Bennett's Cardiac Arrhythmias E-Book

David H. Bennett

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 398

Veröffentlichungsjahr: 2012

Beschreibung

Reviews of previous editions:

"...a well conceived practical guide to the interpretation and treatment of the main cardiac rhythm disturbances."
—Lancet

"This book presents a concise and simplified approach to the diagnosis and management of abnormalities in cardiac rhythm.... One of the book's strengths is the number and quality of electrocardiographic tracings"
—New England Journal of Medicine

"...this book provides an excellent foundation for all those involved in the care of arrhythmia patients"
—British Journal of Hospital Medicine

"…would recommend it unreservedly to anaesthetists who wish to improve their knowledge of cardiac arrhythmias"
—British Journal of Anaesthesia

"This book about cardiac arrhythmias is of much educational value"
—European Heart Journal

A trusted source for junior doctors, students, nurses and cardiac technicians for over 30 years, the new edition of this classic reference continues the winning formula of previous editions while at the same time incorporating essential new content on today's most important clinical topics, including:

• Atrial fibrillation: ablation, drugs, rate control versus rhythm control, risk of systemic embolism, prognosis
• Indications for and management of implantable defibrillators including complications such as arrhythmia storms
• Indications for pacemaker implantation
• Anticoagulant therapy (for atrial fibrillation)
• Long QT syndromes and other channelopathies
• Recently-approved anti-arrhythmia drugs

The 8th edition also features the latest guidelines on ECG screening of athletes and clear guidance for anaesthetists and surgeons dealing with patients with arrhythmias an/or implantable devices. Rich with example ECGs and designed for ease of access to information, Bennett's Cardiac Arrhythmias is the reference you can trust to help you master arrhythmia diagnosis and provide optimal treatment of any patient under your care.

Leseprobe

Contents

Preface

Notes

1 Sinus Rhythm

ECG characteristics

Sinus bradycardia

Sinus tachycardia

Sinus arrhythmia

2 Ectopic Beats

Prematurity

Atrial ectopic beats

Atrioventricular junctional ectopic beats

Ventricular ectopic beats

3 Escape Beats

Timing

Origins

4 Bundle Branch and Fascicular Blocks

Right bundle branch block

Left bundle branch block

Left anterior and posterior fascicular blocks

5 The Supraventricular Tachycardias

Main types

Atrial origin versus atrioventricular re-entry

Effects of supraventricular tachycardias

6 Atrial Fibrillation

ECG characteristics

Causes

Prevalence

Prognosis

Classification

Management

Systemic embolism

Rhythm management

7 Atrial Flutter

Common atrial flutter

Causes

Prevalence

Treatment

Systemic embolism

8 Atrial Tachycardia

ECG characteristics

Causes

Treatment

Multifocal atrial tachycardia

9 Atrioventricular Junctional Re-entrant Tachycardias

Mechanism

ECG characteristics

Clinical features

Treatment

10 Wolff–Parkinson–White Syndrome

Pre-excitation

ECG characteristics

Arrhythmias

Treatment

11 Ventricular Tachyarrhythmias

Ventricular tachycardia

Ventricular fibrillation

Supraventricular versus ventricular tachycardia

12 Monomorphic Ventricular Tachycardia

ECG characteristics

Causes

Mechanisms of ventricular tachycardias

Investigations

Treatment

Coronary heart disease

Hypertrophic cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy

Dilated cardiomyopathy

Ventricular tachycardias not due to structural heart disease

Non-sustained ventricular tachycardia

Accelerated idioventricular rhythm

13 Polymorphic Ventricular Tachycardia and Ventricular Fibrillation

Polymorphic ventricular tachycardia

Torsade de pointes tachycardia

Hereditary long QT syndromes

Ventricular fibrillation

14 Tachycardias with Broad Ventricular Complexes

Causes of a broad complex tachycardia

Useless guidelines

Useful guidelines

15 Atrioventricular Block

Classification

Causes of atrioventricular block

Atrioventricular dissociation

Bilateral bundle branch disease

Clinical aspects of atrioventricular block

Treatment

16 Sick Sinus Syndrome

Causes

ECG characteristics

Clinical features

Diagnosis

Treatment

17 Neurally Mediated Syncope

Malignant vasovagal syndrome

Carotid sinus syndrome

Postural orthostatic tachycardia syndrome

Causes of syncope

18 Arrhythmias Due to Myocardial Infarction

Ventricular fibrillation

Ventricular tachycardia

Reperfusion arrhythmias

Arrhythmias subsequent to recent myocardial infarction

Long-term significance of ventricular arrhythmias

Accelerated idioventricular rhythm

Supraventricular tachycardias

Sinus and junctional bradycardias

Atrioventricular block

19 Antiarrhythmic Drugs

Limitations

Choice of treatment

Modes of action

Notes on individual drugs

Antiarrhythmic drugs during pregnancy

20 Sudden Cardiac Death

Definition

Causes of arrhythmic sudden death

Aborted sudden cardiac death

Athletic activities

21 Cardioversion

Transthoracic cardioversion

Transvenous cardioversion

22 Ambulatory ECG Monitoring

Continuous ECG recording

Intermittent ECG recording

23 Cardiac Pacing

Long-term cardiac pacing

Common indications for long-term pacing

Pacing modes

Pacemaker hardware

Pacemaker implantation

Pacemaker clinic

Electromagnetic interference

Other precautions

Temporary cardiac pacing

24 Implantable Cardioverter Defibrillators

Defibrillator implantation

Indications for ICD implanation

Defibrillator function

Precautions

25 Catheter Ablation

Procedure

Wolff–Parkinson–White syndrome

Typical atrioventricular nodal re-entrant tachycardia

Atrial tachycardia

Atrial flutter

Atrial fibrillation

Atrioventricular nodal ablation

Right ventricular outflow tract tachycardia

Fascicular ventricular tachycardia

Ventricular tachycardia due to structural heart disease

Catheter ablation: what should the patient expect?

26 Arrhythmias for Interpretation

Questions

Interpretations and answers

Index

This edition first published 2013 © 2013 by John Wiley & Sons, Ltd.

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Library of Congress Cataloging-in-Publication Data

Bennett, David H.Bennett’s cardiac arrhythmias : practical notes on interpretation and treatment / David H. Bennett. – 8th ed.p.; cm.Cardiac arrhythmiasRev. ed. of. Cardiac arrhythmias / David H. Bennett. 7th ed., 2006.Includes bibliographical references and index.

ISBN 978-0-470-67493-2 (pbk. : alk. paper)I. Bennett, David H. Cardiac arrhythmias. II. Title. III. Title: Cardiac arrhythmias.[DNLM: 1. Arrhythmias, Cardiac–diagnosis. 2. Arrhythmias, Cardiac–therapy. WG 330]616.1′28–dc23

2012021105

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover image courtesy of the authorCover design by Andrew Magee Design Ltd

Preface

There are several large textbooks which comprehensively cover the field of cardiac arrhythmias with thorough referencing of scientific papers. This book does not attempt to replicate these texts. The purpose of this eighth edition (the first edition was published in 1981, and there have been translations into five other languages) remains the same as that of its predecessors: to provide a concise, up-to-date, practical guide to the diagnosis, investigation and management of the main cardiac arrhythmias, with particular emphasis on the problems commonly faced in practice.

In order to be proficient in the interpretation of arrhythmias it is necessary to study a range of examples of each rhythm disturbance. For this reason, it has always been a purpose of this book to present a large number of electrocardiograms so that the reader can gain experience in ECG interpretation and can test him- or herself out, and thereby gain confidence, during the reading of the book. In this edition there are many new electrocardiograms, and the quiz section has been revised and enlarged to ­provide a challenge to those who may be familiar with previous editions.

The book has been written with junior hospital doctors in mind. They receive little formal training in the management of cardiac arrhythmias and yet, because prompt action is often required, the onus of diagnosis and treatment usually falls on them. It should also be of interest to medical students, who themselves will soon be responsible for dealing with arrhythmias, to nurses working in coronary and intensive care units, to cardiac technicians/physiologists, whose responsibilities nowadays include a major input into arrhythmia management, and to physicians who want a brief review of the practical aspects of cardiac arrhythmias. In recent years there has been a trend to sub-specialisation in cardiology. Whatever the sub-­specialty, cardiac arrhythmias will frequently be encountered. An appreciation of the significance and management of cardiac arrhythmias is required of all who treat patients with cardiac disease.

I am most grateful to my technical, medical and nursing colleagues for their help, and to the staff of my new ­publisher at Wiley-Blackwell for their expertise.

The title of this edition,Bennett’s Cardiac Arrhythmias, was chosen by the publisher to indicate that the author has described the major disturbances of heart rhythm, not, at least to date, that the author has experienced all of them!

The book is dedicated to my family, Irene, Samantha and Sally.

David H. Bennett, MD FRCPSenior Consultant CardiologistUniversity Hospital of South ManchesterManchester, UK

Notes

The electrocardiograms in this book have been recorded at the conventional paper speed of 25 mm/s, unless otherwise indicated. At this speed, each large square represents 0.2 s and each small square represents 0.04 s. Heart rate (beats/minute) can therefore be calculated by dividing the number of large squares between two consecutive complexes into 300, or by dividing the number of small squares between two complexes into 1500.

A single ECG ‘rhythm strip’ may be inadequate for diagnosis. Scrutiny of several ECG leads, preferably recorded simultaneously, may be necessary. For example, atrial activity is often the key to diagnosis but may not be clearly shown in all ECG leads: it is often best seen in leads II and V1. Frequently, a ‘12-lead ECG’ will provide much more information than a rhythm strip.

An ECG recorded during an arrhythmia that is of diagnostic importance should always be safely stored in the patient’s notes. This guideline, which may be very important to the long-term management of a patient, is often ignored, particularly on intensive and coronary care units!

1

Sinus Rhythm

The sinus node lies at the junction of the superior vena cava and right atrium. Atrial activation travels inferiorly from the sinus node to the atrioventricular (AV) node, resulting in a positive P wave in the inferior ECG leads, II, III and aVF. If the QRS complex is preceded by a P wave that is not positive in the ­inferior leads then the rhythm is other than sinus rhythm. The sinus node impulse is conducted relatively slowly via the AV node to reach the His–Purkinje system, which then conducts very rapidly to activate the ventricular myocardium.

   Normal sinus rhythm is characterised by a rate of 60–100 beats/min; PR interval 0.12–0.21 s; QRS duration ≤ 0.10 s; QTc ≤ 0.44 s.

ECG characteristics

The sinus node initiates the electrical impulse that activates atrial and then ventricular myocardium during each normal heartbeat. Sinus node activity itself does not register on the electrocardiogram (ECG).

P wave

Atrial activity, the P wave, is usually apparent in most ECG leads (Figure 1.1). However, occasionally the P wave in some leads is not visible or is of low amplitude, and it may be necessary to inspect all leads of the ECG to establish that there is sinus rhythm (Figure 1.2).

The sinus node lies at the junction of the superior vena cava and right atrium. Atrial activation therefore spreads from the sinus node in an inferior direction (i.e. towards the feet) to the atrioventricular (AV) junction. The P wave, therefore, is upright in those leads that are directed to the inferior surface of the heart (i.e. II, III and aVF), and is inverted in aVR, which faces the superior heart surface (Figure 1.1). If a P wave does not have these characteristics then, even though a P wave precedes each ventricular complex, the sinus node has not activated the atria and the rhythm is abnormal (Figure 1.3).

PR interval

The AV node is the only electrical connection between atria and ventricles: the mitral-­tricuspid valve ring that separates the atria from the ventricles is fibrous and cannot ­conduct electrical impulses. The AV node conducts relatively slowly, thereby delaying conduction of the atrial impulse to the ventricles. Conduction through the AV node does not register on the ECG. The PR interval, which is measured from the onset of the P wave to the onset of the ventricular complex, indicates the time taken for an atrial impulse to reach the ventricles. The normal PR interval ranges from 0.12 to 0.21 s. It should shorten during sinus tachycardia.

Figure 1.1 Sinus rhythm. Atrial activity is clearly seen in the limb leads.

Figure 1.2 Sinus rhythm with low-amplitude P waves (leads I, II, III and V1). Atrial activity is only clearly seen in V1.

QRS complex

After traversing the AV node, the activating impulse reaches the bundle of His, which divides into the right and left bundle branches. The bundle of His, the bundle branches and their ramifications, the Purkinje fibres, constitute the ‘specialised ­intraventricular conducting system’ which facilitates very rapid conduction of the impulse through the ventricular myocardium. Ventricular activation (i.e. depolarisation) is represented by the QRS complex, which is normally no greater than 0.10 s in duration. The amplitude of the QRS complex is larger than that of the P wave because the mass of the ventricles is much greater than that of the atria.

Figure 1.3 Junctional not sinus rhythm: a P wave precedes each QRS complex but is superiorly directed: i.e. it is negative in leads II, III and aVF.

T wave

The T wave is the result of the electrical recovery of ventricular myocardium prior to the next heartbeat, i.e. repolarisation. Sometimes, a low-amplitude wave can be seen following the T wave, termed a U wave. It is thought to result from repolarisation of the Purkinje fibres and is usually seen in leads V2–4.

The QT interval, which is measured from the onset of the QRS complex to the end of the T wave, represents the duration of ventricular activation plus recovery. The QT interval normally shortens with increasing heart rate, partly due to the increase in rate itself and partly due to the increase in sympathetic nervous system activity related to sinus tachycardia. When measuring the QT interval it is necessary to correct the measured interval for heart rate. The corrected QT interval (QTc) is calculated by selecting the ECG lead showing the longest QT interval, and then dividing the square root of the cycle length into the measured QT interval. For example, a patient with a measured QT interval of 0.40 s at a heart rate of 60 beats/min has a cycle length of 1.0 s and therefore also has a QTc of 0.40 s. QT prolongation and a prominent U wave are seen in certain hereditary and acquired conditions.

ECG characteristics of normal sinus rhythm

P wave   Precedes each QRS complex   Upright in leads III, aVF   Inverted in lead aVR

PR interval   Duration 0.12–0.21 s

QRS complex   Duration ≤ 0.10 s

QTc interval   Duration ≤ 0.42 s (men), ≤ 0.44 s (women)

Relative speeds of impulse conduction

Appreciation of the relative speeds of impulse conduction through the heart – slowest through the AV node, fastest through the specialised intraventricular conducting system and at an intermediate rate through ordinary working myocardium – is important in understanding the mechanisms of a number of arrhythmias as well as generation of the normal P-QRS complex.

Speed of impulse conduction

His–Purkinje system > myocardium > AV node

Sinus bradycardia

Sinus bradycardia is sinus rhythm at a rate less then 60 beats/min (Figure 1.4). It may be physiological, as in athletes or during sleep, or it may result from acute myocardial infarction, sick sinus syndrome or from drugs such as beta-adrenoceptor blocking drugs (beta-blockers). Non-cardiac disorders such as hypothyroidism, jaundice and raised intracranial pressure can also cause sinus bradycardia.

Atropine, isoprenaline or pacing can be used to increase the rate but are only necessary when sinus bradycardia causes symptoms or marked hypotension, or leads to tachyarrhythmia.

Sinus tachycardia

Sinus tachycardia is defined as sinus rhythm at a rate greater than 100 beats/min (Figure 1.5). Exercise, anxiety or any disorder that increases sympathetic nervous system activity may cause sinus tachycardia.

Occasionally, sinus tachycardia can be inappropriate. Hyperthyroidism is a possible cause. However, often no cause is found. Young females are most commonly affected. Fast rates are usually persistent and there is an exaggerated response to exercise with rates increasing rapidly almost immediately exertion begins. Rarely, inappropriate sinus tachycardia is due to a primary disorder of the sinus node (sinus node re-entry).

Since sinus tachycardia is usually a physiological response, there is rarely a need for specific treatment. However, if sinus tachycardia is inappropriate, the rate may be slowed by a beta-blocker, or by ivabradine, which is a selective inhibitor of sinus node function.

At rest, the sinus node rate is seldom above 100 beats/min unless the patient is very ill. If there is apparent sinus tachycardia at rest alternative rhythms such as atrial tachycardia or atrial flutter should be considered.

Figure 1.4 Sinus bradycardia (lead II): rate 34 beats/min.

Figure 1.5 Sinus tachycardia during exercise. The rate is 136 beats/min.

Figure 1.6 Sinus arrhythmia.

Sinus arrhythmia

In sinus arrhythmia, which is of no pathological significance, there are alternating periods of slowing and increasing sinus node rate. Usually the rate increases during inspiration (Figure 1.6). Sinus arrhythmia is most commonly seen in the young.

2

Ectopic Beats

The terms ectopic beat, extrasystole and premature contraction are, for practical purposes, synonymous. They refer to an impulse originating from the atria, atrioventricular (AV) junction or ventricles that arises prematurely in the cardiac cycle.

   Usually the AV junction and bundle branches will conduct an atrial ectopic to the ventricles normally, resulting in a narrow QRS complex. The prematurity of an atrial ectopic beat is such that the P wave may be superimposed on the preceding T wave.

   The impulse of a ventricular ectopic beat is not conducted through the ­ventricles via the rapidly conducting His–Purkinje system. The resultant ­complexes are therefore broad (> 0.12 s) and bizarre in shape, and will not be preceded by a premature P wave. Ventricular ectopic beats are often idiopathic but when caused by cardiac disease are associated with an increased cardiovascular mortality that will not be reduced by antiarrhythmic drugs.

Prematurity

The terms ectopic beat, extrasystole and premature contraction are, for practical purposes, synonymous. They refer to an impulse originating from the atria, AV junction (i.e. the AV node together with the bundle of His) or ventricles that arises prematurely in the cardiac cycle (Figures 2.1–2.3).

By definition, an ectopic beat must arise earlier in the cardiac cycle than the next normally timed beat would be expected. Thus the interval between the ectopic beat and the preceding beat, i.e. the coupling interval, is shorter than the cycle length of the main rhythm. If this fact is ignored, other beats with abnormal configurations such as escape beats (Chapter 3) and intermittent bundle branch block (Chapter 4) may be misinterpreted as ectopic beats.