specific cardiac arrest models. A number of resuscitation science centers have been established with translational science breadth and may serve as models for others as they form collaborative teams. The Safar Center for Resuscitation Research in Pittsburgh, the Center for Resuscitation Science in Philadelphia, and the Emergency Resuscitation Center in Chicago serve as exam­ ples of such organizations. Each of these centers comprises resuscitation-focused scientists and clinicians that carry out investigations and programs in cellular laboratories, animal facilities, and clinical trials. Having such collaborations within the same organization will allow for more rapid progress and innovation and neatly fits the NIH vision of translational science.

Opportunities for New Directions: Translational Science There has been a recent appreciation for the importance of translational research in the biosciences, and this will likely have an important influence on careers and funding as it relates to ECC. As described on the NIH "roadmap" Web site: As a field of study, resuscitation science could serve as a prime example for translational research, with its broad focus from basic science to the bedside, and for resuscitation beyond the bedside into the community. The NIH has specifically created special funding for translational research via Clinical and Translational Science Awards (CTSAs) and additional funding mechanisms . But there are those who criticize translational research, citing a lack of mechanistic

To improve human health, scientific discoveries must be translated into practical applications. Such discoveries typically begin at "the bench " with basic research-in which scientists study disease at the molecular or cellular level-then they progress to the clinical level, or the patient's "bedside. " Scientists are increasingly aware that the bench-to-bedside approach to translational research is really a two-way street. Basic scientists provide clinicians with new tools for use in patients and for assessment of their impact, and clinical researchers make novel observations about the nature and progression of disease that often stimulate basic investigation. (http://nihroadmap. nih.govlclinicalresearch/overview­ translational.asp Dec2007)

focus, questioning the quality of the science, and noting that most researchers are not even sure what defines the bound­ aries of translational research. A consideration of what trans­ lational research is, why it may represent a particularly important opportunity for resuscitation science, and describing some models for how translational research can be organized is presented in the following section. What really is translational research? There is general agreement that translational research is still somewhat poorly defined. Wikipedia defines translational research as "a branch of medical research that attempts to more directly connect basic research to patient care" but goes on to say "and is a term whose precise definition is in flux. "; The importance of translational research is growing in the health care industry and the most common notion is that it deals with the advancement of basic science into actual therapies for patients. This is the "bench-to-bedside" defini­ tion and is most often used in referring to drug or device development. However, others use "translational research" to mean something quite different. They refer to the broader dissemination of a therapy into the population or community. This definition often encompasses notions about education and training of providers, knowledge translation to various audiences, dissemination of knowledge, patient-oriented research, and putting known therapies into more common practice in a broad community. The American Heart Association's program "Get With the Guidelines" is termed a translational project under this definition.6

Career Opportunities There are a wide variety of careers that directly impact emergency cardiac care and contribute toward saving lives from cardiac arrest. These career options span a large range of both educational backgrounds as well as areas of focus, including both research and nonresearch endeavors.

Clinical Investigator A daunting number of clinical questions exist in our scien­ tific knowledge of resuscitation and emergency cardiac care. Such questions will require a cadre of clinical scholars who

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practice medicine as well as conduct clinical trials and other human subj ect investigations. Questions that require further elaboration include the development and testing of novel drugs for ACLS and postarrest care, many of which have already been evaluated with promising results in the animal laboratory7•8; the further investigation of postarrest care and development of postarrest care pathways9• 1 0; the implemen­ tation of different methods of CPR and defibrillation4· 1 1 · 12 ; the evaluation of new CPR teaching and measurement tech­ niques3 -1 5 ; and the epidemiologic study of cardiac care processes and disease burden. 16-18 A number of other broad questions exist for aspiring clinical investigators, in such clinical fields as both adult and pediatric emergency medi­ cine, cardiology, critical care, anesthesiology, epidemiology, general internal medicine, and cardiac surgery. Clinical investigators with medical and/or nursing backgrounds will both be required in these endeavors . In addition, EMS physicians, paramedics, and other field responders will be invaluable participants in clinical research processes and should be encouraged to consider study of ECC.

Basic Science Investigator The realm of basic science investigation of cardiac arrest, ischemia-reperfusion, and the modeling of emergency car­ diac conditions is in great need of further scholarship in numerous specific areas, including understanding the mech­ anisms of ischemia-reperfusion injury at the levels of the cell and subcellular organelles 1 9-2 3 ; the modeling and under­ standing of ventricular fibrillation in isolated heart and heart tissues as well as computer models 2 4· 2 \ the evaluation of stem cell technology to improve repair and recovery from organ injury after ischemia-reperfusion2 6· 2 7; the study of hormonal and neurologic influence on cardiac arrest and tis­ sue response 28•2 9; the physiology of CPR/CPR quality; and the impact of potential new therapeutic agents.30·3 1 This list is by no means exhaustive, and investigators with both clin­ ical and laboratory research background will be required to further develop these fields of inquiry. Expertise will be required from such domains as molecular biology, cellular physiology, bioengineering, veterinary critical care, compu­ tational biology, and neuroscience, to name just a few.

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and diabetes management. Positions for such careers exist not just in academia and government bodies, but also in the nonprofit organization sphere, including organizations such as the American Heart Association, the American Red Cross, and other public health-minded groups. Such organ­ izations require individuals with research backgrounds as well as training in communications, marketing, and govern­ ment affairs.

Bioengineering and Industry Careers There are a wide array of careers available in ECC that reside within industry, and thus afford opportunities for those individuals trained in electrical, mechanical, or com­ puter engineering, or marketing and business administra­ tion. ECC is dependent on high-quality industrial partners, and a number of corporate entities maintain important involvement in resuscitation device design, including moni­ tors, defibrillators, and mechanical chest compression tools, drug development, as well as computer algorithms for data evaluation and processing for research and educational pur­ poses. Exciting new frontiers in resuscitation care will include the development of better monitoring and sensors for assessment of physiology during and after arrest as well as optimization of treatment technology such as hypother­ mia equipment and telemedicine communication systems.

Funding Opportunities

Investigators in resuscitation science have historically received funding from a variety of sources, including federal and nonprofit agencies. The qualities of these funding enti­ ties and the nature of their funding programs are detailed below. This list is by no means exhaustive but reflects the collective experience of ECC professionals with regards to recent successful funding for research or other resuscitation­ related proj ects.

Governmental Organizations National Institutes of Health

Public Health Education and Advocacy At the level of policy development and public education, there is an enormous contribution to be made by those with a diverse set of educational and training backgrounds, including those with master's degrees in public policy or public health, advanced training in communications, public relations, government, and economics, to name just a few. Involvement in the legislative and public educational spheres will be critical to improve and broaden CPR education,3 2 strengthen public access defibrillation programs , 3 3 •34 and engender governmental support for such lifesaving pro­ grams. A formidable amount of work also exists to improve public education and legislative support to reduce risk fac­ tors for cardiac emergencies in the community, such as smoking cessation, hypertension screening and treatment,

The NIH has served as a major source of funding for bio­ medical research in the United States. Decisions regarding funds allocation are made by the 27 institutes and centers that make up the NIH (e.g., National Institute for Mental Health [NIMH] , National Institute for Allergy and Infectious Diseases [NIAID] , etc.). While the review process for NIH grants has some complexities and exceptions in unusual cir­ cumstances, grants are typically reviewed by a group of "peer" scientists through the Center for Scientific Review (CSR-termed a "study section"), which is an independent agency that serves primarily to rate each grant for scientific merit. This review process generates a "priority score" for each application as well as a narrative scientific critique. Following review of a grant by CSR, each individual agency will fund the highest-scored applications that are appropriate

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to the agencies' areas of interest and research. Funding appli­ cations for resuscitation science have historically been directed toward the National Heart Lung and Blood Institute (NHLBI), although other institutes might be con­ sidered, depending on specific research proposals. For exam­ ple, a proposal that seeks to evaluate cardiac arrest treatment in the elderly could theoretically be directed to the National Institute of Aging (NIA). The success of a funding applica­ tion depends in part on the "fit" between the described proj­ ect and the goals and priorities of any given specific institute. Program officers within each institute can be consulted regarding the suitability of any given proposal. In general, to be successfully funded, most grants to the NIH must be clearly "hypothesis-driven, " with a testable research ques­ tion. Unless specifically described in a particular grant offer­ ing, the NIH generally does not fund educational or advo­ cacy projects that do not have such hypotheses.

and policy surrounding resuscitation science through the Council for Cardiopulmonary Perioperative and Critical Care (CPCC) and the Emergency Cardiovascular Care (ECC) Committee. The AHA is also a sponsor of the annual Resuscitation Science Symposium (ReSS), held in conjunc­ tion with the American Heart Association S cientific Sessions.

Society for Academic Emergency Medicine This society, composed of emergency medicine (EM) physi­ cians, supports several young investigator, medical student, and resident grant opportunities in partnership with the affiliated Emergency Research Foundation (EMF). While generally preferring to support EM physicians, collabora­ tions with non-EM personnel have been successfully funded as well.

Agency for Health Research and Quality

American Thoracic Society

This agency resides within the Department of Health and Human Services but is separate from the NIH structures described above . Certain resuscitation science proposals might be suitable for application to AHRQ, such as studies of health-care disparities or processes of care on a popula­ tion level. AHRQ also provides competitive funding for small conferences and educational initiatives . Generally speaking, AHRQ does not fund laboratory-based projects, nor is it the optimal source for clinical trial funding.

As the professional society of pulmonary/critical care physi­ cians, this group supports a small grants portfolio that has historically focused on focused aspects of pulmonary/critical care medicine, earmarked for such topics as asthma, cystic fibrosis , etc. Unrestricted grants are also available and potentially might be considered for ECC-related proj ects championed by a pulmonary/critical care physician.

Military Funding Resuscitation science, involving the clinical goal of rapid care of acutely ill patients, has a number of clearly important links to the interests of military funding groups such as the Defense Advanced Research Proj ects Agency (DARPA), and military branch funding sources such as the Office of Naval Research (ONR) or the Army Research Office (ARO) . Resuscitation from traumatic arrest and physiologic moni­ toring of the acutely ill serve as important starting points of interest for these agencies, and a number of resuscitation sci­ entists have been successfully funded through their mecha­ nisms for proj ects that span both clinical and laboratory investigations.

Nongovernmental Organizations

American Association of Critical Care Nurses (AACN ) This organization represents critical care nurses and nursing educators in a wide variety of disciplines, including cardiol­ ogy, pulmonary medicine, medical and surgical critical care, and palliative care. AACN offers a variety of small grants annually, and ECC topics are specifically encouraged for several of these offerings. In addition, the grants portfolio encourages applications in quality of care and technology application to critical care nursing, which could certainly apply to resuscitation science.

Society for Critical Care Medicine With a membership comprising medical intensivists, anes­ thesiologists, and surgical critical care specialists , this organization sponsors several grant opportunities annually that are available to the wide range of specialties repre­ sented.

American Heart Association (AHA)

Robert Wood Johnson (RWJ ) Foundation

The sponsor of the U.S. version of international resuscita­ tion guidelines for basic life support, advanced cardiac life support, and other emergency care protocols, the AHA has historically been a strong supporter of research into ECC and resuscitation science. AHA sponsors a number of fund­ ing opportunities through both the national organization and via regional chapters known as "affiliates." AHA also provides a large variety of opportunities for investigators (both yow1g and senior) to become involved in education

With a focus on health services and clinical research, R\VJ sponsors a number of fellowship training programs nation­ ally as well as hosting a variety of grant offerings. While fel­ lowships and some grants are funding solely through the select institutions with established RWJ programs, other grant opportunities exist for applicants at other centers . Resuscitation topics that address health care costs, dispari­ ties, and systems of care may be appropriate for R\V] con­ sideration.

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Summary For the wide variety of individuals who are interested in sav­ ing lives from cardiac arrest, there are exciting options for career paths, funding, and collaborative models that make resuscitation science a rich and intriguing arena in which to contribute. Given the enormous challenge to increase sur­ vival from such a deadly disease process, the ECC commu­ nity will require the collective strengths of many to harness scientific advances and make them a reality for patients and the communities in which they live.

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14. Abella BS, Edelson DP, Kim S, et a!. CPR quality improvement during in-hospital cardiac arrest using a real-time audiovisual feed­ back system. Resuscitation 2 007; 7 3 ( 1 ) : 54-6 1 . 1 5 . Kramer-Johansen J , Edelson DP, Losert H , et al. Uniform report­ ing of measured quality of cardiopulmonary resuscitation (CPR). Resuscitation 2007; 74(3):406-4 1 7 . 1 6 . Herlitz J, Svensson L, Engdahl J, e t a!. Characteristics of cardiac arrest and resuscitation by age group : an analysis from the Swedish Cardiac Arrest Registry. Am J E11m15 Med 2007;2 5 (9): 1 0 2 5- 1 0 3 1 . 1 7 . Herlitz J, Engdahl ], Svensson L , et a!. Is female sex associated with increased survival after out-of-hospital cardiac arrest? Resuscitation 2 004;60(2): 1 97-2 03 . 1 8 . Nichol G, Valenzuela T, Roe D, et al. Cost effectiveness of defib­ rillation by targeted responders in public settings. Cimdation 2003 ; 1 08(6):697-703 . 1 9 . Vanden Hoek TL, Li C, Shao Z, et al. Significant levels of oxidants are generated by isolated cardiomyocytes during ischemia prior to reperfusion. J Mol Cell Cardiol 1 997;29:2 5 7 1 -2 5 8 3 . 2 0 . Bottiger B , Teschendorf P, Krumnikl J, e t a!. Global cerebral ischemia due to cardiocirculatory arrest in mice causes neuronal degeneration and early induction of transcription factor genes in the hippocampus. Mol B1'ain Res 1 999;6 5 : 1 3 5-142 . 2 1 . An J , Bosnjak ZJ, Jiang MT. Myocardial protection by isoflurane preconditioning preserves Ca l + cycling proteins independent of sarcolemmal and mitochondrial KATP channels. Anestb Analg 2 007 ; 1 05(5): 1 2 07-1 2 1 3 , table of contents. 2 2 . Giacomo CG, Antonio M. Melatonin in cardiac ischemia/reperfu­ sion-induced mitochondrial adaptive changes. Cardiovasc Hematol Disord Drug Tm'gets 2007;7(3): 1 63-1 69. 2 3 . Miyamoto S, Murphy AN, Brown JH. Akt mediates mitochondrial protection in cardiomyocytes through phosphorylation of mito­ chondrial hexokinase-H. Cell Deatb Diffe1' 2 008; 1 5 (3) : 5 2 1-529. 24. Abildskov JA. Additions to the wavelet hypothesis of cardiac fibril­ lation. J Cm,diovasc ElectTopbysiol 1 994; 5(6) : 5 5 3-5 59. 25. Bemus 0, Van Eyck B, Verschelde H, et a!. Transition from ven­ tricular fibrillation to ventricular tachycardia: a simulation study on the role of Ca(2 +)-channel blockers in human ventricular tissue. Pbys Med Biol 2 002 ;47(2 3):41 67-41 79. 2 6 . Kocher AA, Schlechta B, Gasparovicova A, Wolner E, Bonaros N, Laufer G. Stem cells and cardiac regeneration. Transpl Int 2 007;2 0(9) : 7 3 1-746. 2 7 . Gu Y, Yu J, Lum LG, Lee RJ. Tissue engineering and stem cell therapy for myocardial repair. F1'ont Biosci 2007 ; 1 2 : 5 1 5 7-5 1 6 5 . 2 8 . Little RA , Frayn KN , Randall PE, et a!. Plasma catecholamines in the acute phase of the response to myocardial infarction. A1Tb Eme1'g Med 1 986; 3 ( 1 ) : 2 0-2 7 . 2 9 . Kuhar P, Lunder M, Drevensek G. The role of gender and sex hor­ mones in ischemic-reperfusion injury in isolated rat hearts. Ew' J Pbannacol 2007;5 6 1 ( 1 -3): 1 5 1-1 59. 3 0 . Trevino RP, Bisera J, Wei! MH, et a!. End-tidal C02 as a guide to successful cardiopulmonary resuscitation: a preliminary report. O'it Care Med 1 9 8 5 ; 1 3 ( 1 1):9 1 0-9 1 1 . 3 1 . Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal car­ bon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1 987;2 5 7(4): 5 1 2-5 1 5 . 3 2 . Lynch B , Einspruch EL, Nichol G, et al. Effectiveness o f a 3 0-min CPR self-instruction program for lay responders: a controlled ran­ domized study. Resuscitation 2005;67(1): 3 1 -43 . 3 3 . Ornato JP, Hankins DG. Public-access defibrillation. Prebosp Eme1'g Ca1'e 1 999; 3 (4):2 97-3 02 . 34. Riegel B, Mosesso VN, Birnbaum A, et a!. Stress reactions and per­ ceived difficulties of lay responders to a medical emergency. Resuscitation 2 006;70(1):98-1 06.

Page numbers followed by findicate figures; those followed by t indicate tables. A

A waves, 1 3 6, 1 3 6f abandonment issues, 5 7 8 abciximab dosing table in AU/NSTEMI, 8 3 t facilitated PCI and, 5 5 mechanism o f action, 7 9 reteplase with, 8 9 abdominal binding, 1 5 1 Abildgaard, Peter Christian, 1 94 accessory pathway-mediated tachycardias, 3 3 5 acebutolol, toxicology, 449 acetaminophen, toxicity, 454 acetonitrile, 466 acetylsalicylic acid (ASA, aspirin) administration by EMS, 50-5 1 cardiovascular risks of, 1 St clopidogrel versus, 7 6 delay in calling EMS and, 46 dosage, 5 0 GPis with, 89 initial treatment strategies, 73, 75 instructions, 48 ACI-TIP!, risk stratification, 3 0-3 1 acidosis myocardial, 2 3 4f renal tubule, 462 shock and, 1 1 6 sodium bicarbonate in, 467 "Act in Time to Heart Attack Signs" (AHA), 47f action potentials of myocardial cells, 3 0 1 , 3 0 1f of pacemaker cells, 3 02-3 03 phases of, 3 0 1-302 acute care units admissions, 1 1 1 discharge guidelines, 1 I 2 acute coronary syndromes (ACS) algorithm for management of, 9f annual discharges with, 1 atropine use in, 346 cardiac arrest and, 1 cardiogenic shock and, 1 1 5- 1 2 8 chronology, 2 circadian variation, 5 , 1 7 community strategies, 5 3-57 definition of, 2 destination protocols, 5 3-57 differential diagnoses, 2 7-2 8 electrocardiograms, 2 8-3 3 emergency department disposition, 3 7-3 8 emergency department management of, 63-95 EMS ' role, 48--49 imaging modalities, 3 5-3 6 indications for pacing, 3 6 8 indications for sonography, 1 3 4, 1 3 6- 1 3 9 markers o f myocardial injury, 3 3-3 5 mortality within 3 0 days, 1 5 patient evaluation, 2 5 -2 7 in poisoned patients, 445t prehospital management, 5 0-53 progression to, 5 secondary to coronary artery disease, 6t spectrum of disorders, 2 symptom recognition, 43--46

treatment of, 43 1 triage of patients, 5-6 acute decompensated heart failure, 2 7-2 8 acute heart failure syndrome disposition of patients with, I 1 1 precipitants of, 1 0 3 t treatment options, 1 0 6 acute ischemic stroke, 5 5 9 t acute lung injury, tidal volumes and, 43 3 acute myocardial infarction (AMI) cardiac biomarkers and, 70f clinical features and risk of, 26t confirmation based on ECG, 6t ECG features predictive of, 29t prehospital mortality, 43 acute myocardial syndromes, in poisoning, 445t acute pulmonary edema (APE). see also pulmonary edema clinical signs, 1 2 5 disposition o f patients with, I 1 1 ED presentation with, 97 first-line actions, 1 2 5- 1 2 6 i n heart failure, 1 04 with hypotension and shock, 1 2 4-- 1 2 7 second-line actions, 1 2 6 third-line actions, 1 2 6- 1 2 7 acute respiratory failure, causes of, 2 3 4 Adam's apple, 2 3 9 adenosine contraindications, 3 8 3 dosing, 3 83-3 84 drug interactions, 3 84 half-life, 3 8 3 indications, 3 8 3 mechanism o f action, 3 8 3 i n PSVT, 3 3 0 i n refractory PSVT, 3 3 1 side effects, 3 8 3-3 84 for sinus node reentry tachycardia, 3 3 1 in stable tachycardias, 3 2 6 , 3 2 7f Vaughn-Williams classification, 3 8 3 t adrenal dysfunction, 4 3 5 adrenergic agonists, 3 9 8-399 adrenergic receptors alpha adrenoceptors, 3 96-3 98 beta adrenoceptors, 3 98-3 99 mechanisms of action, 3 96-3 98 types of, 3 9 8f adrenergic system, responses, 3 99--400 advance directives ethical issues, 572-5 7 7 forms available for, 574 nonstandard, 575 policies on, 576t advanced cardiac life support (ACLS) airway interventions, 242 BLS and, 1 7 5- 1 7 6 care i n anaphylaxis, 5 3 4 CPR integration, 1 7 5 defibrillation, 1 7 5 for electrical injuries, 5 08-509 medications, 3 8 3 t for poisoned patients, 444, 445t--446t, 447--449 pulseless arrest algorithm, 3 1 Of team concept, 1 7 5 , 1 8 5 team leaders, 1 7 5 use of transcutaneous pacing, 3 66

advanced drowning life support (ADLS), 483-485 advanced life support (ALS) ambulances, 49 advocacy, public education and, 589 aeroallergens, 5 1 4 aeromedical services, 49-50 afterload sensitivity, 97 age/aging heart attacks by gender and, 1 2 2/ heart failure prevalence by, 96f risk of cardiac arrest and, 1 5 stroke incidence and, 545 Agency for Health Research and Quality (AHRQ), 590 agonal gasps, 1 7 9 air ambulances, 49-5 0 aircraft, early defibrillation programs, 2 0 5 airports, early defibrillation programs, 205 airway adjuncts, 2 5 6-2 64 airway control in anaphylaxis, 5 3 3-5 34 for electrical injuries, 508 in poisoned patients, 447 in water rescues, 482-483 Airway Management Device (AMD), 2 67-2 68 airway obstruction in asthma, 5 1 3 , 5 1 3/ determination of, 243 by tongue and epiglottis, 2 5 6f airways ACLS interventions, 242 anatomy of, 2 3 7-240 assessment of, 2 5 6 BLS interventions, 242 difficult, 2 7 3 -293 establishment of, 2 5 6 initial assessment sequence, 242-243 maintenance of, 242-2 52 opening of, 1 79, 1 79f suctioning, 2 5 8-2 59 surgical, 2 9 1 -292 albumin cobalt binding (ACE) test, 7 1 albuterol for anaphylaxis, 53 5 in severe asthma, 5 1 9, 5 2 0 alcohol intake as asthma trigger, 5 1 5 electrical injuries and, 5 0 1 risk o f cardiac arrest and, 1 7 aldosterone antagonists cardiovascular risks of, 1 8t in heart failure, 1 00 alkalinization, of urine, 448 alkyl nitrite, 462 allergens, as asthma triggers, 5 1 4 alpha-adrenergic agonists, 1 5 3 alpha adrenoceptors, 3 96-3 98, 3 96f alteplase (tissue-type plasminogen activator), 52 altered mental status in hypoglycemia, 447 in opioid toxicity, 463 alternative diagnoses, presence of, 3 3 ambulance responders, categories of, 49-50 ambulances, transport by, 46 Ambulatory Pediatrics Association, 5 80-5 8 1 American Academy o f Pediatrics, 580-5 8 1 5 93

594 1

INDEX

American Association of Critical Care Nurses (AACN), 590 American College of Anesthesiologists, 5 80-5 8 1 American College o f Cardiology/American Heart Association (ACC/AHA) adherence to guidelines of, 90 defibrillation guidelines, 49 Guidelines for the management of Patients with Unstable Angina Non-ST Elevation MI, 8 pulmonary artery catheter guidelines, 1 1 6 STEMI guidelines, 46, 5 0 o n ultrasonography, 1 3 4 American College of Emergency Physicians, 5 6 1 An1erican College o f Surgeons, 5 7 9-580 American Heart Association (AHA) ACLS pulseless arrest algorithm, 3 1 Of "Act in Time to Heart Attack Signs, " 47f CPR guidelines, 43 ECC CPR guidelines, 2 05-2 06 on family attendance at codes, 5 S0-5 S 1 guidelines for CPR, 1 S 5 research funding by, 590 on termination of resuscitation, 570 American Heart Association!American Stroke Association, 545, 547 An1erican Society of Echocardiography (ASE), 1 44-145 aminophylline, 347 2 1 -aminosteroids, 1 5 9 amiodarone administration, 3 S2-3 S 3 adverse effects, 3 S3 for atrial fibrillation/flutter, 3 3 2 , 3 3 5 in automatic atrial tachycardias, 3 3 1 in cardiac arrest, 3 S 1 , 3 8 7 cardiovascular effects, 3 97t cardiovascular risks of, 1 St characteristics, 3 S2 t dosing, 3 S2-3 S 3 , 405 in HF patients, 1 1 0 indications, 3 S 1 , 405 for junctional tachycardia, 3 3 5 mechanisms of action, 3 8 1 in refractory PSVf, 3 3 0, 3 3 1 usage, 3 S 1 , 405 Vaughn-Williams classification, 3 S 3 t i n ventricular tachycardia, 3 2 S , 3 3 0 amlopidine toxicology, 45 1 amphetamines, 45 S-460 amygdalin, 466 amyl nitrate, 46 1 , 467 anaphylaxis, 5 3 0-5 3 7 clinical manifestations, 5 3 1-5 3 2 , 5 3 2 t definition, 5 3 0 diagnostic criteria, 5 3 0, 5 3 1 t differential diagnoses, 5 3 2 , 5 3 3 t emergency department management, 5 3 4-5 3 5 epidemiology, 5 3 0-5 3 1 etiologies, 5 3 1 , 5 3 2 t general care for, 5 3 3-5 3 4 pathophysiologic concepts, 5 3 2-5 3 3 prehospital care, 5 3 4 the unstable patient, 5 3 5-5 3 6 Anectine. see succinylcholine anesthesia halothane inhalation, 462 in rapid sequence intubation, 524-5 2 5 sevoflurane, 462 angina, 3 7, 68 angioedema, anaphylaxis and, 5 3 1 angiography

after out-of-hospital arrest, 4 3 1 atheroma burden and, 2 electron-beam computed tomography, 3 6 risk stratification and, 72 Angiomax, outcomes, 7S angiotensin, 4 1 1 angiotensin converting enzyme inhibitors (ACEis) in cardiogenic shock, 1 1 7, 1 2 4 cardiovascular risks of, 1 St complications, 1 07-10S contraindications, I 08t in heart failure, 1 00, 1 04, 1 07-108 initiation of, 7 5 loop diuretics with, 1 06 mechanism of action, 1 0 7 angiotensin II clinical use, 42 1-42 2 dosing, 42 0-42 1 mechanism of action, 42 0-42 1 angiotensin receptor blockers (ARBs), I 00 cardiovascular risks of, 1 St in heart failure, 1 0 S mechanism o f action, 1 0 S side effects, 1 OS anterior circulation stroke, 548 anterior internodal pathway, 3 04 anteromedial nasal septum, 2 5 S antiarrhythmic drugs basic principles of, 3 S0-390 classification of, 3 S 1 contraindicated in HF, 1 1 0 in emergency cardiovascular care, 3 79 proarrhythmic risks of, 3 SO Vaughn-Williams classification, 3 S2 t anticholinergic drugs management of toxicity, 454-45 5 poisoned patients, 446t in severe asthma, 5 2 0 toxicology, 454 anticholinergic symptoms, 445t anticoagulant therapy atrial fibrillation/flutter, 3 3 4-3 3 5 in AU/NSTEMI, 82t-S4t in heart failure, 1 09 initial management strategies and, 7 7-79 inpatient, 1 1 0 for stroke patients, 560-5 6 1 anticonvulsants, 4 3 5 antidromic reciprocating tachycardias, 3 3 5 antidromic tachycardia, 2 9 S antihistamines for anaphylaxis, 5 3 5 anticholinergic symptoms, 454 poisoned patients, 446t antileukotrienes, 52 1 antiplatelet therapy in AU!NSTEMI, S2t-S4t initiation of, 7 5-77 for stroke patients, 562 anti psychotics anticholinergic symptoms, 454 management of toxicity, 45S toxicology, 45S antithrombin III (AT3), 77 aorta, balloon occlusion of, 1 66 aortic arches, 1 3 5/ aortic dissection, 2 7, 1 3 5 apoptosis, inhibition of, 4 3 3 argmme vasopressm clinical trials of, 4 1 3-4 1 8 clinical uses for, 4 1 S-42 0 during CPR, 4 1 2 -4 1 3 , 4 1 2f, 4 1 4f, 4 1 5-4 1 8 epinephrine venus, 4 1 4-4 1 S , 4 1 Sf, 4 1 9t during hemorrhage, 42 1/ .

.

.

during hemorrhagic shock, 42 2/ limitations during CPR, 41 8-4 1 9 pharmacologic effects, 4 1 1-4 1 S amino acid sequence, 4 1 1/ description, 4 1 0 physiology of, 4 1 0-4 1 1 receptors, 4 1 1-4 1 2 arm numbness, reports of, 44-45 arm pain, reports of, 44-45 Army Research Office (ARO), 590 arrhythmias. see also dysrhythmias; specific arrhythmias accessory pathways in, 2 9 S cardiac arrest and, 1 5 causes of, 306 classification of, 2 96-2 99 electric shocks and, 503 electrophysiology of, 3 00-3 0S evaluation, 2 9 5-2 96 fictitious, 297, 297f in hypothermia, 492 monitoring of drug administration, 3 2 7 procainamide in, 3 S9 recognition of, 296-2 99 risk of cardiac arrest and, 1 7 in severe hypothermia, 493 in therapeutic hypothermia, 434 treatment of, 3 2 7-3 3 5 arrhythmic shock, 1 1 6 arterial blood gases, 5 1 7 arterial oxygen content, 2 44 artificial neural networks, 3 1 , 3 2 t aryepiglottic folds, 2 3 7, 2 3 9f arytenoid cartilages, 2 3 9 aspirin. see also acetylsalicylic acid (ASA, aspirin) as asthma trigger, 5 1 4 clopidogrel with, S S dosing table in AU/NSTEMI, S2t unfractionated heparin with, S S assessments cardiovascular, 4S6 CNS, 4S5-4S6, 4S6t electrocardiographic, 3 1 3 initial clinical evaluation, 67 patient histories, 67-6S physical examinations, 67-6S prehospital, 50 pulmonary, 4S6 renal system, 4S7 reperfusion options, S7t in stroke, 5 5 1 , 5 5 2 t, 5 5 3-5 54, 5 5 3 t, 556, 5 5 6t ultrasound, 1 2 9-1 3 9, 1 2 9- 1 4S asthma, severe life-threatening assessing severity of, 5 1 5-5 1 7 , 5 1 6t consensus group guidelines, 5 1 3 differential diagnoses, 2 7 , 5 1 7-5 1 S , 5 1 St difficult to ventilate patients, 5 2 7 ECMO in, 5 2 S emergency department management of, 5 1 S-52 2 epidemiology, 5 1 2-5 1 3 facts about, 5 1 5 ICU admissions, 5 2 3 indications for endotracheal intubation, 524 inhaled beta2 agonists, 5 1 9-52 0 intubated, ventilator-dependent patients, 5 2 6-5 2 7 mechanical ventilation in, 52 5-5 2 7 monitoring, 5 1 7 mortality rate, 5 2 S overview, 5 1 2-5 1 3 pathophysiology, 5 1 3-5 1 4 posttreatu1ent care, 522-5 2 3

IN DEX

prehospital deterioration, 5 1 8 primary therapy, 5 1 9 rapid sequence intubation in, 524--5 2 5 response t o initial treatment, 52 2-52 3 risk factors, 5 1 4f signs and symptoms, 5 1 4 supplemental oxygen in, 5 1 9 triggers for, 5 1 4--5 1 5 , 5 1 4t types of, 5 1 5 vital signs in exacerbation of, 5 1 7 asystole atropine for, 3 84 pulseless arrest and, 3 1 1-3 1 2 , 3 1 1f atelectasis, 1 3 8, 1 3 9 atenolol characteristics, 3 82 t dosing, 3 8 5 Vaughn-Williams classification, 3 8 3 t atheroma burden, 2 atherosclerosis, 548 ATP release, 400 atrial fibrillation anticoagulation in, 3 3 4-3 3 5 cardioversion electrodes, 3 64 causes, 3 3 2 description, 3 3 2 duration-based treatment, 3 3 3 t ECG features, 3 1 6f preexcited, 3 2 6f, 3 3 2-3 3 4, 3 3 4t rate control, 3 3 2 restoration o f sinus rhythm, 3 3 5 in severe hypothermia, 493 stroke and, 5 49 with wide-complex conduction, 3 2 5f atrial flutter anticoagulation in, 3 3 4-3 3 5 causes, 3 3 2 defibrillation energy settings, 3 6 5 description, 3 3 2 duration-based treatment, 3 3 3 t ECG features of, 3 1 8f ibutilide for, 3 87 preexcited, 3 3 4t rate control, 3 3 2 atrial tachycardias automatic, 3 3 1 effect of adenosine, 3 2 7f atrioventricular block 2 : 1 conduction ratio, 3 60 advanced, 3 60 classification of, 348, 3 50 degree of block, 3 5 0 etiologies, 348 first-degree, 3 42-344, 3 50-3 5 1 ECG features of, 3 50t, 3 5 1 pathophysiology, 3 5 1 therapy, 3 5 1 indications for pacing, 3 68 second-degree, 343f, 3 44, 3 5 0t ECG features of, 3 50t second-degree, type I clinical manifestations of, 3 52 t, 3 5 3 , 3 54t description, 3 5 1 ECG features of, 3 52 t, 3 5 3 , 3 5 3f, 3 54t etiologies, 3 5 3 , 3 54t pathophysiology, 3 5 2 , 3 5 2 t, 3 54t therapy, 3 5 2 t, 3 54, 3 54t second-degree, type II clinical manifestations, 3 5 5 description, 3 5 5 ECG criteria, 3 5 5 etiologies, 3 5 5-3 56 pathophysiology, 3 55 therapy, 3 5 6 sinus bradycardia with, 3 47f

sites of, 3 50 third-degree, 343f, 344, 3 5 0t in beta-blocker toxicity, 450 clinical manifestations, 3 5 6, 3 5 7t, 3 59t ECG features of, 3 5 0t, 3 5 6, 3 5 7f, 3 5 7t, 3 5 8, 3 5 9t etiologies, 3 5 7 t, 3 5 8, 3 5 9t pathophysiology, 3 5 6, 3 5 7t, 3 59t therapy, 3 5 7 t, 3 5 8, 3 59t atrioventricular conduction in acute myocardial infarction, 3 69t dissociation, 2 99, 3 60 disturbances in STEMI, 3 70t atrioventricular junction, 3 02 atrioventricular nodal reciprocating tachycardia (AVRT), 3 1 7 , 3 1 9, 3 2 7f atrioventricular nodes conduction through, 3 04 impulse conduction and, 341 atropine adverse effects, 3 8 5 anticholinergic symptoms, 454 for bradycardia, 3 45-346 for calcium channel blocker toxicity, 452 in digoxin toxicity, 453 in disorders of impulse formation, 3 42 dosing, 3 84--3 8 5 endotracheal administration, 3 80 indications, 3 84 mechanism of action, 3 84 in organophosphate toxicity, 468 in rapid sequence intubation, 2 79, 5 2 5 Vaughn-Williams classification, 3 8 3 t atypical angina, 68 auto-PEEP, 525, 5 2 6, 527 automatic atrial tachycardias, 3 3 1 automatic defibrillators, history of, 1 98 automatic external defibrillators (AEDs). see also defibrillation biphasic waveform technology, 2 2 5-2 2 8 i n children, 2 1 3 community access, 43, 2 1 4 compression first vs shock first, 1 74 in dense public spaces, 1 7 0 description, 2 06-207, 206f early defibrillation programs, 2 0 5 i n electrical injuries, 508 first responders and, 2 04 fully vs semiautomated, 207 history of, 1 9 8 home (residential) use, 2 1 4 in hospitals, 1 70, 2 1 3 liability issues, 2 1 4--2 1 5 maintenance, 207 neighborhood access, 2 1 4 nonresidential locations, 2 1 4 operation, 207 pacemaker interference with, 372, 3 74 personal use, 2 1 4 readiness, 207 regulatory issues, 2 1 4--2 1 5 Rochester, MN study, 1 70 Seattle/King County, WA study, 1 7 0 i n severe hypothermia, 493 shock sequences, 17 5 successful law enforcement programs, 49t training in schools, 1 7 2 use by first responders, 48-49 zero-tier responders, 1 72 automatic implanted cardioverter­ defibrillators (AICDs), 3 72-3 7 5 automatic rhythms, 3 1 7-3 1 9 automaticity, rhythm mechanisms and, 3 0 3 , 341 autonomy, principle of, 568, 573

5 95

AutoPulse CPR device, 1 6 5f azotemia, diuretic-induced, 1 04 B

B-type natiuretic peptide (BNP), 3 5 bag-mask devices, 2 60-2 64 bag-mask ventilation (BMV), 2 60-2 63 "successful," 2 8 7 "unsuccessful," 2 8 7 "bagging, " 46 1 balloon occlusion of the aorta, 1 66 barbiturates, poisoned patients, 446t baroreceptors, activation of, 4 1 1 baroreflex, 400 barotrauma, tidal volumes and, 43 3 basic drowning life support (BDLS), on-land, 482-483 basic life support (BLS) ACLS and, 1 7 5-1 76 airway interventions, 242 algorithm for health care providers, 1 7 6f, 1 78-1 80 algorithm for lay-responders, 1 7 8- 1 7 9 algorithms, 1 7 5- 1 85 CPR integration, 1 7 5 defibrillation, 1 7 5 in electrical injuries, 508 indications for withholding of, 569 recent recommendations, 1 7 3-1 7 5 survival and, 1 69-1 9 1 team concept, 1 7 5 , 1 8 5 termination of, 5 7 0 basic life support (BLS) ambulances, 49 basic science investigators, 589 basic water life support (BWLS), 482 basophils, activation of, 5 3 2 Battelli, Frederic, 1 95 Beck, Claude, 1 97- 1 98, 1 9 7f bedside ultrasound cardiac arrest management and, 1 3 9-141 cardiac function assessed by, 13 2 chest pain assessed by, 1 3 4-- 1 3 5 dyspnea assessed by, 1 3 5- 1 3 9 ejection fraction assessed by, 1 3 2 hypotension evaluation, 1 2 9-1 3 4 invasive procedures with, 1 4 1 - 1 44 training in, 1 44-- 1 45 beneficence, principle of, 5 68 benzodiazepines for amphetamine toxicity, 459-460 for cocaine toxicity, 460 for drug-induced seizures, 464, 468 flumazenil in toxicity of, 447 poisoned patients, 446t in rapid sequence intubation, 2 7 9-2 80 for toxicity of antipsychotics, 458 in tricyclic antidepressant toxicity, 456 benzothiazepines, 45 1 benzoylmethylecogonine. see cocaine beta-adrenergic blocking agents. see betablockers beta adrenoceptors, 3 98-3 99 beta blockade cardiogenic shock and, 1 1 9f in disorders of impulse formation, 3 42 heart failure and, 1 1 8 beta-blockers ACC/AHA guidelines, 52 as asthma trigger, 5 1 4 in atrial fibrillation/flutter, 3 3 2 i n automatic atrial tachycardias, 3 3 1 cardiogenic shock and, 1 1 7 cardiovascular risks of, 1 S t contraindications, 1 08t, 3 8 5

596 1

INDEX

beta-blockers (continued) dosing, 3 8 S i n heart failure, 1 00, 1 08-109 initial treatment strategies, 74 for irregular narrow-complex tachycardias, 3 2 7 for junctional tachycardia, 3 3 S management o f toxicity, 4S0--4S l mechanism of action, 3 8 S overdose presentation, 4SO poisoned patients, 446t in PSVT, 3 3 0 side-effects, 3 8 S for sinus node reentry tachycardia, 3 3 1 in torsades de pointes, 3 2 9 toxicology, 449-4SO beta2 agonists, S l 9, S 2 S betaxolol, toxicology, 449 Beth Israel Hospital, 1 9 8 bilevel positive airway pressure (BiPAP), S 2 4 bioengineering careers, S89 bioethics committees, S 7 2 , S 76-S 77 bioimpedance measurements, 1 0 1 biomarkers, prognostic use of, 436 biotrauma, tidal volumes and, 43 3 biphasic positive airway pressure (BiPAP), 1 0 3 bivalirudin, 7 8 , 8 2 t blunt trauma, spinal trauma and, 1 79 Boston criteria for heart failure, 99, 99t Boxt neural nerwork, 3 2 t bradycardia, 3 4 1 -3 6 1 . see also sinus bradycardia assessment, 3 44 atropine for, 3 84 dopamine for, 3 86 evaluation, 3 44 in hypothermia, 49 1-492 indications for pacing, 3 6 8 initial patient stabilization, 3 44 management algorithm, 34Sf in poisoned patients, 44S t therapy, 34S-347 in tricyclic antidepressant toxicity, 4S S Brain airway, 2 6 S Brain Attack Coalition, S 6 2 brain imaging, S S 7 , S 5 9 brain injnry clinical signs of, 42 8 post-cardiac arrest, 42 8 Braunwald Risk Stratification, 8 Brazil, drowning deaths in, 478, 479f breathing ACLS interventions, 2 42 assessment of, 1 7 8f, 1 79 BLS interventions, 2 42 initial assessment sequence, 2 42-243 bretylium, 3 82 t, 3 8 3 t bronchoconstriction, S l 3 , S 1 3f bronchospasm, 4SO Brugada syndrome, 3 2 9 bumetanide, 1 04, l O S t bundle-branch blocks fibrinolytic therapy in, 80 impulse conduction and, 3 4 1 indications for pacing, 3 6 8 bundle branch re-entrant tachycardia, 3 2 4t bundle branches action potentials of, 3 02 conduction through, 3 04 bundle of His, 3 0 2 , 3 04 bupropion, 4S7 burns electrical injuries and, S07f high-voltage, 499f lightning and, 506f

myocardial, S03 transfers for, S09 Bums, Allan, 1 94 butyl nitrate inhalation, 46 1 bystander CPR, ethics of, S69-S 70 c

C-reactive protein (CRP), 1 6, 7 1 caffeine, 3 84 calcium, coronary, 3 6 calcium antagonists, 7 S calcium channel blockers for cocaine toxicity, 460 contraindicated in HF, 1 1 0 in disorders of impulse formation, 3 42 dosing, 3 8 S-3 86 for irregular narrow-complex tachycardias, 3 2 7 for junctional tachycardia, 3 3 5 management of toxicity, 4S l-4S2 mechanisms of action, 3 8 S poisoned patients, 446t for PSVT, 3 3 0 signs o f overdose, 4S l for sinus node reentry tachycardia, 3 3 1 toxicology, 4S l calcium chloride, 4S 1 --4S2 calcium gluconate for arrest in pregnancy, S42 for calcium channel blocker toxicity, 4S l --4S2 calcium salts dosing, 40S indication, 40S usage, 40S "Call 9 1 1 , Call Fast" campaign, 4S capnography, 244--24S basic principles, 24S in cardiac arrest, 246 function, 24S capnometry, 244--2 4S basic principles, 24S in cardiac arrest, 246 colorimetric devices, 24S false-negative results, 246 false-positive results, 24S-246 captopril, side effects, 1 1 8 carbamates, 468--469 carbamazepine, 3 84 carbon dioxide detectors, 2 8 S-2 86 carbon monoxide management of toxicity, 464--4 6 S poisoned patients, 446t toxicology, 464 carbon tetrachloride, 462 carboxyhemoglobinemia management of, 464--46S methylene chloride inhalation and, 462 pulse oxymetry in, 244 cardiac arrest. see also sudden cardiac arrest (SCA) in accidental hypothermia, 490 ACS and, 1 amiodarone in, 3 8 1 arginine vasopressin during CPR, 4 1 3-4 1 8 , 4 1 S t, 4 1 6t from blunt trauma, S 7 1 capnography in, 246 capnometry in, 246 cellular changes, 1 9-2 0 cesarean delivery in, S41-S42 in children, 1 4-- l S , 43 7 controlled reoxygenation after, 432 definitions, 1 1 - 1 2

i n drowning, 482 drug-induced, 3 66 EMS-treated, 1 2 , 1 4f, 1 8f en route to hospital, 46 endotracheal intubation in, 2 7 3 -290 epidemiology of, 1 2 -2 0 epinephrine during CPR, 41 St functional outcomes, 436 hemodynamic instability after, 43 1 high-risk groups, l S- 1 6 hyperthermia after, 43 3 iatrogenic, S79 in-hospital, I S incidence of, 1 3 lidocaine in, 3 87-3 8 8 metabolic abnormalities and, 402 out-of-hospital, 1 9 , 400f, 43 1 pathophysiology of, 1 49-1 60 phases of, 2 04f prehospital management of, 1 3 9 procainamide in, 3 89 prognostication, 43S--436 pulseless, 3 09-3 1 2 pulseless bradyasystolic, 3 66 rescue sequence for, S 40 respiratory arrest vs. , 242 return of spontaneous circulation, 1 S 7-1 S9, 4 1 3 , 4 1 4f, 4 1 Sf, 4 1 6f seizures after, 4 3 3 supplemental oxygen in, 2 S 3 survival, 1 8f, 1 9f survival to discharge and, 4 3 1 termination of resuscitation, 49S--496 triggers for, 1 6-1 8 ultrasound in management of, 1 3 9-1 41 ventricular function after, I S 7 vomiting in, 2 6 3 Cardiac Arrhythmia Suppression Trial (CAST), 3 8 1 cardiac bypass, for beta-blocker toxicity, 4SO cardiac care units (CCUs), goals of, 3 8 cardiac catheterization, prior results, 3 7 cardiac conduction system anatomy of, 3 04--3 0 S , 3 0 Sf ECGs and, 3 06 cardiac function, sonographic assessment, 1 3 6 cardiac glycosides poisoned patients, 446t toxicity, 4S4 cardiac index in left ventricular dysfunction, 1 1 9 postresuscitation, 403f cardiac ischemia, ultrasonography in, 1 3 4-- 1 3 S cardiac markers in ACS secondary to CAD , 6t combinations of, 3 S in diagnosis of Ai\IU, 70-7 1 discordant results, 3 S of myocardial injnry, 3 3-3 S predictive properties of, 3 4t risk stratification and, 3 7 risk stratification in UNNSTEMI, 7t serial measurements of, 37, ?Of cardiac massage minimally invasive direct, 1 66, 1 6 6f open chest, 1 S2 , S42 cardiac output (CO) determinants of, 1 1 6-1 1 7 systemic vascular resistance and, 97 cardiac remodeling, 97 cardiac tamponade traumatic, 1 3 3-1 34, 1 3 4f ultrasonographic assessment, 1 3 2-1 34, 1 3 3f cardiac transplantation, 346 cardiogenic shock

IN DEX

beta-blocker impact on, 52 complicating acute coronary syndromes, 1 1 5- 1 2 8 description of, 1 1 7 in elderly patients, 1 2 2 epidemiology of, 1 1 5-1 1 6 hemodynamic definition of, 1 1 9 hemodynamic parameters of, 1 1 7, 1 1 7t, 1 1 8-1 1 9 incidence of, 1 1 5 initial focus of therapy, 1 1 6 intra-aortic balloon counterpulsation, 1 2 1f pathophysiology of, 1 1 7, 1 1 8f patient transfer in, 1 2 1 prehospital recommendations, 1 2 2 reperfusion in, 1 2 4 treatment of, 1 2 0- 1 2 4 vasodilation and, 1 0 5 cardiomyopathies, segmental wall motion and, 1 3 4 cardiopulmonary arrest in drowning, 483 in pregnancy, 5 3 9t, 542 severe asthma and, 5 1 8 cardiopulmonary bypass (CBP) partial, 1 66 resuscitation of pregnant patients, 542 rewarming, 495 , 495t cardiopulmonary resuscitation (CPR). see also resuscitation in accidental hypothermia, 490 active compression-decompression (ACD-CPR), 1 6 3 - 1 64 American Heart Association guidelines, 4 3 arginine vasopressin during, 412-4 1 3 , 4 1 2f, 41 'if, 4 1 8-4 1 9 i n basic life support, 1 6 9 blood flow during, 1 5 0-1 52 , 1 5 5- 1 5 6 bystander, 1 9, 1 7 1 - 1 7 2 , 1 72 chest compression rates, 1 5 0, 1 5 1 compression-only, 1 87, 1 87t, 2 3 9 compression-ventilation type, 1 5 1 , 1 7 3 - 1 74 coronary perfusion pressures and, 1 52-1 5 3 , 1 54f, 1 5 5- 1 5 6, 1 5 5f, 1 62f, 4 1 7f cough, 1 50, 1 88 crash airway intubation and, 2 7 5 defibrillation and, 1 8 5 DNAR orders and, 5 7 7-5 78, 5 7 8-5 79 duration of, 1 5 6, 5 69-5 70 duty cycle, 1 5 0 early cooling during, 43 3 epinephrine during, 4 1 2f, 4 1 4f ethics of, 568 interposed abdominal compression, 1 6 1 - 1 62 , 1 62f load-distributing-band, 1 64- 1 6 5 LUCAS , 1 6 3 , 1 6 5f mechanical piston devices, 1 62-1 6 3 , 1 6 3f no-flow times, 1 5 6 open chest cardiac massage, 1 65-1 66, 542 over-the-head, 1 8 8 oxygenation during, 2 3 4-2 3 7 perfusion pressure gradients, 1 5 3 phased thoracic-abdominal compressiondecompression (PTACD), 1 65 , 1 6 5f in pregnancy, 5 3 8-543 , 540t prone patients, 1 8 8 i n pulseless cardiac arrest, 309 quality feedback, 1 8 5- 1 8 6 rapid compression rate, 1 62 in severe hypothermia, 493-494 simultaneous ventilation-compression (SVC-CPR), 1 6 3

survival and, 1 5 6-1 5 7 survival t o discharge and, 1 5 1 tidal volumes and, 2 3 6 ventilation during, 2 3 4-2 3 7 vest-like garments, 1 64-1 6 5 withdrawing of, 5 69-5 72 withholding of, 569-572 cardiorespiratory arrest, crash airway intubation for, 2 74-2 76 cardiovascular disease (CVD) causes of death from, 1 5f trends in morbidity and mortality, 1 3 cardiovascular risk factors, U. S . trends, 1 2f cardioversion for atrial fibrillation/flutter, 3 3 5 description, 3 62 history of, 1 9 8 for sinus node reentry tachycardia, 3 3 1 care pathways, development of, 90 carotid artery atherosclerosis, 548-549 carotid artery territory stroke, 548 cartelolol, toxicology, 449 casinos, early defibrillation programs, 205 cassava, 466 catheters, for suctioning, 2 5 8 , 2 5 9f central lines drug administration, 3 80 placement of, 1 4 1 - 1 42 central nervous system, blood flow and, 1 49. see also brain injury central venous pressures (CVPs), 1 3 0, 43 1-432 cerebral metabolic rate for oxygen (CMR02), 43 3 cerebral perfusion pressures (CPPs), 432 cerebrospinal fluid biomarkers, 436 cerebrovascular accident (CVA). see stroke cervical collars, 1 79 cervical spine injury (CSI), 2 5 6-2 5 7 , 482 cesarean delivery 20-week rule, 542 following cardiac arrest, 541-542 "chain of survival" metaphor, 1 70- 1 7 3 , 1 7 1f in drowning, 480-487, 480f in STEMI, 43, 44f in stroke, 547, 547f supporting evidence for, 1 7 1 - 1 72 charcoal, activated for cocaine toxicity, 460 complications, 448 contraindications, 448 gastrointestinal decontamination with, 448 multi-dose, 448 in opioid poisoning, 464 in the poisoned patient, 447-448 charcoal hemoperfusion, 449 chest compressions, 1 8 3 - 1 8 5 , 1 84f AED coordination with, 208-2 09 blood flow and, 400 compression-only CPR, 1 8 7 coronary blood flow and, 4 0 lf chest discomfort prior to Al\ll.I , 45 reports of, 44-45 chest pain bedside ultrasound, 1 3 4-1 3 5 clinical classification of, 68 clinical features of AMI, 26t cocaine-induced, 460 ECG features of AMI, 29t indications for ultrasonography, 1 3 4 morphine sulfate in, 7 3 noncardiac, 68 chest radiography (CXR) heart failure diagnosis and, 99- 1 00 in severe asthma, 5 1 7

597

children cardiac arrest in, 1 4- 1 5 common causes o f cardiac arrest, 43 7 compression-ventilation ratios, 1 74 decision-making for, 5 7 6-5 7 7 defibrillation in, 2 1 2-2 1 3 drowning by, 482 duration of resuscitation efforts, 5 7 1 electrical injuries, 5 0 1 epinephrine for asthma in, 52 1 impacts of deaths of, 4 3 7 junctional tachycardia in, 3 3 5 post -cardiac arrest syndrome in, 4 3 7 severe asthma in, 52 1 sudden deaths in, 1 9 terbutaline for asthma in, 52 1 unexpected death in, 1 9 use o f inhalants, 462 Chlamydia pneumoniae, 5 1 4 chloroform, 462 chlorpromazine, seizures and, 458 cholesterol levels, risks-related to, 16 cholinergic symptoms, 445 t cholinergic toxidrome, 446t, 468 chyn1ase, in anaphylaxis, 5 3 3 cigarette smoke, 1 7 , 5 1 4 Cincinnati prehospital stroke scale (CPSS), 553, 553t circadian rhythms, 5 , 1 7 circulatory arrest, i n anaphylaxis, 5 3 6 citalopram, 457 classification, assessments, 344-345 clinical evaluations, 67. see also physical examination clinical findings, risk stratification, 7 t clinical investigators, 5 88-5 89 clonazepam, for seizures, 43 5 clopidogrel aspirin versus, 7 6 aspirin with, 8 8 cardiovascular risks of, 1 St dosages, 76 dosing table in AU/NSTEMI, 82t initial treatment strategies, 74, 7 5-77 recommendations for, 76 clozapine, seizures and, 45 8 cocaine as asthma trigger, 5 1 5 body stuffers, 46 1 management of toxicity, 460-46 1 poisoned patients, 446t risk of cardiac arrest and, 1 7 toxicology, 460 codes DNAR orders and, 5 7 8 family attendance at, 5 80-5 8 1 cold-water immersions, 482 collapse-to-CPR intervals, 2 02f collapse-to-defibrillation times, 202f colorimetric end-tidal CO detectors, 2 84t Combitube, 2 5 7 , 2 6 5 , 2 66-2 69 insertion, 268f, 269 comet-tail artifacts, ultrasonographic, 13 Sf common carotid arteries, 2 3 5f common oleander (J'fe1'ium oleande1'}, 454 communications death notifications, 5 8 1-5 8 2 , 5 8 1 t quality improvement feedback, 90 competence bedside determination of, 5 7 3 decision-making capacity and, 5 7 3 complete blood counts, 5 1 7 comprehensive stroke centers (CSCs), 562 compression-only CPR, 2 3 9

598 1

INDEX

compression-ventilation CPR in children, 1 74 in infants, 1 74 recent recommendations, 1 74 compression-ventilation ratios oxygen delivery and, 2 3 6f ventilation rates and, 2 3 6-2 3 7 computed tomography electron-beam, 3 6 i n hemorrhagic stroke, 5 5 9 imaging i n stroke patients, 5 5 7 , 5 5 9 i n ischemic stroke, 5 59 risk stratification and, 72 for stroke patients, 5 5 6 conduction delays, i n poisonings, 45 5 conduction system, cardiac, 3 04-3 05 congenital arrhythmias, 1 5 congestive heart failure (CHF) heart sounds in, 2 6-2 7 tissue Doppler imaging, 1 3 6-1 3 7 treatment options, l O S t ultrasonography in, 1 3 6-1 3 7 Conn & Modell neurologic classification, 487t Consolidated Edison, 1 96 continuous arteriovenous rewarming, 495t continuous ECG monitoring, 2 8-2 9 continuous positive airway pressure (CPAP), 1 0 3 Convallaria nzajalis (lily of the valley), 454 coronary angiography after out-of-hospital arrest, 4 3 1 atheroma burden and, 2 risk stratification and, 72 coronary arteries, intravascular ultrasound, 2 coronary artery bypass grafting (CABG), 76 coronary artery disease (CAD) assessment of risk for, 7 cholesterol levels and, 1 6 clinical manifestation, 4f incidence of, 1 3 out-of-hospital cardiac arrest and, 43 1 presentation of ACS secondary to, 6t previous diagnostic testing for, 3 7 risk factors for, 1 5-1 6 coronary artery stenosis, 1 5 6 coronary care units, admission to, 2 5 coronary perfusion pressures adequate, 1 52-1 5 3 cardiopulmonary resuscitation, 1 54f circulatory adjuncts, 1 6 1- 1 6 8 clinical implications, 1 5 3-1 5 5 determinants during CPR, 1 52-1 5 3 measurement of, 1 5 3 perfusion pressure gradients, 1 5 3 resuscitation success and, 400f survival and, 1 5 6-1 5 7 coronary plaques disruption of, 3f formation of, 2 progression, 2f rupture of, 5 , Sf stable, 2-5 , 4f structure of, 3 unstable, 2-5 vulnerable, 3, 4f corticosteroids for anaphylaxis, 53 5 in severe asthma, 5 1 9, 5 2 0 cost effectiveness, treatment strategies and, 72-80 costochondritis differential diagnoses, 2 8 E D diagnoses of, 3 3 costophrenic sulci, fluid in, 1 3 3 cough cardiopulmonary resuscitation, 1 50

cough CPR, 1 8 8 courts, a s decision makers, 5 7 6-5 7 7 crash airway intubation for cardiorespiratory arrest, 2 74-2 7 6 intubation steps, 2 74-2 7 5 "RAPIDS " approach to, 2 7 5-2 7 6 creatine kinase predictive properties of, 3 4t serial measurements of, 70f, 7 1 creatine kinase MB fraction (CK-MB) in myocardial injury, 3 3 predictive properties of, 3 4t serial measurements of, 3 3 , 70f, 7 1 subforms of, 7 1 cricoid cartilage, anatomy, 2 3 9-240 cricoid membranes, 2 9 1f cricoid pressure, 1 8 3 , 1 8 3f, 2 8 1-2 8 2 , 540 in CPR, 48 3 use of, 2 6 3 , 263f cricothyrotomy, 2 9 1 percutaneous dilational, 2 9 1 simple, 2 9 1 surgical, 2 9 1 cuffed endotracheal tubes, 2 7 7 cuffed perilaryngeal sealers (CPLSs), 2 64 cuffed pharyngeal sealers (CPSs), 2 64 cuffiess anatomically preshaped sealers (CAPS), 2 64 cyanide management of toxicity, 467--468 poisoned patients, 446t toxicology, 466--467 cyclooxygenase inhibitors, 1 8t, 7 5 , 76, 1 06 cyproheptadine, 457 cytochrome a3 , 466 D

dalteparin clearance, 7 8 dosage, 7 8 dosing table i n AU/NSTEMI, 82t outcomes, 7 7 dapsone, 466 deaths after unsuccessful resuscitation efforts, 5 82 of children, 437 clinical markers of, 495-496 from drowning, 47 7--47 8, 478t, 48 3 , 485t from electrocution, 499 in hypothermia, 483 lightning-related, 50 1-502, 502f notifications emotional support to families, 5 8 1-5 8 2 , 5 8 1 t harmful phrases, 5 8 1 t helpful phrases, 5 8 1 t termination o f resuscitation and, 5 7 0 decision-making capacity, 5 7 3 classes o f decision makers, 5 7 6-577 surrogates for patients, 5 7 5-5 7 7 deep venous thrombosis, 1 1 0 defasciculating agents, 2 7 9 Defense Advanced Research Projects Agency (DARPA), 590 defibrillation. see also automatic external defibrillators (AEDs) biphasic shocks, 2 2 3 , 224f, 2 2 5 biphasic waveform technology, 2 2 5-2 2 8 , 2 2 5f, 2 2 6f, 2 2 7f, 2 2 8-2 29, 2 2 8f cardiopulmonary resuscitation and, 1 8 5 , 1 8 6f in children, 2 1 2-2 1 3 collapse-to-defibrillation times, 2 02f delayed, 2 04

"early," 2 0 1 -2 0 5 , 202t early instruments, 1 94f electrode positioning, 3 63-3 64, 3 64f electrophysiologic mechanisms, 22 3-22 5 energy settings, 3 6 5 experimental waveforms, 2 2 5 fire hazard and, 3 7 5-3 7 6 lay-responder, 1 9 manual, 2 1 2-2 1 3 medication patches and, 2 1 2 monophasic shocks, 224f monophasic waveforms, 2 2 8-2 2 9, 2 2 8f optimal timing for, 2 04f oxygen delivery and, 2 1 2 pad positioning, 3 64, 3 64f, 3 6 5f pad sizes, 3 64 patient safety during, 3 7 5 i n patients with implanted devices, 2 1 2 in polymorphic ventricular tachycardia, 3 2 8 postresuscitation myocardial dysfunction and, 1 5 8 in practice, 2 0 1 -2 2 1 in pregnancy, 542 provider safety, 3 7 5-3 76 public access defibrillation programs and, 2 1 4f in pulseless cardiac arrest, 3 09-3 1 0 restorating life, 1 93-200 shock waveform, 3 64-3 65 single vs. stacked shocks, 2 09 in wet conditions, 2 1 2 defibrillators. see also automatic external defibrillators (AEDs); implantable cardiac defibrillators (ICDs) automated external, 206-2 07 coordination with chest compressions, 2 0 8-2 09 development of, 1 96-1 9 8 electrodes, 2 09-2 1 1 contact/impedence, 2 1 1 paddles vs, pads, 2 1 1 placement, 2 09-2 1 1 , 2 1 0f size, 2 09 energy levels, 2 1 1-2 1 2 manual, 2 0 6 shock delivery, 2 0 8 waveform analysis, 2 0 8 delays components of, 64f in seeking care, 44t, 45--46 taking ASA and, 46 demographics, of ACS, 2 5 depolarization, electrophysiology, 3 00-3 0 1 desmethylcitalopram, 457 dextrose, in poisoned patients, 447 diabetes atypical AMI symptoms in, 45 risk of cardiac arrest and, 1 6 diagnostic criteria, risk stratification by, 67f dialysis, for poisoned patients, 449 diaphoresis, likelihood of Al\11 and, 2 6t diastolic heart failure, 98 diffusion, pulmonary ventilation and, 2 3 4 digitalis in atrial fibrillation/flutter, 3 3 2 indications, 405 in PSVT, 3 3 0 in refractory PSVT, 3 3 0 Digitalis pzwpurea (foxglove), 454 digoxin in atrial fibrillation/flutter, 3 3 2 cardiovascular risks of, 1 8t in disorders of impulse formation, 3 42 dosage, 1 09 dosing, 3 86

IN DEX

drug interactions, 1 09 in heart failure, 1 09 management of toxicity, 45 3--454 mechanisms of action, 3 86 risk for toxicity, 4 53 toxicity, 1 09 toxicology, 452--45 3 dihydropyridines, toxicology, 45 1 diltiazem for atrial fibrillation/flutter, 3 3 2 , 3 3 5 in automatic atrial tachycardias, 3 3 1 characteristics, 3 82t for cocaine toxicity, 460 dosing, 3 8 5-3 86 mechanism of action, 385 in refractory PSVT, 3 3 0 toxicology, 45 1 Vaughn-Williams classification, 3 8 3 t diphenoxylate-atropine (Lomotil), 463 , 464 diphenylhydramine, 454 dipyridamole, interactions, 3 84 disopyramide for atrial fibrillation/flutter, 3 3 5 characteristics, 3 82 t dosing, 3 86 mechanism of action, 3 86 in monomorphic ventricular tachycardia, 3 2 8 Vaughn-Williams classification, 3 8 3 t distributive shock in anaphylaxis, 53 3 initial focus of therapy, 1 1 6 diuresis, HF protocol-exclusion criteria, 1 1 2f diuretic therapy in cardiogenic shock, 1 1 7 , 12 4 dosing, 406 drug interactions, 1 06 in heart failure, 1 04, 1 06 indications, 406 usage, 406 diurnal patterns, in ACS presentation, 5 DNIR. see do not attempt resuscitation (DNAR) DNR. see do not attempt resuscitation (DNAR) do not attempt resuscitation (DNAR) prehospital directives, 574--5 7 5 tattoos, 5 69 use of, 5 7 7-5 7 8 do-not-hospitalize (DNH) orders, 5 7 8 dobutamine in acute pulmonary edema, 1 2 6 cardiovascular effects, 397t in complicated STEM!, 1 2 4{ dosing, 405 indications, 405 postresuscitation myocardial dysfunction and, 1 5 8-1 59, 403f usage, 405 dofetilide characteristics, 3 82 t Vaughn-Williams classification, 3 8 3 t DONT mnemonic, 444 door-to-balloon time outcomes and, 54 reduction of, 5 6 transport options and, 5 8f door-to-needle time, transport options and, 5 8f dopa, structure, 399f dopamine administration in anaphylaxis, 5 3 5-5 3 6 for bradycardia, 3 46 cardiovascular effects, 397t

in complicated STEMI, 1 2 4f in disorders of impulse formation, 3 42 dosage, 404--4 0 5 dosing, 3 86 indications, 404 mechanisms of action, 3 86, 3 99 structure, 3 99f synthesis of, 3 99f in tricyclic antidepressant toxicity, 456 usage, 404--4 0 5 Vaughn-Williams classification, 3 8 3 t dopamine receptors, 399 doxylamine, 454 drowning, 477--489 abnormal ausculation with rales, 485 cardiovascular assessments, 486 chain of survival, 480--487, 480f classification algorithm, 484{ CNS assessments, 48 5-486, 486t coughing, 485 deaths in Brazil, 478, 479f definitions, 47 8--479 EMS activation, 48 1--482 epidemiology, 477--478 first-responder systems, 478 foam and difficulty breathing, 485 hospitalization, 485 t infections following, 486--487 mortality rates, 48 5t outcomes, 487-488 pathophysiology of, 479--480 physiologic consequences, 480 prevention programs, 480--48 1 , 48 1 t process of, 4 79--480 pulmonary assessments, 486 pulmonary edema with hypotension, 484 pulmonary edema without hypotension, 484 removal of victim from water, 482 renal system assessments, 487 respiratory arrest in, 484 risk factors, 4 7 8 terminology, 4 7 8--4 79 treatment algorithm, 484f uniform clinical reporting, 487, 487f drugs. see pharmacologic agents duloxetine, 457 DUMBEBELS mnemonic, 468 Durable Power of Attorney for Health Care, 574 Dutch Humane Society, 1 94 dyspnea, bedside evaluation of, 1 3 5- 1 3 9 dysrhythmias. see also arrhythmias; specific dysrhythmias cardiac ischemia-reperfusion and, 4 3 1 inhalant abuse and, 463 in tricyclic antidepressant toxicity, 45 5 E

E waves, 1 3 6, 1 3 6f early goal-directed therapy (EGDT), 43 1--432 early hemodynamic optimization, 43 1--43 2 ECGs. see electrocardiograms echocardiography after electric shocks, 503 in cardiogenic shock, 120 in heart failure diagnosis, 99 ecstasy (3 ,3 -methylene dioxymethamphetarnine, ecstasy, MDMA), 459 ectopic atrial tachycardia (EAT), 3 3 1 education, in post-cardiac arrest care, 43 7--43 8 . see also patient education

599

ejection fraction bedside evaluation of, 1 3 2 classification of, 1 3 2 sonographic assessment of, 1 3 6 elderly patients atypical AMI symptoms in, 45 cardiogenic shock in, 1 2 2 presentations with MI, 2 7 electric shocks. see also cardioversion; defibrillation; electrical therapies cardiac effects, 503-5 04 discharge of patients, 5 04 monitoring of patients, 5 04 prognosis after, 5 04 for resuscitation, 1 94-- 1 9 5 electrical-conducting cells, 3 0 0 electrical currents pathway prediction, 5 04 physiological effects, 5 04--5 05 electrical injuries, 498-5 1 1 ACLS for, 508-509 basic life support, 508 ED management of, 509 epidemiology, 499, S OOt, 5 0 1 flashover, 507f out-of-hospital management, 506-507 pathophysiology, 5 04--5 06 physics of, 5 04--506 prevention of, 509-5 1 0 resuscitation in, 508 electrical therapies, 3 62-3 7 7 electrocardiograms (ECGs) ACS evaluation, 2 8-3 3 in ACS secondary to CAD , 6t additional leads, 2 9 after electric shocks, 503 in arrhythmias, 296 cardiac monitoring, 3 07-3 08 classification of ventricular arrhythmias, 3 2 4t clinical correlation, 3 0 7 confirmation of AMI based on, 6t confounders, 2 9 continuous monitoring, 2 8-2 9 criteria for sinus bradycardia, 347 electrode placement, 308f in the emergency department, 2 8 , 66 esophageal lead, 3 2 1-324, 3 2 2[, 3 2 3f features of AV blocks, 3 5 0t function of, 3 05-306 heart block types, 343f in heart failure, 1 04 initial assessments, 3 1 3 normal, 70 pre- and post-conversion, 3 2 7 prehospital, 5 0 rhythm analysis, 3 0 7 rhythm recognition and, 3 07-3 08 right bundle-branch block, 69f risk stratification and, 3 7 risk stratification in UA/NSTEMI, 7t, 69-70 skills development, 3 0 7 ST-segment elevation, 69f surface ECG, 3 06f in triage of possible ACS, 5-6 electrocution childhood, 5 0 1 risk groups for, 499 victim extraction, 507 electroencephalograms, prognostic, 4 3 6 electron-beam coronary tomography (EBCT), 3 6 electrophysiology, cardiac, 3 00-3 03 embolic stroke, 547

600

I

INDEX

Emergency Cardiovascular Care (ECC) 2005 recommendations, 1 7 5 , 1 77 CPR guidelines, 43 on defibrillation, 204 ethical principles, 567 pharmacology in, 3 79-3 94 emergency departments (EDs) diagnosis of HF, 1 04 disposition, 3 7-3 8 heart failure in, 96 management of ACS, 63-95 quality initiatives, 90 shortness of breath in, l l lf stroke assessments, 5 5 6, 5 5 6t termination of resuscitation in, 5 7 0-5 7 1 triage, 64 triage of patients with chest pain, 7 emergency medical practice groups DNAR orders and, 5 7 8-579 well-organized, 90 emergency medical services (EMS). see also prehospital medicine activation of, 1 7 7, 1 7 8f ambulance responder categories, 49-5 0 aspirin administration by, 50 assessments for suspected stroke, 5 5 1 , 5 5 3 automatic defibrillators used by, 1 7 1 , 1 72 basic water life support, 482 cardiac arrest survival and, 203/ cardiac arrest treated by, 1 4/ "chain of survival," 1 70-1 7 3 , 1 7 1f crash airway inmbation by, 2 74-2 76 defibrillation guidelines, 49, 2 0 5-2 06 definition of sudden cardiac death, 1 1 - 1 2 destination protocols, 56, 5 5 5 dispatch, 4 8 , 5 5 1 for drowning victims, 48 1-482 efficacy of resuscitation by, 402 establishing stroke onset times, 5 5 6 facilitated PCI goals and, 5 7 heparin administration by, 50 hospital bypass, 5 5 5 medical dispatch, 1 72 oxygen administration by, 50 prehosital stroke scale, 5 5 3 t prehospital assessments, 5 0 prehospital fibrinolysis, 52-5 3 prehospital initial smdies, 5 5 5 prehospital stroke care, 5 5 1-5 5 5 public-access defibrillation (PAD), 1 72-1 7 3 public education and use of, 46 public safety first responders, 48-49 response times, 1 72 response to DNAR orders, 5 7 5 role o f bystanders, 1 7 2 roles i n acute coronary syndrome, 48-49 termination of resuscitation efforts, 570 treatment delays and, 64 treatment of cardiac arrest, 1 2 use o f transcutaneous pacing, 3 6 6 zero-tier responders, 1 7 3 emergency physicians, collaboration by, 90 Emergency Research Foundation (EMF), 590 end of life care, 572 endothelia clinical use, 42 1-42 2 levels in heart failure, 97 mechanism of action, 42 1-42 2 endotoxin, 41 1 endotracheal inmbation (ETI). see also inmbation assessment of relaxation/flaccidity, 2 8 7 i n cardiac arrest, 2 7 3 -290 checklists for, 2 8 8-2 90 complication prevention, 2 87-2 8 8

complications, 2 64, 2 8 6-2 8 8 confirmation of positioning, 2 82-2 8 7 , 2 8 5f, 2 8 6/ equipment for, 2 8 9 hypotension after, 5 2 7 hypoxia after, 5 2 7 indications for, 2 7 3 neuromuscular blocking agents, 2 74t oral, 2 82-2 8 3 patient paralysis, 2 8 7 patient positioning, 2 8 1-2 8 2 personnel preparation, 2 9 0 postinmbation management, 2 87-2 88 premedication agents, 289 in pulseless cardiac arrest, 3 1 0/ in severe asthma, 524-5 2 5 i n severe hypothermia, 492-493 use of, 263 endotracheal rubes cuffed, 2 7 7 drug administration via, 3 8 0 obstruction of, 5 2 7 placement of, 5 2 7 suctioning procedures, 2 5 9f enhanced elimination, 448-449 enoxaparin adjw1ctive reperfusion therapy with, 89 bleeding risk, 79 clearance, 7 8 dosage, 7 8 , 79 dosing table in AU/NSTEMI, 8 3 t outcomes, 77-7 8 tenecteplase with, 89 environmental factors, cardiac arrests and, 1 7 epicardial fat, on ultrasound, 1 3 3 epiglottal cartilage, 2 3 9, 2 3 9f epinephrine administration in anaphylaxis, 53 5 arginine vasopressin venus, 4 1 4-4 1 8 , 4 1 8f, 4 1 9t for beta-blocker toxicity, 450 for bradycardia, 346 during cardiac arrest, 1 5 3 in cardiac resuscitation, 400-40 1 , 40 1/ cardiovascular effects, 397t, 399-400 during CPR, 4 1 2f, 4 1 4f, 4 1 S t, 4 1 6t dosage, 403-404 endotracheal administration, 3 80 indications, 403 parenteral, 52 1 pharmacology, 52 1 postresuscitation myocardial dysfunction and, 1 5 8 in pregnancy, 5 3 8 strucmre, 399f synthesis of, 3 99/ usage, 403-404 use in anaphylaxis, 5 3 4 vasopressin vs., 40 1 eptifibatide dosing table in AU/NSTEMI, 8 3 t mechanism o f action, 7 9 outcomes, 79-80 tenecteplace with, 89 escape pacemakers, 3 02 escape rhythms, 3 4 1 escitalopram, 4 5 7 esmolol characteristics, 3 82 t dosing, 3 8 5 Vaughn-Williams classification, 3 8 3 t esophageal detector devices (EDDs), 2 84t, 2 8 6 esophageal spasm, 2 7

Esophageal-Tracheal Combimbe (ETC), 2 66-2 69, 2 68f, 2 69t estrogen, hyperemia induced by, 5 3 9 ethacrynic acid in acute pulmonary edema, 1 04 complications, l O S t dosage, l O S t for heart failure, l O S t, 1 06 ethanol, poisoned patients, 446t. see also alcohol intake ethics advance directives, 573-577 decision-making capacity, 573 in emergency cardiovascular care, 567-568 health care professionals' values, 568-569 patient values and, 567-5 68, 568t principle of autonomy, 568 societal values and, 567-5 68, 568t etomidate, 2 80, 5 2 5 etopic atrial tachycardia, ECG, 3 1 8f excito toxins, 4 3 3 exercise protective effects of, 5 risk of cardiac arrest and, 1 7 in stress testing, 3 6 stroke risk and, 5 50 exhaled col detectors, 2 8 5-2 86 extracorporeal membrane oxygenation (ECMO) for beta-blocker toxicity, 450 for calcium charmel blocker toxicity, 45 2 in severe, life-threatening asthma, 5 2 8 F

face, suspected injury to, 2 5 6-2 5 7 face masks oxygen delivery, 2 5 5 , 2 5 5f with oxygen reservoir, 2 5 5 face shields, 1 8 1 , 2 5 9, 2 60f facial droop, 5 5 4f facilitated percutaneous interventions, 8 8 factor Ila, inactivation of, 77 factor Xa inactivation of, 77 inhibition, 79 families attendance at "codes," 580-5 8 1 death notifications and, 5 8 1-582 as decision makers, 5 7 6-5 77 emotional support to, 5 8 1-582 history of cardiac risk factors, 2 5-2 6 fasicular block, 3 68 fatigue, prior to Al\11, 45 fatty acid-binding protein (FABP), 7 1 felodipine, toxicology, 45 1 femoral vein cannulation, 1 42 fentanyl, 2 7 9 ferning, after lightning injury, 506f fibrinolytic therapy ASA with, 5 1 checklist for, 5 60t contraindications, 8 5 t efficacy over time, 8 5-86 indications, 80 outcomes, 8 5 patient transfer and, 5 7 prehospital, 52-5 3 , 5 3 risk assessments, 5 60-5 6 1 for STEM!, 80-8 1 for stroke patients, 5 5 7 stroke patients eligible for, 5 5 7 fire hazard, defibrillation and, 3 7 5-3 76 firefighters, as first responders, 204

IN DEX

first responders AEDs and, 204 in drownings, 478 public-safety, 48-49 flail chest, CPR in, 1 5 0 flecainide for atrial fibrillation/flutter, 3 3 5 in automatic atrial tachycardias, 3 3 1 characteristics, 3 82 t dosing, 3 86-3 87 mechanism of action, 386 in monomorphic ventricular tachycardia, 328 in refractory PSVT, 3 3 0, 3 3 1 Vauglm-Williams classification, 3 8 3 t Flexner, Simon, 1 96 fluid administration in electrical injuries, 508-509 for hypotension, 4 3 1 hypothermia induction using, 434 IV bolus, 3 80 during resuscitation, 406-407 during uncontrolled hemorrhage, 4 1 9-42 0 flumazenil, 447 fondaparinux catheter thrombosis with, 79 dosing table in AU/NSTEMI, 8 3 t i n STEM!, 8 9 foods, anaphylaxis and, 5 3 1 forced expiratory volumes (FEVs) as measure of clinical response, 52 2-52 3 in severe asthma, 5 1 7 foxglove (Digitalis pznpurea), 454 Framingham criteria for heart failure, 99, 99t furosemide in acute pulmonary edema, 1 04, 1 2 5- 1 2 6 i n complicated STEM!, 1 2 4{ complications, 1 0 5 t dosage, l O S t, 1 2 6 for heart failure, 1 0 5 t, 1 06 ototoxicity of, 1 06 G

gasoline, inhalation of, 46 1 gastric inflation, 1 80 gastric lavage complications, 448 indications, 448 gastroesophageal reflux, 2 7 Gastrografin swallow, 46 1 gastrointestinal irrigation, 495 Geddes, John, 1 9 8 gender. see also women atypical AMI symptoms in, 45 diastolic heart failure and, 98 electrical injuries and, 499 heart attacks by age and, 1 2 2/ heart failure prevalence by, 96f risk of cardiac arrest and, 1 6 stroke incidence and, 546 genetic factors, risk of cardiac arrest and, 1 6- 1 7 GHB, poisoned patients, 446t GI cocktail, relief of symptoms with, 2 7 Glasgow Coma Scale, 486 Global Initiative for Asthma, 5 1 2-5 1 3 glottic opening, anatomy of, 240 glottis, tip of, 2 3 7 glucagon for anaphylaxis, 53 5 for beta-blocker toxicity, 450 for bradycardia, 3 46-3 47 for calcium channel blocker toxicity, 452 glucose control, post-cardiac arrest, 4 3 5 glue, inhalation of, 46 1

glycoprotein lib/Ilia inhibitors (GPis), 1 St, 5 5 , 79-80 adjunctive therapy, 78, 89 ASAs with, 89 bleeding risk and, 76 Goldman Risk score, 2 9-3 0, 3 1f, 32t Guerike, Otto von, 193 Guidelines for the management of Patients with Unstable Angina Non-ST Elevation MI (ACC/AHA), 8 gum elastic bougie, 2 7 7-2 7 8, 2 7 7f H

haloperidol, 458 halothane, inhalation of, 462 Hamman's crunch, 2 7 head tilt-chin lift maneuver, 1 79f, 2 5 6f health care professionals BLS algorithm for, 1 7 6f education about death notifications, 582 education about PCAS, 43 7 ICD shocks to, 3 7 5-3 7 6 physician collaboration with, 9 0 values of, 568-569 heart anatomy of, 1 2 2/ conduction through, 3 04-3 05 electrophysiology, 3 00-3 0 3 as target organ in anaphylaxis, 53 3 heart block, types of, 343f heart failure atypical AMI symptoms in, 45 classifications, 97t common causes of, 98t complications of, 1 1 0 costs related to, 96 decompensated, 1 02f diagnosis, 99- 1 02 differential diagnoses, 1 02 , 1 0 3 t discharge home, 1 1 2 disposition guidelines, 1 1 1 t disposition of patients with, 1 1 1 -1 1 2 etiology, 98t general measures in, 1 02 - 1 04 left-sided, 98 pathophysiology, 97-98 prevalence in the U. S . , 96, 96f prognosis, 96-97 right-sided, 98 risk stratification in, 1 1 0-1 1 1 stable, 1 06 stages, 97t systolic vs. diastolic, 97-98 heart rates cardiac output and, 1 1 6 pulse check in SCA, 1 8 3 heart rhythms normal automaticity, 3 0 3 "triggered" automaticity, 3 0 3 heart sounds likelihood of AMI and, 26t myocardial contractility and, 26 S3, 99 helicopter air ambulances, 49-50 heliox, in severe asthma, 5 1 9, 52 1 hemodialysis for the poisoned patient, 449 rewarming, 495t hemofiltration, 449 hemoglobin, oxygen delivery and, 243-244 hemoglobins, abnormal, 2 44 hemoperfusion, charcoal, 449 hemorrhagic shock, 4 1 9-42 0, 42 1f, 42 2f, 42 3

601

hemorrhagic stroke, 548 description, 547 imaging studies in, 5 59 heparin, administration, 5 0-5 1 heroin, as asthma trigger, 5 1 5 HF protocols, 1 1 2/ hiatal hernias, 2 7 high-frequency CPR, 1 62 His-Purkinje network, 3 00, 3 04 histamines in anaphylaxis, 5 3 2-5 3 3 coronary artery vasospasm and, 5 3 3 heart rate and, 5 3 3 HMB coreductase inhibitors, 1 St Hoffa, M., 1 9 5 Hoffmann, Augustus, 1 96 "Hollywood heart attacks," 46 Hooker, Donald, 1 96 Hopkins closed-chest AC defibrillator, 1 97f hospital bypass, by ambulances, 55 5 Howell, W H., 1 96 "huffing," 46 1 Hunter, John, 1 94 hydralazine/isosorbide dinitrate complications, 1 0 8 dosage, 1 0 8 i n heart failure, 1 0 8 hydrocarbon pneumonitis, 462 hydrocarbons, inhalation of, 462 hydroxocobalmin, 466, 467-468 hyoid bone, 2 3 9f hypercapnia, permissive, 5 2 6-52 7 hyperemia, estrogen-induced, 5 3 9 hyperglycemia. see also glucose control in post-cardiac arrest syndrome, 4 3 5 in stroke patients, 5 63 in therapeutic hypothermia, 434 hyperinflation, dynamic, 5 2 6f hyperinsulinemia-euglycemia (HIE) therapy for beta-blocker toxicity, 450 for calcium channel blocker toxicity, 452 hyperkalemia, obstructive nephropathy and, 1 3 9 hyperoxia, damage caused by, 432 hypertension cocaine-induced, 460 diastolic heart failure and, 98 hemorrhagic stroke and, 80 management in stroke patients, 5 5 7 , 5 59t in poisoned patients, 445 t risk of cardiac arrest and, 1 5 stroke and, 5 49 hyperthermia after cardiac arrest, 4 3 3 cocaine-induced, 460 drug-induced, 459 in poisoned patients, 445 t, 449 hypertrophic cardiomyopathy (HCM), 1 05-106 hyperventilation contraindications, 5 1 8 ECG changes, 2 9 hypocalcemia diuretic use and, 1 06 in therapeutic hypothermia, 434 hypoglycemia altered mental status in, 447 arginine vasopressin secretion and, 4 1 1 in beta-blocker toxicity, 450 hypoglycemics, poisoned patients, 446t hypokalemia correction of, 45 3-454 diuretic use and, 1 06 in therapeutic hypothermia, 434 toluene inhalation and, 462

602 1

INDEX

hypomagnesemia diuretic use and, 1 06 in therapeutic hypothermia, 434 hypopharynx, 2 3 7 hypophosphatemia, 434 hypotension acute pulmonary edema, shock and, 1 2 4-- 1 2 7 after intubation, i n asthma, 52 7 after vasodilation, l OSt bedside evaluation of, 1 2 9- 1 3 4 definition, 1 1 6 differential diagnosis of, 1 1 6 fluid balance and, 43 1 hemorrhage-induced, 4 1 9-42 0 likelihood of AMI and, 26t pulmonary edema and, 484 shock and, 1 1 6-1 1 7 symptomatic, 1 04-- 1 0 5 i n tricyclic antidepressant toxicity, 45 5 hypothermia, 490-497 cardiovascular manifestations, 49 1-492 classification of, 490, 49 1 t complicating drowning, 483-484 management algorithm, 494{ neuroprotective effects, 563 in poisoned patients, 445 t prehospital treatment of, 492-493 rewarming, 490, 494--4 95 rewarming in the field, 493 therapeutic, 1 9 , 433-434 cardiac arrest survival and, 19 complications, 434 contraindications, 4 3 4 maintenance phase, 4 3 4 practical application of, 4 34-4 3 5 prognosis after, 436-43 7 recovery period, 4 3 7 rewarming phase, 434 shivering during, 43 3 , 43 5 unintentional, 490 hypovolemia, diastolic ventricular collapse and, 1 3 3 hypovolemic shock in anaphylaxis, 5 3 3 in electrical injuries, 508-509 hemodynamic parameters of, 1 1 7t initial focus of therapy, 1 1 6 volume replacement in, 1 2 0 hypoxia after intubation, in asthma, 5 2 7 arginine vasopressin secretion and, 4 1 1 I

iatrogenic cardiac arrest, 5 7 9 iatrogenic cardiac shock, 1 1 7-1 1 8 , 1 1 8/ ibutilide for atrial fibrillation/flutter, 3 3 5 characteristics, 3 82t dosing, 387 mechanism of action, 387 Vaughn-Williams classification, 3 8 3 t imaging in hemorrhagic stroke, 5 5 9 i n ischemic stroke, 5 59 in stroke patients, 557, 559 impedance threshold valves (lTV), 1 6 3_f, 1 64 implantable cardiac defibrillators (ICDs) electrode placement, 3 74 generator placement, 3 7 3/ hazard ratios, 2 0 8f history of, 1 9 8 , 1 99/ inactivation of, 572 indications, 207

interference with AEDs, 3 74 management in out-of-hospital conditions, 3 74--3 7 5 operation, 207 printout from, 3 7 3f shock to health care providers, 3 7 5-3 76 suspension of tachycardia functions, 3 7 4 impulse conduction disorders of, 3 42-344 effect of adenosine on, 3 2 6 impulse formation, 3 2 6 impulse formation disorders, 34 1-342 , 3 42/ inamrinone. see amiodarone infants compression-ventilation ratios, 1 74 duration of resuscitation efforts, 5 7 1 withholding resuscitation, 5 7 1 infarct-related arteries (IRAs), 1 1 5 infarct sizes, 45 inferior vena cava collapse index (IVC-CI), 1 3 0-1 3 2 inferior vena cava (IVC) dehydrated patient, 1 3 1/ intravascular volume assessment using, 1 3 0-1 3 2 misidentification o n ultrasound, 1 3 1/ sniff test, 1 3 3 well- filled, 1 3 1/ inflammation markers of, 3 5 reduction by hypothermia, 43 3 INH, poisoned patients, 446t inhalants hepatotoxicity, 462 management of toxicity, 462-463 toxicology, 46 1-462 inhaled anesthetics, in severe asthma, 5 2 2 inhalers, 5 1 9-5 2 0 inotropic agents cardiovascular risks of, 1 8t mechanisms of action, 402-403 inpatient telemetry, 3 8 insect stings, anaphylaxis and, 5 3 1 insulin, 43 5 , 563 internal core rewarming, active, 495 , 495t internal jugular vein cannulation, 141-142 , 1 42/ International Liaison Committee on Resuscitation (ILCOR), 50, 1 62 interposed abdominal compression CPR (lAC-CPR), 1 6 1 - 1 6 2 , 1 62/ intra-aortic balloon counterpulsation (IABP) for beta-blocker toxicity, 450 for calcium channel blocker toxicity, 452 in cardiogenic shock, 1 2 0, 1 2 1f occlusion of the aorta, 1 66 intra-atrial reentry tachycardia, 3 3 1-3 3 2 intracerebral hemorrhagic stroke, 548 intracranial hemorrhages, 87f intracranial pressures (ICPs), 42 8 intraosseous access arginine vasoopressin via, 4 1 3 , 4 1 3/ drug administration via, 3 80 in hypothermic patients, 483 intrathoracic pressures, 2 3 5f intravascular volume, ultrasound assessment, 1 3 0-1 3 2 intravenous access arginine vasopressin via, 4 ! 3f drug administration, 3 80 in pulseless cardiac arrest, 3 1 0f intraventricular conduction disturbances, 3 70t intubation. s e e also endotracheal intubation (ETI) for electrical injuries, 508 in pregnancy, 540

ion gradients, 3 00 ipratropatium bromide, 5 1 9, 5 2 0 ischemi-/reperfusion injury after cardiac arrest, 1 9-2 0 ischemia, global, 1 9 ischemia, transient, 1 5 ischemia-modified albumin (IMA) , 7 1 ischemia-reperfusion injury cardiac dysrhythmias and, 43 1-43 2 post-cardiac arrest, 42 8 , 43 0 total-body, 43 5 ischemic discomfort, plaque disruption and, 3f ischemic penumbra, 549 ischemic stroke categories of, 547-548 causes of, 547 definition, 547-548 imaging studies in, 5 5 9 management of hypertension in, 5 59t signs and symptoms, 5 5 1 isobutyl nitrate inhalation, 46 1 isoproterenol for bradycardia, 347 cardiovascular effects, 397t dosing, 387 indications, 3 87 mechanisms of action, 3 87 in torsades de pointes, 3 2 9 Vaughn-Williams classification, 3 83 t isradipine, toxicology, 45 1

J

J -point elevation, 69 jaw-thrust maneuver, 1 79, 2 5 6f Johns Hopkins, defibrillation work, 1 96 jugular vein distension (JVD), 98, 99 junctional tachycardia, 3 1 8, 3 3 5 K

Kerley lines, 1 00 ketamine in rapid sequence intubation, 524--5 2 5 i n severe asthma, 5 2 1 Kiesselbach's plexus, 2 3 7 King Airway, 268 Kite, Charles, 1 94 Kouwenhoven, William B . , 1 9 5 , 1 96/ KvLTQ gene mutation, 1 7 L

labetalol characteristics, 3 82t toxicology, 449 Vaughn-Williams classification, 3 8 3 t lactate levels, ROSC, 43 2 laetrile, 466 LaPlace, law of, 97 laryngeal mask airways (LMAs), 2 5 7 i n anesthesia, 2 6 5 design of, 2 6 5 , 265f insertion steps, 2 66t, 267t models of, 2 6 5 safety of, 2 66 Laryngeal Tube (LT), 268 Laryngeal Tube S (LTS), 2 68-2 69 laryngeal tubes, 2 5 7 , 2 68-2 69 laryngopharynx, 23 7 , 2 3 8 laryngoscopes, 2 7 8 , 2 7 8/ curved blade, 2 7 8 , 2 7 8f patient positioning, 2 8 2 straight blade, 2 7 9f laryngospasm, drowning and, 479-480

IN DEX

larynx anatomy of, 2 3 7, 2 3 9 skeleton of, 2 3 9f "laughing gas" inhalation, 46 1 law enforcement personnel, AED programs, 49, 49f lay providers, algorithms, 1 7 5-1 8 5 lay responders, defibrillation and, 2 1 3 -2 1 8 leading edge sign, 1 3 8 left bundle-branch block (LBBB) ECG confounding by, 29 mortality rates, 69-70 left bundle-branch conduction, 3 04 left ventricular dysfunction after cardiac arrest, 1 5 7 description of, 1 1 9 left ventricular ejection fraction (LVEF) postresuscitation, 402f risk of cardiac arrest and, 1 5 left ventricular shock ECG, 1 2 3f in-hospital outcomes, 1 2 3f left ventricular wall, thickness, 1 3 7 legal knowledge, limitations in, 569 leukotrienes, in anaphylaxis, 5 3 3 levalbuterol, 5 1 9 levetiracetam, for seizure control, 43 5 levosimendan, 503 Levy, A. G., 1 96 Lewis, Thomas, 1 96 Leyden jars, 1 9 3 , 1 94f Lichtenberg figures, 506f lidocaine in arrhythmias, 3 8 8 i n cardiac arrest, 3 87-3 8 8 characteristics, 2 79, 3 82 t for cocaine toxicity, 46 1 for digoxin toxicity, 45 3 dosing, 3 8 8 endotracheal administration, 3 8 0 mechanisms o f action, 3 8 7 i n rapid sequence intubation, 2 7 9 i n torsades d e pointes, 3 2 9 in tricyclic antidepressant toxicity, 456 Vaughn-Williams classification, 3 83 t i n ventricular tachycardias, 3 2 8-3 3 0 life support goaIs of, 5 72 withdrawal of, 5 7 1-572 lighter fluid inhalation, 46 1 lightning, 498-499 ACLS for, 508-509 burns, 506f cardiac effects, 503-504 casualties, 50 1-502 , 502f cloud-to-ground flashes to ground, 5 0 lf ED management of, 509 ground potential, 505f injuries due to, 5 0 1 , 505-506, SOSJ Lichtenberg figures, 506f out-of-hospital management, 5 07-5 08 prevention of, 5 1 0 resuscitation in, 508 triage of multiple victims, 508 upward streamers, 505f lily of the valley (Convallaria majalis), 454 limitation-of-treatment orders, 5 7 8 linanza1·in, 466 Little's area, 2 3 7 liver failure, pericardia! effusion and, 1 3 3f living wills, 574 LOAD mnemonic, 276 Lomotil (diphenoxylate-atropine), 463 , 464 loop diuretics, 1 06

Los Angeles prehospital stroke screen (LAPS S), 5 5 3 , 5 54t low-molecular-weight heparins (LMWHs) adjunctive reperfusion therapy with, 89 cardiac risks, 1 St clearance, 7 8 dosage, 78 initial management strategies and, 7 7-7 8 lower respiratory system anatomy of, 240 Lawn, Bernard, 1 9 8 LUCAS CPR, 1 6 3 , 1 6 5f Ludwig, Carl, 1 9 5 Lw1d University Cardiopulmonary Assist System (LUCAS), 1 6 3 , 1 6 5f lung point sign, 1 3 8 lung sliding, 1 3 8 lungs changes in pregnancy, 5 3 9 sonographic evaluation, 1 3 8 thorax relationship with, 2 3 5 M

MACE, reduction of, 76 MacWilliam, John, 1 9 5 , 1 9 5f, 1 96 magnesium in arrhythmias, 3 8 8 i n atrial fibrillation, 3 3 2 in cardiac arrest, 3 8 8 i n cocaine toxicity, 46 1 in digoxin toxicity, 453 dosing, 3 8 8-3 89 mechanisms of action, 3 88 in reducing shivering, 434 for serotonin syndrome, 457 in severe asthma, 5 1 9, 5 2 0-52 1 for torsades de pointes, 3 2 7 i n tricyclic antidepressant toxicity, 4 5 6 Vaughn-Williams classification, 3 8 3 t i n ventricular arrhythmias, 453-454 magnetic resonance imaging, 5 5 7 malaria, quinidine for, 3 90 malignancies, differential diagnoses, 2 8 masks mouth-to-barrier devices, 2 5 9 nonrebreathing, 2 5 5 one-hand holds, 262t pocket devices, 2 60f, 2 6 lf techniques, 2 6 lf two-hand holds, 2 62 t mast cells, activation of, 5 3 2 MDMA (3 , 3 -methylene dioxymethamphetamine, ecstasy), 459 mean arterial pressures (MAPs), 43 1 -43 2 media campaigns, 45-46 mediastinitis, presentation, 2 7 meperidine, 463 , 464 mesoridazine, 458 metered-dose inhalers, 5 1 9-52 0 methadone, 1 7 , 463 methamphetamines, 459-460 methemoglobinemia alkyl nitrate use and, 462 dapsone-induced, 466 inducers of, 465t management of, 465-466 poisoned patients, 446t pulse oxymetry in, 244 methylene blue, 466 methylene chloride, 462 3 , 3 -methylene dioxyn1ethamphetamine (MDMA, ecstasy), 459 methylprednisone, in severe asthma, 520

603

methylxanthines interaction with adenosine, 3 84 poisoned patients, 446t metolazone, for heart failure, 1 06 metoprolol cardiogenic shock and, 1 1 9f characteristics, 3 82 t death before first discharge and, 7 5f dosing, 3 8 5 initial treatn1ent strategies, 74 prehospital use, 52 timing of treatment with, 80 toxicology, 449 Vaughn-Williams classification, 3 8 3 t microbubbles, a s contrast agents, 1 3 5 microcirculatory perfusion disorders, post-arrest, 4 3 0 midazolam, 2 8 0 middle cerebral artery occlusion, 549f middle internodal pathway, 3 04 milrinone cardiovascular effects, 3 97t dosing, 405 indications, 405 usage, 405 miltifocal atrial tachycardia (MAT), 3 3 1 mirtazapine, 457 mitral valve, inflow velocity, 1 3 6 Mobitz type I heart block, 343f, 344 Mobitz type II heart block, 343f, 3 44 morphine for acute pulmonary edema, 1 04 for cardiogenic shock, 1 1 7, 1 2 0 , 1 2 4 complications, l O S t, 1 09 dosage, 7 3 , l O S t, 1 09 for heart failure, 1 0 5 t, 1 09 initial treatment strategies, 7 3 i n prehospital management, 5 1 -52 for pulmonary edema, 1 2 6 mortality rates, within 3 0 days, 68f mouth, oral cavity and, 2 3 7 mouth-to-barrier devices, 1 8 1 , 2 5 9-2 60 mouth-to-mask techniques, 2 62f mouth-to-mouth rescue breathing, 1 80, 2 5 3 mouth-to-mouth ventilation, 1 80f, 1 8 1 , I S lf, 1 9 7 mouth-to-nose ventilation, 1 8 1 mouth-to-stoma ventilation, 1 8 1 Mower, Morton, 1 98 mucous impaction, in asthma, 5 1 3f multidisciplinary collaboration, 90 muscle strains, 2 8 Musschenbroek, Pietr van, 1 9 3 Mycoplasma pneunzoniae, 5 1 4 myocardial acidosis, 2 3 4f myocardial blood flow, 1 5 5-1 5 6 myocardial contractility, depressed, 1 3 2 myocardial dysfunction post-cardiac arrest, 42 9-430 postresuscitation, 1 5 7-1 5 8 myocardial infarction within 3 0 days, 68f by age and gender, 1 2 2f AV conduction in, 3 69t classic shock paradigm in, 1 1 9f cocaine-induced, 460 indications for pacing, 3 68 "silent, " 68 myocardial ischemia polymorphic VT in, 3 2 9-3 3 0 supplemental oxygen in, 2 5 3-2 54 myocardial necrosis, markers of, 7 1 myocardial perfusion imaging (MPI), 72 myocarditis, segmental wall motion and, 1 3 4

604 1

INDEX

myocardium action potentials of cells, 3 0 1 cell types, 3 00 markers of injury to, 3 3-3 5 predictive properties of, 3 4t myoglobin in myocardial injury, 3 4-3 5 risk stratification and, 70-7 1 serial measurements of, ?Of N

nadroparin, with ASA, 7 7 naloxone, for opioid toxicity, 447, 463--464 nasal cannulas, 2 54-2 5 5 , 2 5 5f nasopharyngeal airways (NPAs), 2 5 7-2 5 S , 2 5 Sf nasopharynx, 2 3 7 , 2 3 S National Asthma Education and Prevention Program, 5 1 2-5 1 3 National Center for Early Defibrillation, 49 National Emergency Airway Registry, 2 S O National Institutes of Health (NIH) Rapid Early Action for Coronary Treatment trial, 44 research funding, 5 S9-5 90 Stroke Scale, 5 SSt National Registry of Myocardial Infarction2 , 45 National Weather Service, 502 natriuretic peptide assay body mass index and, 1 02f cutpoints for decision-making, l O l t i n heart failure diagnosis, 1 00- 1 0 1 , 1 02f mortality in HF and, 1 02f nausea, likelihood of AMI and, 26t nebulizers, in severe asthma, 5 1 9-520 neonates, withholding resuscitation, 5 7 1 nephropathy, obstructive, 1 3 9 Ne,�iznn oleander (common oleander), 454 nesiritide in acute pulmonary edema, 1 04 in complicated STEMI, 1 2 4{ complications, l OSt, 1 0 7 dosage, l OSt, 1 0 7 for heart failure, 1 00, 1 04, l OS t, 107 neuroimaging, prognostic use of, 43 6 neurologic screening, for stroke, 5 5 6-5 5 7 neuromuscular blockade after ROSC, 43 3 in rapid sequence intubation, 2 S O neuropeptide Y, 400 neuroprotection, hypothermia in, 43 3 nicardipine, toxicology, 45 1 nifedipine, toxicology, 45 1 nimodipine, toxicology, 45 1 9 1 1 system calling, 46 dispatch protocols, 4S nisoldipine, toxicology, 45 1 nitrates in cardiogenic shock, 1 2 4 cardiogenic shock and, 1 1 7 contraindications, 1 2 5 initial treatment strategies, 7 3 intravenous, 1 04 side effects, 7 3 nitric oxide, 41 1 , 467 nitroglycerin (NTG) in acute pulmonary edema, 1 04, 1 2 5 cardiovascular effects, 3 9 7 t for cocaine toxicity, 460 complications, 1 05 t, 1 0 7 contraindications, 7 3 dosage, l OSt

dosing, 406 guidelines for use, 46 for heart failure, l O S t, 1 06-1 0 7 indication, 406 initial treatment strategies, 73 patient instructions, 46, 4Sf in prehospital management, 5 1-52 relief of symptoms with, 2 7 routes o f administration, 1 0 7 usage, 406 nitroprusside. see also sodium nitroprusside in acute pulmonary edema, 1 2 6 cardiovascular effects, 397t for cocaine toxicity, 460 complications, l O S t, 107 dosage, l O S t, 1 07 dosing, 406 for heart failure, l O S t, 1 0 7 nitrous oxide inhalation, 46 1 NMS, poisoned patients, 446t non-ST-segment elevation myocardial infarction (NSTEMI) ACS and, 2 cardiogenic shock and, 1 1 5 , 1 1 7 emergency department triage, 66 fibrinolytic therapy, SO ST-segment depression and, 70 TI..LVII risk scores, Sf triage of patients, 6-S nonesterified fatty acids (NEFAs), 1 6 noninvasive positive-pressure ventilation (NPPV), 1 0 3 benefits, 52 3-524 contraindications, 5 2 3 t criteria, 5 2 3 t description, 52 3 initial steps in, 52 3-524 posttreatment for asthma, 522 nonsteroidal antiinflammatory drugs (NSAIDs) as asthma trigger, 5 1 4 contraindications, 1 1 0 drug interactions, 1 0 6 noradrenergic vasopressors, 4 1 0--42 5 Norcuron (vecuronium) characteristics, 2 74t, 2 S l in endotracheal intubation, 2 S O nordextropropoxyphene, 463 norepinephrine arginine vasopressin secretion and, 41 1 for beta-blocker toxicity, 450 cardiovascular effects, 3 97 t dosage, 404 indications, 404 levels in heart failure, 97 structure, 3 99f synthesis of, 3 99f in tricyclic antidepressant toxicity, 456 usage, 404 normeperidine, 463 nuclear imaging, risk stratification and, 72 0

obesity during pregnancy, 5 3 9 risk o f cardiac arrest and, 1 6 observation units admissions for heart failure, 1 1 1 discharge criteria, 1 1 2 Office of Naval Research (ONR), 590 oleander (Ne7'ium oleander), 454 one-sided motor weakness, 5 5 5f open chest cardiac massage (OCCM), 1 65-166

operating rooms, DNAR orders and, 5 79-S SO opioid toxicity airway control in, 447 clinical presentation, 463 management of toxicity, 463--464 naloxone for, 447 poisoned patients, 446t opioids in rapid sequence intubation, 2 7 9 risk of cardiac arrest and, 1 7 toxicology, 463 oral cavity, mouth and, 2 3 7 organophosphates management of toxicity, 46S--469 toxicology, 46S oropharyngeal airways (OPAs), 2 5 7 , 2 5 7f 2 59t oropharynx, 2 3 7 , 2 3 S orthodromic reciprocating tachycardias, 3 3 5 ototoxicity, of furosemide, 1 06 over-the-head CPR, l S S oxprenolol, toxicology, 449 oxycodone, 463 oxygen, supplemental in acute pulmonary edema, 12 5 administration by EMS, 50 assessing need for, 243-246 in cardiac arrest, 2 5 3 defibrillation and, 3 7 5-3 76 delivery devices for, 2 54-2 5 5 , 2 5 5f in drownings, 4S3 in heart failure, 1 02-103 indications, 2 54t during intubation, 2 S2 in myocardial ischemia, 2 5 3 -2 5 4 i n severe asthma, 5 1 9 in severe hypothermia, 492--493 oxygenation during CPR, 2 3 4-2 3 7 hemoglobin and, 243-2 44 principles of, 2 42-243 oxyhemoglobin, monitoring saturation of, 1 2 5 p

P-selectin, inflammation and, 3 5 P waves, amplification of, 3 2 1-3 2 3 PA Express, 267 paced rhythms, ECG confow1ding, 2 9 pacemaker cells, 3 0 0 action potentials of, 3 0 1f 3 02-3 03 groups of, 3 02 pacemaker-defibrillators, placement of, 3 7 1f pacemakers automatic external defibrillators and, 3 72, 3 74 description of, 3 6S-3 69 electrode placement, 3 7 1-3 72, 3 72f electrodes on chest x-rays, 3 72f inactivation of, 572 permanent, 3 6S-3 7 1 pacing. see alro transcutaneous pacing (TCP) for beta-blocker toxicity, 450 for bradycardia, 3 46 in disorders of impulse formation, 3 42 history of, 3 65-3 66, 3 6 S modern refinements, 3 6 S i n torsades de pointes, 3 2 9 pain characteristics likelihood of AMI and, 26t risk stratification in UAINSTEMI, 7t Pantridge, J. Frank, 19S paralytic agents in crash airway intubation, 2 7 5 i n rapid sequence intubation, 2 SO, 5 2 5

IN DEX

paramedic protocols, on aspirin, 50-5 1 paramedics, ambulance responders, 49-5 0 paroxysmal supraventricular tachycardia (PSVT) atropine for, 3 8 3 defibrillation energy settings, 3 6 5 description, 3 3 0 ECG features, 3 1 7, 3 1 7f refractory to standard treatment, 3 3 0-3 3 1 treatment of, 3 3 0 partial cardiopulmonary bypass, 1 66 passive smoking, cardiac arrest and, 1 7 paternalism, 568 patient education, 46, 48f patient history in ACS secondary to CAD , 6t of arrhythmias, 296 cardiac risk factors, 2 5-2 6 heart failure diagnosis and, 99, 99t initial assessments and, 67-68 likelihood of AMI and, 26t risk stratification in UA/NSTEMI, 7t stroke-focused, 5 5 3 t patient profiles, ACS patients, 63-66 patient transfers in cardiogenic shock, 1 2 1 destination hospital protocols, 1 2 1 patient values, 567-568, 568t peak expiratory flow rates (PEFRs) as measure of clinical response, 52 2-52 3 in severe asthma, 5 1 7 peak flow meters, 5 1 7 pediatric patients. see children PEEP, 5 2 5 penbutolol, toxicology, 449 Pensile Galvanic Pile, 1 9 5 pentazocine, toxicity, 464 percutaneous coronary interventions (PCis). see also specific interventions certification programs, 5 7 door-to-balloon time, 54 facilitated, 55, 5 5 t post-cardiac arrest syndromes and, 43 1 in STEM! patients, 5 1 percutaneous transluminal coronary angioplasty (PTCA), 8 5 perfusion pressure gradients, 1 5 3 pericardia! effusion (PE) cardiac tamponade and, 2 7 , 1 3 2-1 3 4, 1 3 2f false-positive diagnoses, 1 3 3 pericardia! sac, aspiration of, 143 pericardia! tamponade, 27 pericardiocentesis, 142-143 peripheral venous cannulation, 3 80 peritoneal lavage, rewarming, 495 , 495t permanent form of junctional reciprocating tachycardia (PJRT), 3 1 9 permissive hypercapnia, ventilation with, 5 2 6-52 7 pharmacologic agents. see also specific drugs as asthma trigger, 5 1 4 cardiovascular toxicity of, 449-458 for heart failure therapy, 1 06-1 07 overdose limits, 444 prehospital management, 5 0-5 3 risk of cardiac arrest and, 1 7- 1 8 pharynx, divisions of, 2 3 7 , 2 3 8f phencyclidine, poisoned patients, 446t phenobarbital, for seizures, 464, 468 phentolamine, for cocaine toxicity, 460 phenylalkylamines, toxicology, 45 1 phenylephrine, 3 97t phenytoin in automatic atrial tachycardias, 3 3 1 contraindications, 45 8

in digoxin toxicity, 453 dosing, 3 89 mechanisms of action, 3 89 in polymorphic ventricular tachycardia, 3 3 0 phosphodiesterase inhibitors dosing, 405 indications, 405 nitrate contraindications and, 1 2 5 usage, 405 physical activity, 5 50. see also exercise physical examination in ACS secondary to CAD, 6t in arrhythmias, 296 cardiac risk factors, 2 6-2 7 heart failure diagnosis and, 99, 99t initial assessments and, 67-68 physicians, as decision makers, 5 7 6-5 7 7 physostigmine adverse effects, 4 5 5 for anticholinergic poisoning, 4 5 5 pindolol, toxicology, 449 plaques. see coronary plaques plasminogen activator, recombinant (reteplase), 52 plasminogen activator, tissue-type (alteplase) checklist for fibrinolytic therapy, 5 60t intra-arterial, 562 intravenous, 5 60-5 6 1 in ischemic stroke, 5 5 7 PCI and, 5 5 prehospital use, 5 2 risk assessment, 5 60-5 6 1 Plasmodium falciparum, 3 90 platelet activating factor, 53 3 platelet activation, markers of, 3 5 pleural effusion false-positive evaluations, 1 3 8- 1 3 9 thoracentesis and, 1 3 9 ultrasonographic image, 1 3 9f pleural fluid, pericardia! fluid versus, 1 3 3 pleural lavage, rewarming, 495 pleural sliding, 1 3 8 pleurocentesis, ultrasound-guided, 1 44 pneumothorax presentation, 2 7 sonographic evaluation, 1 3 8- 1 3 9 poison centers, 444 poisoned patients approach to, 444-449 diagnosis of, 444f differential diagnoses, 445 t extracorporeal measures, 449 general considerations for, 44 7-449 interventions, 445 t management of, 444f policies. see also protocols out-of-hospital advance directives, 576t review of, 90 pollutants, as asthma trigger, 5 1 4 polyunsaturated fatty acids (PUFAs), 1 6 pomum Adami, 2 3 9 "poppers," inhalation of, 46 1 positive end-expiratory pressure (PEE), 483 positive pressure ventilation in cardiogenic shock, 1 1 7 in drownings, 483 post-cardiac arrest syndrome (PCAS), 42 7-442 adrenal dysfunction after, 4 3 5 background, 42 8 brain injury in, 42 8 clinical manifestations of, 42 9t epidemiology of, 42 8 glucose control, 43 5 implementation of care, 43 7-43 8

605

monitoring options, 430t pathophysiology of, 42 8, 42 9t in pediatric patients, 4 3 7 phases of, 43 6f precipitating pathology, 43 0 prognostication, 43 5-43 6 quality improvement, 43 7-43 8 therapeutic hypothermia, 4 3 4-4 3 5 therapeutic strategies, 43 0-43 5 treatments, 42 9t posterior circulation stroke, 548 posterior internodal pathway, 3 04 postresuscitation myocardial dysfunction mechanism of, 1 5 7-1 5 8 potential treatments for, 1 5 8- 1 5 9 potassium action potentials and, 3 0 1 digoxin toxicity and, 452 serum levels, 496 potassium ATP channel activators, 1 5 9 power lines, electrical injury and, 499 pralidoxime, 468-469 precordial thump cardioversion, 3 6 3 preexcitation rhythms, 2 9 7-2 98, 2 9 8f, 3 3 2-3 3 4, 3 3 4t pregnancy 5 -minute rule and delivery, 541-542 airway changes, 5 3 9 cardiopulmonary resuscitation in, 5 3 8-543 , 540t cardiovascular changes, 540 defibrillation in, 542 gastrointestinal changes, 5 3 9 hematologic changes, 540 maternal mortality, 5 3 9 obesity and, 5 3 9 pulmonary changes, 5 3 9 prehospital directives, 5 74--5 7 5 prehospital medicine. see also emergency medical services (EMS) care in anaphylaxis, 5 3 4 recommendations i n cardiogenic shock, 1 2 2 preload sensitivity, 9 8 premature ventricular contractions (PVCs), 1 1 0, 3 80 Prevost, Jean Louis, 1 9 5 primary percutaneous intervention (PPCis) fibrinolysis ve1·sus, 8 1 , 8 5 thrombolytic therapy versus, 86f procainamide in arrhythmias, 3 89 for atrial fibrillation/flutter, 3 3 5 in automatic atrial tachycardias, 3 3 1 in cardiac arrest, 3 89 characteristics, 3 82 t contraindications, 3 89 dosing, 3 89 mechanisms of action, 3 89 in monomorphic ventricular tachycardia, 3 2 8 i n polymorphic ventricular tachycardia, 3 3 0 in refractory PSvr, 3 3 0, 3 3 1 Vaughn-Williams classification, 3 8 3 t prodromal symptoms incidence of, 45 infarct size and, 45 propafenone for atrial fibrillation/flutter, 3 3 5 in automatic atrial tachycardias, 3 3 1 characteristics, 3 82 t contraindications, 3 89 dosing, 390 indications, 3 89

606 1

INDEX

propafenone (continued) mechanism of action, 3 89-3 90 in monomorphic ventricular tachycardia, 3 2 8 i n refractory PSVT, 3 3 0, 3 3 1 Vaughn-Williams classification, 3 8 3 t propofol for drug-induced seizures, 464 in rapid sequence intubation, 5 2 5 for seizure control, 43 5 in ventilator-dependent patients, 5 2 7 propoxyphene, 463 cardiotoxicity of, 464 seizures in toxicity, 464 propranolol characteristics, 3 82 t toxicology, 449 Vaughn-Williams classification, 3 8 3 t prostacyclin, 400 prostaglandin D2, 5 3 3 protamine sulfate, 79 protein-contractile structures, 3 00 protocols. see also policies destination hospitals, 5 3-5 7, 56, 5 5 5 development of, 90 in heart failure, 1 1 2f in post-cardiac arrest care, 43 7-43 8 provocative testing, risk stratification and, 72 Prunus spp., 466 public-access defibrillation (PAD), 1 72-1 7 3 , 2 04, 2 0 5 cost-effectiveness, 2 1 3 device deployment, 2 1 5-2 1 6 equipment, 2 1 6 incident follow-up, 2 1 7 lay-responders and, 2 1 3-2 1 8, 2 1 4f maintenance issues, 2 1 7 personnel, 2 1 6 program coordination, 2 1 5 program leadership, 2 1 5 quality improvement for programs, 2 1 7-2 1 8 quality programs for, 2 1 5-2 1 8 response planning, 2 1 5 site assessment, 2 1 5 standard operating guidelines, 2 1 5-2 1 6 supplies for, 2 1 6 signage, 2 1 6-2 1 7 storage, 2 1 6-2 1 7 training, 2 1 6 public education roles of, 589 on symptom recognition, 45-46 trial outcomes, 46 public safety first responders, 48-49 pulmonary artery catheters, 1 1 6 pulmonary capillary wedge pressures (PCWPs), 99, 1 00 pulmonary crackles, 2 6t pulmonary edema. see also acute pulmonary edema (APE) in drowning, 484 opioid-induced, 447 , 463 pulmonary emboli presentation, 2 7 sonographic assessment, 1 3 7-1 3 8 pulmonary ventilation, definition of, 2 3 4 pulse checks, 1 8 3 , 3 1 0f pulse oxymetry accuracy of, 2 44 basic physics of, 243 basic principles, 243 conditions affecting, 244 limitations, 244 precautions, 244

safety considerations, 244 in severe asthma, 5 1 7 pulseless cardiac arrest algorithm, 3 09-3 1 2 , 3 1 0f pulseless electrical activity (PEA) atropine for, 3 84 in cardiac arrest, 140- 1 4 1 prognosis, 3 1 2 pulseless arrest and, 3 1 1-3 1 2 reversible causes, 3 1 2 , 3 1 2 t i n severe hypothermia, 493-494 sonographic findings in, 1 40t treatment, 3 1 2 Purkinj e system, action potentials of, 3 02

Q

Q-wave myocardial infarction, 2 7 Q waves, in heart failure, 1 04 QRS complexes appearance in tachycardias, 297 in hypothermia, 492f narrow, 3 1 5f, 3 1 9-3 2 0 preexcitation rhythms, 2 97-298, 298f ST-segment elevation, 2 9 uniformity of, 298-2 99 wide, 3 2 0-3 24 QT intervals antipsychotics and, 45 8 in beta-blocker toxicity, 450 diuretic use and, 106 prolonged magnesium for, 461 SSRI toxicity and, 457 tricyclic antidepressants and, 45 5 quality-adjusted life years (QALYs), 2 1 3-2 1 4 quality improvement in cardiopulmonary resuscitation, 1 85-186 feedback for, 90 in post-cardiac arrest care, 43 7-43 8 support for initiatives for, 90 quinidine for atrial fibrillation/flutter, 3 3 5 in automatic atrial tachycardias, 3 3 1 dosing, 3 90 mechanism of action, 3 90 in monomorphic ventricular tachycardia, 3 2 8 Quinlan, Karen Ann, 5 7 6 R

race heart attack experience and, 44-45 risk of cardiac arrest and, 1 5 , 1 7 stroke incidence and, 546 railway lines, electrical injury and, 499 rapid compression rate CPR, 1 62 Rapid Early Action for Coronary Treatment (REACT) trial, 44, 46 rapid sequence intubation (RSI), 2 74, 2 7 5-2 8 3 description, 2 7 6-2 8 3 intubation steps, 2 7 6 precautions i n severe asthma, 5 2 4 i n pregnancy, 5 3 8, 540 seven "Ps" of, 2 7 6-2 8 3 i n severe asthma, 524-5 2 5 reanimation chair, 1 9 5f Reece, Richard, 1 94 reentry components of, 3 04 mechanism of, 3 03-3 04, 3 0 3f shock therapy and, 3 62 reentry tachycardia, 2 9 8

refractory periods, portions of, 3 0 3 refusals of care, 5 7 8 registration clerks, ACS identification, 65 t renal tubule acidosis, 462 ReoPro, mechanism of action, 79 reoxygenation, after cardiac arrest, 43 2 reperfusion adjunctive therapy, 8 8-89 in cardiogenic shock, 1 2 0-1 2 1 checklist, 5 3-54, 54f initial treatment goals, 5 8f options, 8 7 t selection of strategy for, 85-88 repolarization, 3 0 1-3 02 rescue breaths, 1 80 in drownings, 483 without chest compressions, 1 8 3 resource utilization, treatment strategies and, 72-80 respiration components of, 2 3 4 lung-thorax relationship, 2 3 5 respiratory arrest cardiac arrest vs., 242 in drowning, 484 severe asthma and, 5 1 8 respiratory infections, 2 7 respiratory physiology, 2 3 4 respiratory system anatomy, 2 3 8f resting sestamibi imaging, 3 5-3 6 resuscitation. see also cardiopulmonary resuscitation (CPR) crash airway intubation and, 2 7 5-2 76 duration of, 5 7 1 electric shocks for, 1 94- 1 9 5 i n electrical injuries, 508 family attendance at codes, 5 80-5 8 1 in-hospital, 5 7 1-572, 579 in-water, 482 in lightning injuries, 508 out-of-hospital, 5 7 8-579 postresuscitation hemodynamics, 402-403 in pregnancy, 540-542 termination of, 495-496, 5 3 6, 570 translational science and, 5 8 8 unsuccessful, 582 vaspopressors used in, 400-40 1 resuscitation medicine careers, 5 8 7-5 9 1 Resuscitation Outcomes Consortium (ROC), 2 0 resuscitation science care and, 5 8 8 funding for, 5 8 9-590 reteplase (recombinant plasminogen activator) with abciximab, 89 facilitated PCI and, 55 prehospital use, 52 return of spontaneous circulation (ROSC), 1 62 after cardiac arrest, 1 5 7-1 59, 4 1 3 , 4 1 4f, 4 1 5f, 4 1 6f brain edema after, 42 8 defibrillation timing and, 3 1 Of lactate levels after, 432 mortality after, 42 7, 42 8 neuromuscular block after, 43 3 sedation after, 43 3 seizures after, 43 5 therapeutic hypothermia after, 43 3 revascularization, within 30 days, 68f rewarming active internal core, 495t in drownings, 482 in hypothermia, 494-495 in severe hypothermia, 492-493

IN DEX

rhabdomyolysis, 454 for amphetamine toxicity, 45 9-460 in cocaine toxicity, 46 1 right bundle-branch block (RBBB) 1 2 -lead ECG, 69f right bundle-branch conduction, 3 04 right coronary artery anatomy, 1 2 2f thrombosis, 1 2 2f right ventricle, end-diastolic dimensions, 1 3 7 right ventricular shock, 1 2 2 - 1 2 4 in-hospital outcomes, 1 2 3f mortality rate, 1 1 5 risk stratification of the ACS patient, 66-72 algorithms ACI-TIPI, 3 0-3 1 artificial neural networks, 3 1 clinical criteria in, 3 2 t Goldman Risk score, 2 9-3 0, 3 1f resting sestamibi imaging in, 3 5-3 6 TIMI risk scores, 3 1 , 3 3 electrocardiography in, 69-70 mortality rates and, 66f previous testing for CAD , 3 7 prior catheterization results in, 3 7 shortness of breath in the ED, 1 1 1f risperidone, 458 Robert Wood Johnson (RWJ) Foundation, 590 rocuroium (Zemuron) characteristics, 2 74t, 2 8 1 in endotracheal intubation, 2 8 0 i n rapid sequence intubation, 5 2 5 Royal Humane Society for the Apparently Dead, 1 94 "ruptured plaque," stroke and, 548-549 s

Safar, Peter, 1 9 7 Saikewicz case, 5 7 6 salbutamol, 5 1 9 salicylate overdoses, 448 schools AED training in, 1 72 BLS training in, 1 72 SCN5A genes, 1 7 sedation, after ROSC, 4 3 3 sedatives end of life care, 572 in rapid sequence intubation, 2 79-2 80, 2 80, 524-5 2 5 seizures after cardiac arrest, 43 3 , 436 for amphetamine toxicity, 45 9-460 antipsychotics and, 45 8 cocaine-induced, 460 in cocaine toxicity, 46 1 control of, 43 6, 46 1 in opioid toxicity, 464 in organophosphate toxicity, 468 in poisoned patients, 445t prevention of, 43 6 in tricyclic antidepressant toxicity, 456 self-determination, principle of, 568 Sellick's technique in CPR, 483 in rapid sequence intubation, 280 use of, 263f sepsis, shock and, 1 1 9- 1 2 0 septal velocity, assessment of, 1 3 6 septum motion of, 1 3 7f

paradoxical motion of, 1 3 4 serotonin-specific reuptake inhibitors (SSRis) management of toxicity, 45 7-45 8 toxicology, 45 6-457 serotonin syndrome management of, 457 poisoned patients, 446t sestamibi testing, 3 7, 72 sevoflurane, 462 shock characterization of, 1 1 6 differential diagnoses, 1 1 6 hypotension, acute pulmonary edema, and, 1 2 4- 1 2 7 i n poisoned patients, 445t short-stay units, discharge guidelines, 1 1 2 shortness of breath in the emergency department, 1 1 1f prior to AMI 45 reports of, 44 risk stratification, 1 1 1/ Sicilian Gambit, 3 8 1 sildenafil (Viagra), 1 2 6 sinus arrest, 3 4 1 sinus bradycardia, 3 4 1 i n beta-blocker toxicity, 4 5 0 clinical manifestations, 3 4 7, 349t ECG criteria, 3 47, 3 49t etiologies, 3 47-348, 3 49t pathophysiology, 347, 349t therapy, 348, 349t transcutaneous pacing in, 3 6 7f sinus node action potentials of, 3 02 conduction through, 3 04 reentry tachycardia, 3 3 1-3 3 2 sinus pause, 3 4 1 sinusitis, a s asthma trigger, 5 1 4 sleep disturbances, prior to AMI 45 smoking, risks of, 1 7 "sniffing," 46 1 social factors, cardiac arrest and, 1 7 societal values, ECC and, 5 67-5 68, 568t Society for Academic Emergency Medicine, 590 Society for Critical Care Medicine, 590 sodium bicarbonate in acidosis, 467 for beta-blocker toxicity, 450 for cardiopulmonary arrest, 542 in cocaine toxicity, 46 1 for diphenhydramine toxicity, 455 in tricyclic antidepressant toxicity, 45 6 sodium ions, fast channel entry, 3 00-3 0 1 sodium nitrite, i n cyanide poisoning, 467 sodium nitroprusside, 466. see also nitroprusside dosing, 406 indications, 406 usage, 406 sodium/potassiwn ion pumps, 3 02 sodium thiosulfate, 467 somatosensory evoked potentials (SSEPs), 43 6 sonography, indications for, 1 3 0 sotalol for atrial fibrillation/flutter, 3 3 5 characteristics, 3 82 t dosing, 3 90 mechanism of action, 390 in monomorphic ventricular tachycardia, 328 i n polymorphic ventricular tachycardia, 330 in refractory PSVT, 3 3 0, 3 3 1 ,

,

607

toxicology, 449-450 Vaughn-Williams classification, 3 8 3 t spine immobilization, 1 79 spironolactone adverse effects, 1 09 contraindications, 1 09 dosage, 1 09 in heart failure, 1 09 spray paint inhalation, 46 1 ST-segment depression differential diagnoses with, 3 0t high-risk UNNSTEMI, 70 ST-segment elevation on 1 2 -lead electrocardiograms, 69f in detection of AMI, 2 8 differential diagnoses with, 3 0t fibrinolytic therapy, 80 myocardial injury and, 69 ST-segment elevation myocardial infarction (STEM!) ACC/AHA guidelines, 46 ACS and, 2 adjunctive reperfusion therapy, 8 8-89 ASA in, 5 1 atypical symptoms, 45 beta-blocker recommendations, 74 cardiogenic shock and, 1 1 5 chain of survival metaphor, 43 , 44f community programs, 5 6-57 conduction disturbances in, 3 70t ED prioritization, 65-66, 65t emergency management of, 1 2 4f ]-point elevation, 69 left bundle-branch block and, 69-70 prehospital morphine in, 5 1-52 prehospital nitroglycerine in, 5 1-52 reasons for delay in treatment, 44t reperfusion goals, 5 Sf reperfusion therapy, 80-88 risk stratification, 2 8 significant ECG features, 2 8 t transportation options, 5 8f triage of patients, 6 statutory surrogates, 5 7 6-5 77 stents, PCI and, 55 sternotomy, sequela, 1 3 4 steroids, inhaled, 5 2 0 Stor111 Data, 502 street drugs, cardiac arrest and, 1 7 streptokinase, ASA with, 5 1 stress testing for exercise-induced angina, 3 7 risk stratification and, 3 6, 72 stretch receptor activation, 41 1 stroke, 545-5 66. see also hemorrhagic stroke; ischemic stroke algorithm for management, 5 5 2f chain of survival, 546, 547f checklist for fibrinolytic therapy, 5 60t classification by vascular supply, 548 definition, 547 ED assessments, 5 5 6 facts a bout, 5 46 fibrinolytic therapy, 5 60-5 6 1 general care in, 5 6 3 hyperglycemia in, 5 6 3 in-hospital management, 5 5 5-563 management of, 5 5 1-562 modifying risk of, 55 Ot mortality rates, 546 NIH Stroke Scale, 5 5 6-5 5 7 , 5 5 8 t pathophysiology of, 548-549 postocclusioin dynamics, 549 prehospital assessments, 5 52f, 55 5 prehospital care, 5 5 1-5 5 5

608 1

INDEX

stroke (continued) risk factors, 549 7 "D"s of care, 546-547, 547t severity of, 5 5 6-5 5 7 temperature control in, 5 6 3 "time i s brain," 549 time of onset, 55 6 transition to critical care, 5 63 treatment centers, 5 5 1 types of, 547, 547/ stroke volume, cardiac output and, 1 1 6 stylets, 2 7 7 subarachnoid hemorrhagic stroke, 548 subclavian vein (SVC) cannulation, 1 42 , 143/ subglottic airways, 2 5 3-2 72 succinylcholine (Anectine) adverse effects, 2 8 l t characteristics, 2 74t complications, 2 8 l t in crash airway intubation, 2 7 6 i n endotracheal intubation, 2 8 0 paralysis time, 2 8 0 pharmacology of, 2 80-2 8 1 in rapid sequence intubation, 2 80, 5 2 5 sudden cardiac arrest (SCA). see also cardiac arrest 1 -shock vs. three-shock sequence, 1 7 5 agonal gasps and, 1 79 compression first vs shock first, 1 74 early defibrillation outcomes, 2 0 1 -2 02 incidence of, 1 69 research studies, 1 7 0 sudden cardiac death (SCD), 1 1-24 ACS and, 1 definitions, 1 1 - 1 2 risk factors for, 1 2 risk of, !f syndromes associated with, 2 "sudden sniffing death," 462 supraglottic airways, 2 5 7 definition, 2 64 ventilation using, 263-2 64 supraventricular arrhythmias cardioversion history, 1 9 8 tachycardias, 3 1 5-3 2 6 supraventricular tachycardia (SVT) defibrillation energy settings, 3 6 5 recognition of, 2 9 6 V T versus, 2 9 9 surgical airways, 2 9 1 surrogate decision makers, 5 7 5-577 swallow tests, 5 63 sweating, reports of, 44 sympathetic surge, 447 sympathomimetic toxidromes, 459 sympathomimetics, poisoned patients, 446t symptom recognition in acute myocardial infarction, 43-48 media campaigns, 45-46 public education, 45-46 self-triage and, 63-64 synchronized electrical shock. see cardioversion systemic inflammatory response syndrome (SIRS), 1 1 9- 1 2 0 systenlic vascular resistance index (SVRI), 403/ systemic vascular resistance (SVR), 97 systolic dysfunction, definition of, 97 systolic heart failure, 97 T

T-wave abnormalities acute myocardial infarction and, 6t from hyperventilation, 2 9 T-wave inversions, 3 0t

tachycardias 1 2 -lead ECG, 3 1 3 accessory pathway-mediated, 3 3 5 classification of, 2 97-298, 299 etopic atrial, 3 1 8/ hemodynamically stable management of, 3 3 6t treatment of, 3 2 6-3 3 5 long-RP, 3 1 9 monitoring of drug administration, 3 2 7 narrow-complex diagnosis of, 3 1 9-3 2 0 differential diagnoses, 3 1 5 , 3 ! 6t irregular, 3 1 6 reentry arrhythmias, 3 1 6-3 1 7 regular, 3 1 6 treatment, 3 2 7 in poisoned patients, 445 t with pulses, 3 1 3-340, 3 1 4f shock and, 1 1 6 short-RP, 3 1 9 in tricyclic antidepressant toxicity, 45 5 wide-QRS-complex, 299, 3 2 0-3 24 atrial fibrillation with, 3 2 5f, 3 2 6f with a capture complex, 3 2 5/ clinical clues, 3 2 0 description, 3 2 0 differential diagnoses, 3 2 1/ ECG features, 3 2 0-3 2 1 , 3 2 1-324 inappropriately synchronized shock, 3 6 3/ irregular, 3 2 4-3 26, 3 2 6f lidocaine for, 3 8 8 presentations with, 2 95-296 regular, 3 2 4 tachypnea, shock and, 1 1 6 Task Force of Epidemiology of Drowning (TFED), 479 tattoos, DNAR-type, 569 team coordination, in PCA, 3 1 Of technetium sestamibi. see resting sestamibi imaging telemetry, inpatient, 3 8 temperature, tympanic, 483 temperature control, in stroke, 563 tenecteplase, 89 tension pneumothorax in mechanical ventilation, 5 2 7 presentation, 2 7 terbutaline parenteral, 52 1 in severe asthma, 52 1 terminal sedation, 5 7 2 theobromine, 3 84 theophylline, 3 84 thermal regulation, poisoned patient, 449 Thevetia peruviana (yellow oleander), 454 thiocyanate, 466 thiopental, for seizure control, 43 5 thioridazine, overdose, 458 thoracentesis pleural effusion and, 1 3 9 ultrasound-guided, 143-144 thoracic lavage, rewarming, 495t thoracic pump mechanism, 1 50- 1 52 thorax, lung relationship with, 2 3 5 threshold potentials, 3 02 thrombin, direct inhibitors of, 7 8-79 thrombolysis in myocardial infarction. see TIMI thrombolytic therapy cardiovascular risks of, 1 St PPCI ve7Ttts, 86f thrombotic stroke, 547 thromboxane A, 400 Thumper, 1 6 2 , 1 6 3/

thyroid cartilage, 2 3 9-240, 2 3 9/ ticlopidine, dosing, 82t tidal volumes CPR and, 2 3 6 high, 43 3 "time is brain," 549 time-to-reperfusion, 86 time-to-treatment, 56 TIMI risk scores outcomes and, 68/ risk stratification, 3 1 , 3 2 t, 3 3 , 66 in triage of patients with UNNSTEMI, 8 for UNNSTEMI, 8f unstable angina and, 3 3 t, 66f tirofiban dosing table in AU/NSTEMI, 84t mechanism of action, 79 outcomes, 79-80 tissue Doppler imaging (TDI), 1 3 6-1 3 7 tissue necrosis factor, 97 toluene inhalation, 462 torsades de pointes description, 3 2 8-329, 3 2 9 ECG features, 3 2 4t isoproterenol for, 3 8 7 magnesium for, 3 2 7 , 46 1 QRS appearance, 3 2 5 toxicology, 43 3-476 tracheostomy, 2 9 1-292 training in CPR, 1 87 electrocardiography, 307 in ultrasonography, 1 44-145 tramadol, 463 , 464 transabdominal ultrasound, 1 3 5 transalveolar drug absorption, 3 80 transcutaneous pacing (TCP) in drug-induced cardiac arrest, 3 66 emergency pacing, 3 66 in pulseless bradyasystolic cardiac arrest, 3 66 in sinus bradycardia, 3 6 7/ standby pacing, 3 66 temporary, 3 66-3 68 transdermal patches, 2 1 2 transfer protocols in cardiogenic shock, 1 2 1 destination hospital, 1 2 1 in electrical injuries, 509 for PCI, 86-88 for STEMI, 86 transient ischemic attacks (TIAs), 548 transIationa! science careers, 5 88-5 89 transportation. see also transfer protocols self-transport issues, 5 8/ to a skilled PCI laboratory, 86-88 of STEMI patients, 5 8/ use of ambulances, 46 transthoracic echocardiography (TTE), 1 3 4- 1 3 5 transvenous pacemaker capture by, 1 44 ultrasound-guided insertion, 1 44 trauma center models, 56 trazodone, 457 treatment, withdrawal of, 572 triage 1 2 -lead ECGs, 66 ACS identification guidelines, 65t initial, 63-66 of patients with possible ACS, 5-6 trichloroethane, 462 trichloroethylene, 462 tricyclic antidepressants (TCAs) anticholinergic syn1ptoms, 454

IN DEX

management of toxicity, 456 poisoned patients, 446t toxicology, 45 5--456 trismus, cold induced, 492 troponins, cardiac (cTnT, cTni) in myocardial injury, 34 predictive properties of, 3 4t serial measurements of, 70f, 7 1 tryptases, in anaphylaxis, 5 3 3 tubes, 2 5 9 . see also Combitube; endotracheal intubation (ETI); laryngeal tubes tumor necrosis factor-alpha, 5 3 3 tympanic temperatures, 4S3 tyrosine, structure, 399[ u

ultrasonography. see also bedside ultrasound; echocardiography; transabdominal ultrasound; transthoracic echocardiography (TTE) adjunctive uses, 1 4 1 - 1 44 assessment of acute chest pain, 1 3 4- 1 3 5 bedside assessments, 1 2 9-1 3 9 i n central line placement, 1 4 1 - 1 42 comet-tail artifacts, 1 3 S, 1 3 8[ in emergency cardiovascular care, 1 2 9-148 intravascular, 2 lung, 1 3 8 training issues, 1 44-145 unconscious patients, decision-making capacity of, 5 7 3 unfractionated heparin (UFH) aspirin with, S 8 dosages, 77 dosing table in AU/NSTEMI, S 3 t initial management strategies and, 7 7 patient monitoring, 7 7 unstable angina/NSTEMI (UAINSTEMI) algorithm for initial strategy, 8 1f anti platelet and anticoagulant therapy, 82t-84t triage of patients, 6-8 unstable angina pectoris ACS and, 2 emergency department triage, 66 incidence, 2 8 prodromal symptoms, 45 ST-segment depression and, 70 TIMI risk scores, 8f, 3 3 t, 66f unsynchronized shock. see defibrillation upper airway, aligning axes of, 2S2 upper respiratory system, anatomy of, 2 3 7, 2 3 8[ urine alkalinization of, 448 impact of shock on output, 1 1 6 urticaria, anaphylaxis and, 5 3 1 uterine displacement position, 541 v

vagal maneuvers in PSVT, 3 3 0 in refractory PSVT, 3 3 1 for sinus node reentry tachycardia, 3 3 1 in stable tachycardias, 3 2 6 valproate, for seizure control, 43 5 vascular resistance, cardiac output and, 1 1 6 vascular tone, cardiac function and, 3 95--409 vasoactive drugs, in cardiogenic shock, 1 2 0 vasodilation complications of, 1 04-106 contraindications, 1 04-1 06 HF protocol-exclusion criteria, 1 1 2[

vasodilators cardiogenic shock and, 1 1 7 for heart failure therapy, 1 06 vasogenic shock, parameters of, 1 1 7t vasopressm cardiovascular effects, 3 97t dosage, 404 epinephrine vs., 40 1 indications, 404 levels in heart failure, 97 mechanisms of action, 40 1 usage, 404 vasopressors administration in anaphylaxis, 5 3 5-5 3 6 for calcium channel blocker toxicity, 452 in tricyclic antidepressant toxicity, 456 used in resuscitation, 400--40 1 Vaughn-Williams classification of ACLS medications, 3 8 3 t o f antiarrhythmic drugs, 3 8 1 , 3 82 t cardiovascular risks of, 1 St vecuronium (Norcuron) characteristics, 2 74t in endotracheal intubation, 2 8 0 i n rapid sequence intubation, 2 8 0 vena cava, prominent, 1 00 venlafaxine, 457 venovenus rewarming modality, 495t ventilation with advanced airways, 1 82-1 8 3 after cardiac arrest, 43 2-43 3 in anaphylaxis, 5 3 6 assessing need for, 243-2 46 with bag and mask, 1 8 1- 1 8 2 , 1 S2f during CPR, 2 3 4-2 3 7 mouth-to-barrier, 1 8 1 mouth-to-mouth, 1 80 mouth-to-nose, 1 8 1 mouth-to-stoma, 1 S 1 principles of, 242-243 rates, 2 3 6-2 3 7 in severe asthma, 52 5-5 2 7 sudden patient deterioration, 52 5 supplemental oxygenation and, 2 5 3 tidal volumes, 1 80 ventilation tidal volumes, 1 80 ventilation-compression ratio guidelines, 1 S 5 ventilation-perfusion ratios, 2 3 5 ventricles, conduction through, 3 0 5 ventricular arrhythmias in beta-blocker toxicity, 450 classification by disease, 3 2 4t classification by ECG, 3 2 4t classification of, 3 2 3 t clinical presentation, 3 2 3 t defibrillation energy settings, 3 6 5 i n poisoned patients, 445t ventricular fibrillation/ventricular tachycardia (VF/VT), 1 3 ventricular fibrillation (VF) amiodarone in, 3 8 1 arginine vasopressin with epinephrine, 42 3[ beta-blocker impact on, 52 cardioversion history, 198 cell lack of synchrony, 224 cough CPR in, 1 50 CPR in, 1 S 5 defibrillation shocks, 209 early defibrillation and, 2 0 1 ECG features, 3 2 4t in electrical injuries, 508 electrophysiologic mechanisms, 222-2 2 3

609

EMS and estimated survival, 2 0 3f, 2 0 3 t i n hypothermia, 492 incidence of, 1 4f myocardial acidosis and, 2 3 4[ neurologically-intact survival, 2 02 phases of arrest, 2 04[ prehospital mortality, 4 3 pulseless arrest and, 3 09-3 1 1 QRS in, 297 in severe hypothermia, 493 sudden cardiac death and, 1 69 surface ECG, 209[ types of, 2 2 2 ventricular flutter, E C G features, 3 2 4t ventricular function, after cardiac arrest, 1 5 7 ventricular tachycardia (VT) amiodarone in, 3 8 1 assessment of, 3 2 8 bidirectional, 3 2 4t cardiac arrest and, 1 3 in heart failure, 1 1 0 hemodynamically stable, 3 2 7-3 2 8 monomorphic, 2 99f, 3 2 S morphologies of, 2 99[ nonsustained, 3 2 4t polymorphic, 299f, 3 2 S-329, 3 2 9[ prehospital mortality, 4 3 pulseless, 1 69 pulseless arrest and, 3 09-3 1 1 QRS in, 297 risk through antiarrhythmics, 3 SO with RV dissociation, 3 2 2[ supraventricular tachycardias venus, 299 sustained, 3 2 4t terminated by shock, 3 6 3[ Venturi mask system, 2 5 5 verapamil in atrial fibrillation/flutter, 3 3 2 i n automatic atrial tachycardias, 3 3 1 characteristics, 3 82 t dosing, 3 8 5-3 86 mechanism of action, 3 S 5 i n refractory PSVT, 3 3 0 toxicology, 45 1 Vaughn-Williams classification, 3 8 3 t vertebrovasilar artery atherosclerosis, 548-549 vertebrovasilar artery territory stroke, 548 virtual electrode polarization (VEP), 222-2 2 3 , 2 2 4[ viruses, as asthma triggers, 5 1 4 vitamin B 1 7, 466 vocal cords anatomy of, 240 visualization of, 240f, 2 S 2 , 2 8 3[ Volta, Alexandra, 1 94 volume replacement, 1 2 0, 1 2 4. see also fluid administration volutrauma, tidal volumes and, 43 3 vomiting in cardiac arrest, 2 6 3 endotracheal intubation and, 2 S6 w

warfarin cardiovascular risks of, 1 S t i n heart failure, 1 09 weakness, prior to Alvil, 45 Wenckebach heart block, 343f, 3 44. see also atrioventricular block, second-degree wheezing, asthma severity and, 5 1 5 "whippets," inhalation of, 46 1 whole-bowel irrigation, 44S , 464

610 1

INDEX

wide-complex tachycardias. see tachycardias Wiggers, Carl, 1 96, 1 9 7 withdrawal states, poisoned patients, 446t Wolff-Parkinson-White syndrome, 3 3 5 , 3 8 6 women. see also gender presentations with MI, 2 7 prodromal syn1ptoms in, 45

X

z

xenobiotocs, cardiotoxic, 444

Zemuron (rocuroium) characteristics, 2 74t in endotracheal intubation, 2 8 1 in rapid sequence intubation, 5 2 5 Zener diodes, 3 6 8 , 3 69 zero-tier responders, 1 7 3 Zoll, Paul, 1 9 8

y

yellow oleander (Tbevetia pe1"1tviana), 454