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Authors: Rosenthal, Law rence S.

Title: DX/RX: Arrhythmias, 1st Edition

Copyright2008 Jones and Bartlett Publishers

2008

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Sudbury, MA 01776

978-0-7637-2354-5

0-7637-2354-1

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ISBN-13: 978-0-7637-2354-5

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The authors, editor, and publisher have made every effort to provide accurate information.

However, they are not responsible for errors, omissions, or for any outcomes related to the

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described. Treatments and side effects described in this book may not be applicable to all

patients; likewise, some patients may require a dose or experience a side effect that is not

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described herein. The reader should confer with his or her own physician regarding specific

treatments and side effects. Drugs and medical devices are discussed that may have limited

availability controlled by the Food and Drug Administration (FDA) for use only in a research

study or clinical trial. The drug information presented has been derived from reference

sources, recently published data, and pharmaceutical research data. Research, clinical

practice, and government regulations often change the accepted standard in this field. When

consideration is being given to use of any drug in the clinical setting, the health care provider

or reader is responsible for determining FDA status of the drug, reading the package insert,reviewing prescribing information for the most up-to-date recommendations on dose,

precautions, and contraindications, and determining the appropriate usage for the product.

This is especially important in the case of drugs that are new or seldom used.

Library of Congress Cataloging-in-Publication Data

Rosenthal, Lawrence S.

Dx/Rx. Arrhythmias / Lawrence S. Rosenthal.

p. ; cm. (Jones and Bartlett publishers Dx/Rx cardiology series)

Includes bibliographical references and index.

ISBN-13: 978-0-7637-2354-5 (pbk. : alk. paper)

ISBN-10: 0-7637-2354-1 (pbk. : alk. paper)

1. ArrhythmiaHandbooks, manuals, etc. I. Title. II. Title:Arrhythmias. III. Series.

[DNLM: 1. Tachycardia

diagnosis

Handbooks. 2. Anti-Arrhythmia Agents

Handbooks. 3.ArrhythmiaHandbooks. 4. TachycardiatherapyHandbooks.

WG 39 R815d 2008]

RC685.A65R55 2008

616.1 8dc22

2007028853

Production Credits

Executive Publisher: Christopher Davis

Acquisitions Editor: Janice Hackenberg

Associate Editor: Kathy Richardson

Production Director: Amy Rose

Production Editor: Carolyn F. Rogers

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Associate Marketing Manager: Rebecca Wasley

Manufacturing Buyer: Therese Connell

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Cover Design: Anne Spencer

Composition: ATLIS Graphics

Printing and Binding: Malloy, Inc.

Cover Printing: Malloy, Inc.

Printed in the United States of America

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> Front of Book > Authors

Author

Law rence S. Rosenthal MD, PhD, FACC

Associate Professor of Medicine

Director, Section Cardiac Pacing and Electrophysiology

Division of Cardiology

UMass Memorial Medical Center

Worcester, Massachusetts

Series Editor:Dennis A. Tighe MD, FACC, FACP

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> Front of Book > Editor's Preface

Editor's Preface

Cardiac arrhythmias are commonly encountered in both inpatient and outpatient settings.

They are seen in a variety of patients and may reflect a severe underlying cardiac disorder or

represent a cardiac response to a non-cardiac disorder. To the nonspecialist, the diagnosis and

management of cardiac arrhythmias can sometimes present diagnostic and/or therapeutic

dilemmas. In this monograph, Dr. Lawrence Rosenthal shares his experience and presents a

concise and practical approach to the diagnosis and treatment of cardiac arrhythmias. The

text is well supplemented with tables and illustrations of the various cardiac arrhythmias. I am

most grateful to Larry for his excellent contribution to this series. Any healthcare professional

who deals with cardiac patients will find this book to be most informative and helpful.

Dennis A. Tighe

Worcester, M

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> Back of Book > Appendix I - Drug Trials and Device Therapy in Patients with Ventricular Arrhythmias

Appendix IDrug Trials and Device Therapy in Patients with

Ventricular Arrhythmias

n Several clinical trials have helped to clarify the indications for drug therapy in various

subgroups of patients with ventricular arrhythmias.

Ventricular Ectopic Activity and Sudden Cardiac Death:Post-MI

n Following MI there is no indication to treat isolated premature ventricular beats.

BHAT (Beta-Blocker Heart Attack Trial)

n The BHAT trial examined the usefulness of beta-blockers in the prevention of sudden

cardiac death (SCD).

n This randomized, double-blind, placebo-controlled study tested whether the administration

of propranolol in patients with a history of at least one myocardial infarction could reduce

subsequent mortality.

n A total of 3,837 patients were randomized to receive propranolol (180 or 200 mg/d) or a

placebo.

n The trial was stopped nine months before the planned termination date because of the

significant improvement in total mortality in the beta-blocker treatment group.

n Total mortality at 25.1 months was 7.2% in the propranolol-treated patients and 9.8% in the

placebo group.

n SCD was significantly less frequent in the propranolol-treated patients (3.3% in the

propranolol-treated group versus 4.6% in the placebo group).

n Patients with a history of congestive heart failure experienced a 47% reduction in SCD

(5.5% in the propanolol treated group versus 10.4% in the placebo group).

References

Beta-Blocker Heart Attack Trial Research Group. A randomized trial of propranolol in

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patients with acute myocardial infarction, I: mortality results. JAMA. 1982;247:1707-1714.

Chadda K, Goldstein S, Byington R, Curb JD. Effect of propranolol after acute myocardial

infarction in patients with congestive heart failure. Circulation. 1986;73:503-510.

CAST I and II (Cardiac Arrhythmia Suppression Trial)

n In patients with coronary artery disease and LV function of less than 40%, the suppression of

ventricular ectopic beats with flecainide, encainide, and moricizine was associated with

an increased risk of mortality.

References

Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving

encainide, flecainide, or placebo: the Cardiac Arrhythmia Suppression Trial. N Engl J

Med. 1991; 324:781-788.

The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic

agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227-233.

BASIS (Basel Antiarrhythmic Study of Infarct Survival)

n This is the only study supporting the suppression of ventricular ectopy with antiarrhythmic

drugs post-MI.

n Amiodarone therapy was associated with an improved survival even after the drug was

discontinued.

n Most experts, however, do not recommend amiodarone for the treatment of isolated

ventricular ectopy.

Reference

Burkart F, Pfisterer M, Kiowski W, Follath F, Burckhardt D. Effect of antiarrhythmic

therapy on mortality in survivors of myocardial infarction with asymptomatic complex

ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS). J Am Coll

Cardiol. 1990;16:1711-1718.

CAMIAT (Canadian Amiodarone MyocardialInfarction Arrhythmia Trial)

n The use of amiodarone in post-MI patients with ventricular ectopic activity was associated

with a decrease in sudden death. However, this study did not include enough patients and

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did not follow them long enough to show an improvement in survival.

Reference

Cairns JA, Connolly SJ, Roberts R, Gent M. Randomised trial of outcome after myocardial

infarction in patients with frequent or repetitive ventricular premature depolarisations:

CAMIAT. Lancet. 349(9053):675-682.

EMIAT (European Myocardial Infarction AmiodaroneTrial)

n The European Myocardial Infarct Amiodarone Trial (EMIAT) was designed to study the

efficacy of amiodarone in reducing mortality in patients with decreased left ventricular

function after myocardial infarction.

n

This trial enrolled 1,486 patients.

n Patients were enrolled 5 to 21 days after myocardial infarction if their left ventricular

ejection fraction (LVEF) was less than or equal to 40%.

n Patients were randomized to receive treatment with amiodarone or placebo.

n There was no difference in all-cause mortality (the primary end point of the study) or in

cardiac mortality.

n Arrhythmic death was reduced from 7.0% in the placebo group to 4.0% in the amiodarone

group (P = .05).

n Retrospective analysis of the data demonstrated a significant reduction in cardiac deaths in

amiodarone-treated patients who were also treated with beta-blockers; this suggests that

beta-blockers confer an additional benefit beyond that provided by amiodarone alone.

n The failure of an improvement in arrhythmic death to translate into an improvement in

cardiac or all-cause mortality may be related to the limited power of the study.

Reference

Julian DG, Camm AJ, Frangin G, et al. Randomised trial of effect of amiodarone on

mortality in patients with left-ventricular dysfunction after recent myocardial infarction:

EMIAT: European Myocardial Infarct Amiodarone Trial Investigators. Lancet. 1997;349: 667-

674.

SWORD (Survival With Oral D-Sotalol)

n The SWORD trial was designed to test the hypothesis that d-sotalol would reduce mortality

in high-risk survivors of a myocardial infarction.

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n This study enrolled patients with an LVEF of less than or equal to 40% and a history of

myocardial infarction with heart failure.

n The study was designed to enroll 6400 patients but was stopped after the enrollment of

3400 patients because excess mortality in the d-sotalol group was observed.

l The mortality rate was 4.6% in the sotalol group and 2.7% in the placebo group (P

= .005).

Reference

Waldo AL, Camm AJ, deRuyter H, et al. Effect of d-sotalol on mortality in patients with

left ventricular dysfunction after recent and remote myocardial infarction: the SWORD

Investigators: Survival With Oral d-Sotalol. Lancet. 1996;348:7-12.

Congestive Heart Failure

CHF-STAT (Survival Trial of Antiarrhythmic Therapy inCongestive Heart Failure)

n This study enrolled 674 patients with the following conditions: symptoms of congestive

heart failure, cardiac enlargement, 10 or more PVCs/min, and an LVEF of less than or equal

to 40%.

n

Patients were randomly assigned to receive amiodarone or a placebo.

n The primary end point of this study was total mortality, and the median follow-up was 45

months.

n Treatment with amiodarone was effective in suppressing ventricular ectopy but did not

result in a substantial reduction

in the combined endpoint of cardiac death or hospitalizations for heart failure.

ReferenceSingh S, Fletcher R, Fisher S, Singh B. Amiodarone in patients with congestive heart

failure and asymptomatic ventricular arrhythmia: Survival Trial of Amiodarone in Patients

with Congestive Heart Failure. N Engl J Med. 1995;333:77-82.

GESICA (Grupo de Estudio de la Sobrevida en la

Insuficiecia Cardiaca en Argentina)n This trial examined the prophylactic use of amiodarone in SCD prevention in patients at

risk because of heart failure.

n This study randomized 516 patients with advanced heart failure to treatment with

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amiodarone and standard heart failure therapy or to standard heart failure therapy alone.

n At an average follow-up of 13 months, mortality was 41.4% in the control group and 33.5%

in the amiodaronetreated patients (P = .02).

n Treatment with amiodarone resulted in a 28% risk reduction for mortality attributable both

to arrhythmic death and to progressive heart failure.

l These results are divergent from those of CHF-STAT; no consensus exists in the United

States to treat CHF patients with PVCs.

Reference

Doval HC, Nul DL, Grancelli HO, et al. Randomized trial of low-dose amiodarone in severe

congestive heart failure. Lancet. 1994;344:493-498.

Nonsustained Ventricular Tachycardia: PrimaryPrevention of SCD

n Nonsustained ventricular tachycardia is considered an independent predictor of mortality

after a myocardial infarction.

n In certain groups, treatment may improve survival.

MADIT (Multicenter Automatic DefibrillatorImplantation Trial)

n Among post-MI patients with an LVEF of less than 35%, nonsustained ventricular tachycardia,

and inducible but not suppressible sustained VTach at EPS, a 50% reduction in mortality was

observed with ICD therapy as compared to therapy with antiarrhythmic drugs (primarily

amiodarone).

Reference

Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in

patients with coronary disease at high risk for ventricular arrhythmia: Multicenter

Automatic Defibrillator Implantation Trial Investigators. N Engl J Med. 1996;335:1933-

1940.

MUSTT (Multicenter UnSustained Tachycardia Trial)

n The Multicenter UnSustained Tachycardia Trial (MUSTT) was a primary prevention trial that

examined the ability of electrophysiologically guided antiarrhythmic therapy to reduce

mortality rates in patients with coronary artery disease, LVEF of less than or equal to 40%,

and asymptomatic nonsustained ventricular tachycardia.

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n Patients with inducible sustained ventricular tachycardia had a high mortality rate, which

was lowered by implantable ICDs but not by antiarrhythmic drug therapy.

Reference

Buxton AE, Lee KL, Fisher JD, et al., for the Multicenter UnSustained Tachycardia Trial

Investigators. A randomized study of the prevention of sudden death in patients with

coronary artery disease. N Engl J Med. 1999;341:1882-1890.

MADIT II (Multicenter Automatic DefibrillatorImplantation Trial II)

n This trial evaluated whether prophylactic defibrillator implantation would offer a survival

benefit in patients with prior MI and advanced left ventricular dysfunction who did not

have manifest ventricular arrhythmias and

who did not have a requirement for electrophysiologic study.

n The rationale was that the scarred myocardium in such patients would serve as a substrate

for malignant ventricular arrhythmias and increase the risk of sudden death.

n All patients had an ejection fraction of 0.30 or less within a 3-month period prior to study

entry; these ejection fractions were documented by angiography, radionuclide scanning, or

echocardiography.

n Follow-up averaged 20 months with a range of 6 days to 53 months.

n The data and safety monitoring board recommended termination of the trial due to the

superiority of implantable defibrillation in terms of survival.

l Mortality rates were 19.8% in the conventional therapy group and 14.2% in the

defibrillator group.

l The hazard ratio for risk of death from any cause in the defibrillator group was 0.69 (CI

95%, 0.51-0.93; p = 0.016) when compared to the medical treatment group, representing

a 31% reduction in the risk of death for defibrillator patients.

Reference

Moss A, Zareba W, Hall J, et al. Prophylactic implantation of a defibrillator in patients

with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346

(12):877-883.

SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial)

n Patients with class II and class III heart failure (52% ischemic in origin and 48% nonischemic)

with ejection fractions of less than 35% were randomly assigned to receive an ICD,

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amiodarone, or a placebo.

n The 2,252 patients were followed for an average of 40 months.

n There was 23% less death in the ICD group regardless of the etiology of the heart disease

(ischemic or nonischemic). In addition, amiodarone was no better than the placebo.

Reference

Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, et al. Sudden Cardiac Death

in Heart Failure Trial (SCD-HeFT) Investigators. N Engl J Med. 2005;352(3):225-237.

Sustained Ventricular Arrhythmia: SecondaryPrevention of SCD

AVID (Antiarrhythmics Versus Implantable Defibrillators)n Survivors of cardiac arrest or symptomatic ventricular tachycardia were randomized to ICD

therapy or antiarrhythmic therapy (amiodarone or sotalol).

n A statistically significant 28% reduction in death was associated with ICD therapy.

Reference

Antiarrhythmics Versus Implantable Defibrillators (AVID) Investigators. A comparison of

antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from

near-fatal ventricular arrhythmias. N Engl J Med. 1997;337:1576-1583.

ESVEM (Electrophysiologic Study VersusElectrocardiographic Monitoring)

n Survivors of cardiac arrest, symptomatic ventricular tachycardia, or syncope with inducible

arrhythmia at EPS and ventricular ectopic activity (more than 10 PCs/hr on 24-hour ECGmonitoring) were randomized to ventricular premature beat (VPB) suppression (24-hour

ECG and exercise treadmill testing [ETT]) or noninducibility at EPS with seven

antiarrhythmic drugs.

n Neither strategy was superior for predicting arrhythmia recurrence or death, but sotalol

appeared to be a superior antiarrhythmic agent.

Reference

Mason JW for the Electrophysiologic Study versus Electrocardiographic Monitoring

Investigators. A comparison of electrophysiologic testing with Holter monitoring to

predict antiarrhythmic-drug efficacy for ventricular tachyarrhythmias. N Engl J Med.

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1993;329:445-451.

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> Back of Book > Appendix II - 2005 Changes to the AHA's BLS and ACLS Guidelines

Appendix II2005 Changes to the AHA's BLS and ACLS

Guidelines

Survival for an out of hospital cardiac arrest is less 5% in the US. This is likely due, in part, to

inconsistencies in the delivery of effective CPR, the availability of Automatic External

defibrillators (AEDs), as well as early intervention. Thus in 2005 changes were made in the BLSand ACLS algorithms by the American Heart Association. The goal was to simplify resuscitation

training and improve outcomes.

Major changes include:

1. Changing compression rate to 100 per minute in all victims except newborns in order to

achieve effective coronary and cerebral perfusion

2. When attempting defibrillation, deliver a single shock followed by 5 cycles of CPR (2

minutes) beginning with chest compressions. After delivering a shock, rhythm analysis by

AEDs can take as long as 37 seconds, during which no CPR would potentially be delivered.

3. The delivery of normal breaths over one second, because longer breaths reduce coronary

blood flow and oppose chest compressions

4. Using a 30:2 compression to breath ratio for all victims except newborns

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