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"…A significant resource of information for medical students and junior medical staff, as well as for those wishing to refresh their knowledge." By Perfusion, Apr 2015

      • Clinically-orientated with a quick reference list of cardiovascular conditions
      • Builds on the basic knowledge outlined in the classic ECG Made Easy
      • Emphasises the individuality of every ECG and uses full 12-lead ECG recordings to provide a realistic reproduction of the clinical environment.
      • The unique page size allows presentation of all 12-lead ECGs across a single page for clarity.
      • Each chapter begins with a brief account of the relevant history and examination and ends with a short account of what might be done once the ECG has been interpreted.

    Now integrated throughout the book is text on electrophysiology and electrical devices. With pacemakers and implanted defibrillators now common among patients on general medical take, this material guides the reader in recognising their purpose and making a preliminary analysis of any malfunction.

    Categories:
    Year:
    2013
    Edition:
    6
    Publisher:
    Churchill Livingstone
    Language:
    english
    Pages:
    376 / 378
    ISBN 10:
    0702046434
    ISBN 13:
    9780702046438
    File:
    PDF, 32.44 MB
    Download (pdf, 32.44 MB)

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    You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read. Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them.
    08 May 2017 (16:25) 

    You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read. Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them.
    The
    
    ECG
    In Practice
    
    For Elsevier
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    1
    
    The
    
    ECG
    In Practice
    
    SIXTH EDITION
    
    John R. Hampton
    DM MA DPhil FRCP FFPM FESC
    Emeritus Professor of Cardiology,
    University of Nottingham, UK
    With contributions by
    
    David Adlam
    
    BA BM BCh DPhil MRCP
    
    Senior Lecturer in Acute and Interventional
    Cardiology and Honorary Consultant
    Cardiologist, University of Leicester, UK
    
    EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY TORONTO 2013
    
    Notices
    Knowledge and best practice in this field are constantly changing. As
    new research and experience broaden our understanding, changes in
    research methods, professional practices, or medical treatment may
    become necessary.
    © 2013 Elsevier Ltd. All rights reserved.
    No part of this publication may be reproduced or transmitted in
    any form or by any means, electronic or mechanical, including
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    system, without permission in writing from the publisher. Details on
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    the Copyright Clearance Center and the Copyright Licensing Agency,
    can be found at our website: www.elsevier.com/permissions.
    This book and the individual contributions contained in it are
    protected under copyright by the publisher (other than as may be
    noted herein).
    First edition 1986
    Second edition 1992
    Third edition 1997
    
    Fourth edition 2003
    Fifth edition 2008
    Sixth edition 2013
    
    ISBN 978-0-7020-4643-8
    International ISBN 978-0-7020-4644-5
    e-book ISBN 978-0-7020-5244-6
    British Library Cataloguing in Publication Data
    A catalogue record for this book is available from the British Library
    
    Practitioners and researchers must always rely on their own experience
    and knowledge in evaluating and us; ing any information, methods,
    compounds, or experiments described herein. In using such information
    or methods they should be mindful of their own safety and the safety
    of others, including parties for whom they have a professional
    responsibility.
    With respect to any drug or pharmaceutical products identified,
    readers are advised to check the most current information provided
    (i) on procedures featured or (ii) by the manufacturer of each product
    to be administered, to verify the recommended dose or formula, the
    method and duration of administration, and contraindications. It is the
    responsibility of practitioners, relying on their own experience and
    knowledge of their patients, to make diagnoses, to determine dosages
    and the best treatment for each individual patient, and to take all
    appropriate safety precautions.
    To the fullest extent of the law, neither the publisher nor the authors,
    contributors, or editors, assume any liability for any injury and/or
    damage to persons or property as a matter of products liability,
    negligence or otherwise, or from any use or operation of any methods,
    products, instructions, or ideas contained in the material herein.
    
    Library of Congress Cataloging in Publication Data
    A catalog record for this book is available from the Library of Congress
    
    Printed in China
    
    www.cambodiamed.blogspot.com | Best Medical Books | Chy Yong
    
    1
    
    Preface
    WHAT TO EXPECT OF THIS BOOK
    I assume that the reader of this book will have the level
    of knowledge of the ECG that is contained in The ECG
    Made Easy, to which this is a companion volume. The
    ECG is indeed easy in principle, but the variations in
    pattern seen both in normal people and in patients with
    cardiac and other problems can make the ECG seem
    more complex than it really is. This book concentrates
    on these variations, and contains several examples of
    each abnormality. It is intended for anyone who understands the basics, but now wants to use the ECG to its
    maximum potential as a clinical tool.
    The ECG is not an end in itself, but is an extension
    of the history and physical examination. Patients do
    not visit the doctor wanting an ECG, but come either
    for a health check or because they have symptoms.
    Therefore, this book is organized according to clinical
    situations, and the chapters cover the ECG in healthy
    subjects and in patients with palpitations, syncope,
    chest pain, breathlessness or non-cardiac conditions.
    To emphasize that the ECG is part of the general
    assessment of a patient, each chapter begins with
    a brief section on history and examination and ends
    
    with a short account of what might be done once the
    ECG has been interpreted.
    This sixth edition continues the philosophy of its
    predecessors in that the patient is considered more
    important than the ECG. However, the ECG is a vital
    part of diagnosis and, increasingly, dictates treatment.
    Electrical devices of various sorts are standard treatment in cardiology, and patients with such devices
    are now commonly seen in patients who present
    with non-cardiological problems. Those who are not
    specialists in cardiology need to understand them.
    Therefore there is a series of changes in the text compared with previous editions, and the sections on pacemakers, defibrillators and electrophysiology have been
    integrated into the relevant chapters.
    
    WHAT TO EXPECT OF THE ECG
    The ECG has its limitations. Remember that it provides
    a picture of the electrical activity of the heart, but gives
    only an indirect indication of the heart’s structure and
    function. It is, however, invaluable for assessing
    patients whose symptoms may be due to electrical
    
    v
    
    Preface
    malfunction in the heart, including patients with conduction problems and those with arrhythmias.
    In healthy people, finding an apparently normal
    ECG may be reassuring. Unfortunately the ECG can
    be totally normal in patients with severe coronary
    disease. Conversely the range of normality is such that
    a healthy subject may quite wrongly be labelled as
    having heart disease on the basis of the ECG. Some
    ECG patterns that are undoubtedly abnormal (for
    example, right bundle branch block) are seen in perfectly healthy people. It is a good working principle
    that it is the individual’s clinical state that matters, not
    the ECG.
    When a patient complains of palpitations or
    syncope, the diagnosis of a cardiac cause is only certain
    if an ECG is recorded at the time of symptoms – but
    even when the patient is symptom-free, the ECG may
    provide a clue for the prepared mind. In patients with
    chest pain the ECG may indicate the diagnosis, and
    treatment can be based upon it, but it is essential to
    remember that the ECG may remain normal for a few
    hours after the onset of a myocardial infarction. In
    breathless patients a totally normal ECG probably
    rules out heart failure, but it is not a good way of
    diagnosing lung disease or pulmonary embolism.
    Finally, it must be remembered that the ECG can be
    
    vi
    
    quite abnormal in a patient with a variety of noncardiac conditions, and one must not jump to the
    conclusion that an abnormal ECG indicates cardiac
    pathology.
    
    ACKNOWLEDGEMENTS
    In this sixth edition of The ECG in Practice I have
    been helped by many people. In particular, I am grateful to David Adlam for providing many illustrations,
    and for contributing the sections on devices and
    electrophysiology, which takes the book beyond the
    routine ECG into the realm of sophisticated diagnosis
    and electrical treatments – which are nevertheless
    based on an understanding of the ECG. I am also
    extremely grateful to my copy-editor, Alison Gale, for
    her enormous attention to detail that led to many
    improvements in the text. I am also grateful to Laurence Hunter and his team at Elsevier for their encouragement and patience. As before, I am grateful to
    many friends and colleagues who have helped me to
    find the wide range of examples of normal and abnormal ECGs that form the backbone of the book.
    John Hampton
    Nottingham, 2013
    
    1
    
    Contents
    
    12-lead ECGs
    1. The ECG in healthy people
    2. The ECG in patients with palpitations and syncope: between attacks
    
    viii
    1
    58
    
    3. The ECG when the patient has a tachycardia
    
    101
    
    4. The ECG when the patient has a bradycardia
    
    169
    
    5. The ECG in patients with chest pain
    
    208
    
    6. The ECG in patients with breathlessness
    
    287
    
    7. The effect of other conditions on the ECG
    
    316
    
    8. Conclusions: four steps to making the most of the ECG
    
    346
    
    Index
    
    350
    
    vii
    
    12-lead ECGs
    
    viii
    
    AAI pacing 196
    Accelerated idionodal rhythm 48
    Accelerated idioventricular rhythm 28
    Anorexia nervosa 342
    Aortic stenosis, severe, left ventricular
    hypertrophy with 298
    Aortic stenosis and left bundle branch block 296
    Atrial fibrillation 124, 178
    Atrial fibrillation, uncontrolled 290
    Atrial fibrillation and anterior ischaemia 244
    Atrial fibrillation and coupled ventricular
    extrasystoles 290
    Atrial fibrillation and digoxin effect at rest 280
    Atrial fibrillation and digoxin effect on exercise
    280
    Atrial fibrillation and inferior infarction 140
    Atrial fibrillation and left bundle branch block
    128, 130
    Atrial fibrillation and right bundle branch block
    134
    Atrial fibrillation and Wolff–Parkinson-White
    syndrome 148
    
    Atrial flutter and 1:1 conduction 120
    Atrial flutter and 2:1 block 118
    Atrial flutter and 4:1 block 120
    Atrial flutter and intermittent VVI pacing 194
    Atrial flutter and variable block 176
    Atrial flutter in hypothermia 318
    Atrial septal defect and right bundle branch block
    326
    Atrial tachycardia 110, 116
    Atrioventricular nodal re-entry tachycardia
    (AVNRT) 122
    Atrioventricular nodal re-entry tachycardia
    (AVNRT) and anterior ischaemia 244
    Bifascicular block 90
    Biventricular pacing 314
    Broad complex tachycardia of uncertain origin
    136, 138
    Brugada syndrome 80
    Chronic lung disease 310
    Complete heart block 180
    
    12-lead ECGs
    Complete heart block and Stokes–Adams attack
    182
    Congenital long QT syndrome 76
    DDD pacing, atrial tracking 200
    DDD pacing, atrial and ventricular pacing 198
    DDD pacing, intermittent 200
    Dextrocardia 10
    Dextrocardia, leads reversed 10
    Digoxin effect 334
    Digoxin effect and ischaemia 262
    Digoxin toxicity 336
    Ebstein’s anomaly, right atrial hypertrophy and
    right bundle branch block 324
    Ectopic atrial rhythm 8
    Electrical alternans 328
    Exercise, digoxin effect, atrial fibrillation 280
    Exercise-induced ischaemia 272
    Exercise-induced ST segment depression 278
    Exercise-induced ST segment elevation 274
    Exercise testing, normal ECG 272, 278
    Fallot’s tetralogy, right ventricular hypertrophy in
    324
    Fascicular tachycardia 136
    First degree block 84
    First degree block and left bundle branch block
    88
    First degree block and right bundle branch block
    90, 174, 182
    Friedreich’s ataxia 344
    Hyperkalaemia 330
    Hyperkalaemia, corrected 332
    Hypertrophic cardiomyopathy 68, 300
    
    Hypokalaemia 334
    Hypothermia 318
    Hypothermia, atrial flutter 318
    Hypothermia, re-warming after 320
    Intermittent VVI pacing 192
    Ischaemia, anterior 242
    Ischaemia, anterior and atrial fibrillation 244
    Ischaemia, anterior and AV nodal re-entry
    tachycardia 244
    Ischaemia, anterior and inferior infarction and
    right bundle branch block 238
    Ischaemia, anterior and possible old inferior
    infarction 240
    Ischaemia, anterior and right bundle branch block
    238
    Ischaemia, anterolateral 242
    Ischaemia, digoxin effect and 262
    Ischaemia, exercise-induced 272
    Ischaemia, ?left ventricular hypertrophy 300
    Ischaemia, probable 298
    Junctional tachycardia with right bundle branch
    block 136
    Left anterior hemiblock 88, 302
    Left atrial hypertrophy 70
    Left atrial hypertrophy and left ventricular
    hypertrophy 292
    Left axis deviation 86
    Left bundle branch block 66, 234
    Left bundle branch block and aortic stenosis 296
    Left bundle branch block and ?right ventricular
    overload 234
    Left posterior hemiblock 92
    Left ventricular hypertrophy 64, 252, 260, 294,
    
    ix
    
    12-lead ECGs
    296, 322
    Left ventricular hypertrophy and ?ischaemia 300
    Left ventricular hypertrophy and left atrial
    hypertrophy 292
    Left ventricular hypertrophy and severe aortic
    stenosis 298
    Lithium treatment 340
    Long QT syndrome, congenital 76
    Long QT syndrome, drug toxicity 146
    Lown–Ganong–Levine syndrome 74
    
    x
    
    Malignant pericardial effusion 328
    Mediastinal shift 22
    Mitral stenosis and pulmonary hypertension 292
    Myocardial infarction, acute anterior and old
    inferior 232
    Myocardial infarction, acute anterolateral, with
    left axis deviation 222
    Myocardial infarction, acute inferior 214
    Myocardial infarction, acute inferior and anterior
    ischaemia 230
    Myocardial infarction, acute inferior (STEMI) and
    anterior NSTEMI 232
    Myocardial infarction, acute inferior and old
    anterior 230
    Myocardial infarction, acute inferior and RBBB 236
    Myocardial infarction, acute lateral 220
    Myocardial infarction, anterior 218
    Myocardial infarction, anterior, ?age 274
    Myocardial infarction, anterior NSTEMI 240
    Myocardial infarction, anterolateral, ?age 224
    Myocardial infarction, evolving inferior 216
    Myocardial infarction, inferior and atrial
    fibrillation 140
    Myocardial infarction, inferior and right bundle
    branch block 236
    
    Myocardial infarction, inferior and right bundle
    branch block and ?anterior ischaemia 238
    Myocardial infarction, inferior and right
    ventricular infarction 228
    Myocardial infarction, inferior and ventricular
    tachycardia 140
    Myocardial infarction, lateral (after 3 days) 222
    Myocardial infarction, old anterior 224
    Myocardial infarction, old anterolateral NSTEMI
    260
    Myocardial infarction, old inferior (possible) and
    anterior ischaemia 240
    Myocardial infarction, old posterior 254
    Myocardial infarction, posterior 226
    Myocardial infarction, posterior infarct with
    normal QT interval 78
    Normal ECG 8, 12, 272, 278
    Normal ECG, accelerated idionodal rhythm 48
    Normal ECG, black people 42
    Normal ECG, child 52
    Normal ECG, ectopic atrial rhythm 8
    Normal ECG, exercise testing 272, 278
    Normal ECG, high take-off ST segment 32
    Normal ECG, junctional escape beat 4
    Normal ECG, left axis deviation 50
    Normal ECG, ‘leftward’ limit of normality 16
    Normal ECG, notched (bifid) P wave 12
    Normal ECG, notched S wave (V2) 26
    Normal ECG, P wave, bifid (notched) 12
    Normal ECG, P wave inversion 8, 40
    Normal ECG, P wave inversion (lead VR, VL) 40
    Normal ECG, partial right bundle branch block
    pattern 34
    Normal ECG, PR interval variation 48
    Normal ECG, pre-exercise 282
    
    12-lead ECGs
    Normal ECG, R wave, tall (voltage criteria and) 294
    Normal ECG, R wave dominance (lead II) 14
    Normal ECG, R wave dominance (V1) 22, 308
    Normal ECG, R wave dominance (V3) 20
    Normal ECG, R wave dominance (V4) 18
    Normal ECG, R wave dominance (V5) 20, 24
    Normal ECG, R wave dominance (V6) 18
    Normal ECG, R wave size 14
    Normal ECG, right axis deviation 16
    Normal ECG, ‘rightward’ limit of normality 14
    Normal ECG, R–R interval variation 2
    Normal ECG, RSR1 pattern 26
    Normal ECG, RSR1S1 pattern 26
    Normal ECG, S wave dominance (lead I) 16
    Normal ECG, S wave dominance (lead III) 16
    Normal ECG, S wave dominance (V1) 18
    Normal ECG, S wave dominance (V2) 20, 24
    Normal ECG, S wave dominance (V3) 18
    Normal ECG, S wave dominance (V4) 20
    Normal ECG, septal Q wave 28, 50
    Normal ECG, small Q wave 30, 38
    Normal ECG, ST segment, isoelectric and sloping
    upward 30
    Normal ECG, ST segment depression 34
    Normal ECG, ST segment depression (nonspecific)
    36
    Normal ECG, ST segment elevation 32
    Normal ECG, T wave, biphasic 34, 40, 52
    Normal ECG, T wave, peaked 332
    Normal ECG, T wave, tall peaked 44
    Normal ECG, T wave flattening 44
    Normal ECG, T wave inversion (lead III) 38
    Normal ECG, T wave inversion (lead V1) 38
    Normal ECG, T wave inversion (lead V2) 40
    Normal ECG, T wave inversion (lead V3) 42
    Normal ECG, T wave inversion (lead VR) 36
    
    Normal ECG, T wave inversion (lead VR, V1–V2) 40
    Normal ECG, T wave inversion (lead VR, VL) 40, 42
    Normal ECG, T wave inversion in black people 42
    Normal ECG, U wave, prominent/large 46, 50
    Pericardial effusion, malignant 328
    Pericarditis 250
    Pre-exercise normal ECG 282
    Prolonged QT interval due to amiodarone 78, 338
    Pseudonormalization 276
    Pulmonary embolus 246, 248, 250, 310
    Pulmonary hypertension and mitral stenosis 292
    Pulmonary stenosis 322
    Re-warming after hypothermia 320
    Right atrial hypertrophy 304
    Right atrial hypertrophy and right bundle branch
    block, in Ebstein’s anomaly 324
    Right atrial hypertrophy and right ventricular
    hypertrophy 304
    Right bundle branch block and acute inferior
    infarction 236
    Right bundle branch block and anterior infarction
    236
    Right bundle branch block and anterior ischaemia
    238
    Right bundle branch block and atrial septal defect
    326
    Right bundle branch block and inferior infarction,
    ?anterior ischaemia 238
    Right bundle branch block and right atrial
    hypertrophy, in Ebstein’s anomaly 324
    Right ventricular hypertrophy 66, 308
    Right ventricular hypertrophy, marked 306
    Right ventricular hypertrophy in Fallot’s tetralogy
    324
    
    xi
    
    12-lead ECGs
    Right ventricular hypertrophy and right atrial
    hypertrophy 304
    Right ventricular outflow tract ventricular
    tachycardia (RVOT-VT) 104, 144
    RSR1 pattern 26, 80
    RSR1S1 pattern 26
    Second degree block (2:1) 86, 180
    Second degree block (Wenckebach) 84
    Second degree block and left anterior hemiblock
    94
    Second degree block and left anterior hemiblock
    and right bundle branch block 94
    Sick sinus syndrome 172
    Sinus arrhythmia 2, 112
    Sinus bradycardia 4, 170, 172
    Sinus rhythm, after cardioversion 118, 122, 138
    Sinus rhythm, in Wolff–Parkinson-White
    syndrome type A 108
    Sinus rhythm and left bundle branch block 128
    Sinus rhythm and normal conduction,
    post-cardioversion 138
    Sinus tachycardia 4, 112
    ST segment, nonspecific changes 210
    ST segment depression, exercise-induced 278
    ST segment elevation, exercise-induced 274
    Subarachnoid haemorrhage 344
    Supraventricular extrasystole 6, 114
    
    xii
    
    Supraventricular tachycardia 106
    T wave, nonspecific changes 210
    T wave, nonspecific flattening 262
    T wave, unexplained abnormality 258
    Thyrotoxicosis 326
    Trauma 342
    Trifascicular block 92
    Ventricular extrasystole 6, 114
    Ventricular extrasystoles, coupled and atrial
    fibrillation 290
    Ventricular fibrillation 162
    Ventricular tachycardia 132, 134
    Ventricular tachycardia, fusion and capture beats
    142
    Ventricular tachycardia and inferior infarction
    140
    VVI pacing, bipolar 190
    VVI pacing, intermittent 192
    VVI pacing, unipolar 192
    VVI pacing in complete block 194
    Wolff–Parkinson-White syndrome and atrial
    fibrillation 148
    Wolff–Parkinson-White syndrome type A 70, 72,
    148, 256, 302
    Wolff–Parkinson-White syndrome type B 74, 258
    
    The ECG in healthy people
    
    1
    
    The ‘normal’ ECG
    
    2
    
    What to do
    
    54
    
    The normal cardiac rhythm
    
    2
    
    The range of normality
    
    54
    
    The heart rate
    
    2
    
    Extrasystoles
    
    7
    
    The prognosis of patients with an
    abnormal ECG
    
    54
    
    The P wave
    
    7
    
    Further investigations
    
    56
    
    Treatment of asymptomatic ECG
    abnormalities
    
    56
    
    The PR interval
    
    13
    
    The QRS complex
    
    15
    
    The ST segment
    
    31
    
    The T wave
    
    37
    
    The QT interval
    
    48
    
    The ECG in athletes
    
    48
    
    The ECG in pregnancy
    
    52
    
    The ECG in children
    
    52
    
    Frequency of ECG abnormalities
    in healthy people
    
    54
    
    For the purposes of this chapter, we shall assume that
    the subject from whom the ECG was recorded is
    asymptomatic, and that physical examination has
    revealed no abnormalities. We need to consider the
    range of normality of the ECG, but of course we
    cannot escape from the fact that not all disease causes
    symptoms or abnormal signs, and a subject who
    appears healthy may not be so and may therefore have
    an abnormal ECG. In particular, individuals who
    present for screening may well have symptoms about
    which they have not consulted a doctor, so it cannot
    
    1
    
    The ECG in healthy people
    be assumed that an ECG obtained through a screening
    programme has come from a healthy subject.
    The range of normality in the ECG is therefore
    debatable. We first have to consider the variations in
    the ECG that we can expect to find in completely
    healthy people, and then we can think about the significance of ECGs that are undoubtedly ‘abnormal’.
    
    rate is increased) during inspiration, and this is called
    sinus arrhythmia (Fig. 1.1). When sinus arrhythmia is
    marked, it may mimic an atrial arrhythmia. However,
    in sinus arrhythmia each P–QRS–T complex is normal,
    and it is only the interval between them that changes.
    Sinus arrhythmia becomes less marked with increasing age of the subject, and is lost in conditions such
    as diabetic autonomic neuropathy due to impairment
    of the vagus nerve function.
    
    THE ‘NORMAL’ ECG
    THE NORMAL CARDIAC RHYTHM
    
    THE HEART RATE
    
    Sinus rhythm is the only normal sustained rhythm. In
    young people the R–R interval is reduced (i.e. the heart
    
    Fig. 1.1
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    2
    
    There is no such thing as a normal heart rate, and the
    terms ‘tachycardia’ and ‘bradycardia’ should be used
    
    The heart rate
    with care. There is no point at which a high heart rate
    in sinus rhythm has to be called ‘sinus tachycardia’
    and there is no upper limit for ‘sinus bradycardia’.
    Nevertheless, unexpectedly fast or slow rates do need
    an explanation.
    
    SINUS TACHYCARDIA
    The ECG in Figure 1.2 was recorded from a young
    woman who complained of a fast heart rate. She had
    no other symptoms, but was anxious. There were no
    other abnormalities on examination, and her blood
    count and thyroid function tests were normal.
    Box 1.1 shows possible causes of sinus rhythm with
    a fast heart rate.
    
    1
    
    Box 1.1 Possible causes of sinus rhythm with a fast
    heart rate
    
    • Pain, fright, exercise
    • Hypovolaemia
    • Myocardial infarction
    • Heart failure
    • Pulmonary embolism
    • Obesity
    • Lack of physical fitness
    • Pregnancy
    • Thyrotoxicosis
    • Anaemia
    • Beri-beri
    • CO retention
    • Autonomic neuropathy
    • Drugs:
    2
    
    –
    –
    –
    –
    
    sympathomimetics
    salbutamol (including by inhalation)
    caffeine
    atropine
    
    Sinus arrhythmia
    Note
    
    • Marked variation in R–R interval
    • Constant PR interval
    • Constant shape of P wave and QRS complex
    
    3
    
    The ECG in healthy people
    Fig. 1.2
    
    Fig. 1.3
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    4
    
    The heart rate
    Sinus tachycardia
    Note
    
    • Normal P–QRS–T waves
    • R–R interval 500 ms
    • Heart rate 120/min
    
    1
    
    SINUS BRADYCARDIA
    The ECG in Figure 1.3 was recorded from a young
    professional footballer. His heart rate was 44/min, and
    at one point the sinus rate became so slow that a
    junctional escape beat appeared.
    The possible causes of sinus rhythm with a slow
    heart rate are summarized in Box 1.2.
    
    Box 1.2 Possible causes of sinus rhythm with a slow
    heart rate
    
    Sinus bradycardia
    Note
    Sinus rhythm
    Rate 44/min
    One junctional escape beat
    
    •
    •
    •
    
    • Physical fitness
    • Vasovagal attacks
    • Sick sinus syndrome
    • Acute myocardial infarction, especially inferior
    • Hypothyroidism
    • Hypothermia
    • Obstructive jaundice
    • Raised intracranial pressure
    • Drugs:
    
    – beta-blockers (including eye drops for glaucoma)
    – verapamil
    – digoxin
    
    Junctional escape beat
    
    5
    
    The ECG in healthy people
    Fig. 1.4
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    Fig. 1.5
    
    II
    
    6
    
    The P wave
    Supraventricular extrasystole
    Note
    
    • In supraventricular extrasystoles the QRS complex and
    •
    
    the T wave are the same as in the sinus beat
    The fourth beat has an abnormal P wave and therefore
    an atrial origin
    
    Early abnormal P wave
    
    1
    
    EXTRASYSTOLES
    Supraventricular extrasystoles, either atrial or junctional (AV nodal), occur commonly in normal people
    and are of no significance. Atrial extrasystoles (Fig.
    1.4) have an abnormal P wave; in junctional extrasystoles either there is no P wave or the P wave may
    follow the QRS complex.
    Ventricular extrasystoles are also commonly seen
    in normal ECGs (Fig. 1.5).
    In healthy people, normal sinus rhythm may be
    replaced by what are, in effect, repeated atrial extrasystoles. This is sometimes called an ‘ectopic atrial
    rhythm’ and it is of no particular significance
    (Fig. 1.6).
    
    THE P WAVE
    
    Ventricular extrasystole
    Note
    Sinus rhythm, with one ventricular extrasystole
    Extrasystole has a wide and abnormal QRS complex and
    an abnormal T wave
    
    •
    •
    
    Ventricular extrasystole
    
    In sinus rhythm, the P wave is normally upright in all
    leads except VR. When the QRS complex is predominantly downward in lead VL, the P wave may also be
    inverted (Fig. 1.7).
    In patients with dextrocardia the P wave is inverted
    in lead I (Fig. 1.8). In practice this is more often seen
    if the limb leads have been wrongly attached, but
    dextrocardia can be recognized if leads V5 and V6,
    which normally ‘look at’ the left ventricle, show a
    predominantly downward QRS complex.
    If the ECG of a patient with dextrocardia is repeated
    with the limb leads reversed, and the chest leads are
    placed on the right side of the chest instead of the left,
    in corresponding positions, the ECG becomes like that
    of a normal patient (Fig. 1.9).
    A notched or bifid P wave is the hallmark of left
    atrial hypertrophy, and peaked P waves indicate right
    atrial hypertrophy – but bifid or peaked P waves can
    also be seen with normal hearts (Fig. 1.10).
    
    7
    
    The ECG in healthy people
    Fig. 1.6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    Fig. 1.7
    
    8
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The P wave
    
    1
    
    Normal variant: ectopic atrial rhythm
    Note
    Sinus rhythm
    Inverted P wave in leads II–III, VF, V4–V6
    Constant PR interval
    
    •
    •
    •
    
    Inverted P waves in lead II
    
    Normal ECG
    Note
    
    • In both leads VR and VL the P wave is inverted, and the
    QRS complex is predominantly downward
    
    Inverted P wave in lead VL
    
    9
    
    The ECG in healthy people
    Fig. 1.8
    
    Fig. 1.9
    
    10
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The P wave
    
    1
    
    Dextrocardia
    Note
    Inverted P wave in lead I
    No left ventricular complexes seen in leads V5–V6
    
    •
    •
    
    Inverted P wave
    and dominant S
    wave in lead I
    
    Persistent S wave
    in lead V6
    
    Dextrocardia, leads reversed
    Note
    Same patient as in Figure 1.8
    P wave in lead I upright
    QRS complex upright in lead I
    Typical left ventricular complex in lead V6
    
    •
    •
    •
    •
    
    Upright P wave and
    QRS complex in lead I
    
    Normal QRS complex
    in lead V6
    
    11
    
    The ECG in healthy people
    Fig. 1.10
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    Fig. 1.11
    
    12
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The PR interval
    
    1
    
    Normal ECG
    Note
    Sinus rhythm
    Bifid P waves, best seen in leads V2–V4
    Peaked T waves and U waves, best seen in leads
    V2–V3 – normal variants
    
    •
    •
    •
    
    Bifid P wave in lead V3
    
    THE PR INTERVAL
    
    Normal ECG
    Note
    
    • PR interval 170 ms
    • PR interval constant in all leads
    • Notched P wave in lead V is often normal
    5
    
    PR interval 170 ms
    
    In sinus rhythm, the PR interval is constant and its
    normal range is 120–200 ms (3–5 small squares of
    ECG paper) (Fig. 1.11). In atrial extrasystoles, or
    ectopic atrial rhythms, the PR interval may be short,
    and a PR interval of less than 120 ms suggests
    pre-excitation.
    A PR interval of longer than 220 ms may be due
    to first degree block, but the ECGs of healthy individuals, especially athletes, may have PR intervals of
    slightly longer than 220 ms – which can be ignored in
    the absence of any other indication of heart disease.
    PR interval ‘abnormalities’ will be discussed further
    in the context of normal people in Chapter 2.
    
    13
    
    The ECG in healthy people
    Fig. 1.12
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Fig. 1.13
    
    14
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The QRS complex
    Normal ECG
    Note
    
    • QRS complex upright in leads I–III
    • R wave tallest in lead II
    
    Normal ECG
    Note
    
    • This record shows the ‘rightward’ limit of normality of
    the cardiac axis
    
    • R and S waves equal in lead I
    
    1
    
    THE QRS COMPLEX
    THE CARDIAC AXIS
    There is a fairly wide range of normality in the direction of the cardiac axis. In most people the QRS
    complex is tallest in lead II, but in leads I and III the
    QRS complex is also predominantly upright (i.e. the
    R wave is greater than the S wave) (Fig. 1.12).
    The cardiac axis is still perfectly normal when the
    R wave and S wave are equal in lead I: this is common
    in tall people (Fig. 1.13).
    When the S wave is greater than the R wave in lead
    I, right axis deviation is present. However, this is very
    common in perfectly normal people. The ECG in
    Figure 1.14 is from a professional footballer.
    It is common for the S wave to be greater than the
    R wave in lead III, and the cardiac axis can still be
    considered normal when the S wave equals the R wave
    in lead II (Fig. 1.15). These patterns are common in
    fat people and during pregnancy.
    When the depth of the S wave exceeds the height
    of the R wave in lead II, left axis deviation is present
    (see Figs 2.25 and 2.26).
    
    15
    
    The ECG in healthy people
    Fig. 1.14
    
    Fig. 1.15
    
    16
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The QRS complex
    
    1
    
    ?Normal ECG
    Note
    Right axis deviation: S wave greater than R wave
    in lead I
    Upright QRS complexes in leads II–III
    
    •
    •
    
    Dominant S wave in lead I
    
    Normal ECG
    Note
    
    • This shows the ‘leftward’ limit of normality of the
    cardiac axis
    
    • S wave equals R wave in lead II
    • S wave greater than R wave in lead III
    
    S wave = R
    wave in lead II
    
    S wave > R
    wave in lead III
    
    17
    
    The ECG in healthy people
    Fig. 1.16
    
    Fig. 1.17
    
    18
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The QRS complex
    
    1
    
    Normal ECG
    Note
    
    • Lead V
    •
    
    1 shows a predominantly downward complex,
    with the S wave greater than the R wave
    Lead V6 shows an upright complex, with a dominant R
    wave and a tiny S wave
    
    S wave > R
    wave in lead V1
    
    Dominant R
    wave in lead V6
    
    THE SIZE OF R AND S WAVES IN THE CHEST
    LEADS
    
    Normal ECG
    Note
    
    • In lead V there is a dominant S wave
    • In lead V there is a dominant R wave
    • The transition point is between leads V
    3
    4
    
    3
    
    and V4
    
    In lead V1 there should be a small R wave and a deep
    S wave, and the balance between the two should
    change progressively from V1 to V6. In lead V6 there
    should be a tall R wave and no S wave (Fig. 1.16).
    Typically the ‘transition point’, when the R and S
    waves are equal, is seen in lead V3 or V4 but there is
    quite a lot of variation. Figure 1.17 shows an ECG in
    which the transition point is somewhere between leads
    V3 and V4.
    
    19
    
    The ECG in healthy people
    Fig. 1.18
    
    Fig. 1.19
    
    20
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The QRS complex
    Normal ECG
    Note
    
    • Dominant S wave in lead V
    • R wave just bigger than S wave in lead V
    4
    
    5
    
    Normal ECG
    Note
    
    • Dominant S wave in lead V
    • Dominant R wave in lead V
    • The transition point is between leads V
    2
    
    1
    
    Figure 1.18 shows an ECG with a transition point
    between leads V4 and V5, and Figure 1.19 shows an
    ECG with a transition point between leads V2 and V3.
    The transition point is typically seen in lead V5 or
    even V6 in patients with chronic lung disease (see Ch.
    6), and this is called ‘clockwise rotation’. In extreme
    cases, the chest lead needs to be placed in the posterior
    axillary line, or even further round to the back (leads
    V7–V9) before the transition point is demonstrated. A
    similar ECG pattern may be seen in patients with an
    abnormal chest shape, particularly when depression of
    the sternum shifts the mediastinum to the left, although
    in this case the term ‘clockwise rotation’ is not used.
    The patient from whom the ECG in Figure 1.20 was
    recorded had mediastinal shift.
    Occasionally the ECG of a totally normal subject
    will show a ‘dominant’ R wave (i.e. the height of the R
    wave exceeds the depth of the S wave) in lead V1. There
    will thus, effectively, be no transition point, and this is
    called ‘counterclockwise rotation’. The ECG in Figure
    1.21 was recorded from a healthy footballer with a
    normal heart. However, a dominant R wave in lead V1
    is usually due to either right ventricular hypertrophy
    (see Ch. 6) or a true posterior infarction (see Ch. 5).
    
    3
    
    2
    
    and V3
    
    21
    
    The ECG in healthy people
    Fig. 1.20
    
    Fig. 1.21
    
    22
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The QRS complex
    V7
    
    1
    
    Mediastinal shift
    Note
    ‘Abnormal’ ECG, but a normal heart
    Shift of the mediastinum means that the transition point
    is under lead V6
    Ventricular complexes are shown in leads round the left
    side of the chest, in positions V7–V9
    
    •
    •
    •
    V8
    
    V9
    
    Normal ECG
    Note
    
    • Dominant R waves in lead V
    
    1
    
    Dominant R wave in lead V1
    
    23
    
    The ECG in healthy people
    Fig. 1.22
    
    Fig. 1.23
    
    I
    
    VR
    
    V1
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    II
    
    VL
    
    V2
    
    V4
    
    V4
    
    V5
    
    III
    
    VF
    
    V3
    V6
    
    24
    
    The QRS complex
    Normal ECG
    Note
    
    • S wave in lead V
    
    2
    
    is 36 mm
    
    Although the balance between the height of the R
    wave and the depth of the S wave is significant for the
    identification of cardiac axis deviation, or right ventricular hypertrophy, the absolute height of the R wave
    provides little useful information. Provided that the
    ECG is properly calibrated (1 mV causes 1 cm of vertical deflection on the ECG), the limits for the sizes of
    the R and S waves in normal subjects are usually said
    to be:
    
    •
    •
    •
    S wave > 25 mm in lead V2
    
    Normal ECG
    Note
    R wave in lead V5 is 42 mm
    
    •
    
    R wave > 25 mm in lead V5
    
    1
    
    25 mm for the R wave in lead V5 or V6
    25 mm for the S wave in lead V1 or V2
    Sum of R wave in lead V5 or V6 plus S wave in
    lead V1 or V2 should be less than 35 mm.
    
    However, R waves taller than 25 mm are commonly seen in leads V5–V6 in fit and thin young people,
    and are perfectly normal. Thus, these ‘limits’ are not
    helpful. The ECGs in Figures 1.22 and 1.23 were both
    recorded from fit young men with normal hearts.
    
    THE WIDTH OF THE QRS COMPLEX
    The QRS complex should be less than 120 ms in duration (i.e. less than 3 small squares) in all leads. If it is
    longer than this, then either the ventricles have
    been depolarized from a ventricular rather than a
    supraventricular focus (i.e. a ventricular rhythm is
    present), or there is an abnormality of conduction
    within the ventricles. The latter is most commonly
    due to bundle branch block. An RSR1 pattern, resembling that of right bundle branch block but with a
    narrow QRS complex, is sometimes called ‘partial
    right bundle branch block’ and is a normal variant
    (Fig. 1.24). An RSR1S1 pattern is also a normal variant
    (Fig. 1.25), and is sometimes called a ‘splintered’
    complex.
    
    25
    
    The ECG in healthy people
    Fig. 1.24
    
    Fig. 1.25
    
    26
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    V4
    
    V1
    
    V2
    
    V3
    
    V5
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The QRS complex
    
    1
    
    Normal ECG
    Note
    
    • RSR pattern in lead V
    • QRS complex duration 100 ms
    • Partial right bundle branch block pattern
    1
    
    2
    
    RSR1 pattern and QRS complex 100 ms in lead V1
    
    Normal ECG
    Note
    
    • RSR S pattern in lead V
    • Notched S wave in lead V
    • QRS complex duration 100 ms
    • Partial right bundle branch block pattern
    1 1
    
    1
    
    2
    
    RSR1S1 pattern in
    lead V1
    
    Notched S wave
    in lead V2
    
    27
    
    The ECG in healthy people
    Fig 1.26
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    Fig. 1.27
    
    28
    
    I
    
    VR
    
    V1
    
    II
    
    VL
    
    V2
    
    III
    
    VF
    
    V3
    
    V4
    
    V5
    
    V6
    
    The QRS complex
    Accelerated idioventricular rhythm
    Note
    
    • Sinus rhythm
    • First and last beats are ventricular extrasystoles
    • The fifth beat starts a run of ventricular rhythm at about
    80/min
    
    1
    
    In perfectly normal hearts the normal rhythm may
    be replaced by an accelerated idioventricular rhythm,
    which looks like a run of regular ventricular extrasystoles, with wide QRS complexes (Fig. 1.26).
    
    Q WAVES
    The normal depolarization of the interventricular
    septum from left to right causes a small ‘septal’ Q
    wave in any of leads II, VL or V5–V6. Septal Q waves
    are usually less than 3 mm deep and less than 1 mm
    across (Fig. 1.27).
    A small Q wave is also common in lead III in normal
    people, in which case it is always narrow but can be
    more than 3 mm deep. Occasionally there will be a
    similar Q wave in lead VF (Fig. 1.28). These ‘normal’
    Q waves become much less deep, and may disappear
    altogether, on deep inspiration (see Fig. 1.36).
    
    Idioventricular rhythm in lead II
    
    Normal ECG
    Note
    
    • Septal Q waves in leads I, II, V –V
    4
    
    6
    
    Septal Q wave in lead V5
    
    29
    
    The ECG in healthy people
    Fig. 1.28
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    V4
    
    V1
    
    V2
    
    V5
    
    V3
    
    V6
    
    Fig. 1.29
    
    30
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The ST segment
    
    1
    
    THE ST SEGMENT
    
    Normal ECG
    Note
    
    • Narrow but quite deep Q wave in lead III
    • Smaller Q wave in lead VF
    
    Narrow Q wave in lead III
    
    Normal ECG
    
    The ST segment (the part of the ECG between the S
    wave and the T wave) should be horizontal and ‘isoelectric’, which means that it should be at the same
    level as the baseline of the record between the end of
    the T wave and the next P wave. However, in the chest
    leads the ST segment often slopes upwards and is not
    easy to define (Fig. 1.29).
    An elevation of the ST segment is the hallmark
    of an acute myocardial infarction (see Ch. 5), and
    depression of the ST segment can indicate ischaemia
    or the effect of digoxin. However, it is perfectly
    normal for the ST segment to be elevated following
    an S wave in leads V2–V5. This is sometimes called a
    ‘high take-off ST segment’. The ECGs in Figures 1.30
    and 1.31 were recorded from perfectly healthy young
    men.
    The ST segment is apparently raised when there is
    ‘early repolarization’, which causes the ST segment to
    be arched, and is usually only seen in the anterior
    leads, not the limb leads (see Fig. 1.39).
    
    Note
    
    • ST segment is isoelectric but slopes upwards in
    leads V2–V5
    
    Upward-sloping ST segment in
    lead V4
    
    31
    
    The ECG in healthy people
    Fig. 1.30
    
    Fig. 1.31
    
    32
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The ST segment
    
    1
    
    Normal ECG
    Note
    
    • In lead V
    
    4 there is an S wave followed by a raised ST
    segment. This is a ‘high take-off’ ST segment
    
    High take-off ST segment in lead V4
    
    Normal ECG
    Note
    
    • Marked ST segment elevation in lead V
    
    3
    
    follows an S
    
    wave
    
    High take-off ST segment in lead V3
    
    33
    
    The ECG in healthy people
    Box 1.3 shows the possible causes of ST segment
    elevation, other than myocardial infarction.
    ST segment depression is measured relative to the
    baseline (between the T and P waves), 60–80 ms after
    the ‘J’ point, which is the point of inflection at the
    junction of the S wave and the ST segment. Minor
    depression of the ST segment is not uncommon in
    normal people, and is then called ‘nonspecific’; the
    
    Fig. 1.32
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    VF
    
    V3
    
    V6
    
    III
    
    34
    
    advantage of using this word is that it leaves the way
    open for a later change of diagnosis. ST segment
    depression in lead III but not VF is likely to be nonspecific (Fig. 1.32). Nonspecific ST segment depression
    should not be more than 2 mm (Fig. 1.33), and the
    segment often slopes upwards. Horizontal ST segment
    depression of more than 2 mm indicates ischaemia (see
    Ch. 5).
    
    The ST segment
    
    1
    
    Box 1.3 Causes of ST segment elevation other than
    myocardial infarction
    
    • Normal variants (high take-off and early repolarization)
    • Left bundle branch block
    • Acute pericarditis and myocarditis
    • Hyperkalaemia
    • Brugada syndrome
    • Arrhythmogenic right ventricular cardiomyopathy
    • Pulmonary embolism
    
    Normal ECG
    Note
    
    • ST segment depression in lead III but not VF
    • Biphasic T wave (i.e. initially inverted but then upright)
    in lead III but not VF
    
    • Partial right bundle branch block pattern
    
    ST segment depression and
    biphasic T wave in lead III
    
    35
    
    The ECG in healthy people
    Fig. 1.33
    
    I
    
    VR
    
    V1
    
    II
    
    VL
    
    V2
    
    VF
    
    V3
    
    III
    
    Fig. 1.34
    
    36
    
    V4
    
    V5
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The T wave
    
    1
    
    Possibly normal ECG
    Note
    ST segment depression of 1 mm in leads V3–V6
    In a patient with chest pain this would raise suspicions
    of ischaemia but, particularly in women, such changes
    can be nonspecific
    
    •
    •
    
    Nonspecific ST segment depression in lead V5
    
    Normal ECG
    Note
    
    • T wave is inverted in lead VR but is upright in all
    other leads
    
    THE T WAVE
    In a normal ECG the T wave is always inverted in lead
    VR, and often in lead V1, but is usually upright in all
    the other leads (Fig. 1.34).
    The T wave is also often inverted in lead III but not
    VF. However, its inversion in lead III may be reversed
    on deep inspiration (Figs 1.35 and 1.36).
    
    Inverted T wave in lead VR
    
    37
    
    The ECG in healthy people
    Fig. 1.35
    
    I
    
    VR
    
    II
    
    VL
    
    VF
    
    III
    
    V4
    
    V1
    
    V5
    
    V2
    
    V6
    
    V3
    
    Fig. 1.36
    
    Normal ECG during inspiration
    Inspiration
    Note
    
    III
    
    • ECG recorded from same patient as in
    Figure 1.35, but during deep inspiration
    
    • Q wave in lead III disappears
    • T wave becomes upright
    
    38
    
    The T wave
    
    1
    
    Normal ECG
    Note
    
    • Small Q wave in lead III but not VF
    • Inverted T wave in lead III but upright T wave in VF
    • Inverted T wave in lead V
    1
    
    Q wave and inverted
    T wave in lead III
    
    T wave inversion in lead VL as well as in VR can
    be normal, particularly if the P wave in lead VL is
    inverted. The ECG in Figure 1.37 was recorded from
    a completely healthy young woman.
    T wave inversion in leads V2–V3 as well as in V1
    occurs in pulmonary embolism and in right ventricular
    hypertrophy (see Chs 5 and 6) but it can be a normal
    variant. This is particularly true in black people. The
    ECG in Figure 1.38 was recorded from a healthy
    young white man, and that shown in Figure 1.39 from
    a young black professional footballer. The ECG in
    Figure 1.40 was recorded from a middle-aged black
    woman with rather nonspecific chest pain, whose
    coronary arteries and left ventricle were shown to be
    entirely normal on catheterization.
    Box 1.4 summarizes the situations in which T wave
    inversion is seen.
    
    Inverted T wave in
    lead V1
    
    Box 1.4 Causes of T wave inversion
    
    • Normal in leads VR, V –V and V , in black people
    • Normal in lead III when the T wave in lead VF is upright
    • Ventricular extrasystoles and other ventricular rhythms
    • Bundle branch block (right or left)
    • Myocardial infarction
    • Right or left ventricular hypertrophy
    • The Wolff–Parkinson–White syndrome
    1
    
    2
    
    3
    
    39
    
    The ECG in healthy people
    Fig. 1.37
    
    Fig. 1.38
    
    40
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    V1
    
    V4
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    V2
    
    V3
    
    V5
    
    V6
    
    The T wave
    
    1
    
    Normal ECG
    Note
    
    • Inverted T waves in leads VR, VL
    • Inverted P waves in leads VR, VL
    Inverted P and T waves in lead VL
    
    Normal ECG
    Note
    
    • T wave inversion in leads VR, V –V
    • Biphasic T wave in lead V
    1
    
    2
    
    3
    
    Inverted T wave in lead V2
    
    41
    
    The ECG in healthy people
    Fig. 1.39
    
    Fig. 1.40
    
    42
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The T wave
    
    1
    
    Normal ECG, from a black man
    Note
    T wave inversion in leads VR, V1–V3
    Early repolarization in leads V2–V3
    
    •
    •
    
    Inverted T wave in lead V3
    
    Normal ECG, from a black woman
    Note
    
    • Sinus rhythm
    • T wave inversion in lead VL and all chest leads
    • Presumably a normal variant: coronary angiography and
    echocardiography were normal
    
    43
    
    The ECG in healthy people
    Fig. 1.41
    
    Fig. 1.42
    
    44
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The T wave
    
    1
    
    Possibly normal ECG
    Note
    Sinus rhythm
    Normal axis
    Normal QRS complexes
    T wave flattening in all chest leads
    T wave inversion in leads III, VF
    In an asymptomatic patient, these changes are not
    necessarily significant
    
    •
    •
    •
    •
    •
    •
    
    Flattened T wave in lead V3
    
    Normal ECG
    Note
    
    • Sinus rhythm
    • Normal axis
    • Normal QRS complexes
    • Very tall and peaked T wave
    
    Tall peaked T wave in lead V3
    
    Generalized flattening of the T waves with a normal
    QT interval is best described as ‘nonspecific’. In
    a patient without symptoms and whose heart is
    clinically normal, the finding has little prognostic
    significance. This was the case with the patient
    whose ECG is shown in Figure 1.41. In patients with
    symptoms suggestive of cardiovascular disease,
    however, such an ECG would require further
    investigation.
    Peaked T waves are one of the features of hyperkalaemia, but they can also be very prominent in
    healthy people (Fig. 1.42). Tall and peaked T waves
    are sometimes seen in the early stages of a myocardial
    infarction, when they are described as ‘hyperacute’.
    They are, however, an extremely unreliable sign of
    infarction.
    The T wave is the most variable part of the ECG.
    It may become inverted in some leads simply by hyperventilation associated with anxiety.
    
    45
    
    The ECG in healthy people
    Fig. 1.43
    
    Fig 1.44
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    II
    
    46
    
    V6
    
    V3
    
    V6
    
    The T wave
    Normal ECG
    Note
    
    • Prominent U waves following normal T waves in
    leads V2–V4
    
    1
    
    An extra hump on the end of the T wave, a ‘U’
    wave, is characteristic of hypokalaemia. However, U
    waves are commonly seen in the anterior chest leads
    of normal ECGs (Fig. 1.43), where they can be
    remarkably prominent (Fig. 1.44). It is thought that
    they represent repolarization of the papillary muscles.
    A U wave is probably only important if it follows a
    flat T wave.
    
    U wave in lead V3
    
    Normal ECG
    Note
    
    • Very large U waves following normal T waves in leads
    V1–V4
    
    Very large U wave in lead V3
    
    47
    
    The ECG in healthy people
    THE QT INTERVAL
    The QT interval (from the Q wave to the end of the
    T wave) varies with the heart rate, gender and time of
    day. There are several different ways of correcting the
    QT interval for heart rate, but the simplest is Bazett’s
    formula. In this, the corrected QT interval (QT c) is
    calculated by:
    
    QTc =
    
    THE ECG IN ATHLETES
    
    QT
    (R − R interval)
    
    An alternative is Fridericia’s correction, in which QT c
    is the QT interval divided by the cube root of the R–R
    
    Fig. 1.45
    
    Any of the normal variations discussed above can
    be found in athletes. There can be changes in rhythm
    and/or ECG pattern, and the ECGs of athletes may
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    48
    
    interval. It is uncertain which of the corrections is
    clinically more important.
    The upper limit of the normal QT c interval is
    longer in women than in men, and increases with age.
    Its precise limit is uncertain, but is usually taken
    (following Bazett’s correction) as 450 ms for adult
    men and 470 ms for adult women.
    
    The ECG in athletes
    also show some features that might be considered
    abnormal in non-athletic subjects, but are normal in
    athletes (see Box 1.5). Figure 1.45 shows the short and
    varying PR interval of an ‘accelerated idionodal
    rhythm’ (also known as a ‘wandering atrial pacemaker’). Here the sinus node rate has slowed, and the
    heart rate is controlled by the AV node, which is discharging faster than the SA node.
    The ECGs in Figures 1.45, 1.46 and 1.47 were all
    recorded during the screening examinations of healthy
    young footballers.
    
    1
    
    Box 1.5 Possible ECG features of healthy athletes
    Variations in rhythm
    Sinus bradycardia
    Marked sinus arrhythmia
    Junctional rhythm
    ‘Wandering’ atrial pacemaker
    First degree block
    Wenckebach phenomenon
    Second degree block
    
    •
    •
    •
    •
    •
    •
    •
    
    Variations in ECG pattern
    
    • Tall P waves
    • Prominent septal Q waves
    • Tall R waves and deep S waves
    • Counterclockwise rotation
    • Slight ST segment elevation
    • Tall symmetrical T waves
    • T wave inversion, especially in lateral leads
    • Biphasic T waves
    • Prominent U waves
    
    Normal ECG with accelerated idionodal
    rhythm
    Note
    
    • SA node stimulates the atria at a constant rate of
    50/min
    
    • Ventricular rate is slightly faster than the atrial rate
    • Narrow QRS complexes, originating in the AV node
    • QRS complexes appear to ‘overtake’ the P waves, which
    are not suppressed – causing an apparent variation in
    the PR interval
    Variation of PR interval
    
    49
    
    The ECG in healthy people
    Fig. 1.46
    
    Fig. 1.47
    
    50
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    V4
    
    V1
    
    V5
    
    V2
    
    V6
    
    V3
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The ECG in athletes
    
    1
    
    Normal ECG
    Note
    
    • Heart rate 53/min
    • Sinus rhythm
    • Prominent U waves in leads V –V
    • Inverted T waves in lead VL
    2
    
    5
    
    U wave in lead V3
    
    Normal ECG
    Note
    
    • Sinus rhythm
    • Left axis deviation
    • Septal Q waves in leads V –V
    5
    
    6
    
    51
    
    The ECG in healthy people
    Fig. 1.48
    
    I
    
    VR
    
    V1
    
    V4R
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    THE ECG IN PREGNANCY
    Minor changes in the ECG are commonly seen in
    pregnancy (see Box 1.6). Ventricular extrasystoles are
    almost universal.
    
    THE ECG IN CHILDREN
    
    52
    
    The normal heart rate in the first year of life is
    140–160/min, falling slowly to about 80/min by
    puberty. Sinus arrhythmia is usually quite marked in
    children.
    At birth, the muscle of the right ventricle is as thick
    as that of the left ventricle. The ECG of a normal child
    in the first year of life has a pattern that would indicate
    right ventricular hypertrophy in an adult. The ECG in
    Figure 1.48 was recorded from a normal 1-month-old
    child.
    
    Box 1.6 Possible ECG features in pregnancy
    
    • Sinus tachycardia
    • Supraventricular and ventricular extrasystoles
    • Nonspecific ST segment/T wave changes
    The changes suggestive of right ventricular hypertrophy disappear during the first few years of life. All
    the features other than the inverted T waves in leads
    V1 and V2 should have disappeared by the age of
    2 years, and the adult ECG pattern should have developed by the age of 10 years. In general, if the infant
    ECG pattern persists beyond the age of 2 years, then
    right ventricular hypertrophy is indeed present. If the
    normal adult pattern is present in the first year of life,
    then left ventricular hypertrophy is present.
    The ECG changes associated with childhood are
    summarized in Box 1.7.
    
    The ECG in children
    
    1
    
    Normal ECG, from a child 1 month old
    Note
    Heart rate 170/min
    Sinus rhythm
    Normal axis
    Dominant R waves in lead V1
    Inverted T waves in leads V1–V2
    Biphasic T waves in lead V3
    Lead V4R (a position on the chest equivalent to V4, but
    on the right side) has been recorded instead of V4
    
    •
    •
    •
    •
    •
    •
    •
    
    Box 1.7 The ECG in normal children
    At birth
    
    • Sinus tachycardia
    • Right axis deviation
    • Dominant R waves in lead V
    • Deep S waves in lead V
    • T waves inverted in leads V –V
    
    At 2 years of age
    Normal axis
    S waves greater than R waves in lead V1
    T waves inverted in leads V1–V2
    
    •
    •
    •
    
    1
    
    6
    
    1
    
    4
    
    At 1 year of age
    Sinus tachycardia
    Right axis deviation
    Dominant R waves in lead V1
    T waves inverted in leads V1–V2
    
    •
    •
    •
    •
    
    At 5 years of age
    Normal QRS complexes
    T waves still inverted in leads V1–V2
    
    •
    •
    
    At 10 years of age
    Adult pattern
    
    •
    
    53
    
    The ECG in healthy people
    FREQUENCY OF ECG ABNORMALITIES IN
    HEALTHY PEOPLE
    The ECG findings we have discussed so far can all be
    considered to be within the normal range. Certain
    findings are undoubtedly abnormal as far as the ECG
    is concerned, yet do occur in apparently healthy
    people.
    The frequency with which abnormalities are
    detected depends on the population studied: most
    abnormalities are found least often in healthy young
    people recruited to the armed services, and become
    progressively more common in populations of increasing age. An exception to this rule is that frequent
    ventricular extrasystoles are very common in pregnancy. The frequency of right and left bundle branch
    block has been found to be 0.3% and 0.1% respectively in populations of young recruits to the services,
    but in older working populations these abnormalities
    have been detected in 2% and 0.7% respectively of
    apparently healthy people.
    
    WHAT TO DO
    When an apparently healthy subject has an ECG
    record that appears abnormal, the most important
    thing is not to cause unnecessary alarm. There are four
    questions to ask:
    
    54
    
    1. Does the ECG really come from that individual?
    If so, is he or she really asymptomatic and are the
    findings of the physical examination really
    normal?
    2. Is the ECG really abnormal or is it within the
    normal range?
    3. If the ECG is indeed abnormal, what are the
    implications for the patient?
    4. What further investigations are needed?
    
    THE RANGE OF NORMALITY
    Normal variations in the P waves, QRS complexes and
    T waves have been described in detail. T wave changes
    usually give the most trouble in terms of ECG interpretation, because changes in repolarization occur in
    many different circumstances, and in any individual,
    and variations in T wave morphology can occur from
    day to day.
    Box 1.8 lists some of the ECG patterns that can be
    accepted as normal in healthy patients, and some that
    must be regarded with suspicion.
    
    THE PROGNOSIS OF PATIENTS WITH AN
    ABNORMAL ECG
    In general, the prognosis is related to the patient’s
    clinical history and to the findings on physical
    examination, rather than to the ECG. An abnormal
    ECG is much more significant in a patient with
    symptoms and signs of heart disease than it is in a truly
    healthy subject. In the absence of any other evidence
    of heart disease, the prognosis of an individual with
    one of the more common ECG abnormalities is as
    follows.
    
    CONDUCTION DEFECTS
    First degree block (especially when the PR interval is
    only slightly prolonged) has little effect on prognosis.
    Second and third degree block indicate heart disease
    and the prognosis is worse, though the congenital
    form of complete block is less serious than the acquired
    form in adults.
    Left anterior hemiblock has a good prognosis, as
    does right bundle branch block (RBBB). The presence
    of left bundle branch block (LBBB) in the absence of
    other manifestations of cardiac disease is associated
    
    The prognosis of patients with an abnormal ECG
    
    1
    
    Box 1.8 Variations in the normal ECG in adults
    Rhythm
    Marked sinus arrhythmia, with escape beats
    Lack of sinus arrhythmia (normal with increasing age)
    Supraventricular extrasystoles
    Ventricular extrasystoles
    
    •
    •
    •
    •
    
    P wave
    
    • Normally inverted in lead VR
    • May be inverted in lead VL
    Cardiac axis
    
    • Minor right axis deviation in tall people
    QRS complexes in the chest leads
    Slight dominance of R wave in lead V1, provided there is
    no other evidence of right ventricular hypertrophy or
    posterior infarction
    The R wave in the lateral chest leads may exceed 25 mm
    in thin fit young people
    Partial right bundle branch block (RSR1 pattern, with QRS
    complexes less than 120 ms)
    Septal Q waves in leads III, VL, V5–V6
    
    •
    
    ST segment
    Raised in anterior leads following an S wave (high take-off
    ST segment)
    Depressed in pregnancy
    Nonspecific upward-sloping depression
    
    •
    •
    •
    
    T wave
    
    • Inverted in lead VR and often in V
    • Inverted in leads V –V , or even V in black people
    • May invert with hyperventilation
    • Peaked, especially if the T waves are tall
    1
    
    2
    
    3
    
    4
    
    U wave
    Normal in anterior leads when the T wave is not flattened
    
    •
    
    •
    •
    •
    
    with about a 30% increase in the risk of death compared with that of individuals with a normal ECG.
    The risk of death doubles if a subject known to have
    a normal ECG suddenly develops LBBB, even if there
    are no symptoms – the ECG change presumably indicates progressive cardiac disease, probably most
    often ischaemia. Bifascicular block seldom progresses
    to complete block, but is always an indication of
    underlying heart disease – the prognosis is therefore
    relatively poor compared to that of patients with
    LBBB alone.
    
    ARRHYTHMIAS
    Supraventricular extrasystoles are of no importance whatsoever. Ventricular extrasystoles are almost
    
    universal, but when frequent or multiform they indicate
    populations with a statistically increased risk of death,
    presumably because in some people they indicate subclinical heart disease. The increased risk to an individual is, however, insignificant and there is no
    evidence that treating ventricular extrasystoles prolongs survival.
    Atrial fibrillation is frequently the result of rheumatic or ischaemic heart disease or cardiomyopathy,
    and the prognosis is then relatively poor. In about one
    third of individuals with atrial fibrillation no cardiac
    disease can be demonstrated. However, even in these
    people the risk of death is increased by three or four
    times, and the risk of stroke is increased perhaps
    tenfold, compared with people of the same age whose
    hearts are in sinus rhythm.
    
    55
    
    The ECG in healthy people
    FURTHER INVESTIGATIONS
    Complex and expensive investigations are seldom justified in asymptomatic patients whose hearts are clinically normal, but who have been found to have an
    abnormal ECG.
    An echocardiogram should be recorded in all
    patients with bundle branch block, to assess the size
    and function of the individual heart chambers. Patients
    with LBBB may have a dilated cardiomyopathy, and
    the echocardiogram will then show a dilated left ventricle which contracts poorly. Alternatively they may
    have ischaemia, and the echocardiogram will show
    some segments of the left ventricle failing to contract
    or contracting poorly. Patients with LBBB may also
    have unsuspected aortic stenosis. Patients with RBBB
    may have an atrial septal defect or pulmonary hypertension, but quite frequently the echocardiogram
    shows no abnormality.
    Echocardiography may be helpful in establishing
    the cause of T wave inversion, which might be due to
    ischaemia, ventricular hypertrophy or cardiomyopathy.
    Patients with frequent ventricular extrasystoles
    seldom need detailed investigation, but if there is any
    question of underlying heart disease an echocardiogram may help to exclude the possibility of a cardiomyopathy. It is also worth checking their blood
    haemoglobin level.
    In patients with atrial fibrillation, an echocardiogram is useful for defining or excluding structural
    
    56
    
    abnormalities, and for studying left ventricular function. An echocardiogram is indicated if there is anything that might suggest rheumatic heart disease.
    Since atrial fibrillation can be the only manifestation
    of thyrotoxicosis, thyroid function must be checked.
    Atrial fibrillation may also be the result of alcoholism,
    and this may be denied by the patient, so it may be
    fair to check liver function.
    Table 1.1 shows investigations that should be
    considered in the case of various cardiac rhythms
    and indicates which underlying diseases may be
    present.
    
    TREATMENT OF ASYMPTOMATIC
    ECG ABNORMALITIES
    It is always the patient who should be treated, not the
    ECG. The prognosis of patients with complete heart
    block is improved by permanent pacing, but that of
    patients with other degrees of block is not. Ventricular
    extrasystoles should not be treated because of the risk
    of the pro-arrhythmic effects of antiarrhythmic drugs.
    Atrial fibrillation need not be treated if the ventricular
    rate is reasonable, but anticoagulation must be considered in all cases. In the case of patients with valve
    disease and atrial fibrillation, however, anticoagulant
    treatment is essential.
    
    Treatment of asymptomatic ECG abnormalities
    
    1
    
    Table 1.1 Investigations in apparently healthy people with an abnormal ECG
    ECG appearance
    
    Diagnosis to be excluded
    
    Possible investigations
    
    Sinus tachycardia
    
    Thyrotoxicosis
    Anaemia
    Changes in heart size
    Heart failure
    Systolic dysfunction
    
    Thyroid function
    Haemoglobin
    
    }
    
    Echocardiogram
    
    Sinus bradycardia
    
    Myxoedema
    
    Thyroid function
    
    Frequent ventricular extrasystoles
    
    Left ventricular dysfunction
    Anaemia
    
    Echocardiogram
    Haemoglobin
    
    Right bundle branch block
    
    Heart size
    Lung disease
    Atrial septal defect
    
    Echocardiogram
    
    Left bundle branch block
    
    Heart size
    Aortic stenosis
    Cardiomyopathy
    Ischaemia
    
    Echocardiogram
    
    T wave abnormalities
    
    High or low potassium or calcium
    Ventricular systolic dysfunction
    Hypertrophic cardiomyopathy
    Ischaemia
    
    Electrolytes
    
    Atrial fibrillation
    
    Thyrotoxicosis
    Alcoholism
    Valve disease, ventricular
    and left atrial dimensions
    Myxoma
    
    }
    
    Echocardiogram
    Exercise test
    Myocardial perfusion scan
    Thyroid function
    Liver function
    
    }
    
    Echocardiogram
    
    57
    
    2
    
    58
    
    The ECG in patients with
    palpitations and syncope:
    between attacks
    
    The clinical history and physical
    examination
    
    59
    
    Palpitations
    
    59
    
    Dizziness and syncope
    
    60
    
    Physical examination
    
    64
    
    The ECG
    
    64
    
    Syncope due to cardiac disease other
    than arrhythmias
    
    64
    
    Patients with possible tachycardias
    
    69
    
    Patients with possible bradycardias
    
    82
    
    Ambulatory ECG recording
    
    96
    
    The ECG is of paramount importance for the diagnosis of arrhythmias. Many arrhythmias are not noticed
    by the patient, but often they cause symptoms. These
    symptoms are often transient, and the patient may be
    completely well at the time he or she consults a doctor.
    Obtaining an ECG during a symptomatic episode is
    then the only certain way of making a diagnosis, but
    as always the history and physical examination are
    also extremely important. The main purpose of the
    history and examination is to help decide whether a
    patient’s symptoms could be the result of an arrhythmia, and whether the patient has a cardiac or other
    disease that may cause an arrhythmia.
    
    Palpitations
    THE CLINICAL HISTORY AND
    PHYSICAL EXAMINATION
    
    •
    
    PALPITATIONS
    ‘Palpitations’ mean different things to different
    patients, but a general definition would be ‘an awareness of the heartbeat’. Arrhythmias, fast or slow, can
    cause poor organ perfusion and so lead to syncope (a
    word used to describe all sorts of collapse), breathlessness and angina. Some rhythms can be identified from
    a patient’s description, such as:
    
    •
    
    A patient recognizes sinus tachycardia because it
    feels like the palpitations that he or she associates
    with anxiety or exercise.
    
    •
    
    2
    
    Extrasystoles are described as the heart ‘jumping’
    or ‘missing a beat’. It is not possible to
    distinguish between supraventricular and
    ventricular extrasystoles from a patient’s
    description, although they can be differentiated
    from an ECG.
    A paroxysmal tachycardia begins suddenly and
    sometimes stops suddenly. The heart rate is often
    ‘too fast to count’. Severe attacks are associated
    with dizziness, breathlessness and chest pain.
    
    Table 2.1 compares the symptoms associated with
    sinus tachycardia and a paroxysmal tachycardia, and
    shows how a diagnosis can be made from the history.
    Note that a heart rate between 140/min and 160/min
    may be associated with either sinus or paroxysmal
    tachycardia.
    
    Table 2.1 Diagnosis of sinus tachycardia or paroxysmal tachycardia from a patient’s symptoms
    Symptoms
    
    Sinus tachycardia
    
    Paroxysmal tachycardia
    
    Timing of initial attack
    
    Attacks probably began recently
    
    Attacks probably began in teens or early
    adult life
    
    Associations of attack
    
    Exercise, anxiety
    
    Usually no associations, but occasionally
    exercise-induced
    
    Rate of start of palpitations
    
    Slow build-up
    
    Sudden onset
    
    Rate of end of palpitations
    
    ’Die away’
    
    Classically sudden, but often ‘die away’
    
    Heart rate
    
    <140/min
    
    >160/min
    
    Associated symptoms
    
    Paraesthesia due to hyperventilation
    
    Chest pain
    Breathlessness
    Dizziness
    Syncope
    
    Ways of terminating attacks
    
    Relaxation
    
    Breath holding
    Valsalva’s manoeuvre
    
    59
    
    The ECG in patients with palpitations and syncope: between attacks
    DIZZINESS AND SYNCOPE
    These symptoms may have a cardiovascular or a
    neurological cause. Remember that cerebral hypoxia,
    however caused, may lead to a seizure, and that can
    make the differentiation between cardiac and neurological syncope very difficult. Syncope is defined as ‘a
    transient loss of consciousness characterized by unresponsiveness and loss of postural tone, with spontaneous recovery and not requiring specific resuscitative
    intervention’.
    Figure 2.1 shows an EEG that was being recorded
    in a 46-year-old woman with episodes of limb shaking,
    suspected of being generalized tonic–clonic seizures. She
    lost awareness during events, and had violent limb
    shaking for several seconds as she came round. She felt
    nauseated, but was rapidly reorientated. By chance, she
    had one of her ‘attacks’ while her EEG was being
    recorded, and from the ECG being routinely recorded
    in parallel, it became clear that the problem was not
    seizures, but periods of asystole – in this case lasting
    about 15 s. The numbered arrows in Figure 2.1 mark
    significant features. The recording begins with a routine
    period of hyperventilation, with the EEG showing an
    
    60
    
    eye blink in the anterior leads and the ECG showing
    sinus rhythm. There are then (at arrow 1 on the record)
    one (or possibly two) ventricular extrasystoles, followed by a narrow complex beat (probably sinus) and
    another ventricular extrasystole, with a different configuration from the previous ones. Asystole follows, and
    after 7–8 s (at arrow 2) there is global EEG slowing,
    and the patient became unresponsive. After 4 s (at
    arrow 3), there is global attenuation (reduction in
    signals) in the EEG and after another 3 s, there is an
    escape beat whose morphology suggests a ventricular
    origin. This is followed by a beat with a narrow QRS
    complex and possibly an inverted T wave, and then
    there is gross artefact due to the ECG lead being
    checked. During that period, sinus rhythm was restored.
    There was then (at arrow 4) global EEG slowing for
    5 s, followed by (at arrow 5) violent limb thrashing for
    about 12 s as the patient regained consciousness – these
    movements were not clonic, and were thought to represent anxiety or fear. Normal EEG and ECG activity
    were then resumed (at arrow 6).
    Some causes of syncope are summarized in Box 2.1.
    Table 2.2 shows some clinical features of syncope,
    and possible causes.
    
    Dizziness and syncope
    Box 2.1 Cardiovascular causes of syncope
    Obstructed blood flow in heart or lungs
    
    • Aortic stenosis
    • Pulmonary embolus
    • Pulmonary hypertension
    • Hypertrophic cardiomyopathy
    • Pericardial tamponade
    • Atrial myxoma
    Arrhythmias
    
    • Tachycardias: patient is usually aware of a fast heartbeat
    before becoming dizzy
    • Bradycardias: slow heart rates are often not appreciated.
    A classical cause of syncope is a Stokes–Adams attack,
    due to a very slow ventricular rate in patients with
    complete heart block. A Stokes–Adams attack can be
    recognized because the patient is initially pale but
    flushes red on recovery
    
    Postural hypotension, occurring immediately on
    standing
    Seen with:
    Loss of blood volume
    Autonomic nervous system disease (e.g. diabetes,
    Shy–Drager syndrome, amyloid neuropathy)
    Patients being treated with antihypertensive drugs
    
    •
    •
    •
    
    Neurally-mediated reflex syncopal syndromes
    Vasovagal (neurocardiogenic) (simple faints)
    Situational (e.g. after coughing, sneezing,
    gastrointestinal stimulation of various sorts,
    post-micturition)
    Carotid sinus hypersensitivity
    
    •
    •
    •
    
    2
    
    Table 2.2 Diagnosis of causes of syncope
    Symptoms and signs
    
    Possible diagnosis
    
    Family history of sudden
    death
    
    Long QT syndrome,
    Brugada syndrome,
    hypertrophic
    cardiomyopathy
    
    Caused by unpleasant stimuli,
    prolonged standing, hot
    places (situational syncope)
    
    Vasovagal syncope
    
    Occurs within seconds or
    minutes of standing
    
    Orthostatic hypotension
    
    Temporal relation to
    medication
    
    Orthostatic hypotension
    
    Occurs during exertion
    
    Obstruction to blood
    flow (e.g. aortic stenosis,
    pulmonary hypertension)
    
    Occurs with head rotation or
    pressure on neck
    
    Carotid sinus
    hypersensitivity
    
    Confusion for more than
    5 min afterwards
    
    Seizure
    
    Tonic–clonic movements,
    automatism
    
    Seizure
    
    Frequent attacks, usually
    unobserved, with somatic
    symptoms
    
    Psychiatric illness
    
    Symptoms or signs
    suggesting cardiac disease
    
    Cardiac disease
    
    61
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.1
    
    EEG recorded during a syncopal attack
    1
    
    2
    
    Fp2 F8
    F8 T4
    T4 T6
    T6 O2
    Fp1 F7
    F7 T3
    T3 T5
    T5 O1
    Fp2 F4
    F4 C4
    C4 P4
    P4 O2
    Fp1 F3
    F3 C3
    C3 P3
    P3 O1
    ECG
    lead I
    
    (a)
    
    62
    
    (b)
    
    3
    
    Dizziness and syncope
    
    2
    
    Courtesy of Dr A. Michell, Addenbrooke’s Hospital, Cambridge
    
    4
    
    5
    
    6
    
    Note
    EEG and ECG lead I (lower trace)
    Paper speed five times normal ECG speed
    (a) Sinus rhythm at about 70/min, ventricular extrasystoles
    interrupted by one narrow complex beat, then asystole
    (b) Asystole followed by an escape beat, a narrow complex beat,
    and gross artefact
    (c) Sinus rhythm restored, with a period of limb thrashing before
    resumption of a normal record
    
    •
    •
    •
    •
    (c)
    
    •
    
    63
    
    The ECG in patients with palpitations and syncope: between attacks
    continuously, in the hope that an episode of the
    arrhythmia will be detected.
    
    PHYSICAL EXAMINATION
    If the patient has no symptoms at the time of the
    examination, look for:
    
    •
    •
    •
    •
    
    Evidence of any heart disease that might cause an
    arrhythmia
    Evidence of non-cardiac disease that might cause
    an arrhythmia
    Evidence of cardiovascular disease that might
    cause syncope without an arrhythmia
    Evidence (from the history or examination) of
    neurological disease.
    
    It is only possible to make a confident diagnosis
    that an arrhythmia is the cause of palpitations or
    syncope if an ECG recording of the arrhythmia can be
    obtained at the time of the patient’s symptoms. If the
    patient is asymptomatic at the time of examination, it
    may be worth arranging for an ECG to be recorded
    during an attack of palpitations, or to be recorded
    
    THE ECG
    Even when the patient is asymptomatic, the resting
    ECG can be very helpful, as summarized in Table 2.3.
    
    SYNCOPE DUE TO CARDIAC DISEASE OTHER
    THAN ARRHYTHMIAS
    The ECG may indicate that syncopal attacks have a
    cardiovascular cause other than an arrhythmia.
    ECG evidence of left ventricular hypertrophy
    or of left bundle branch block may suggest that
    syncope is due to aortic stenosis. The ECGs in Figures
    2.2 and 2.3 were recorded from patients who had
    syncopal attacks on exercise due to severe aortic
    stenosis.
    
    Fig. 2.2
    
    64
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Syncope due to cardiac disease other than arrhythmias
    
    2
    
    Table 2.3 ECG features between attacks of palpitations or syncope
    ECG appearance
    
    Possible cause of symptoms
    
    ECG completely normal
    
    Symptoms may not be due to a primary arrhythmia – consider anxiety,
    epilepsy, atrial myxoma or carotid sinus hypersensitivity
    
    ECGs that suggest cardiac disease
    
    Left ventricular hypertrophy or left bundle branch block – aortic stenosis
    Right ventricular hypertrophy – pulmonary hypertension
    Anterior T wave inversion – hypertrophic cardiomyopathy
    
    ECGs that suggest intermittent tachyarrhythmia
    
    Left atrial hypertrophy – mitral stenosis, so possibly atrial fibrillation
    Pre-excitation syndromes
    Long QT syndrome
    Flat T waves suggest hypokalaemia
    Digoxin effect – ?digoxin toxicity
    
    ECGs that suggest intermittent bradyarrhythmia
    
    Second degree block
    First degree block plus bundle branch block
    Digoxin effect
    
    Left ventricular hypertrophy
    Note
    Sinus rhythm
    Bifid P waves suggest left atrial hypertrophy (best seen
    in leads V4–V5)
    Normal axis
    Tall R waves and deep S waves
    T waves inverted in leads I, VL, V5–V6
    
    •
    •
    •
    •
    •
    
    Tall R wave, inverted T wave in lead V5
    
    65
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.3
    
    I
    
    VR
    
    II
    
    VL
    
    V1
    
    V2
    
    V4
    
    V5
    
    V3
    III
    
    Fig. 2.4
    
    66
    
    V6
    
    VF
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Syncope due to cardiac disease other than arrhythmias
    Left bundle branch block
    Note
    
    • Sinus rhythm
    • Slight PR interval prolongation (212 ms)
    • Broad QRS complexes
    • ‘M’ pattern in lateral leads
    • T wave inversion in leads I, VL, V –V
    5
    
    6
    
    M pattern of left bundle
    branch block in lead VL
    
    2
    
    ECG evidence of right ventricular hypertrophy suggests thromboembolic pulmonary hypertension. The
    ECG in Figure 2.4 is that of a middle-aged woman
    with dizziness on exertion, due to multiple pulmonary
    emboli.
    Syncope due to hypertrophic cardiomyopathy (Fig.
    2.5) may be associated with a characteristic ECG
    (Fig. 2.6) that resembles that of patients with an anterior non-ST segment elevation myocardial infarction
    (NSTEMI) (compare with Fig. 5.23, p. 240). With
    hypertrophic cardiomyopathy, the T wave inversion is
    usually more pronounced than with an NSTEMI, but
    differentiation really depends on the clinical picture,
    not on the ECG appearance. Hypertrophic cardiomyopathy can cause syncope due to obstruction to outflow
    from the left ventricle, or can cause symptomatic
    arrhythmias.
    
    Right ventricular hypertrophy
    Note
    Sinus rhythm
    Right axis deviation
    Dominant R waves in lead V1
    Inverted T waves in leads V1–V4
    
    •
    •
    •
    •
    
    Dominant R wave in lead V1
    
    67
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig 2.5
    
    MR image of a heart with hypertrophic
    cardiomyopathy
    
    RV
    Septum
    RA
    
    LV
    LV
    Free wall
    
    Note
    RA – right atrium
    RV – right ventricular cavity
    Septum – interventricular septum
    LV – left ventricular cavity
    LA – left atrium
    LV free wall – left ventricular myocardium
    
    •
    •
    •
    •
    •
    •
    
    LA
    
    Fig. 2.6
    
    68
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible tachycardias
    PATIENTS WITH POSSIBLE TACHYCARDIAS
    MITRAL STENOSIS
    Mitral stenosis leads to atrial fibrillation, but when the
    heart is still in sinus rhythm the presence of the characteristics of left atrial hypertrophy on the ECG may
    give a clue that paroxysmal atrial fibrillation is occurring (Fig. 2.7).
    
    PRE-EXCITATION SYNDROMES
    Normal conduction between the atria and ventricles
    involves the uniform spread of the depolarization
    wave front in a constant direction, down the bundle
    of His. In the pre-excitation syndromes, an abnormal
    additional pathway, or multiple pathways, connect the
    atria and ventricles. These accessory pathways bypass
    the AV node, where normal conduction is delayed, and
    
    Hypertrophic cardiomyopathy
    Note
    
    • Sinus rhythm
    • Marked T wave inversion in leads V –V
    3
    
    6
    
    2
    
    therefore conduct more rapidly than the normal
    pathway. The anatomical combination of the normal
    AV node–His bundle pathway and the accessory
    pathway creates a potential circuit around which excitation may spread, causing a ‘re-entry’ tachycardia
    (Ch. 3, p. 105).
    The Wolff–Parkinson–White syndrome
    In the Wolff–Parkinson–White (WPW) syndrome, an
    accessory pathway (the ‘bundle of Kent’) connects
    either the left atrium and left ventricle, or the right
    atrium and right ventricle. Conduction may at times
    occur only through the normal His bundle pathway,
    so the QRS complexes will be normal and narrow; the
    accessory pathway is then said to be concealed. At
    other times, conduction may occur through both pathways simultaneously, but the heart will remain in sinus
    rhythm if conduction occurs in a forward direction
    via both the AV node–His bundle pathway and the
    accessory pathway. The faster conduction down
    the accessory pathway causes part of the ventricle to
    depolarize early, resulting in a short PR interval and a
    slurred upstroke to the QRS complex (delta wave),
    causing a wide QRS complex.
    With a left-sided accessory pathway, the ECG
    shows a dominant R wave in lead V1. This is called
    the ‘type A’ pattern (Fig. 2.8). This pattern can easily
    be mistaken for right ventricular hypertrophy, the differentiation being made by the presence or absence of
    a short PR interval.
    
    Inverted T wave in lead V4
    
    69
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.7
    
    I
    
    II
    
    III
    
    Fig. 2.8
    
    70
    
    VR
    
    V1
    
    V4
    
    VL
    
    V2
    
    V5
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible tachycardias
    
    2
    
    Left atrial hypertrophy
    Note
    Sinus rhythm
    Bifid P waves, most clearly seen in leads I, II, V3–V5
    
    •
    •
    
    Bifid P wave in lead II
    
    The Wolff–Parkinson–White syndrome,
    type A
    Note
    
    • Sinus rhythm
    • Short PR interval
    • Broad QRS complexes
    • Dominant R wave in lead V
    • Slurred upstroke to QRS complexes – the delta wave
    • Inverted T waves in leads II, III, VF, V –V
    1
    
    1
    
    4
    
    Delta wave in lead III
    
    71
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.9
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    The ECG in Figure 2.9 is from a young man
    who complained of symptoms that sounded like paroxysmal tachycardia. His ECG shows the WPW
    syndrome type A, but it would be quite easy to
    miss the short PR interval unless the whole of the
    12-lead trace were carefully inspected. The short PR
    interval and delta waves are most obvious in leads V4
    and V5.
    When the accessory pathway is on the right side of
    the heart, there is no dominant R wave in lead V1, and
    this is called the ‘type B’ pattern (Fig. 2.10).
    ECGs indicating pre-excitation of the WPW type
    are found in approximately 1 in every 3000 healthy
    young people. Only half of these ever have an episode
    
    72
    
    of tachycardia, and many have only very occasional
    attacks.
    The ECG features associated with the WPW syndrome are summarized in Box 2.2.
    The Lown–Ganong–Levine syndrome
    Where an accessory pathway connects the atria to the
    bundle of His rather than to the right or left ventricle,
    there will be a short PR interval but the QRS complex
    will be normal. This is called the Lown–Ganong–Levine
    (LGL) syndrome (Fig. 2.11). This syndrome must be
    differentiated from accelerated idionodal rhythm,
    where the PR interval varies (see p. 49 and Fig. 1.45).
    
    Patients with possible tachycardias
    
    2
    
    The Wolff–Parkinson–White syndrome,
    type A
    Note
    
    • Sinus rhythm
    • Short PR interval, especially obvious in leads V –V
    • Slurred upstroke to QRS complexes, obvious in leads
    3
    
    5
    
    V3–V5 but not obvious in the limb leads
    
    • Dominant R wave in lead V
    • No T wave inversion in the anterior leads (cf. Fig. 2.8)
    1
    
    Delta wave in lead V5
    
    Box 2.2 The Wolff–Parkinson–White syndrome:
    ECG features
    
    • Short PR interval
    • Wide QRS complexes with delta wave with normal
    terminal segment
    • ST segment/T wave changes
    • Left-sided pathway (type A): dominant R waves in leads
    V –V
    • Right-sided pathway (type B): dominant S wave in lead
    V , and sometimes, anterior T wave inversion
    • Arrhythmias (narrow or wide complex)
    • Arrhythmia with wide, irregular complex suggests the
    1
    
    6
    
    1
    
    WPW syndrome with atrial fibrillation
    
    73
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.10
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    VF
    
    V3
    
    V6
    
    III
    
    Fig. 2.11
    
    74
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible tachycardias
    
    2
    
    The Wolff–Parkinson–White syndrome, type B
    Note
    Sinus rhythm
    Short PR interval
    Broad QRS complexes with delta waves
    No dominant R waves in lead V1 (cf. Figs 2.8 and 2.9)
    T wave inversion in leads III, VF, V3
    
    •
    •
    •
    •
    •
    
    Short PR interval; broad QRS complex in lead III
    
    The Lown–Ganong–Levine syndrome
    Note
    Sinus rhythm
    Short PR interval
    Normal QRS complexes and P waves
    
    •
    •
    •
    
    Short PR interval in lead II
    
    75
    
    The ECG in patients with palpitations and syncope: between attacks
    THE LONG QT SYNDROME
    Delayed repolarization occurs for a variety of reasons
    (Box 2.3), and causes a long QT interval. A prolonged
    QT interval is associated with paroxysmal ventricular
    tachycardia, and therefore can be the cause of episodes
    of collapse or even sudden death. The ventricular
    tachycardia associated with a prolonged QT interval
    usually involves a continual change from upright to
    
    downward QRS complexes. This is called ‘torsade de
    pointes’ (Fig. 2.12), and it usually occurs at times of
    increased sympathetic nervous system activity.
    Several genetic abnormalities have been described
    that lead to familial prolongation of the QT interval.
    The ECG in Figure 2.13 is from a 10-year-old girl who
    suffered from ‘fainting’ attacks. Her sister had died
    suddenly; three other siblings and both parents had
    normal ECGs.
    
    Fig. 2.12
    
    Torsade de pointes ventricular tachycardia
    
    Note
    
    • Broad complex tachycardia at 300/min
    • Continually changing shape of QRS complexes
    Fig. 2.13
    
    76
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible tachycardias
    Box 2.3 Possible causes of a prolonged QT interval
    Congenital
    Jervell–Lange–Nielson syndrome
    Romano–Ward syndrome
    
    •
    •
    
    Antiarrhythmic drugs
    
    • Quinidine (of historical interest only)
    • Procainamide
    • Disopyramide
    • Amiodarone
    • Sotalol
    Other drugs
    
    • Tricyclic antidepressants
    • Erythromycin
    Plasma electrolyte abnormality
    
    • Low potassium
    • Low magnesium
    • Low calcium
    
    2
    
    The most common cause of QT prolongation is
    drug therapy. The ECG in Figure 2.14 is from a patient
    who had a posterior myocardial infarction (see Ch. 5).
    He was treated with amiodarone because of recurrent
    ventricular tachycardias, and developed a prolonged
    QT interval. Figure 2.15 shows his record 4 months
    later: the prolonged QT interval reverted to normal
    when the amiodarone treatment was stopped.
    Episodes of symptomatic ventricular tachycardia
    occur in about 8% of affected subjects each year, and
    the annual death rate due to arrhythmias is about 1%
    of patients with a long QT syndrome. The precise
    relationship between QT c interval prolongation and
    the risk of sudden death is unknown; neither is it clear
    whether prolongation of the QT or QT c interval is
    more significant. There is no absolute threshold of
    risk. However, torsade de pointes ventricular tachycardia seems rare when the QT or QT c interval is less
    than 500 ms.
    
    Congenital long QT syndrome
    Note
    Sinus rhythm
    Normal axis
    QT interval 520 ms
    Marked T wave inversion in leads V2–V4
    
    •
    •
    •
    •
    
    Long QT interval and inverted T wave in lead V3
    
    77
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.14
    
    Fig. 2.15
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    V4
    
    V1
    
    V2
    
    V5
    
    V6
    
    V3
    
    V4
    
    V1
    
    V2
    
    78
    
    V5
    
    V3
    
    V6
    
    Patients with possible tachycardias
    
    2
    
    Prolonged QT interval due to amiodarone
    Note
    
    • Sinus rhythm
    • Normal axis
    • Dominant R waves in lead V due to posterior infarction
    • QT interval 800 ms
    • Bizarre T wave shape in anterior leads
    1
    
    Long QT interval and bizarre T wave in lead V2
    
    Posterior infarct with normal QT interval
    Note
    Same patient as in Figure 2.14
    Sinus rhythm
    Normal axis
    Dominant R waves in lead V1
    Ischaemic ST segment depression
    Normal QT interval
    
    •
    •
    •
    •
    •
    •
    
    ST segment depression in lead V2
    
    79
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.16
    
    Fig. 2.17
    
    80
    
    I
    
    VR
    
    II
    
    VL
    
    III
    
    VF
    
    V4
    
    V1
    
    V2
    
    V3
    
    V5
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible tachycardias
    
    2
    
    Brugada syndrome
    Note
    
    • Sinus rhythm
    • Normal axis
    • Normal QRS complex duration
    • RSR pattern in leads V –V
    • No wide S wave in lead V
    • Raised, downward-sloping ST segment in leads V –V
    1
    
    1
    
    2
    
    6
    
    1
    
    2
    
    RSR1 pattern and raised ST segment in lead V2
    
    Brugada syndrome
    Note
    Same patient as in Figure 2.16
    Normal ECG
    
    •
    •
    
    Normal appearance in lead V2
    
    THE BRUGADA SYNDROME
    Sudden collapse due to ventricular tachycardia and
    fibrillation occurs in a congenital disorder of sodium
    ion transport called the Brugada syndrome. Between
    attacks, the ECG superficially resembles that associated with right bundle branch block (RBBB), with an
    RSR1 pattern in leads V1 and V2 (Fig. 2.16). However,
    the ST segment in these leads is raised, and there is no
    wide S wave in lead V6 as there is in RBBB. The
    changes are seen in the right ventricular leads because
    the abnormal sodium channels are predominantly
    found in the right ventricle. The ECG abnormality can
    be transient – the ECG in Figure 2.17 was taken a day
    later from the same patient as in Figure 2.16.
    
    81
    
    The ECG in patients with palpitations and syncope: between attacks
    PATIENTS WITH POSSIBLE BRADYCARDIAS
    When a patient is asymptomatic, an intermittent bradycardia can be suspected if the ECG shows any evidence
    of an escape rhythm or a conduction defect. However,
    it must be remembered that conduction defects and
    escape rhythms are quite common in healthy people,
    and their presence may be coincidental.
    
    ESCAPE RHYTHMS
    Myocardial cells are only depolarized when they are
    stimulated, but the cells of the SA node, those around
    
    the AV node (the ‘junctional’ cells) and those of the
    conducting pathways all possess the property of spontaneous depolarization or ‘automaticity’.
    The automaticity of any part of the heart is
    suppressed by the arrival of a depolarization wave,
    and so the heart rate is controlled by the region
    with the highest automatic depolarization frequency.
    Normally the SA node controls the heart rate because
    it has thehighest frequency of discharge, but if for
    any reason this fails, the region with the next
    highest intrinsic depolarization frequency will emerge
    as the pacemaker and set up an ‘escape’ rhythm.
    The atria and the junctional region have automatic
    
    Fig. 2.18
    
    Junctional escape beat
    Note
    
    • After two sinus beats there is no P wave
    • After an interval there is a narrow QRS complex, with
    •
    •
    
    the same configuration as that of the sinus beats but
    without a preceding P wave
    This is a junctional beat (arrowed)
    Sinus rhythm then reappears
    
    Fig. 2.19
    
    Junctional (escape) rhythm
    P
    
    Note
    
    • Two sinus beats are followed by an interval with no P
    waves
    
    • A junctional rhythm then emerges (with QRS complexes
    the same as in sinus rhythm)
    
    • A P wave (arrowed) can be seen as a hump on the T
    wave of the junctional beats: the atria have been
    depolarized retrogradely
    
    82
    
    Patients with possible bradycardias
    depolarization frequencies of about 50/min, compared
    with the normal SA node frequency of 60–70/min.
    If both the SA node and the junctional region fail
    to depolarize, or if conduction to the ventricles
    fails, a ventricular focus may emerge, with a rate of
    30–40/min; this is classically seen in complete heart
    block.
    Escape beats may be single or may form sustained
    rhythms. They have the same ECG appearance as the
    corresponding extrasystoles, but appear late rather
    than early (Fig. 2.18).
    In sustained junctional escape rhythms, atrial activation may be seen as a P wave following the QRS
    
    2
    
    complex (Fig. 2.19). This occurs if depolarization
    spreads in the opposite direction from normal, from
    the AV node to the atria, and is called ‘retrograde’
    conduction. Figure 2.20 also shows a junctional escape
    rhythm.
    Figure 2.21 shows a ventricular escape beat.
    
    Fig. 2.20
    
    Junctional (escape) rhythm
    
    Note
    
    • No P waves
    • Narrow QRS complexes and normal T waves
    Fig. 2.21
    
    Ventricular escape beat
    Note
    
    • Three sinus beats are followed by a pause
    • There is then a single ventricular beat with a wide QRS
    complex and an inverted T wave
    
    • Sinus rhythm is then restored
    83
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.22
    
    Fig. 2.23
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    84
    
    Patients with possible bradycardias
    First degree block
    Note
    Sinus rhythm
    PR interval 380 ms
    T wave inversion in leads III and VF suggests ischaemia
    
    •
    •
    •
    
    Long PR interval in lead III
    
    2
    
    SYNCOPE
    In a patient with syncopal attacks, ECG changes that
    would be ignored in a healthy person take on a greater
    significance. First degree block, itself of no clinical
    importance, may point to intermittent complete block,
    and complete block is much more likely when the ECG
    of a currently asymptomatic patient shows second
    degree block. The ECGs in Figures 2.22, 2.23 and 2.24
    are from patients with syncopal attacks, all of whom
    needed permanent pacemakers.
    Left axis deviation usually indicates left anterior
    hemiblock, but a minor degree of left axis deviation
    with a narrow QRS complex can be accepted as a
    normal variant (Fig. 2.25). A QRS complex near the
    upper limit of the normal width with marked left axis
    deviation represents the full pattern of left anterior
    hemiblock (Fig. 2.26).
    
    Second degree block (Wenckebach)
    Note
    Sinus rhythm
    PR interval lengthens progressively from 360 ms to
    440 ms and then a P wave is not conducted
    Small Q wave and inverted T wave in leads III and VF
    suggest an old inferior infarct
    
    •
    •
    •
    
    P waves
    
    85
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.24
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    Fig. 2.25
    
    86
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible bradycardias
    
    2
    
    Second degree block (2 : 1)
    Note
    Sinus rhythm
    Alternate beats conducted and not conducted
    Lateral T wave inversion in leads I, VL, V6 suggests
    ischaemia
    
    •
    •
    •
    
    P waves
    
    Left axis deviation
    Note
    
    • Sinus rhythm
    • Dominant S waves in leads II and III: left axis deviation
    • Normal QRS complex duration
    • Lateral T wave inversion
    
    Dominant S waves in leads II and III
    
    87
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.26
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    VF
    
    V3
    
    V6
    
    III
    
    Fig. 2.27
    
    88
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible bradycardias
    
    2
    
    Combinations of conduction abnormalities
    
    Left anterior hemiblock
    Note
    Sinus rhythm
    Left axis deviation
    Broad QRS complexes (122 ms)
    Inverted T waves in lead VL
    
    •
    •
    •
    •
    
    Dominant S
    waves and broad
    QRS complexes
    in leads II and III
    
    First degree block and left bundle branch
    block (LBBB)
    Note
    Sinus rhythm
    PR interval 300 ms
    LBBB pattern
    Broad QRS complexes
    
    •
    •
    •
    •
    
    Long PR interval
    in leads II and III
    
    ECG evidence of atrioventricular conduction abnormalities will not be associated with syncope unless there
    is intermittent second or third degree heart block with
    a bradycardia. It is, however, important to recognize
    the clinically less common conduction defects because
    they may be pointers to the cause of syncopal attacks.
    When first degree block is associated with left
    bundle branch block (Fig. 2.27), conduction must be
    delayed in either the AV node, the His bundle or the
    right bundle branch as well as in the left bundle
    branch. The combination of first degree block and
    right bundle branch block (RBBB) (Fig. 2.28) shows
    that conduction has failed in the right bundle branch
    and is also beginning to fail elsewhere.
    A combination of left anterior hemiblock and
    RBBB means that conduction into the ventricles is only
    passing through the posterior fascicle of the left bundle
    branch (Fig. 2.29). This is called ‘bifascicular block’.
    A combination of left anterior hemiblock, RBBB and
    first degree block suggests that there is disease in the
    remaining conducting pathway – either in the main His
    bundle or in the posterior fascicle of the left bundle
    branch. This is sometimes called ‘trifascicular block’
    (Fig. 2.30). Complete conduction block in the right bundle
    and in both fascicles of the left bundle would, of course,
    cause complete (third degree) heart block.
    Right axis deviation is not necessarily a feature of
    left posterior hemiblock, but, when combined with
    other evidence of conducting tissue disease such as first
    degree block (Fig. 2.31), it usually is.
    A combination of second degree (2 : 1) block with
    left anterior hemiblock (Fig. 2.32) or with both left
    anterior hemiblock and RBBB (Fig. 2.33) suggests
    widespread conduction tissue disease.
    
    89
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.28
    
    Fig. 2.29
    
    90
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible bradycardias
    
    2
    
    First degree block and right bundle branch
    block (RBBB)
    Note
    Sinus rhythm
    PR interval 328 ms
    Right axis deviation
    Broad QRS complexes
    RBBB pattern
    
    •
    •
    •
    •
    •
    
    Long PR interval and RBBB pattern in lead V1
    
    Bifascicular block
    Note
    Sinus rhythm
    PR interval normal (176 ms)
    Left anterior hemiblock
    RBBB
    
    •
    •
    •
    •
    
    Left axis deviation
    and broad QRS
    complex in lead II
    
    RBBB in lead V1
    
    91
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.30
    
    Fig. 2.31
    
    92
    
    V1
    
    V4
    
    I
    
    VR
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible bradycardias
    
    2
    
    Trifascicular block
    Note
    Sinus rhythm
    PR interval 224 ms
    Left anterior hemiblock
    RBBB
    
    •
    •
    •
    •
    
    Left axis deviation
    in lead II
    
    RBBB in lead V1
    
    Left posterior hemiblock
    Note
    Sinus rhythm
    First degree block (PR interval 320 ms)
    Right axis deviation
    This could represent right ventricular hypertrophy, but
    there is no dominant R wave in lead V1
    
    •
    •
    •
    •
    
    Long PR interval and deep S wave in lead I
    
    93
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.32
    
    Fig. 2.33
    
    94
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    Patients with possible bradycardias
    
    2
    
    Second degree block and left anterior
    hemiblock
    Note
    
    • Sinus rhythm
    • Second degree block (2 : 1 type)
    • Left anterior hemiblock
    • Poor R wave progression suggests possible old anterior
    infarct
    
    P waves in lead II
    
    Second degree block, left anterior
    hemiblock and right bundle branch block
    (RBBB)
    Note
    Sinus rhythm
    Second degree block (2 : 1 type)
    Left anterior hemiblock
    RBBB
    
    •
    •
    •
    •
    
    P waves and RBBB in lead V1
    
    95
    
    The ECG in patients with palpitations and syncope: between attacks
    AMBULATORY ECG RECORDING
    The only way to be certain that a patient’s symptoms
    are due to an arrhythmia is to show that an arrhythmia is present at the time of the symptoms. If symptoms occur frequently – say two or three times a
    week – a 24-h tape recording (called a ‘Holter’ record
    after its inventor) may show the abnormality. When
    symptoms are infrequent ‘event recorders’ are more
    useful, and these can either be patient-activated or
    programmed to detect rate or rhythm changes. Table
    2.4 shows examples of these devices, and some of their
    advantages and disadvantages.
    Figures 2.34, 2.35 and 2.36 show examples of
    ambulatory records obtained from patients who complained of syncopal attacks, but whose hearts were in
    sinus rhythm at the time they were first seen.
    
    When an ambulatory record shows arrhythmias
    which are not accompanied by symptoms, it is difficult
    to be certain of their significance. When 24-h recordings are made from healthy volunteers, extrasystoles
    are found in about two-thirds of them, and a few
    will even show the R on T phenomenon. Episodes of
    supraventricular tachycardia are seen in about 3% of
    apparently healthy subjects, and ventricular tachycardia in about 1%.
    If an ECG can be recorded at the time when the
    patient has symptoms, then there can be little doubt
    about the relationship between the symptoms and the
    cardiac rhythm, and the next two chapters deal with
    ECGs that may be recorded when a patient has either
    a tachycardia or a bradycardia.
    
    Fig. 2.34
    
    Ventricular tachycardia
    
    Note
    
    • Ambulatory recording
    • Initially sinus rhythm with ventricular extrasystoles
    • Then salvos (three beats) of extrasystoles, leading to a broad complex
    tachycardia
    
    • The change in the QRS complex configuration suggests that the tachycardia is
    ventricular, but a 12-lead ECG would be necessary to be certain
    
    96
    
    Ambulatory ECG recording
    
    2
    
    Fig. 2.35
    
    Ventricular standstill
    
    Note
    
    • Ambulatory recording
    • Top strip shows sinus rhythm with normal AV
    conduction
    
    • Second strip shows SA block, which was asymptomatic
    • Third strip shows second degree block, which was also
    asymptomatic
    
    • Bottom strip shows a ventricular extrasystole followed
    by ventricular standstill. The patient lost consciousness
    due to this Stokes–Adams attack
    
    97
    
    Table 2.4 Ambulatory cardiac monitoring devices
    Monitoring device
    
    Mode of use
    
    Holter monitor
    Usually three electrodes placed on
    chest wall for maximal signal;
    activation button can be used in
    association with patient diary to
    highlight symptomatic events
    
    Cardiac memo
    Device placed directly on to the
    skin by patient when symptomatic,
    or can be adapted to use with
    electrodes; traces can be
    downloaded by telephone
    
    Loop recorder
    Usually three electrodes placed on
    chest wall; position of electrodes
    may require rotation, especially if
    there is skin reaction
    
    Implantable loop recorder
    Requires subcutaneous
    implantation, a procedure taking
    around 20 min and with a low risk
    of infection
    Can be patient-activated
    
    98
    
    Duration and mode of recording
    
    Applications
    
    Comments
    
    Usually 24 h, but up to 7 days
    Usually 1–2 channels, but up to 12 leads
    possible
    
    Suitable for palpitations, syncope or
    presyncope occurring fairly frequently
    (e.g. daily)
    
    Analysis time-consuming, but
    aided by software
    
    10–20 recordings of 30–60 s
    
    Suitable for palpitations lasting for
    several minutes, enabling patient to
    apply device and record trace
    
    Not suitable for syncope, because
    patient activation required
    
    Recording period programmable; usually
    4 min pre- and post-activation
    Can record 2000–3000 periods (‘loops’) of
    ECG records, including patient-activated
    and autoactivated episodes
    Autoactivation function programmable,
    based on heart rate and on QRS complex
    duration and irregularity
    
    Increasingly replacing memo devices
    Useful for diagnosis of palpitations or
    syncope
    
    Can be kept in place for long
    periods, although batteries may
    need replacing periodically
    
    Highly programmable; autoactivation can be
    based on heart rate and on QRS complex
    duration and irregularity
    
    Especially useful for the diagnosis of
    rare rhythm disturbances and syncope
    
    Orientation and site of
    implantation can be optimized
    prior to implantation
    Up to 14 months’ battery life
    Surgical removal needed
    
    99
    
    The ECG in patients with palpitations and syncope: between attacks
    Fig. 2.36
    
    Sudden death due to ventricular fibrillation
    
    Note
    
    • Ambulatory recording
    • First strip shows sinus rhythm
    • Sinus bradycardia then develops, with inversion of the
    T wave suggesting ischaemia
    
    • Short runs of ventricular tachycardia (VT) lead to
    polymorphic VT
    
    • Ventricular fibrillation then develops
    
    100
    
    The ECG when the patient
    has a tachycardia
    
    Mechanism of tachycardias
    
    102
    
    3
    
    Tachycardias associated with the Wolff–
    Parkinson–White syndrome
    
    147
    
    Enhanced automaticity and triggered
    activity
    
    102
    
    Management of arrhythmias
    
    150
    
    Abnormalities of cardiac rhythm due to
    re-entry
    
    105
    
    What to do when an arrhythmia is
    suspected
    
    150
    
    Differentiation between re-entry and
    enhanced automaticity
    
    111
    
    What to do when an arrhythmia is
    recorded
    
    150
    
    Tachycardias with symptoms
    
    113
    
    Extrasystoles
    
    152
    
    Sinus rhythm causing symptoms
    
    113
    
    Sinus tachycardia
    
    154
    
    Extrasystoles causing symptoms
    
    115
    
    Atrial tachycardia
    
    154
    
    Narrow complex tachycardias causing
    symptoms
    
    117
    
    Atrioventricular nodal re-entry
    tachycardia (AVNRT, junctional tachycardia)
    
    154
    
    Broad complex tachycardias causing
    symptoms
    
    126
    
    Atrial fibrillation and flutter
    
    154
    
    Ventricular tachycardia
    
    155
    
    The Wolff–Parkinson–White syndrome
    
    155
    
    Special forms of ventricular tachycardia in
    patients with symptoms
    
    144
    
    101
    
    The ECG when the patient has a tachycardia
    Electrophysiology and catheter ablation
    
    155
    
    Cardiac arrest
    
    162
    
    The endocardial ECG
    
    156
    
    Management of cardiac arrest
    
    164
    
    Catheter ablation
    
    157
    
    Causes of cardiac arrest
    
    165
    
    Arrhythmias amenable to ablation
    
    158
    
    Indications for electrophysiology
    
    162
    
    Implanted cardioverter defibrillator
    (ICD) devices
    
    165
    
    The only tachycardia that can be (reasonably) reliably
    diagnosed from the patient’s history is sinus tachycardia. A patient may notice the irregularity of atrial
    fibrillation, but it is easy to confuse this with multiple
    extrasystoles. The heart rate may give a clue to the
    nature of the arrhythmia (Table 3.1) but there is really
    no substitute for the ECG.
    
    MECHANISM OF TACHYCARDIAS
    
    102
    
    Electrophysiology is the process of recording the ECG
    from inside the heart, using electrodes inserted via a
    peripheral vein. This is a highly specialized area, and
    yields additional information to that obtained from a
    conventional 12-lead ECG.
    The main purpose of electrophysiological studies is
    to identify the site of origin of an arrhythmia. Arrhythmias occur either because of an abnormality of focal
    depolarization of the heart, or because of re-entry
    circuits. If the origin can be localized, the arrhythmia
    may be prevented permanently by ablation. This technique uses local endocardial (or more rarely epicardial)
    cautery burns to abolish areas of abnormal cardiac
    electrical activity, or to interrupt re-entry circuits.
    Before the advent of electrical (ablation) therapy,
    the cause of arrhythmias was a fairly esoteric subject.
    Now, however, it is essential to understand the underlying electrical mechanisms, because they form the
    basis of ablation therapy.
    
    ENHANCED AUTOMATICITY AND
    TRIGGERED ACTIVITY
    If the intrinsic frequency of depolarization of the
    atrial, junctional or ventricular conducting tissue is
    increased, an abnormal rhythm may occur. This phenomenon is called ‘enhanced automaticity’. Single
    early beats, or extrasystoles, may be due to enhanced
    automaticity arising from a myocardial focus. The
    most common example of a sustained rhythm due to
    enhanced automaticity is ‘accelerated idioventricular
    rhythm’, which is common after acute myocardial
    infarction. The ECG appearance (Fig. 3.1) resembles
    that of a slow ventricular tachycardia, and that is the
    old-fashioned name for this condition. This rhythm
    causes no symptoms, and should not be treated.
    If the junctional intrinsic frequency is increased to
    a point at which it approximates to that of the SA
    node, an ‘accelerated idionodal rhythm’ results. This
    may appear to ‘overtake’ the P waves (Fig. 3.2). This
    rhythm used to be called a ‘wandering pacemaker’.
    The term ‘focal junctional tachycardia’ is used in the
    (probably rare) instances of a supraventricular tachycardia originating around the AV node, by mechanisms other than re-entry.
    Enhanced automaticity is also thought to be the
    mechanism causing some non-paroxysmal tachycardias, particularly those due to digoxin intoxication.
    
    Enhanced automaticity and triggered activity
    
    3
    
    Table 3.1 Physical signs and arrhythmias
    Pulse
    
    Heart rate (beats/min)
    
    Possible nature of any arrhythmia
    
    < 50
    
    Sinus bradycardia
    Second or third degree block
    Atrial flutter with 3 : 1 or 4 : 1 block
    Idionodal rhythm (junctional escape), with or without
    sick sinus syndrome
    Probable sinus rhythm
    Sinus tachycardia or an arrhythmia
    Probable atrial flutter with 2 : 1 block
    Atrial tachycardia
    Atrioventricular re-entry tachycardia (AVRT)
    Atrioventricular nodal re-entry tachycardia (AVNRT;
    junctional (nodal) tachycardia)
    Ventricular tachycardia
    Probable ventricular tachycardia
    Atrial flutter with 1 : 1 conduction
    
    Arterial pulse
    Regular
    
    60–140
    140–160
    150
    140–170
    
    > 180
    300
    Irregular
    
    Marked sinus arrhythmia
    Extrasystoles (supraventricular or ventricular)
    Atrial fibrillation
    Atrial flutter with variable block
    Rhythm varying between sinus rhythm and any
    arrhythmia or conduction defect
    
    Jugular venous pulse
    More pulsations visible than heart rate
    
    Second or third degree block
    Cannon waves – third degree block
    
    Fig. 3.1
    
    Accelerated idioventricular rhythm
    
    Note
    
    • After two sinus beats, there are four beats of ventricular
    origin with a rate of 75/min
    
    • Sinus rhythm is then restored
    
    103
    
    The ECG when the patient has a tachycardia
    Fig. 3.2
    
    Accelerated idionodal rhythm
    
    Note
    
    • After three sinus beats, the sinus rate slows slightly
    • A nodal rhythm appears and ‘overtakes’ the P waves
    
    Fig. 3.3
    
    I
    
    VR
    
    V1
    
    V4
    
    II
    
    VL
    
    V2
    
    V5
    
    III
    
    VF
    
    V3
    
    V6
    
    II
    
    104
    
    Abnormalities of cardiac rhythm due to re-entry
    
    3
    
    Fig. 3.4
    
    Re-entry pathways in the pre-excitation syndromes
    The Wolff–Parkinson–White
    syndrome type A
    
    The Lown–Ganong–Levine
    syndrome
    
    LA
    RA
    
    LA
    LV
    
    RA
    
    LV
    Note
    
    RV
    
    RV
    
    • Broken lines indicate the
    potential re-entry pathways in
    AVRT
    
    Right ventricular outflow tract ventricular
    tachycardia (RVOT-VT)
    Note
    Broad complex tachycardia
    Left bundle branch block and right axis deviation,
    typical of RVOT-VT
    
    •
    •
    
    ‘Triggered activity’ results from late depolarizations
    which occur after normal depolarization, during what
    would normally be a period of repolarization. Like
    enhanced automaticity, this can cause extrasystoles or
    a sustained a