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  • 1. ABC OFCLINICAL ELECTRO- CARDIOGRAPHY FRANCIS MORRIS JUNE EDHOUSE WILLIAM J BRADY JOHN CAMM BMJ Books
  • 2. ABC OFCLINICAL ELECTROCARDIOGRAPHY
  • 3. ABC OFCLINICAL ELECTROCARDIOGRAPHY Edited by FRANCIS MORRIS Consultant in Emergency Medicine, Northern General Hospital, Sheffield JUNE EDHOUSE Consultant in Emergency Medicine, Stepping Hill Hospital, Stockport WILLIAM J BRADY Associate Professor, Programme Director, and Vice Chair, Department of Emergency Medicine, University of Virginia, Charlottesville, VA, USA and JOHN CAMM Professor of Clinical Cardiology, St George’s Hospital Medical School, London
  • 4. © BMJ Publishing Group 2003All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording and/or otherwise, without the prior written permission of the publishers. First published in 2003 by BMJ Books, BMA House, Tavistock Square, London WC1H 9JR www.bmjbooks.com British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library ISBN 0 7279 1536 3 Typeset by BMJ Electronic Production Printed and bound in Spain by GraphyCems, Navarra Cover image depicts a chest x ray and electrocardiogram traceComposite image of an electrocardiogram trace showing termination of atrioventricular nodal re-entrant tachycardia, overlaid onto a false-coloured chest x ray With permission from Sheila Terry/Science Photo Library
  • 5. Contents Contributors vi Preface vii1 Introduction. I—Leads, rate, rhythm, and cardiac axis 1 Steve Meek, Francis Morris2 Introduction. II—Basic terminology 5 Steve Meek, Francis Morris3 Bradycardias and atrioventricular conduction block 9 David Da Costa, William J Brady, June Edhouse4 Atrial arrhythmias 13 Steve Goodacre, Richard Irons5 Junctional tachycardias 17 Demas Esberger, Sallyann Jones, Francis Morris6 Broad complex tachycardia—Part I 21 June Edhouse, Francis Morris7 Broad complex tachycardia—Part II 25 June Edhouse, Francis Morris8 Acute myocardial infarction—Part I 29 Francis Morris, William J Brady9 Acute myocardial infarction—Part II 33 June Edhouse, William J Brady, Francis Morris10 Myocardial ischaemia 37 Kevin Channer, Francis Morris11 Exercise tolerance testing 41 Jonathan Hill, Adam Timmis12 Conditions affecting the right side of the heart 45 Richard A Harrigan, Kevin Jones13 Conditions affecting the left side of the heart 49 June Edhouse, R K Thakur, Jihad M Khalil14 Conditions not primarily affecting the heart 53 Corey Slovis, Richard Jenkins15 Paediatric electrocardiography 57 Steve Goodacre, Karen McLeod16 Cardiac arrest rhythms 61 Robert French, Daniel DeBehnke, Stephen Hawes17 Pacemakers and electrocardiography 66 Richard Harper, Francis Morris18 Pericarditis, myocarditis, drug effects, and congenital heart disease 70 Chris A Ghammaghami, Jennifer H Lindsey Index 75 v
  • 6. ContributorsWilliam J Brady Jonathan HillAssociate Professor, Programme Director, and Vice Chair, Specialist Registrar in Cardiology, Barts and the LondonDepartment of Emergency Medicine, University of Virginia, NHS TrustCharlottesville, VA, USA Richard IronsKevin Channer Consultant in Accident and Emergency Medicine, Princess ofConsultant Cardiologist, Royal Hallamshire Hospital, Sheffield Wales Hospital, BridgendDavid Da Costa Richard JenkinsConsultant Physician, Northern General Hospital, Sheffield Specialist Registrar in General Medicine and Endocrinology, Northern General Hospital, SheffieldDaniel De BehnkeDepartment of Emergency Medicine, Medical College of Kevin JonesWisconsin, Milwaukee, WI, USA Consultant Chest Physician, Bolton Royal HospitalJune Edhouse Sallyann JonesConsultant in Emergency Medicine, Stepping Hill Hospital, Specialist Registrar in Accident and Emergency Medicine,Stockport Queen’s Medical Centre, NottinghamDemas Esberger Jihad M KhalilConsultant in Accident and Emergency Medicine, Queen’s Thoracic and Cardiovascular Institute, Michigan StateMedical Centre, Nottingham University, Lancing, MI, USARobert French Jennifer H LindseyDepartment of Emergency Medicine, Medical College of Fellow, Division of Cardiology, Department of Pediatrics,Wisconsin, Milwaukee, WI, USA University of Virginia Health System, Charlottesville, VA, USAChris A Ghammaghami Karen McLeodAssistant Professor of Emergency and Internal Medicine, Consultant Paediatric Cardiologist, Royal Hospital forDirector, Chest Pain Centre, Department of Emergency Sick Children, GlasgowMedicine, University of Virginia Health System, Charlottesville,VA, USA Steve Meek Consultant in Emergency Medicine, Royal United Hospitals,Steve Goodacre BathHealth Services Research Fellow, Accident and EmergencyDepartment, Northern General Hospital, Sheffield Francis Morris Consultant in Emergency Medicine, Northern GeneralRichard Harper Hospital, SheffieldAssistant Professor, Department of Emergency Medicine,Oregon Health and Science University, Portland, Corey SlovisOregon, USA Professor of Emergency Medicine and Medicine, Vanderbilt University Medical Center, Department of EmergencyRichard A Harrigan Medicine, Nashville, TN, USAAssociate Professor of Emergency Medicine, Temple UniversitySchool of Medicine, Associate Research Director, Division of R K ThakurEmergency Medicine, Temple University Hospital, Professor of Medicine, Thoracic and Cardiovascular Institute,Philadelphia, PA, USA Michigan State University, Lancing, MI, USAStephen Hawes Adam TimmisDepartment of Emergency Medicine, Wythenshaw Hospital, Consultant Cardiologist, London Chest Hospital, Barts and theManchester London NHS Trustvi
  • 7. PrefaceTo my mind electrocardiogram interpretation is all about pattern recognition. This collection of 18 articles covers all the importantpatterns encountered in emergency medicine. Whether you are a novice or an experienced clinician, I hope that you find this bookenjoyable and clinically relevant. Francis Morris Sheffield 2002 vii
  • 8. 1 Introduction. I—Leads, rate, rhythm, and cardiac axisSteve Meek, Francis MorrisElectrocardiography is a fundamental part of cardiovascularassessment. It is an essential tool for investigating cardiacarrhythmias and is also useful in diagnosing cardiac disorderssuch as myocardial infarction. Familiarity with the wide range ofpatterns seen in the electrocardiograms of normal subjects andan understanding of the effects of non-cardiac disorders on thetrace are prerequisites to accurate interpretation. The contraction and relaxation of cardiac muscle resultsfrom the depolarisation and repolarisation of myocardial cells. Sinoatrial node Electrically inertThese electrical changes are recorded via electrodes placed on atrioventricular Left regionthe limbs and chest wall and are transcribed on to graph paper Right atriumto produce an electrocardiogram (commonly known as an atriumECG). Left bundle branch The sinoatrial node acts as a natural pacemaker and initiates Atrioventricular nodeatrial depolarisation. The impulse is propagated to the Left Left anterior Right hemifascicleventricles by the atrioventricular node and spreads in a ventricle ventriclecoordinated fashion throughout the ventricles via thespecialised conducting tissue of the His-Purkinje system. Thus,after delay in the atrioventricular mode, atrial contraction is Left posteriorfollowed by rapid and coordinated contraction of the ventricles. hemifascicle The electrocardiogram is recorded on to standard paper Right bundle branchtravelling at a rate of 25 mm/s. The paper is divided into largesquares, each measuring 5 mm wide and equivalent to 0.2 s. The His-Purkinje conduction systemEach large square is five small squares in width, and each smallsquare is 1 mm wide and equivalent to 0.04 s. Throughout this article the duration of waveforms will be expressed as 0.04 s = 1 mm = 1 small square Speed : 25 mm/s Gain : 10 mm/mVStandard calibration signal V5 The electrical activity detected by the electrocardiogrammachine is measured in millivolts. Machines are calibrated sothat a signal with an amplitude of 1 mV moves the recordingstylus vertically 1 cm. Throughout this text, the amplitude ofwaveforms will be expressed as: 0.1 mV = 1 mm = 1 smallsquare. The amplitude of the waveform recorded in any lead maybe influenced by the myocardial mass, the net vector ofdepolarisation, the thickness and properties of the interveningtissues, and the distance between the electrode and themyocardium. Patients with ventricular hypertrophy have arelatively large myocardial mass and are therefore likely to have V5high amplitude waveforms. In the presence of pericardial fluid,pulmonary emphysema, or obesity, there is increased resistanceto current flow, and thus waveform amplitude is reduced. The direction of the deflection on the electrocardiogramdepends on whether the electrical impulse is travelling towardsor away from a detecting electrode. By convention, an electrical Role of body habitus and disease on the amplitude of the QRS complex.impulse travelling directly towards the electrode produces an Top: Low amplitude complexes in an obese woman with hypothyroidism.upright (“positive”) deflection relative to the isoelectric baseline, Bottom: High amplitude complexes in a hypertensive manwhereas an impulse moving directly away from an electrodeproduces a downward (“negative”) deflection relative to the 1
  • 9. ABC of Clinical Electrocardiographybaseline. When the wave of depolarisation is at right angles tothe lead, an equiphasic deflection is produced. The six chest leads (V1 to V6) “view” the heart in thehorizontal plane. The information from the limb electrodes iscombined to produce the six limb leads (I, II, III, aVR, aVL, andaVF), which view the heart in the vertical plane. Theinformation from these 12 leads is combined to form astandard electrocardiogram. Wave of depolarisation Wave of depolarisation. Shape of QRS complex in any lead depends on orientation of that lead to vector of depolarisation V1 V2 V3 V6 aVR aVL V4 V5Position of the six chest electrodes for standard 12 leadelectrocardiography. V1: right sternal edge, 4th intercostal Ispace; V2: left sternal edge, 4th intercostal space; V3:between V2 and V4; V4: mid-clavicular line, 5th space; V5: V6anterior axillary line, horizontally in line with V4; V6:mid-axillary line, horizontally in line with V4 V5 V1 V2 V3 V4 The arrangement of the leads produces the followinganatomical relationships: leads II, III, and aVF view the inferiorsurface of the heart; leads V1 to V4 view the anterior surface;leads I, aVL, V5, and V6 view the lateral surface; and leads V1 III aVF IIand aVR look through the right atrium directly into the cavityof the left ventricle. Vertical and horizontal perspective of the leads. The limb leads “view” the heart in the vertical plane and the chest leads in the horizontal planeRateThe term tachycardia is used to describe a heart rate greater Anatomical relations of leads in a standard 12 leadthan 100 beats/min. A bradycardia is defined as a rate less than electrocardiogram60 beats/min (or < 50 beats/min during sleep). II, III, and aVF: inferior surface of the heart One large square of recording paper is equivalent to 0.2 V1 to V4: anterior surfaceseconds; there are five large squares per second and 300 per I, aVL, V5, and V6: lateral surfaceminute. Thus when the rhythm is regular and the paper speed V1 and aVR: right atrium and cavity of left ventricleis running at the standard rate of 25 mm/s, the heart rate canbe calculated by counting the number of large squares betweentwo consecutive R waves, and dividing this number into 300.Alternatively, the number of small squares between twoconsecutive R waves may be divided into 1500. Waveforms mentioned in this article (for Some countries use a paper speed of 50 mm/s as standard; example, QRS complex, R wave, P wave)the heart rate is calculated by dividing the number of large are explained in the next articlesquares between R waves into 600, or the number of smallsquares into 3000. “Rate rulers” are sometimes used to calculate heart rate;these are used to measure two or three consecutive R-R IIintervals, of which the average is expressed as the rateequivalent. When using a rate ruler, take care to use the correct scaleaccording to paper speed (25 or 50 mm/s); count the correctnumbers of beats (for example, two or three); and restrict thetechnique to regular rhythms. When an irregular rhythm is present, the heart rate may be Regular rhythm: the R-R interval is two large squares. The rate is 150calculated from the rhythm strip (see next section). It takes one beats/min (300/2=150)2
  • 10. Introduction. I—Leads, rate, rhythm, and cardiac axissecond to record 2.5 cm of trace. The heart rate per minute canbe calculated by counting the number of intervals between QRScomplexes in 10 seconds (namely, 25 cm of recording paper)and multiplying by six.A standard rhythm strip is 25 cm long (that is, 10 seconds). The rate in this strip (showing an irregular rhythm with 21 intervals) is therefore126 beats/min (6×21). Scale is slightly reduced hereRhythmTo assess the cardiac rhythm accurately, a prolonged recordingfrom one lead is used to provide a rhythm strip. Lead II, whichusually gives a good view of the P wave, is most commonly used Cardinal features of sinus rhythmto record the rhythm strip. x The P wave is upright in leads I and II The term “sinus rhythm” is used when the rhythm originates x Each P wave is usually followed by a QRS complexin the sinus node and conducts to the ventricles. x The heart rate is 60-99 beats/min Young, athletic people may display various other rhythms,particularly during sleep. Sinus arrhythmia is the variation inthe heart rate that occurs during inspiration and expiration.There is “beat to beat” variation in the R-R interval, the rateincreasing with inspiration. It is a vagally mediated response tothe increased volume of blood returning to the heart during Normal findings in healthy individualsinspiration. x Tall R waves x Prominent U waves x ST segment elevation (high-take off, benign early repolarisation)Cardiac axis x Exaggerated sinus arrhythmia x Sinus bradycardiaThe cardiac axis refers to the mean direction of the wave of x Wandering atrial pacemakerventricular depolarisation in the vertical plane, measured from x Wenckebach phenomenona zero reference point. The zero reference point looks at the x Junctional rhythmheart from the same viewpoint as lead I. An axis lying above x 1st degree heart blockthis line is given a negative number, and an axis lying below theline is given a positive number. Theoretically, the cardiac axismay lie anywhere between 180 and − 180°. The normal rangefor the cardiac axis is between − 30° and 90°. An axis lyingbeyond − 30° is termed left axis deviation, whereas an axis > 90° is termed right axis deviation. -90˚ -120˚ -60˚ Conditions for which determination of the axis is helpful in -150˚ -30˚ diagnosis aVR aVL x Conduction defects—for example, left anterior hemiblock x Ventricular enlargement—for example, right ventricular hypertrophy 180˚ 0˚ I x Broad complex tachycardia—for example, bizarre axis suggestive of ventricular origin x Congenital heart disease—for example, atrial septal defects x Pre-excited conduction—for example, Wolff-Parkinson-White 150˚ 30˚ syndrome x Pulmonary embolus 120˚ 60˚ III II 90˚ aVFHexaxial diagram (projection of six leads in verticalplane) showing each lead’s view of the heart 3
  • 11. ABC of Clinical Electrocardiography Several methods can be used to calculate the cardiac axis, I aVRthough occasionally it can prove extremely difficult todetermine. The simplest method is by inspection of leads I, II,and III.Calculating the cardiac axis Right axis Left axis Normal axis deviation deviationLead I Positive Negative Positive II aVLLead II Positive Positive or Negative negativeLead III Positive or Positive Negative negative A more accurate estimate of the axis can be achieved if all III aVFsix limb leads are examined. The hexaxial diagram shows eachlead’s view of the heart in the vertical plane. The direction ofcurrent flow is towards leads with a positive deflection, awayfrom leads with a negative deflection, and at 90° to a lead withan equiphasic QRS complex. The axis is determined as follows:x Choose the limb lead closest to being equiphasic. The axislies about 90° to the right or left of this lead Determination of cardiac axis using the hexaxial diagram (see previousx With reference to the hexaxial diagram, inspect the QRS page). Lead II (60°) is almost equiphasic and therefore the axis lies at 90° tocomplexes in the leads adjacent to the equiphasic lead. If the this lead (that is 150° to the right or −30° to the left). Examination of the adjacent leads (leads I and III) shows that lead I is positive. The cardiac axislead to the left side is positive, then the axis is 90° to the therefore lies at about −30°equiphasic lead towards the left. If the lead to the right side ispositive, then the axis is 90° to the equiphasic lead towards theright.4
  • 12. 2 Introduction. II—Basic terminologySteve Meek, Francis MorrisThis article explains the genesis of and normal values for theindividual components of the wave forms that are seen in anelectrocardiogram. To recognise electrocardiographicabnormalities the range of normal wave patterns must beunderstood.P wave P waveThe sinoatrial node lies high in the wall of the right atrium andinitiates atrial depolarisation, producing the P wave on theelectrocardiogram. Although the atria are anatomically twodistinct chambers, electrically they act almost as one. They haverelatively little muscle and generate a single, small P wave. Pwave amplitude rarely exceeds two and a half small squares Complex showing P wave highlighted(0.25 mV). The duration of the P wave should not exceed threesmall squares (0.12 s). The wave of depolarisation is directed inferiorly andtowards the left, and thus the P wave tends to be upright inleads I and II and inverted in lead aVR. Sinus P waves areusually most prominently seen in leads II and V1. A negative Pwave in lead I may be due to incorrect recording of theelectrocardiogram (that is, with transposition of the left and Right atriumright arm electrodes), dextrocardia, or abnormal atrial rhythms. I Sinoatrial node Wave of depolarisation Atrioventricular node Left atrium Atrial depolarisation gives rise to the P wave II Characteristics of the P waveP waves are usually more obvious in lead II than in lead I x Positive in leads I and II x Best seen in leads II and V1 The P wave in V1 is often biphasic. Early right atrial forces x Commonly biphasic in lead V1are directed anteriorly, giving rise to an initial positive x < 3 small squares in durationdeflection; these are followed by left atrial forces travelling x < 2.5 small squares in amplitudeposteriorly, producing a later negative deflection. A largenegative deflection (area of more than one small square)suggests left atrial enlargement. Normal P waves may have a slight notch, particularly in theprecordial (chest) leads. Bifid P waves result from slight Rasynchrony between right and left atrial depolarisation. Apronounced notch with a peak-to-peak interval of > 1 mm(0.04 s) is usually pathological, and is seen in association with aleft atrial abnormality—for example, in mitral stenosis. PR segmentPR interval P T UAfter the P wave there is a brief return to the isoelectric line,resulting in the “PR segment.” During this time the electricalimpulse is conducted through the atrioventricular node, the Q PR intervalbundle of His and bundle branches, and the Purkinje fibres. S The PR interval is the time between the onset of atrialdepolarisation and the onset of ventricular depolarisation, and Normal duration of PR interval is 0.12-0.20 s (three to five small squares) 5
  • 13. ABC of Clinical Electrocardiographyit is measured from the beginning of the P wave to the first Nomenclature in QRS complexesdeflection of the QRS complex (see next section), whether this Q wave: Any initial negative deflectionbe a Q wave or an R wave. The normal duration of the PR R wave: Any positive deflectioninterval is three to five small squares (0.12-0.20 s). S wave: Any negative deflection after an R waveAbnormalities of the conducting system may lead totransmission delays, prolonging the PR interval. Non-pathological Q waves are oftenQRS complex present in leads I, III, aVL, V5, and V6The QRS complex represents the electrical forces generated byventricular depolarisation. With normal intraventricularconduction, depolarisation occurs in an efficient, rapid fashion.The duration of the QRS complex is measured in the lead withthe widest complex and should not exceed two and a half smallsquares (0.10 s). Delays in ventricular depolarisation—for R waveexample, bundle branch block—give rise to abnormally wideQRS complexes (>0.12 s). The depolarisation wave travels through the interventricularseptum via the bundle of His and bundle branches and reachesthe ventricular myocardium via the Purkinje fibre network. Theleft side of the septum depolarises first, and the impulse thenspreads towards the right. Lead V1 lies immediately to the right Q waveof the septum and thus registers an initial small positive S wavedeflection (R wave) as the depolarisation wave travels towardsthis lead. Composition of QRS complex When the wave of septal depolarisation travels away fromthe recording electrode, the first deflection inscribed is negative.Thus small “septal” Q waves are often present in the lateralleads, usually leads I, aVL, V5, and V6. These non-pathological Q waves are less than two smallsquares deep and less than one small square wide, and shouldbe < 25% of the amplitude of the corresponding R wave. The wave of depolarisation reaches the endocardium at theapex of the ventricles, and then travels to the epicardium,spreading outwards in all directions. Depolarisation of the right Sinoatrial nodeand left ventricles produces opposing electrical vectors, but theleft ventricle has the larger muscle mass and its depolarisation Left Right atriumdominates the electrocardiogram. atrium In the precordial leads, QRS morphology changes Atrioventricular nodedepending on whether the depolarisation forces are moving Righttowards or away from a lead. The forces generated by the free ventriclewall of the left ventricle predominate, and therefore in lead V1 a Left ventriclesmall R wave is followed by a large negative deflection (S wave).The R wave in the precordial leads steadily increases inamplitude from lead V1 to V6, with a corresponding decreasein S wave depth, culminating in a predominantly positivecomplex in V6. Thus, the QRS complex gradually changes frombeing predominantly negative in lead V1 to beingpredominantly positive in lead V6. The lead with an equiphasic Wave of depolarisation spreading throughout ventricles gives rise to QRSQRS complex is located over the transition zone; this lies complexbetween leads V3 and V4, but shifts towards the left with age. The height of the R wave is variable and increasesprogressively across the precordial leads; it is usually < 27 mmin leads V5 and V6. The R wave in lead V6, however, is often Transitional zonesmaller than the R wave in V5, since the V6 electrode is furtherfrom the left ventricle. The S wave is deepest in the right precordial leads; itdecreases in amplitude across the precordium, and is oftenabsent in leads V5 and V6. The depth of the S wave should notexceed 30 mm in a normal individual, although S waves and R V1 V2 V3 V4 V5 V6waves > 30 mm are occasionally recorded in normal youngmale adults. Typical change in morphology of QRS complex from leads V1 to V66
  • 14. Introduction. II—Basic terminologyST segmentThe QRS complex terminates at the J point or ST junction. TheST segment lies between the J point and the beginning of the Twave, and represents the period between the end of ventriculardepolarisation and the beginning of repolarisation. The ST segment should be level with the subsequent “TP ST segment TP segmentsegment” and is normally fairly flat, though it may slopeupwards slightly before merging with the T wave. In leads V1 to V3 the rapidly ascending S wave mergesdirectly with the T wave, making the J point indistinct and theST segment difficult to identify. This produces elevation of the J pointST segment, and this is known as “high take-off.” Non-pathological elevation of the ST segment is also The ST segment should be in the same horizontal plane as the TP segment;associated with benign early repolarisation (see article on acute the J point is the point of inflection between the S wave and ST segmentmyocardial infarction later in the series), which is particularlycommon in young men, athletes, and black people. Interpretation of subtle abnormalities of the ST segment isone of the more difficult areas of clinical electrocardiography;nevertheless, any elevation or depression of the ST segmentmust be explained rather than dismissed. V2 V2 V4 V6 V3 Change in ST segment morphology across the precordial leads The T wave should generally be at least 1/8 but less than 2/3 of theComplexes in leads V2 and V3 showing high take-off amplitude of the corresponding R wave; T wave amplitude rarely exceeds 10 mmT waveVentricular repolarisation produces the T wave. The normal Twave is asymmetrical, the first half having a more gradual slopethan the second half. T wave orientation usually corresponds with that of theQRS complex, and thus is inverted in lead aVR, and may beinverted in lead III. T wave inversion in lead V1 is also common.It is occasionally accompanied by T wave inversion in lead V2,though isolated T wave inversion in lead V2 is abnormal. Twave inversion in two or more of the right precordial leads isknown as a persistent juvenile pattern; it is more common inblack people. The presence of symmetrical, inverted T waves is T wavehighly suggestive of myocardial ischaemia, though asymmetricalinverted T waves are frequently a non-specific finding. No widely accepted criteria exist regarding T waveamplitude. As a general rule, T wave amplitude correspondswith the amplitude of the preceding R wave, though the tallestT waves are seen in leads V3 and V4. Tall T waves may be seenin acute myocardial ischaemia and are a feature of Complex showing T wave highlightedhyperkalaemia. 7
  • 15. ABC of Clinical ElectrocardiographyQT intervalThe QT interval is measured from the beginning of the QRScomplex to the end of the T wave and represents the total timetaken for depolarisation and repolarisation of the ventricles. V1 aVL The QT interval is measured in lead V2 aVL as this lead does not have QT interval prominent U waves (diagram is scaled up) The QT interval lengthens as the heart rate slows, and thuswhen measuring the QT interval the rate must be taken intoaccount. As a general guide the QT interval should be 0.35-0.45 s, and should not be more than half of the interval betweenadjacent R waves (R-R interval). The QT interval increases V3slightly with age and tends to be longer in women than in men.Bazett’s correction is used to calculate the QT interval correctedfor heart rate (QTc): QTc = QT/√R-R (seconds). Prominent U waves can easily be mistaken for T waves, Obvious U waves in leads V1 to V3 in patient with hypokalaemialeading to overestimation of the QT interval. This mistake canbe avoided by identifying a lead where U waves are notprominent—for example, lead aVL.U waveThe U wave is a small deflection that follows the T wave. It isgenerally upright except in the aVR lead and is often mostprominent in leads V2 to V4. U waves result fromrepolarisation of the mid-myocardial cells—that is, thosebetween the endocardium and the epicardium—and theHis-Purkinje system. Many electrocardiograms have no discernible U waves.Prominent U waves may be found in athletes and are associatedwith hypokalaemia and hypercalcaemia.8
  • 16. 3 Bradycardias and atrioventricular conduction blockDavid Da Costa, William J Brady, June EdhouseBy arbitrary definition, a bradycardia is a heart rate of < 60beats/min. A bradycardia may be a normal physiological Many patients tolerate heart rates of 40 beats/min surprisingly well, but atphenomenon or result from a cardiac or non-cardiac disorder. lower rates symptoms are likely to include dizziness, near syncope, syncope, ischaemic chest pain, Stokes-AdamsSinus bradycardia attacks, and hypoxic seizuresSinus bradycardia is common in normal individuals duringsleep and in those with high vagal tone, such as athletes andyoung healthy adults. The electrocardiogram shows a P wavebefore every QRS complex, with a normal P wave axis (that is,upright P wave in lead II). The PR interval is at least 0.12 s. Pathological causes of sinus bradycardia The commonest pathological cause of sinus bradycardia is x Acute myocardial infarctionacute myocardial infarction. Sinus bradycardia is particularly x Drugs—for example, blockers, digoxin, amiodaroneassociated with inferior myocardial infarction as the inferior x Obstructive jaundice x Raised intracranial pressuremyocardial wall and the sinoatrial and atrioventricular nodes x Sick sinus syndromeare usually all supplied by the right coronary artery. x Hypothermia x HypothyroidismSick sinus syndromeSick sinus syndrome is the result of dysfunction of the sinoatrialnode, with impairment of its ability to generate and conductimpulses. It usually results from idiopathic fibrosis of the node Conditions associated with sinoatrial nodebut is also associated with myocardial ischaemia, digoxin, and dysfunctioncardiac surgery. x Age The possible electrocardiographic features include x Idiopathic fibrosispersistent sinus bradycardia, periods of sinoatrial block, sinus x Ischaemia, including myocardial infarction x High vagal tonearrest, junctional or ventricular escape rhythms, x Myocarditistachycardia-bradycardia syndrome, paroxysmal atrial flutter, and x Digoxin toxicityatrial fibrillation. The commonest electrocardiographic featureis an inappropriate, persistent, and often severe sinusbradycardia. Severe sinus bradycardia Sinoatrial block is characterised by a transient failure ofimpulse conduction to the atrial myocardium, resulting inintermittent pauses between P waves. The pauses are the lengthof two or more P-P intervals. Sinus arrest occurs when there is transient cessation ofimpulse formation at the sinoatrial node; it manifests as aprolonged pause without P wave activity. The pause is unrelatedto the length of the P-P cycle. Sinoatrial block (note the pause is twice the P-P interval) Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat 9
  • 17. ABC of Clinical Electrocardiography Escape rhythms are the result of spontaneous activity from a A junctional escape beat has a normal QRS complex shapesubsidiary pacemaker, located in the atria, atrioventricular with a rate of 40-60 beats/min. A ventricular escape rhythmjunction, or ventricles. They take over when normal impulse has broad complexes and is slow (15-40 beats/min)formation or conduction fails and may be associated with anyprofound bradycardia.Atrioventricular conduction block Tachycardia-bradycardia syndromeAtrioventricular conduction can be delayed, intermittently x Common in sick sinus syndrome x Characterised by bursts of atrial tachycardia interspersed withblocked, or completely blocked—classified correspondingly as periods of bradycardiafirst, second, or third degree block. x Paroxysmal atrial flutter or fibrillation may also occur, and cardioversion may be followed by a severe bradycardiaFirst degree blockIn first degree block there is a delay in conduction of the atrialimpulse to the ventricles, usually at the level of theatrioventricular node. This results in prolongation of the PR Causes of atrioventricular conduction blockinterval to > 0.2 s. A QRS complex follows each P wave, and the x Myocardial ischaemia or infarctionPR interval remains constant. x Degeneration of the His-Purkinje system x Infection—for example, Lyme disease, diphtheria x Immunological disorders—for example, systemic lupusSecond degree block erythematosusIn second degree block there is intermittent failure of x Surgeryconduction between the atria and ventricles. Some P waves are x Congenital disordersnot followed by a QRS complex. There are three types of second degree block. Mobitz type Iblock (Wenckebach phenomenon) is usually at the level of the V2atrioventricular node, producing intermittent failure oftransmission of the atrial impulse to the ventricles. The initialPR interval is normal but progressively lengthens with each First degreesuccessive beat until eventually atrioventricular transmission is heart (atrioventricular)blocked completely and the P wave is not followed by a QRS blockcomplex. The PR interval then returns to normal, and the cyclerepeats. Mobitz type II block is less common but is more likely toproduce symptoms. There is intermittent failure of conductionof P waves. The PR interval is constant, though it may benormal or prolonged. The block is often at the level of thebundle branches and is therefore associated with wide QRScomplexes. 2:1 atrioventricular block is difficult to classify, but itis usually a Wenckebach variant. High degree atrioventricular Mobitz type I block (Wenckebach phenomenon)block, which occurs when a QRS complex is seen only afterevery three, four, or more P waves, may progress to completethird degree atrioventricular block.Third degree blockIn third degree block there is complete failure of conductionbetween the atria and ventricles, with complete independence ofatrial and ventricular contractions. The P waves bear no relation Mobitz type II block—a complication of an inferior myocardial infarction.to the QRS complexes and usually proceed at a faster rate. The PR interval is identical before and after the P wave that is not conductedThird degree heart block. A pacemaker in the bundle of His produces a narrow QRS complex (top), whereas more distal pacemakers tend to producebroader complexes (bottom). Arrows show P waves10
  • 18. Bradycardias and atrioventricular conduction block A subsidiary pacemaker triggers ventricular contractions, Conditions associated with right bundle branch blockthough occasionally no escape rhythm occurs and asystolicarrest ensues. The rate and QRS morphology of the escape x Rheumatic heart disease x Cor pulmonale/right ventricular hypertrophyrhythm vary depending on the site of the pacemaker. x Myocarditis or cardiomyopathy x Ischaemic heart disease x Degenerative disease of the conduction systemBundle branch block and fascicular x Pulmonary embolusblock x Congenital heart disease—for example, in atrial septal defectsThe bundle of His divides into the right and left bundlebranches. The left bundle branch then splits into anterior andposterior hemifascicles. Conduction blocks in any of thesestructures produce characteristic electrocardiographic changes.Right bundle branch blockIn most cases right bundle branch block has a pathologicalcause though it is also seen in healthy individuals. When conduction in the right bundle branch is blocked,depolarisation of the right ventricle is delayed. The left ventricle Sinoatrial nodedepolarises in the normal way and thus the early part of theQRS complex appears normal. The wave of depolarisation then Leftspreads to the right ventricle through non-specialised Right atriumconducting tissue, with slow depolarisation of the right ventricle atriumin a left to right direction. As left ventricular depolarisation is Atrioventricular nodecomplete, the forces of right ventricular depolarisation areunopposed. Thus the later part of the QRS complex is Left Right ventricleabnormal; the right precordial leads have a prominent and late ventricleR wave, and the left precordial and limb leads have a terminal Swave. These terminal deflections are wide and slurred.Abnormal ventricular depolarisation is associated withsecondary repolarisation changes, giving rise to changes in theST-T waves in the right chest leads. Right bundle branch block, showing the wave of depolarisation spreading toDiagnostic criteria for right bundle branch block the right ventricle through non-specialised conducting tissuex QRS duration >0.12 sx A secondary R wave (R’) in V1 or V2x Wide slurred S wave in leads I, V5, and V6Associated featurex ST segment depression and T wave inversion in the right precordial I aVR V1 V4 leadsLeft bundle branch blockLeft bundle branch block is most commonly caused bycoronary artery disease, hypertensive heart disease, or dilatedcardiomyopathy. It is unusual for left bundle branch block toexist in the absence of organic disease. II aVL V2 V5 The left bundle branch is supplied by both the anteriordescending artery (a branch of the left coronary artery) and theright coronary artery. Thus patients who develop left bundlebranch block generally have extensive disease. This type ofblock is seen in 2-4% of patients with acute myocardialinfarction and is usually associated with anterior infarction. III aVF V3 V6Diagnostic criteria for left bundle branch blockx QRS duration of >0.12 sx Broad monophasic R wave in leads 1, V5, and V6x Absence of Q waves in leads V5 and V6Associated featuresx Displacement of ST segment and T wave in an opposite direction to the dominant deflection of the QRS complex (appropriate discordance)x Poor R wave progression in the chest leadsx RS complex, rather than monophasic complex, in leads V5 and V6x Left axis deviation—common but not invariable finding Right bundle branch block 11
  • 19. ABC of Clinical Electrocardiography In the normal heart, septal depolarisation proceeds from leftto right, producing Q waves in the left chest leads (septal Qwaves). In left bundle branch block the direction of depolarisationof the intraventricular septum is reversed; the septal Q waves arelost and replaced with R waves. The delay in left ventriculardepolarisation increases the duration of the QRS complex to > 0.12 s. Abnormal ventricular depolarisation leads to secondary Sinoatrial noderepolarisation changes. ST segment depression and T waveinversion are seen in leads with a dominant R wave. ST segment Left Right atriumelevation and positive T waves are seen in leads with a dominant atriumS wave. Thus there is discordance between the QRS complex andthe ST segment and T wave. Atrioventricular node LeftFascicular blocks Right ventricle ventricleBlock of the left anterior and posterior hemifascicles gives riseto the hemiblocks. Left anterior hemiblock is characterised by amean frontal plane axis more leftward than − 30° (abnormalleft axis deviation) in the absence of an inferior myocardialinfarction or other cause of left axis deviation. Left posteriorhemiblock is characterised by a mean frontal plane axis of > 90° in the absence of other causes of right axis deviation. Left bundle branch block, showing depolarisation spreading from the right Bifascicular block is the combination of right bundle branch to left ventricleblock and left anterior or posterior hemiblock. Theelectrocardiogram shows right bundle branch block with left orright axis deviation. Right bundle branch block with left I aVR V1 V4anterior hemiblock is the commonest type of bifascicular block.The left posterior fascicle is fairly stout and more resistant todamage, so right bundle branch block with left posteriorhemiblock is rarely seen. Trifascicular block is present when bifascicular block isassociated with first degree heart block. If conduction in thedysfunctional fascicle also fails completely, complete heart blockensues. I aVR V1 V4 II aVL V2 V5 II aVL V2 V5 III aVF V3 V6 III aVF V3 V6Trifascicular block (right bundle branch block, left anterior hemiblock, andfirst degree heart block) Left bundle branch block12
  • 20. 4 Atrial arrhythmiasSteve Goodacre, Richard IronsIn adults a tachycardia is any heart rate greater than 100 beats Supraventricular tachycardiasper minute. Supraventricular tachycardias may be divided intotwo distinct groups depending on whether they arise from the From the atria or sinoatrial nodeatria or the atrioventricular junction. This article will consider x Sinus tachycardia x Atrial fibrillationthose arising from the atria: sinus tachycardia, atrial fibrillation, x Atrial flutteratrial flutter, and atrial tachycardia. Tachycardias arising from x Atrial tachycardiare-entry circuits in the atrioventricular junction will be From the atrioventricular nodeconsidered in the next article in the series. x Atrioventricular re-entrant tachycardia x Atrioventricular nodal re-entrant tachycardiaClinical relevanceThe clinical importance of a tachycardia in an individual patientis related to the ventricular rate, the presence of any underlyingheart disease, and the integrity of cardiovascular reflexes. Electrocardiographic characteristics of atrial arrhythmiasCoronary blood flow occurs during diastole, and as the heart Sinus tachycardiarate increases diastole shortens. In the presence of coronary x P waves have normal morphologyatherosclerosis, blood flow may become critical and x Atrial rate 100-200 beats/min x Regular ventricular rhythmanginal-type chest pain may result. Similar chest pain, which is x Ventricular rate 100-200 beats/minnot related to myocardial ischaemia, may also occur. Reduced x One P wave precedes every QRS complexcardiac performance produces symptoms of faintness or Atrial tachycardiasyncope and leads to increased sympathetic stimulation, which x Abnormal P wave morphologymay increase the heart rate further. x Atrial rate 100-250 beats/min As a general rule the faster the ventricular rate, the more x Ventricular rhythm usually regularlikely the presence of symptoms—for example, chest pain, x Variable ventricular ratefaintness, and breathlessness. Urgent treatment is needed for Atrial flutterseverely symptomatic patients with a narrow complex x Undulating saw-toothed baseline F (flutter) wavestachycardia. x Atrial rate 250-350 beats/min x Regular ventricular rhythm x Ventricular rate typically 150 beats/min (with 2:1 atrioventricularElectrocardiographic features block) x 4:1 is also common (3:1 and 1:1 block uncommon)Differentiation between different types of supraventricular Atrial fibrillationtachycardia may be difficult, particularly when ventricular rates x P waves absent; oscillating baseline f (fibrillation) wavesexceed 150 beats/min. x Atrial rate 350-600 beats/min x Irregular ventricular rhythm Knowledge of the electrophysiology of these arrhythmias x Ventricular rate 100-180 beats/minwill assist correct identification. Evaluation of atrial activity onthe electrocardiogram is crucial in this process. Analysis of theventricular rate and rhythm may also be helpful, although thisrate will depend on the degree of atrioventricular block.Increasing atrioventricular block by manoeuvres such as carotidsinus massage or administration of intravenous adenosine may Electrocardiographic analysis shouldbe of diagnostic value as slowing the ventricular rate allows include measurement of the ventricularmore accurate visualisation of atrial activity. Such manoeuvres rate, assessment of the ventricularwill not usually stop the tachycardia, however, unless it is due to rhythm, identification of P F, or f waves , ,re-entry involving the atrioventricular node. measurement of the atrial rate, and establishment of the relation of P waves to the ventricular complexesSinus tachycardiaSinus tachycardia is usually a physiological response but may beprecipitated by sympathomimetic drugs or endocrinedisturbances. The rate rarely exceeds 200 beats/min in adults. The rateincreases gradually and may show beat to beat variation. Each Pwave is followed by a QRS complex. P wave morphology andaxis are normal, although the height of the P wave may increasewith the heart rate and the PR interval will shorten. With a fasttachycardia the P wave may become lost in the preceding Twave. Recognition of the underlying cause usually makesdiagnosis of sinus tachycardia easy. A persistent tachycardia in Sinus tachycardia 13
  • 21. ABC of Clinical Electrocardiographythe absence of an obvious underlying cause should prompt Causes of sinus tachycardiaconsideration of atrial flutter or atrial tachycardia. Rarely the sinus tachycardia may be due to a re-entry Physiological—Exertion, anxiety, pain Pathological—Fever, anaemia, hypovolaemia, hypoxiaphenomenon in the sinoatrial node. This is recognised by Endocrine—Thyrotoxicosisabrupt onset and termination, a very regular rate, and absence Pharmacological—Adrenaline as a result of phaeochromocytoma;of an underlying physiological stimulus. The salbutamol; alcohol, caffeineelectrocardiographic characteristics are otherwise identical. Therate is usually 130-140 beats/min, and vagal manoeuvres maybe successful in stopping the arrhythmia. Causes of atrial fibrillation x Ischaemic heart disease x Cardiomyopathy (dilated or x Hypertensive heart disease hypertrophic)Atrial fibrillation x Rheumatic heart disease x Sick sinus syndrome x Thyrotoxicosis x Post-cardiac surgeryThis is the most common sustained arrhythmia. Overall x Alcohol misuse (acute or x Chronic pulmonary diseaseprevalence is 1% to 1.5%, but prevalence increases with age, chronic) x Idiopathic (lone)affecting about 10% of people aged over 70. Causes are varied,although many cases are idiopathic. Prognosis is related to theunderlying cause; it is excellent when due to idiopathic atrialfibrillation and relatively poor when due to ischaemiccardiomyopathy. Right atrium Atrial fibrillation is caused by multiple re-entrant circuits or“wavelets” of activation sweeping around the atrial myocardium.These are often triggered by rapid firing foci. Atrial fibrillation Sinoatrial nodeis seen on the electrocardiogram as a wavy, irregular baselinemade up of f (fibrillation) waves discharging at a frequency of350 to 600 beats/min. The amplitude of these waves varies Left atrium Atrioventricular nodebetween leads but may be so coarse that they are mistaken forflutter waves. Atrial fibrillation is the result of multiple wavelets of depolarisation (shown Conduction of atrial impulses to the ventricles is variable by arrows) moving around the atria chaotically, rarely completing aand unpredictable. Only a few of the impulses transmit through re-entrant circuitthe atrioventricular node to produce an irregular ventricularresponse. This combination of absent P waves, fine baseline fwave oscillations, and irregular ventricular complexes ischaracteristic of atrial fibrillation. The ventricular rate dependson the degree of atrioventricular conduction, and with normalconduction it varies between 100 and 180 beats/min. Slowerrates suggest a higher degree of atrioventricular block or thepatient may be taking medication such as digoxin. Fast atrial fibrillation may be difficult to distinguish from Atrial fibrillation waves seen in lead V1 Rhythm strip in atrial fibrillationother tachycardias. The RR interval remains irregular, however,and the overall rate often fluctuates. Mapping R waves against apiece of paper or with calipers usually confirms the diagnosis. Atrial fibrillation may be paroxysmal, persistent, or Right atriumpermanent. It may be precipitated by an atrial extrasystole orresult from degeneration of other supraventricular tachycardias,particularly atrial tachycardia and/or flutter. Sinoatrial node Left atriumAtrial flutter Atrioventricular nodeAtrial flutter is due to a re-entry circuit in the right atrium withsecondary activation of the left atrium. This produces atrialcontractions at a rate of about 300 beats/min—seen on theelectrocardiogram as flutter (F) waves. These are broad andappear saw-toothed and are best seen in the inferior leads andin lead V1. The ventricular rate depends on conduction through the Atrial flutter is usually the result of a single re-entrant circuit in the rightatrioventricular node. Typically 2:1 block (atrial rate to atrium (top); atrial flutter showing obvious flutter waves (bottom)14
  • 22. Atrial arrhythmiasventricular rate) occurs, giving a ventricular rate of 150beats/min. Identification of a regular tachycardia with this rateshould prompt the diagnosis of atrial flutter. Thenon-conducting flutter waves are often mistaken for or mergedwith T waves and become apparent only if the block isincreased. Manoeuvres that induce transient atrioventricular Rhythm strip in atrial flutter (rate 150 beats/min)block may allow identification of flutter waves.Atrial flutter (rate 150 beats/min) with increasing block (flutter waves revealed after administration of adenosine)Atrial flutter with variable block The causes of atrial flutter are similar to those of atrialfibrillation, although idiopathic atrial flutter is uncommon. Itmay convert into atrial fibrillation over time or, afteradministration of drugs such as digoxin.Atrial tachycardiaAtrial tachycardia typically arises from an ectopic source in theatrial muscle and produces an atrial rate of 150-250beats/min—slower than that of atrial flutter. The P waves may beabnormally shaped depending on the site of the ectopicpacemaker. Right atrium Sinoatrial node Atrioventricular node Left atrium Atrial tachycardia is initiated by an ectopic atrial focus (the P wave morphology therefore differs from that of sinus rhythm)Atrial tachycardia with 2:1 block (note the inverted P waves) The ventricular rate depends on the degree ofatrioventricular block, but when 1:1 conduction occurs a rapidventricular response may result. Increasing the degree of block Types of atrial tachycardiawith carotid sinus massage or adenosine may aid the diagnosis. x Benign There are four commonly recognised types of atrial x Incessant ectopictachycardia. Benign atrial tachycardia is a common arrhythmia x Multifocalin elderly people. It is paroxysmal in nature, has an atrial rate of x Atrial tachycardia with block (digoxin toxicity)80-140 beats/min and an abrupt onset and cessation, and isbrief in duration. 15
  • 23. ABC of Clinical Electrocardiography Incessant ectopic atrial tachycardia is a rare chronicarrhythmia in children and young adults. The rate depends onthe underlying sympathetic tone and is characteristically100-160 beats/min. It can be difficult to distinguish from a sinustachycardia. Diagnosis is important as it may lead to dilatedcardiomyopathy if left untreated. Multifocal atrial tachycardia occurs when multiple sites inthe atria are discharging and is due to increased automaticity. It Multifocal atrial tachycardiais characterised by P waves of varying morphologies and PRintervals of different lengths on the electrocardiographic trace.The ventricular rate is irregular. It can be distinguished fromatrial fibrillation by an isoelectric baseline between the P waves. Conditions associated with atrial tachycardiaIt is typically seen in association with chronic pulmonary x Cardiomyopathydisease. Other causes include hypoxia or digoxin toxicity. x Chronic obstructive pulmonary disease Atrial tachycardia with atrioventricular block is typically x Ischaemic heart diseaseseen with digoxin toxicity. The ventricular rhythm is usually x Rheumatic heart diseaseregular but may be irregular if atrioventricular block is variable. x Sick sinus syndrome x Digoxin toxicityAlthough often referred to as “paroxysmal atrial tachycardiawith block” this arrhythmia is usually sustained.Atrial tachycardia with 2:1 block in patient with digoxin toxicity16
  • 24. 5 Junctional tachycardiasDemas Esberger, Sallyann Jones, Francis MorrisAny tachyarrhythmia arising from the atria or theatrioventricular junction is a supraventricular tachycardia. Inclinical practice, however, the term supraventricular tachycardia Atrioventricular nodeis reserved for atrial tachycardias and arrhythmias arising fromthe region of the atrioventricular junction as a result of are-entry mechanism (junctional tachycardias). The most Slow Fastcommon junctional tachycardias are atrioventricular nodal pathway pathwayre-entrant tachycardia and atrioventricular re-entranttachycardia.Atrioventricular nodal re-entranttachycardia His bundleThis is the most common cause of paroxysmal regular narrowcomplex tachycardia. Affected individuals are usually young andhealthy with no organic heart disease.Mechanism Mechanism of atrioventricular nodal re-entrantIn atrioventricular nodal re-entrant tachycardia there are two tachycardia showing the slow and fast conduction routesfunctionally and anatomically different distinct pathways in the and the final common pathway through the lower partatrioventricular node, with different conduction velocities and of the atrioventricular node and bundle of Hisdifferent refractory periods. They share a final commonpathway through the lower part of the atrioventricular nodeand bundle of His. One pathway is relatively fast and has a longrefractory period; the other pathway is slow with a shortrefractory period. In sinus rhythm the atrial impulse is Atrialconducted through the fast pathway and depolarises the beat prematureventricles. The impulse also travels down the slow pathway butterminates because the final common pathway is refractory. The slow pathway has a short refractory period and recovers Slow Fast Slow Fast Circusfirst. An atrioventricular nodal re-entrant tachycardia is initiated, pathway pathway pathway motion pathwayfor example, if a premature atrial beat occurs at the criticalmoment when the fast pathway is still refractory. The impulse isconducted through the slow pathway and is then propagated ina retrograde fashion up the fast pathway, which has by nowrecovered from its refractory period. Thus a re-entry throughthe circuit is created. This type of “slow-fast” re-entry circuit is found in 90% ofpatients with atrioventricular nodal re-entrant tachycardia. Mostof the rest have a fast-slow circuit, in which the re-entranttachycardia is initiated by a premature ventricular contraction,and the impulse travels retrogradely up the slow pathway. Thisuncommon form of atrioventricular nodal re-entranttachycardia is often sustained for very long periods and is then A premature atrial impulse finds the fast pathway refractory, allowing conduction only down the slow pathway (left). By the time the impulseknown as permanent junctional re-entrant tachycardia and is reaches the His bundle, the fast pathway may have recovered, allowingrecognised by a long RP1 interval. retrograde conduction back up to the atria—the resultant “circus movement” gives rise to slow-fast atrioventricular nodal re-entrant tachycardia (right)Electrocardiographic findingsDuring sinus rhythm the electrocardiogram is normal. Duringthe tachycardia the rhythm is regular, with narrow QRScomplexes and a rate of 130-250 beats/min. Atrial conductionproceeds in a retrograde fashion producing inverted P waves inleads II, III, and aVF. However, since atrial and ventriculardepolarisation often occurs simultaneously, the P waves arefrequently buried in the QRS complex and may be totallyobscured. A P wave may be seen distorting the last part of theQRS complex giving rise to a “pseudo” S wave in the inferiorleads and a “pseudo” R wave in V1. An atrioventricular nodal re-entrant tachycardia 17
  • 25. ABC of Clinical Electrocardiography In the relatively uncommon fast-slow atrioventricular nodal Fast-slow atrioventricular nodal re-entrantre-entrant tachycardia, atrial depolarisation lags behind tachycardia is known as long RP1depolarisation of the ventricles, and inverted P waves may tachycardia, and it may be difficult tofollow the T wave and precede the next QRS complex. distinguish from an atrial tachycardiaTermination of atrioventricular nodal re-entrant tachycardiaClinical presentationEpisodes of atrioventricular nodal re-entrant tachycardia maybegin at any age. They tend to start and stop abruptly and canoccur spontaneously or be precipitated by simple movements.They can last a few seconds, several hours, or days. The Symptoms are commonest in patientsfrequency of episodes can vary between several a day, or one with a very rapid heart rate andepisode in a lifetime. Most patients have only mild symptoms, pre-existing heart diseasesuch as palpitations or the sensation that their heart is beatingrapidly. More severe symptoms include dizziness, dyspnoea,weakness, neck pulsation, and central chest pain. Some patientsreport polyuria.Atrioventricular re-entrant tachycardiaAtrioventricular re-entrant tachycardias occur as a result of an The commonest kind of atrioventricularanatomically distinct atrioventricular connection. This accessory re-entrant tachycardia occurs as part ofconduction pathway allows the atrial impulse to bypass the the Wolff-Parkinson-White syndromeatrioventricular node and activate the ventricles prematurely(ventricular pre-excitation). The presence of the accessorypathway allows a re-entry circuit to form and paroxysmalatrioventricular re-entrant tachycardias to occur.Wolff-Parkinson-White syndromeIn this syndrome an accessory pathway (the bundle of Kent)connects the atria directly to the ventricles. It results from afailure of complete separation of the atria and ventricles duringfetal development. The pathway can be situated anywhere around the groove Bundlebetween the atria and ventricles, and in 10% of cases more than of Kentone accessory pathway exists. The accessory pathway allows the In theformation of a re-entry circuit, which may give rise to either a Wolff-Parkinson-White Early activation syndrome the bundle ofnarrow or a broad complex tachycardia, depending on whether of the ventricle Kent provides a separatethe atrioventricular node or the accessory pathway is used for electrical conduit betweenantegrade conduction. the atria and the ventriclesElectrocardiographic featuresIn sinus rhythm the atrial impulse conducts over the accessorypathway without the delay encountered with atrioventricularnodal conduction. It is transmitted rapidly to the ventricularmyocardium, and consequently the PR interval is short.However, because the impulse enters non-specialisedmyocardium, ventricular depolarisation progresses slowly atfirst, distorting the early part of the R wave and producing thecharacteristic delta wave on the electrocardiogram. This slow In sinus rhythm conductiondepolarisation is then rapidly overtaken by depolarisation over the accessory pathwaypropagated by the normal conduction system, and the rest of gives rise to a short PRthe QRS complex appears relatively normal. interval and a delta wave18
  • 26. Junctional tachycardias Commonly, the accessory pathway is concealed—that is, it iscapable of conducting only in a retrograde fashion, from Classification of Wolff-Parkinson-White syndromeventricles to atria. During sinus rhythm pre-excitation does notoccur and the electrocardiogram is normal. Type A (dominant R wave in V1 lead) may be confused with: x Right bundle branch block Traditionally the Wolff-Parkinson-White syndrome has been x Right ventricular hypertrophyclassified into two types according to the electrocardiographic x Posterior myocardial infarctionmorphology of the precordial leads. In type A, the delta wave Type B (negative QRS complex in V1 lead) may be confused with:and QRS complex are predominantly upright in the precordial x Left bundle branch blockleads. The dominant R wave in lead V1 may be misinterpreted x Anterior myocardial infarctionas right bundle branch block. In type B, the delta wave and QRScomplex are predominantly negative in leads V1 and V2 andpositive in the other precordial leads, resembling left bundlebranch block. Type A V1 V2 V3 V4 V5 V6 Type B V1 V2 V3 V4 V5 V6Wolff-Parkinson-White, type A and type B, characterised by morphology of the recording from leads V1 to V6Mechanism of tachycardia formationOrthodromic atrioventricular re-entrant tachycardias accountfor most tachycardias in the Wolff-Parkinson-White syndrome.A premature atrial impulse is conducted down theatrioventricular node to the ventricles and then in a retrogradefashion via the accessory pathway back to the atria. The impulsethen circles repeatedly between the atria and ventricles,producing a narrow complex tachycardia. Since atrialdepolarisation lags behind ventricular depolarisation, P wavesfollow the QRS complexes. The delta wave is not observedduring the tachycardia, and the QRS complex is of normalduration. The rate is usually 140-250 beats/min. Mechanisms for orthodromic (left) and antidromic (right) atrioventricular re-entrant tachycardiaOrthodromic atrioventricular re-entrant tachycardia (left) showing clearly visible inverted P waves following the QRS complex, and antidromicatrioventricular re-entrant tachycardia (right) in the Wolff-Parkinson-White syndrome showing broad complexes 19
  • 27. ABC of Clinical Electrocardiography Antidromic atrioventricular re-entrant tachycardia isrelatively uncommon, occurring in about 10% of patients withthe Wolff-Parkinson-White syndrome. The accessory pathway Orthodromic atrioventricular re-entrant tachycardia occurs with antegrade conduction through the atrioventricularallows antegrade conduction, and thus the impulse is conducted nodefrom the atria to the ventricles via the accessory pathway.Depolarisation is propagated through non-specialised Antidromic atrioventricular re-entrant tachycardia occursmyocardium, and the resulting QRS complex is broad and with retrograde conduction through the atrioventricularbizarre. The impulse then travels in a retrograde fashion via the nodeatrioventricular node back to the atria.Atrial fibrillationIn patients without an accessory pathway the atrioventricularnode protects the ventricles from the rapid atrial activity that In some patients the accessory pathway allows very rapidoccurs during atrial fibrillation. In the Wolff-Parkinson-White conduction, and consequently very fast ventricular ratessyndrome the atrial impulses can be conducted via the accessory (in excess of 300 beats/min) may be seen, with thepathway, causing ventricular pre-excitation and producing broad associated risk of deterioration into ventricularQRS complexes with delta waves. Occasionally an impulse will be fibrillationconducted via the atrioventricular node and produce a normalQRS complex. The electrocardiogram has a characteristicappearance, showing a rapid, completely irregular broad complextachycardia but with occasional narrow complexes. Atrial fibrillation in the Wolff-Parkinson-White syndromeClinical presentationThe Wolff-Parkinson-White syndrome is sometimes anincidental electrocardiographic finding, but often patientspresent with tachyarrhythmias. Episodes tend to be morecommon in young people but may come and go through life.Patients may first present when they are old. When rapid arrhythmias occur in association with atrialfibrillation, patients may present with heart failure orhypotension. Drugs that block the atrioventricular node—forexample, digoxin, verapamil, and adenosine—may be dangerousin this situation and should be avoided. These drugs decreasethe refractoriness of accessory connections and increase thefrequency of conduction, resulting in a rapid ventricularresponse, which may precipitate ventricular fibrillation.20
  • 28. 6 Broad complex tachycardia—Part IJune Edhouse, Francis MorrisBroad complex tachycardias occur by various mechanisms and Varieties of broad complex tachycardiamay be ventricular or supraventricular in origin. In theemergency setting most broad complex tachycardias have a Ventricularventricular origin. However, an arrhythmia arising from the Regularatria or the atrioventricular junction will produce a broad x Monomorphic ventricular tachycardia x Fascicular tachycardiacomplex if associated with ventricular pre-excitation or bundle x Right ventricular outflow tract tachycardiabranch block. The causes of ventricular and supraventricular Irregulartachycardias are generally quite different, with widely differing x Torsades de pointes tachycardiaprognoses. Most importantly, the treatment of a broad complex x Polymorphic ventricular tachycardiatachycardia depends on the origin of the tachycardia. This Supraventriculararticle describes monomorphic ventricular tachycardias; other x Bundle branch block with aberrant conductionventricular tachycardias and supraventricular tachycardias will x Atrial tachycardia with pre-excitationbe described in the next article.TerminologyVentricular tachycardia is defined as three or more ventricularextrasystoles in succession at a rate of more than 120beats/min. The tachycardia may be self terminating but isdescribed as “sustained” if it lasts longer than 30 seconds. Theterm “accelerated idioventricular rhythm” refers to ventricularrhythms with rates of 100-120 beats/min. Ventricular tachycardia is described as “monomorphic” when the QRS complexes have the same general appearance, and “polymorphic” if there is wide beat to beat variation in QRS morphology. Monomorphic ventricular tachycardia is the commonest form of Non-sustained ventricular tachycardia (top) and accelerated idioventricular sustained ventricular tachycardia rhythm (bottom) Monomorphic PolymorphicMonomorphic and polymorphic ventricular tachycardiaMechanisms of ventricular arrhythmiasThe mechanisms responsible for ventricular tachycardia includere-entry or increased myocardial automaticity. The tachycardia The electrophysiology of a re-entry circuit was described in last week’s articleis usually initiated by an extrasystole and involves two pathwaysof conduction with differing electrical properties. The re-entrycircuits that support ventricular tachycardia can be “micro” or 21
  • 29. ABC of Clinical Electrocardiography“macro” in scale and often occur in the zone of ischaemia or Triggered automaticity of a group of cellsfibrosis surrounding damaged myocardium. can result from congenital or acquired Ventricular tachycardia may result from direct damage to heart disease. Once initiated, thesethe myocardium secondary to ischaemia or cardiomyopathy, or tachycardias tend to accelerate but slowfrom the effects of myocarditis or drugs—for example, class 1 markedly before stoppingantiarrhythmics (such as flecainide, quinidine, anddisopyramide). Monomorphic ventricular tachycardia usuallyoccurs after myocardial infarction and is a sign of extensive Ventricular tachycardia in a patient withmyocardial damage; there is a high inhospital mortality, more chronic ischaemic heart disease isoften resulting from impaired ventricular function than probably caused by a re-entryrecurrence of the arrhythmia. phenomenon involving infarct scar tissue, and thus the arrhythmia tends to be recurrentElectrocardiographic findings inmonomorphic ventricular tachycardiaElectrocardiographic diagnosis of monomorphic ventriculartachycardia is based on the following features.Duration and morphology of QRS complexIn ventricular tachycardia the sequence of cardiac activation isaltered, and the impulse no longer follows the normalintraventricular conduction pathway. As a consequence, themorphology of the QRS complex is bizarre, and the duration of Ventricular tachycardia with very broad QRS complexesthe complex is prolonged (usually to 0.12 s or longer). As a general rule the broader the QRS complex, the morelikely the rhythm is to be ventricular in origin, especially if thecomplexes are greater than 0.16 s. Duration of the QRScomplex may exceed 0.2 s, particularly if the patient haselectrolyte abnormalities or severe myocardial disease or istaking antiarrhythmic drugs, such as flecainide. If thetachycardia originates in the proximal part of the His-Purkinje Fascicular tachycardia with narrow QRS complexessystem, however, duration can be relatively short—as in afascicular tachycardia, where QRS duration ranges from 0.11 sto 0.14 s. The QRS complex in ventricular tachycardia often has aright or left bundle branch morphology. In general, atachycardia originating in the left ventricle produces a rightbundle branch block pattern, whereas a tachycardia originatingin the right ventricle results in a left bundle branch blockpattern. The intraventricular septum is the focus of the Sinoatrial nodearrhythmia in some patients with ischaemic heart disease, andthe resulting complexes have a left bundle branch block Left Right atriummorphology. atrium Atrioventricular nodeRate and rhythmIn ventricular tachycardia the rate is normally 120-300 Rightbeats/minute. The rhythm is regular or almost regular ( < 0.04 s ventriclebeat to beat variation), unless disturbed by the presence ofcapture or fusion beats (see below). If a monomorphic broadcomplex tachycardia has an obviously irregular rhythm themost likely diagnosis is atrial fibrillation with either aberrantconduction or pre-excitation.Frontal plane axis Ventricular tachycardia showing abnormal direction of wave ofIn a normal electrocardiogram the QRS axis in the mean depolarisation, giving rise to bizarre axisfrontal plane is between − 30° and + 90°, with the axis mostcommonly lying at around 60°. With the onset of ventricular Axis changetachycardia the mean frontal plane axis changes from that seenin sinus rhythm and is often bizarre. A change in axis of morethan 40° to the left or right is suggestive of ventriculartachycardia. Lead aVR is situated in the frontal plane at − 210°, andwhen the cardiac axis is normal the QRS complex in this lead isnegative; a positive QRS complex in aVR indicates an Change in axis with onset of monomorphic ventricular tachycardia in leadextremely abnormal axis either to the left or right. When the aVR22
  • 30. Broad complex tachycardia—Part IQRS complex in lead aVR is entirely positive the tachycardiaoriginates close to the apex of the ventricle, with the wave ofdepolarisation moving upwards towards the base of the heart. In some patients the atrioventricular node allows retrograde conduction ofDirect evidence of independent atrial activity ventricular impulses to the atria. TheIn ventricular tachycardia, the sinus node continues to initiate resulting P waves are inverted and occuratrial contraction. Since this atrial contraction is completely after the QRS complex, usually with aindependent of ventricular activity, the resulting P waves are constant RP interval.dissociated from the QRS complexes and are positive in leads Iand II. The atrial rate is usually slower than the ventricular rate,though occasionally 1:1 conduction occurs.Atrioventricular dissociation in monomorphic ventricular tachycardia (note P waves, arrowed) Although evidence of atrioventricular dissociation is It is important to scrutinise the tracingsdiagnostic for ventricular tachycardia, a lack of direct evidence from all 12 leads of theof independent P wave activity does not exclude the diagnosis. electrocardiogram, as P waves may beThe situation may be complicated by artefacts that simulate evident in some leads but not in othersP wave activity. However, beat to beat differences, especially of the STsegment, suggest the possibility of independent P wave activity,even though it may be impossible to pinpoint the independentP wave accurately.Indirect evidence of independent atrial activityCapture beatOccasionally an atrial impulse may cause ventriculardepolarisation via the normal conduction system. The resultingQRS complex occurs earlier than expected and is narrow. Sucha beat shows that even at rapid rates the conduction system isable to conduct normally, thus making a diagnosis ofsupraventricular tachycardia with aberrancy unlikely. Capture beats are uncommon, and though they confirm a Capture beatdiagnosis of ventricular tachycardia, their absence does notexclude the diagnosis.Fusion beatsA fusion beat occurs when a sinus beat conducts to theventricles via the atrioventricular node and fuses with a beatarising in the ventricles. As the ventricles are depolarised partlyby the impulse conducted through the His-Purkinje system andpartly by the impulse arising in the ventricle, the resulting QRScomplex has an appearance intermediate between a normalbeat and a tachycardia beat. Like capture beats, fusion beats are uncommon, and though Fusion beatthey support a diagnosis of ventricular tachycardia, theirabsence does not exclude the diagnosis.QRS concordance throughout the chest leadsConcordance exists when all the QRS complexes in the chest Concordance can be eitherleads are either predominantly positive or predominantly positive or negativenegative. The presence of concordance suggests that the tachycardiahas a ventricular origin. 23
  • 31. ABC of Clinical Electrocardiography Positive concordance probably indicates that the origin ofthe tachycardia lies on the posterior ventricular wall; the wave of V1 V2 V3depolarisation moves towards all the chest leads and producespositive complexes. Similarly, negative concordance is thoughtto correlate with a tachycardia originating in the anteriorventricular wall.V1 V2 V3 V4 V5 V6V4 V5 V6 Positive concordanceNegative concordance: ventricular tachycardia in a 90 year old woman incongestive cardiac failure24
  • 32. 7 Broad complex tachycardia—Part IIJune Edhouse, Francis MorrisThis article continues the discussion, started last week, on I aVR V1 V4ventricular tachycardias and also examines how to determinewhether a broad complex tachycardia is ventricular orsupraventricular in origin.Ventricular tachycardias II aVL V2 V5Fascicular tachycardiaFascicular tachycardia is uncommon and not usually associatedwith underlying structural heart disease. It originates from theregion of the posterior fascicle (or occasionally the anteriorfascicle) of the left bundle branch and is partly propagated bythe His-Purkinje network. It therefore produces QRScomplexes of relatively short duration (0.11-0.14 s). III aVF V3 V6Consequently, this arrhythmia is commonly misdiagnosed as asupraventricular tachycardia. The QRS complexes have a right bundle branch blockpattern, often with a small Q wave rather than primary R wavein lead V1 and a deep S wave in lead V6. When the tachycardia Fascicular ventricular tachycardia (note the right bundle branch blockoriginates from the posterior fascicle the frontal plane axis of pattern and left axis deviation)the QRS complex is deviated to the left; when it originates fromthe anterior fascicle, right axis deviation is seen. I aVR V1 V4Right ventricular outflow tract tachycardiaThis tachycardia originates from the right ventricular outflowtract, and the impulse spreads inferiorly. The electrocardiogramtypically shows right axis deviation, with a left bundle branchblock pattern. The tachycardia may be brief and self terminating II aVL V2 V5or sustained, and it may be provoked by catecholamine release,sudden changes in heart rate, and exercise. The tachycardiausually responds to drugs such as blockers or calciumantagonists. Occasionally the arrhythmia stops with adenosinetreatment and so may be misdiagnosed as a supraventriculartachycardia. III aVF V3 V6Torsades de pointes tachycardiaTorsades de pointes (“twisting of points”) is a type ofpolymorphic ventricular tachycardia in which the cardiac axisrotates over a sequence of 5-20 beats, changing from onedirection to another and back again. The QRS amplitude variessimilarly, such that the complexes appear to twist around thebaseline. In sinus rhythm the QT interval is prolonged andprominent U waves may be seen. Torsades de pointes is not usually sustained, but it will recur Right ventricular outflow track tachycardiaunless the underlying cause is corrected. Occasionally it may beprolonged or degenerate into ventricular fibrillation. It isassociated with conditions that prolong the QT interval. Torsades de pointes may be drug induced or secondary to Transient prolongation of the QT interval is often seen in electrolyte disturbancesthe acute phase of myocardial infarction, and this may lead to Torsades de pointes 25
  • 33. ABC of Clinical Electrocardiographytorsades de pointes. Ability to recognise torsades de pointes is Causes of torsades de pointesimportant because its management is different from themanagement of other ventricular tachycardias. Drugs Electrolyte disturbances x Antiarrhythmic drugs: class x Hypokalaemia Ia (disopyramide, x HypomagnesaemiaPolymorphic ventricular tachycardia procainamide, quinidine);Polymorphic ventricular tachycardia has the electrocardiographic Congenital syndromes class III (amiodarone, x Jervell and Lange-Nielsencharacteristics of torsades de pointes but in sinus rhythm the QT bretylium, sotalol) syndromeinterval is normal. It is much less common than torsades de x Antibacterials: x Romano-Ward syndromepointes. If sustained, polymorphic ventricular tachycardia often erythromycin, fluoquinolones, Other causesleads to haemodynamic collapse. It can occur in acute myocardial trimethoprim x Ischaemic heart diseaseinfarction and may deteriorate into ventricular fibrillation. x Other drugs: terfenadine, x MyxoedemaPolymorphic ventricular tachycardia must be differentiated from cisapride, tricyclic x Bradycardia due to sick sinusatrial fibrillation with pre-excitation, as both have the appearance antidepressants, haloperidol, syndrome or complete heartof an irregular broad complex tachycardia with variable QRS lithium, phenothiazines, blockmorphology (see last week’s article). chloroquine, thioridazine x Subarachnoid haemorrhage Polymorphic ventricular tachycardia deteriorating into ventricular fibrillationBroad complex tachycardias of Differentiation between ventricular tachycardia andsupraventricular origin supraventricular tachycardia with bundle branch block If the tachycardia has a right bundle branch block morphology (aIn the presence of aberrant conduction or ventricular predominantly positive QRS complex in lead V1), a ventricular origin ispre-excitation, any supraventricular tachycardia may present as suggested if there is:a broad complex tachycardia and mimic ventricular tachycardia. x QRS complex with duration > 0.14 s x Axis deviation x A QS wave or predominantly negative complex in lead V6Atrial tachycardia with aberrant conduction x Concordance throughout the chest leads, with all deflectionsAberrant conduction is defined as conduction through the positiveatrioventricular node with delay or block, resulting in a broader x A single (R) or biphasic (QR or RS) R wave in lead V1QRS complex. Aberrant conduction usually manifests as left or x A triphasic R wave in lead V1, with the initial R wave taller than theright bundle branch block, both of which have characteristic secondary R wave and an S wave that passes through the isoelectricfeatures. The bundle branch block may predate the tachycardia, lineor it may be a rate related functional block, occurring when If the tachycardia has a left bundle branch block morphology (aatrial impulses arrive too rapidly for a bundle branch to predominantly negative deflection in lead V1), a ventricular origin isconduct normally. When atrial fibrillation occurs with aberrant suggested if there is: x Axis deviationconduction and a rapid ventricular response, a totally irregular x QRS complexes with duration > 0.16 sbroad complex tachycardia is produced. x A QS or predominantly negative deflection in lead V6 x Concordance throughout the chest leads, with all deflections negative x An rS complex in lead V1V6 IAtrial fibrillation and left bundle branch block Atrial flutter with left bundle branch block, giving rise to broad complex tachycardiaWolff-Parkinson-White syndromeBroad complex tachycardias may also occur in theWolff-Parkinson-White syndrome, either as an antidromic The Wolff-Parkinson-White syndrome isatrioventricular re-entrant tachycardia or in association with discussed in more detail in an earlieratrial flutter or fibrillation. article, on junctional tachycardias26
  • 34. Broad complex tachycardia—Part IIAntidromic atrioventricular re-entrant tachycardiaIn this relatively uncommon tachycardia the impulse is conductedfrom the atria to the ventricles via the accessory pathway. Theresulting tachycardia has broad, bizarre QRS complexes.Atrial fibrillationIn patients without an accessory pathway the atrioventricularnode protects the ventricles from the rapid atrial activity thatoccurs during atrial fibrillation. In the Wolff-Parkinson-White Antidromic atrioventricular re-entrant tachycardia,syndrome the atrial impulses are conducted down the accessory giving rise to broad complex tachycardiapathway, which may allow rapid conduction and consequentlyvery fast ventricular rates. The impulses conducted via the accessory pathway produce Drugs that block the atrioventricularbroad QRS complexes. Occasionally an impulse will be node—such as digoxin, verapamil, andconducted via the atrioventricular node and produce a normal adenosine—should be avoided as they canQRS complex or a fusion beat. The result is a completely produce an extremely rapid ventricularirregular and often rapid broad complex tachycardia with a responsefairly constant QRS pattern, except for occasional normalcomplexes and fusion beats. Atrial fibrillation in patient with Wolff-Parkinson-White syndrome (note irregularity of complexes)Differentiating between ventricularand supraventricular originClinical presentationAge is a useful factor in determining the origin of a broadcomplex tachycardia: a tachycardia in patients aged over 35years is more likely to be ventricular in origin. A history thatincludes ischaemic heart disease or congestive cardiac failure is Danger of misdiagnosis90% predictive of ventricular tachycardia. x The safest option is to regard a broad complex tachycardia of The symptoms associated with broad complex tachycardia uncertain origin as ventricular tachycardia unless good evidencedepend on the haemodynamic consequences of the suggests a supraventricular originarrhythmia—that is, they relate to the heart rate and the x If a ventricular tachycardia is wrongly treated as supraventricular tachycardia, the consequences may be extremely seriousunderlying cardiac reserve rather than to the origin of the x Giving verapamil to a patient with ventricular tachycardia mayarrhythmia. It is wrong to assume that a patient with ventricular result in hypotension, acceleration of the tachycardia, and deathtachycardia will inevitably be in a state of collapse; somepatients look well but present with dizziness, palpitations,syncope, chest pain, or heart failure. In contrast, asupraventricular tachycardia may cause collapse in a patientwith underlying poor ventricular function. Clinical evidence of atrioventricular dissociation—that is,“cannon” waves in the jugular venous pulse or variable intensityof the first heart sound—indicates a diagnosis of a ventriculartachycardia The absence of these findings, however, does notexclude the diagnosis.Electrocardiographic differencesDirect evidence of independent P wave activity is highlysuggestive of ventricular tachycardia, as is the presence of fusion In ventricular tachycardia the rhythm isbeats or captured beats. The duration of QRS complexes is also regular or almost regular; if the rhythm isa key differentiating feature: those of > 0.14 s generally indicate obviously irregular the most likely diagnosis is atrial fibrillation with eithera ventricular origin. Concordance throughout the chest leads aberrant conduction or pre-excitationalso indicates ventricular tachycardia. 27
  • 35. ABC of Clinical Electrocardiography A previous electrocardiogram may give valuableinformation. Evidence of a myocardial infarction increases thelikelihood of ventricular tachycardia, and if the mean frontalplane axis changes during the tachycardia (especially if thechange is > 40° to the left or right) this points to a ventricularorigin. I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Left axis deviation and right bundle branch block in man with previous inferior myocardial infarction I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Monomorphic ventricular tachycardia in same patient, showing a shift of axis to right of >40° (note positive concordance) Ventricular tachycardia and supraventricular tachycardia Adenosine can also be used to blockwith bundle branch block may produce similar conduction temporarily through theelectrocardiograms. If a previous electrocardiogram shows a atrioventricular node to ascertain thebundle branch block pattern during sinus rhythm that is similar origin of a broad complex tachycardia,to or identical with that during the tachycardia, the origin of the but failure to stop the tachycardia doestachycardia is likely to be supraventricular. But if the QRS not necessarily indicate a ventricularmorphology changes during the tachycardia, a ventricular originorigin is indicated. The emergency management of a broad complextachycardia depends on the wellbeing of the patient and theorigin of the arrhythmia. Vagal stimulation—for example,carotid sinus massage or the Valsalva manoeuvre—does notusually affect a ventricular tachycardia but may affectarrhythmias of supraventricular origin. By transiently slowing orblocking conduction through the atrioventricular node, anatrioventricular nodal re-entrant tachycardia or atrioventricularre-entrant tachycardia may be terminated. In atrial fluttertransient block may reveal the underlying flutter waves.28
  • 36. 8 Acute myocardial infarction—Part IFrancis Morris, William J BradyIn the clinical assessment of chest pain, electrocardiography Indications for thrombolytic treatmentis an essential adjunct to the clinical history and physicalexamination. A rapid and accurate diagnosis in patients with x ST elevation > 1 mm in two contiguous limb leads or > 2 mm inacute myocardial infarction is vital, as expeditious reperfusion two contiguous chest leads x Posterior myocardial infarctiontherapy can improve prognosis. The most frequently used x Left bundle branch blockelectrocardiographic criterion for identifying acute myocardialinfarction is ST segment elevation in two or more anatomically ST segment depression or enzymatic change are not indications for thrombolytic treatmentcontiguous leads. The ST segment elevation associated with anevolving myocardial infarction is often readily identifiable, but aknowledge of the common “pseudo” infarct patterns is essentialto avoid the unnecessary use of thrombolytic treatment. In the early stages of acute myocardial infarction theelectrocardiogram may be normal or near normal; less thanhalf of patients with acute myocardial infarction have cleardiagnostic changes on their first trace. About 10% of patients Normalwith a proved acute myocardial infarction (on the basis ofclinical history and enzymatic markers) fail to develop STsegment elevation or depression. In most cases, however, serial Peaked T waveelectrocardiograms show evolving changes that tend to followwell recognised patterns. Degrees of ST segment elevationHyperacute T wavesThe earliest signs of acute myocardial infarction are subtle Q wave formation and loss of R waveand include increased T wave amplitude over the affected area.T waves become more prominent, symmetrical, and pointed(“hyperacute”). Hyperacute T waves are most evident in the T wave inversionanterior chest leads and are more readily visible when an oldelectrocardiogram is available for comparison. These changesin T waves are usually present for only five to 30 minutes after Sequence of changes seen during evolution of myocardial infarctionthe onset of the infarction and are followed by ST segmentchanges.ST segment changes V1 V4In practice, ST segment elevation is often the earliest recognisedsign of acute myocardial infarction and is usually evident withinhours of the onset of symptoms. Initially the ST segment maystraighten, with loss of the ST-T wave angle . Then the T wavebecomes broad and the ST segment elevates, losing its normal V2 V5concavity. As further elevation occurs, the ST segment tends tobecome convex upwards. The degree of ST segment elevationvaries between subtle changes of < 1 mm to gross elevation of > 10 mm. V3 V6V1 V2 V3 Hyperacute T waves Sometimes the QRS complex, the ST segment, and the T wave fuse to form a single monophasic deflection, calledV4 V5 V6 a giant R wave or “tombstone” Anterior myocardial infarction with gross ST segment elevation (showing “tombstone” R waves) 29
  • 37. ABC of Clinical ElectrocardiographyPathological Q wavesAs the acute myocardial infarction evolves, changes to the QRScomplex include loss of R wave height and the development of I aVR V1 V4pathological Q waves. Both of these changes develop as a result of the loss ofviable myocardium beneath the recording electrode, and theQ waves are the only firm electrocardiographic evidence ofmyocardial necrosis. Q waves may develop within one to twohours of the onset of symptoms of acute myocardial infarction, II aVL V2 V5though often they take 12 hours and occasionally up to 24hours to appear. The presence of pathological Q waves,however, does not necessarily indicate a completed infarct. IfST segment elevation and Q waves are evident on theelectrocardiogram and the chest pain is of recent onset, thepatient may still benefit from thrombolysis or directintervention. III aVF V3 V6 When there is extensive myocardial infarction, Q waves actas a permanent marker of necrosis. With more localisedinfarction the scar tissue may contract during the healingprocess, reducing the size of the electrically inert area andcausing the disappearance of the Q waves.Resolution of changes in ST segment Pathological Q waves in inferior and anterior leadsand T wavesAs the infarct evolves, the ST segment elevation diminishes andthe T waves begin to invert. The ST segment elevationassociated with an inferior myocardial infarction may take up totwo weeks to resolve. ST segment elevation associated withanterior myocardial infarction may persist for even longer, and V1 V2 V3if a left ventricular aneurysm develops it may persist indefinitely.T wave inversion may also persist for many months andoccasionally remains as a permanent sign of infarction.Reciprocal ST segment depressionST segment depression in leads remote from the site of an V4 V5 V6acute infarct is known as reciprocal change and is a highlysensitive indicator of acute myocardial infarction. Reciprocalchanges are seen in up to 70% of inferior and 30% of anteriorinfarctions. Long standing ST segment elevation and T wave inversion associated with a Typically, the depressed ST segments tend to be horizontal previous anterior myocardial infarction (echocardiography showed a leftor downsloping. The presence of reciprocal change is ventricular aneurysm)particularly useful when there is doubt about the clinicalsignificance of ST segment elevation. I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 An inferolateral myocardial infarction with reciprocal changes in leads I, aVL, V1, and V230
  • 38. Acute myocardial infarction—Part I Reciprocal change strongly indicates acute infarction, with asensitivity and positive predictive value of over 90%, though its I aVR V1 V4absence does not rule out the diagnosis. The pathogenesis of reciprocal change is uncertain.Reciprocal changes are most frequently seen when the infarct islarge, and they may reflect an extension of the infarct or occur II aVL V2 V5as a result of coexisting remote ischaemia. Alternatively, it maybe a benign electrical phenomenon. The positive potentials thatare recorded by electrodes facing the area of acute injury areprojected as negative deflections in leads opposite the injuredarea, thus producing a “mirror image” change. Extensivereciprocal ST segment depression in remote regions oftenindicates widespread arterial disease and consequently carries III aVF V3 V6a worse prognosis.Localisation of site of infarction Reciprocal changes: presence of widespread ST segment depression in theThe distribution of changes recorded in acute myocardial anterolateral leads strongly suggests that the subtle inferior ST segment elevation is due to acute infarctioninfarction allows the area of infarction to be localised, thusindicating the site of arterial disease. Proximal arterialocclusions tend to produce the most widespreadelectrocardiographic abnormalities. The anterior and inferioraspects of the heart are the areas most commonly subject to Anatomical relationship of leadsinfarction. Anteroseptal infarcts are highly specific indicators of Inferior wall—Leads II, III, and aVFdisease of the left anterior descending artery. Isolated inferior Anterior wall—Leads V1 to V4infarcts—changes in leads II, III, and aVF—are usually associated Lateral wall—Leads I, aVL, V5, and V6with disease in the right coronary or distal circumflex artery. Non-standard leadsDisease in the proximal circumflex artery is often associated Right ventricle—Right sided chest leads V1R to V6R Posterior wall—Leads V7 to V9with a lateral infarct pattern—that is, in leads I, aVL, V5, and V6.Right ventricular infarctionRight ventricular infarction is often overlooked, as standard12 lead electrocardiography is not a particularly sensitiveindicator of right ventricular damage. Right ventricularinfarction is associated with 40% of inferior infarctions. It mayalso complicate some anterior infarctions but rarely occurs asan isolated phenomenon. On the standard 12 leadelectrocardiogram right ventricular infarction is indicated by V2R V1Rsigns of inferior infarction, associated with ST segment V6Relevation in lead V1. It is unusual for ST segment elevation in V3R V5R V4Rlead V1 to occur as an isolated phenomenon. Right sided chest leads are much more sensitive to thepresence of right ventricular infarction. The most useful lead islead V4R (an electrode is placed over the right fifth intercostalspace in the mid-clavicular line). Lead V4R should be recordedas soon as possible in all patients with inferior infarction, as ST Placement of right sided chest leadssegment elevation in right ventricular infarction may be shortlived. I aVR V1 V4R II aVL V2 V5 III aVF V3 V6 Acute inferior myocardial infarction with associated right ventricular infarction 31
  • 39. ABC of Clinical Electrocardiography I aVR V1R V4R The diagnosis of right ventricular infarction is important as it may be associated with hypotension. Treatment II aVL V2R V5R with nitrates or diuretics may compound the hypotension, though the patient may respond to a fluid challenge III aVF V3R V6RAcute inferior myocardial infarction with right ventricular involvement Right ventricular infarction usually results from occlusionof the right coronary artery proximal to the right ventricularmarginal branches, hence its association with inferior infarction.Less commonly, right ventricular infarction is associated withocclusion of the circumflex artery, and if this vessel is dominantthere may be an associated inferolateral wall infarction. ScapulaPosterior myocardial infarctionPosterior myocardial infarction refers to infarction of the V7 V8 V9posterobasal wall of the left ventricle. The diagnosis is oftenmissed as the standard 12 lead electrocardiography does notinclude posterior leads. Early detection is important asexpeditious thrombolytic treatment may improve the outcome Position of V7, V8, and V9for patients with posterior infarction. on posterior chest wall The changes of posterior myocardial infarction are seenindirectly in the anterior precordial leads. Leads V1 to V3 facethe endocardial surface of the posterior wall of the left ventricle.As these leads record from the opposite side of the heartinstead of directly over the infarct, the changes of posteriorinfarction are reversed in these leads. The R waves increase insize, becoming broader and dominant, and are associated withST depression and upright T waves. This contrasts with the Qwaves, ST segment elevation, and T wave inversion seen in acuteanterior myocardial infarction. Ischaemia of the anterior wall ofthe left ventricle also produces ST segment depression in leads I aVR V1 V4V1 to V3, and this must be differentiated from posteriormyocardial infarction. The use of posterior leads V7 to V9 willshow ST segment elevation in patients with posterior infarction.These additional leads therefore provide valuable information,and they help in identfying the patients who may benefit fromurgent reperfusion therapy. II aVL V2 V5 V8 III aVF V3 V6 V9 Isolated posterior infarction with no associated inferior changes (note STST segment elevation in posterior chest leads V8 and V9 segment depression in leads V1 to V3)32
  • 40. 9 Acute myocardial infarction—Part IIJune Edhouse, William J Brady, Francis MorrisThis article describes the association of bundle branch blockwith acute myocardial infarction and the differential diagnosisof ST segment elevation. I aVR V1 V4Bundle branch blockAcute myocardial infarction in the presence of bundle branchblock carries a much worse prognosis than acute myocardialinfarction with normal ventricular conduction. This is true bothfor patients whose bundle branch block precedes the infarctionand for those in whom bundle branch block develops as a result II aVL V2 V5of the acute event. Thrombolytic treatment produces dramaticreductions in mortality in these patients, and the greatestbenefits are seen in those treated early. It is therefore essentialthat the electrocardiographic identification of acute myocardialinfarction in patients with bundle branch block is both timelyand accurate.Left bundle branch blockLeft bundle branch block is most commonly seen in patients III aVF V3 V6with coronary artery disease, hypertension, or dilatedcardiomyopathy. The left bundle branch usually receives bloodfrom the left anterior descending branch of the left coronaryartery and from the right coronary artery. When new leftbundle branch block occurs in the context of an acutemyocardial infarction the infarct is usually anterior andmortality is extremely high. The electrocardiographic changes of acute myocardialinfarction can be difficult to recognise when left bundle branch Appropriate discordance in uncomplicated left bundle branch block (noteblock is present, and many of the conventional diagnostic ST elevation in leads V1 to V3)criteria are not applicable. Abnormal ventricular depolarisation in left bundle branchblock leads to secondary alteration in the recovery process (seeearlier article about bradycardias and atrioventricularconduction block). This appears on the electrocardiogram asrepolarisation changes in a direction opposite to that of themain QRS deflection—that is, “appropriate discordance” I aVR V1 V4between the QRS complex and the ST segment. Thus leads with a predominantly negative QRS complexshow ST segment elevation with positive T waves (anappearance similar to that of acute anterior myocardialinfarction). II aVL V2 V5Recognition of acute ischaemiaMany different electrocardiographic criteria have beenproposed for identifying acute infarction in left bundle branchblock, but none has yet proved sufficiently sensitive to be usefulin the acute setting. However, some features are specific III aVF V3 V6indicators of acute ischaemia. ST segment elevation in association with a positive QRScomplex, or ST segment depression in leads V1, V2, or V3(which have predominantly negative QRS complexes), is notexpected in uncomplicated left bundle branch block and istermed “inappropriate concordance.” Inappropriate concordance strongly indicates acute Acute myocardial infarction and left bundle branch block. Note that the STischaemia. Extreme ST segment elevation (>5 mm) in leads V1 segments are elevated in leads V5 and V6 (inappropriate concordance) andand V2 also suggests acute ischaemia. If doubt persists, serial grossly elevated (> 5 mm) in leads V2, V3, and V4; note also the ST segmentelectrocardiograms may show evolving changes. depression in leads III and aVF 33
  • 41. ABC of Clinical Electrocardiography I aVR V1 V4 A II aVL V2 V5 B Inappropriate concordance in lead III aVF V3 V6 C V1 in patient with left bundle branch block (A); inappropriate concordance in lead V6 in patient with left bundle branch block (B); and exaggeration of appropriate discordance in lead V1 in patientST segment depression in precordial leads in 68 year old man with chest pain with left bundle branch block (C) I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 Development of left bundle branch block in same man shortly after admission (note ST segment depression in lead V3; this is an example of inappropriate concordance)Right bundle branch blockRight bundle branch block is most commonly seen inassociation with coronary artery disease, but in many cases no The Brugada syndrome, which is familial,organic heart disease is present. Uncomplicated right bundle occurs particularly in young men and isbranch block usually causes little ST segment displacement and characterised by right bundle branchneither causes nor masks Q waves. Thus it does not generally block and ST segment elevation in theinterfere with the diagnosis of acute myocardial infarction, right precordial leads. There is a highthough it may mask a posterior myocardial infarction. instance of death as a result of ventricular tachyarrhythmiasDifferential diagnosis of ST segmentelevationST segment elevation has numerous possible causes. It may be avariant of normal or be due to cardiac or non-cardiac disease. A Causes of ST segment elevationcorrect diagnosis has obvious advantages for the patient but isalso particularly important before the use of thrombolytic x Acute myocardial infarction x “High take-off ”treatment so that unnecessary exposure to the risks of x Benign early repolarisationthrombolytic drugs can be avoided. x Left bundle branch block The interpretation of ST segment elevation should always x Left ventricular hypertrophybe made in the light of the clinical history and examination x Ventricular aneurysmfindings. There are often clues in the electrocardiogram to x Coronary vasospasm/Printzmetal’s anginadifferentiate the ST segment elevation of acute ischaemia from x Pericarditis x Brugada syndromeother causes; for example, reciprocal changes (see last week’s x Subarachnoid haemorrhagearticle) may be present, which strongly indicate acute ischaemia.34
  • 42. Acute myocardial infarction—Part IISerial electrocardiography or continuous ST segmentmonitoring is also useful as ischaemic ST segment elevation V1 V2 V3evolves over time. Old electrocardiograms are also useful forcomparison.“High take-off ”Care is required when interpreting ST segment elevation inright sided chest leads as the ST segments, particularly in leadsV2 and V3, tend to be upsloping rather than flat. Isolated STsegment elevation in these leads should be interpreted withcaution. (For more information on “high take-off” see thesecond article in this series.) V4 V5 V6Benign early repolarisationA degree of ST segment elevation is often present in healthyindividuals, especially in young adults and in people of African Benign early repolarisationdescent. This ST segment elevation is most commonly seen inthe precordial leads and is often most marked in lead V4. It isusually subtle but can sometimes be pronounced and can easilybe mistaken for pathological ST segment elevation. Benign early repolarisation can be recognised by its V1 V2 V3characteristic electrocardiographic features: elevation of the Jpoint above the isoelectric line, with high take-off of the STsegment; a distinct notch at the junction of the R wave and Swave, the J point; an upward concavity of the ST segment; andsymmetrical, upright T waves, often of large amplitude.Antecedent myocardial infarction V4 V5 V6The ST segment elevation associated with acute infarctionusually resolves within two weeks of the acute event, but it maypersist indefinitely, especially when associated with anteriormyocardial infarction. In these patients a diagnosis of left Persistent ST segment elevation in anterior chest leads in association withventricular aneurysm should be considered. Care should be left ventricular aneurysmtaken when interpreting the electrocardiogram within twoweeks of an acute event, and comparison with oldelectrocardiograms may be useful.Acute pericarditisAcute pericarditis is commonly mistaken for acute myocardial I aVR V1 V4infarction as both cause chest pain and ST segment elevation.In pericarditis, however, the ST segment elevation is diffuserather than localised, often being present in all leads exceptaVR and V1. The elevated ST segments are concave upwards,rather than convex upwards as seen in acute infarction.Depression of the PR segment may also be seen. ST segment elevation in pericarditis is thought to be due tothe associated subepicardial myocarditis. The zone of injured II aVL V2 V5tissue causes abnormal ST vectors; the end result is that leadsfacing the epicardial surface record ST segment elevation,whereas those facing the ventricular cavity (leads aVR and V1)record ST segment depression. The absence of widespreadreciprocal change, the presence of PR segment depression, andabsence of Q waves may be helpful in distinguishing pericarditisfrom acute myocardial infarction.Other causes of ST segment elevation III aVF V3 V6The characteristic features of left ventricular hypertrophy arealso often misinterpreted as being caused by acute ischaemia.ST segment elevation in the precordial leads is a feature of leftventricular hypertrophy and is due to secondary repolarisationabnormalities. ST segment abnormalities are seen in association withintracranial (particularly subarachnoid) haemorrhage. ST Acute pericarditis with widespread ST segment elevation and PR segmentsegment elevation or depression may be seen; a putative depression (see lead II) 35
  • 43. ABC of Clinical Electrocardiographyexplanation is that altered autonomic tone affects the durationof ventricular repolarisation, producing these changes. Printzmetal’s angina (vasospastic angina) is associated withST segment elevation. As the changes are due to coronaryartery spasm rather than acute infarction, they may becompletely reversible if treated promptly. ST segmentabnormalities may be seen in association with cocaine use and I aVR V1 V4are probably due to a combination of vasospasm andthrombosis. II aVL V2 V5Reversible ST segment elevation associated withcoronary artery spasm III aVF V3 V6 ST segment elevation in leads V1 to V3 in patient with left ventricular hypertrophy36
  • 44. 10 Myocardial ischaemiaKevin Channer, Francis MorrisIn clinical practice electrocardiography is most often used toevaluate patients with suspected ischaemic heart disease. When Electrocardiography is not sufficiently specific or sensitive to be used without ainterpreted in the light of the clinical history, patient’s clinical historyelectrocardiograms can be invaluable in aiding selection of themost appropriate management. Electrocardiography has limitations. A trace can suggest, forexample, that a patient’s heart is entirely normal when in fact heor she has severe and widespread coronary artery disease. Inaddition, less than half of patients presenting to hospital with anacute myocardial infarction will have the typical and diagnosticelectrocardiographic changes present on their initial trace, andas many as 20% of patients will have a normal or near normal Normalelectrocardiogram. Myocardial ischaemia causes changes in the ST-T wave, butunlike a full thickness myocardial infarction it has no direct Tall T waveeffects on the QRS complex (although ischaemia may give riseto bundle branch blocks, which prolongs the QRS complex). When electrocardiographic abnormalities occur in Biphasic T waveassociation with chest pain but in the absence of frankinfarction, they confer prognostic significance. About 20% ofpatients with ST segment depression and 15% with T waveinversion will experience severe angina, myocardial infarction, Inverted T waveor death within 12 months of their initial presentation,compared with 10% of patients with a normal trace. Changes in the ST segment and T waves are not specific for Flat T wave T wave changes associated withischaemia; they also occur in association with several other ischaemiadisease processes, such as left ventricular hypertrophy,hypokalaemia, and digoxin therapy.T wave changesMyocardial ischaemia can affect T wave morphology in a varietyof ways: T waves may become tall, flattened, inverted, orbiphasic. Tall T waves are one of the earliest changes seen in V1 V4acute myocardial infarction, most often seen in the anteriorchest leads. Isolated tall T waves in leads V1 to V3 may also bedue to ischaemia of the posterior wall of the left ventricle (themirror image of T wave inversion). V2 V5 V3 V6Tall T waves in leads V2 and V3 in patient with recentinferoposterior myocardial infarction, indicatingposterior ischaemia Tall T waves in myocardial ischaemia 37
  • 45. ABC of Clinical Electrocardiography As there are other causes of abnormally tall T waves and no Suggested criteria for size of T wavecommonly used criteria for the size of T waves, these changes x 1/8 size of the R waveare not always readily appreciated without comparison with a x < 2/3 size of the R waveprevious electrocardiogram. Flattened T waves are often seen in x Height < 10 mmpatients with myocardial ischaemia, but they are verynon-specific. Myocardial ischaemia may also give rise to T wave inversion,but it must be remembered that inverted T waves are normal in T wave inversionleads III, aVR, and V1 in association with a predominantly x T wave inversion can be normalnegative QRS complex. T waves that are deep and x It occurs in leads III, aVR, and V1 (and in V2, but only in association with T wave inversion in leadsymmetrically inverted (arrowhead) strongly suggest myocardial V1)ischaemia. V1 V4 V1 V4 V2 V5 V3 V6 V2 V5Arrowhead T wave inversion in patient with unstableangina In some patients with partial thickness ischaemia theT waves show a biphasic pattern. This occurs particularly V3 V6in the anterior chest leads and is an acute phenomenon.Biphasic T wave changes usually evolve and are often followedby symmetrical T wave inversion. These changes occur inpatients with unstable or crescendo angina and strongly suggestmyocardial ischaemia. Biphasic T waves in man aged 26 with unstable anginaST segment depressionTypically, myocardial ischaemia gives rise to ST segmentdepression. The normal ST segment usually blends with theT wave smoothly, making it difficult to determine where the A BST segment ends and the T wave starts. One of the first and ST changes with ischaemia showingmost subtle changes in the ST segment is flattening of the normal wave form (A); flattening ofsegment, resulting in a more obvious angle between the ST ST segment (B), making T wavesegment and T wave. more obvious; horizontal (planar) ST segment depression (C); and C D downsloping ST segment depression (D)Subtle ST segment change in patient with ischaemic chest pain: when no Substantial ST segment depressionpain is present (top) and when in pain (bottom) in patient with ischaemic chest pain38
  • 46. Myocardial ischaemia More obvious changes comprise ST segment depressionthat is usually planar (horizontal) or downsloping. Whereashorizontal ST depression strongly suggests ischaemia,downsloping changes are less specific as they are also found in V1 V4association with left ventricular hypertrophy and in patientstaking digoxin. The degree of ST segment depression in anygiven lead is related to the size of the R wave. Thus, ST segmentdepression is usually most obvious in leads V4 to V6 of the 12lead electrocardiogram. Moreover, because the height of theR wave varies with respiration, the degree of ST depression inany one lead may vary from beat to beat. ST segment V2 V5depression is usually not as marked in the inferior leadsbecause here the R waves tend to be smaller. Substantial(>2 mm) and widespread (>2 leads) ST depression is a graveprognostic finding as it implies widespread myocardialischaemia from extensive coronary artery disease. ST segmentdepression may be transient, and its resolution with treatment isreassuring. Modern equipment allows continuous ST segment V3 V6monitoring. Serial changes in the electrocardiogram over a fewhours or days, especially when the changes are associated withrecurrent chest pain, are extremely helpful in confirming thepresence of ischaemic heart disease; serial changes confer aworse prognosis, indicating the need for increased drug Widespread ST segment depression in patient withtreatment or revascularisation interventions. unstable anginaST segment elevationTransient ST segment elevation in patients with chest pain is afeature of ischaemia and is usually seen in vasospastic (variantor Prinzmetal’s) angina. A proportion of these patients,however, will have substantial proximal coronary artery stenosis.When ST segment elevation has occurred and resolved it maybe followed by deep T wave inversion even in the absence ofenzyme evidence of myocardial damage. In patients with previous Q wave myocardial infarction thehallmark of new ischaemia is often ST segment elevation. Thisis thought to be associated with a wall motion abnormality, orbulging of the infarcted segment. It rarely indicates reinfarctionin the same territory. When an electrocardiogram showspersistent T wave inversion accompanying the changes of aprevious acute myocardial infarction, ischaemia in the same Non-ischaemic ST segment changes: in patient taking digoxin (top) andterritory may cause “normalisation” of the T waves (return to an in patient with left ventricularupright position). Alternatively, further ischaemia may make the hypertrophy (bottom)T wave inversion more pronounced. Normalisation of longstanding inverted T waves in patient with chest painArrhythmias associated with acutemyocardial ischaemia or infarction Reversible ST segment changes in patient with chest pain; the ST segment elevation returns to normal as theVentricular myocardial ischaemia may be arrhythmogenic, and chest pain settlesextrasystoles are common. It used to be thought that frequentextrasystoles of multifocal origin, bigeminy, couplets, orextrasystoles that fell on the T wave (R on T) conferred a badprognosis in the early hours of myocardial infarction and 39
  • 47. ABC of Clinical Electrocardiographypredicted the onset of ventricular fibrillation. Clinical trials have Short runs of ventricular tachycardia areclearly shown, however, that their suppression by a bad prognostic sign and shouldantiarrhythmic drugs had no effect on the frequency of probably be treatedsubsequent ventricular fibrillation.R on T, giving rise to ventricular fibrillationVentricular fibrillation is the commonest unheralded fatal Tachycardias of supraventricular origin,arrhythmia in the first 24 hours of acute myocardial infarction. with the exception of atrial fibrillation,The prognosis depends almost entirely on the patient’s are uncommon after myocardialproximity to skilled medical help when the arrhythmia occurs. infarction. Atrial fibrillation occurs inCardiac arrest from ventricular fibrillation outside hospital is about 10% of patients and is moreassociated with a long term survival of about 10%, compared common in those with heart failure,with an initial survival of 90% when cardiac arrest occurs after diabetes, and valvular heart disease. Itadmission to a coronary care unit. Studies have shown that the may be transient or persistent and iskey factor in prognosis is the speed with which electrical often a marker of haemodynamicdefibrillation is delivered. instabilityHeart blockThe artery supplying the atrioventricular node is usually abranch of the right coronary artery; less commonly it originatesfrom the left circumflex artery. In patients with proximalocclusion of the right coronary artery causing an inferior When completeinfarction, the atrioventricular node’s arterial supply may be atrioventricular blockcompromised resulting in various degrees of heart block. occurs in association withAtrioventricular block may be severe at first but usually acute anterior myocardialimproves over subsequent days. Complete atrioventricular block infarction, transvenoususually gives way to second degree and then first degree block. cardiac pacing isAlthough temporary transvenous cardiac pacing may be recommendednecessary for patients who are haemodynamicallycompromised, it is not mandatory in stable patients.Acute myocardial infarction with complete heart block Profound bradycardia or atrioventricular block resultingfrom ischaemia may provoke an escape rhythm. Such rhythmsare the result of spontaneous activity from a subsidiarypacemaker located within the atria, atrioventricular junction, orventricles. An atrioventricular junction escape beat has anormal QRS complex morphology, with a rate of 40-60beats/min. A ventricular escape rhythm is broad complex andgenerally slower (15-40 beats/min).40
  • 48. 11 Exercise tolerance testingJonathan Hill, Adam TimmisExercise tolerance testing is an important diagnostic andprognostic tool for assessing patients with suspected or known ST segment depression (horizontal or downsloping) is the most reliableischaemic heart disease. During exercise, coronary blood flow indicator of exercise-induced ischaemiamust increase to meet the higher metabolic demands of themyocardium. Limiting the coronary blood flow may result inelectrocardiographic changes. This article reviews theelectrocardiographic responses that occur with exercise, both innormal subjects and in those with ischaemic heart disease.Clinical relevance Diagnostic indications for exercise testingExercise tolerance testing (also known as exercise testing or x Assessment of chest pain in patients with intermediate probabilityexercise stress testing) is used routinely in evaluating patients for coronary artery disease x Arrhythmia provocationwho present with chest pain, in patients who have chest pain on x Assessment of symptoms (for example, presyncope) occurringexertion, and in patients with known ischaemic heart disease. during or after exercisePrognostic indications for exercise testingx Risk stratification after myocardial infarctionx Risk stratification in patients with hypertrophic cardiomyopathyx Evaluation of revascularisation or drug treatmentx Evaluation of exercise tolerance and cardiac functionx Assessment of cardiopulmonary function in patients with dilated cardiomyopathy or heart failurex Assessment of treatment for arrhythmia Exercise testing has a sensitivity of 78% and a specificity of70% for detecting coronary artery disease. It cannot thereforebe used to rule in or rule out ischaemic heart disease unless theprobability of coronary artery disease is taken into account. Forexample, in a low risk population, such as men aged under 30years and women aged under 40, a positive test result is morelikely to be a false positive than true, and negative results addlittle new information. In a high risk population, such as thoseaged over 50 with typical angina symptoms, a negative resultcannot rule out ischaemic heart disease, though the results maybe of some prognostic value. Exercise testing is therefore of greatest diagnostic value inpatients with an intermediate risk of coronary artery disease. Patient exercising on treadmillThe testProtocolThe Bruce protocol is the most widely adopted protocol andhas been extensively validated. The protocol has seven stages,each lasting three minutes, resulting in 21 minutes’ exercise fora complete test. In stage 1 the patient walks at 1.7 mph (2.7 km)up a 10% incline. Energy expenditure is estimated to be Workload4.8 METs (metabolic equivalents) during this stage. The speed x Assessment of workload is measured by metabolic equivalentsand incline increase with each stage. A modified Bruce protocol (METs)is used for exercise testing within one week of myocardial x Workload is a reflection of oxygen consumption and hence energyinfarction. use x 1 MET is 3.5 ml oxygen/kg per minute, which is the oxygenPreparing the patient consumption of an average individual at rest x To carry out the activities of daily living an exercise intensity of at Blockers should be discontinued the day before the test, and least 5 METs is requireddixogin (which may cause false positive results, with ST segmentabnormalities) should be stopped one week before testing. The patient is first connected to the exerciseelectrocardiogram machine. Resting electrocardiograms, both 41
  • 49. ABC of Clinical Electrocardiographysitting and standing, are recorded as electrocardiographic Maximum predicted heart ratechanges, particularly T wave inversion, may occur as the patientstands up to start walking on the treadmill. A short period of x By convention, the maximum predicted heart rate is calculated as 220 (210 for women) minus the patient’s ageelectrocardiographic recording during hyperventilation is also x A satisfactory heart rate response is achieved on reaching 85% ofvaluable for identifying changes resulting from hyperventilation the maximum predicted heart raterather than from coronary ischaemia. x Attainment of maximum heart rate is a good prognostic sign During the test the electrocardiogram machine provides acontinuous record of the heart rate, and the 12 leadelectrocardiogram is recorded intermittently. Blood pressuremust be measured before the exercise begins and at the end ofeach exercise stage. Blood pressure may fall or remain staticduring the initial stage of exercise. This is the result of an Contraindications for exercise testinganxious patient relaxing. As the test progresses, however, x Acute myocardial infarction (within 4-6 days)systolic blood pressure should rise as exercise increases. A level x Unstable angina (rest pain in previous 48 hours)of up to 225 mm Hg is normal in adults, although athletes can x Uncontrolled heart failurehave higher levels. Diastolic blood pressure tends to fall slightly. x Acute myocarditis or pericarditis x Acute systemic infectionThe aim of the exercise is for the patient to achieve their x Deep vein thrombosismaximum predicted heart rate. x Uncontrolled hypertension (systolic blood pressure > 220 mm Hg, diastolic > 120 mm Hg)Safety x Severe aortic stenosisIf patients are carefully selected for exercise testing, the rate of x Severe hypertrophic obstructive cardiomyopathy x Untreated life threatening arrhythmiaserious complications (death or acute myocardial infarction) is x Dissecting aneurysmabout 1 in 10 000 tests (0.01%). The incidence of ventricular x Recent aortic surgerytachycardia or fibrillation is about 1 in 5000. Fullcardiopulmonary resuscitation facilities must be available, andtest supervisors must be trained in cardiopulmonaryresuscitation.LimitationsThe specificity of ST segment depression as the main indicatorof myocardial ischaemia is limited. ST segment depression hasbeen estimated to occur in up to 20% of normal individuals onambulatory electrocardiographic monitoring. There are manycauses of ST segment changes apart from coronary arterydisease, which confound the result of exercise testing. If theresting electrocardiogram is abnormal, the usefulness of anexercise test is reduced or may even be precluded. J pointRepolarisation and conduction abnormalities—for example, leftventricular hypertrophy, left bundle branch block,pre-excitation, and effects of digoxin—preclude accurateinterpretation of the electrocardiogram during exercise, and asa result, other forms of exercise test (for example, adenosine ordobutamine scintigraphy) or angiography are required toevaluate this group of patients.Normal trace during exerciseThe J point (the point of inflection at the junction of the S waveand ST segment) becomes depressed during exercise, withmaximum depression at peak exercise. The normal ST segment Top: At rest. Bottom: Pathological ST segment depression as measured 80 ms from J pointduring exercise therefore slopes sharply upwards. A B CNormal changes from rest (A), after three minutes’ exercise (B), and after six minutes’ exercise (C). Note the upsloping ST segments42
  • 50. Exercise tolerance testing By convention, ST segment depression is measured relativeto the isoelectric baseline (between the T and P waves) at a Apoint 60-80 ms after the J point. There is intraobserver variationin the measurement of this ST segment depression, andtherefore a computerised analysis that accompanies the exercisetest can assist but not replace the clinical evaluation of the test. BNormal electrocardiographic changes during exercisex P wave increases in heightx R wave decreases in heightx J point becomes depressedx ST segment becomes sharply upsloping Cx Q-T interval shortensx T wave decreases in heightAbnormal changes during exerciseThe standard criterion for an abnormal ST segment response is Dhorizontal (planar) or downsloping depression of > 1 mm. If0.5 mm of depression is taken as the standard, the sensitivity ofthe test increases and the specificity decreases (vice versa if2 mm of depression is selected as the standard). Other recognised abnormal responses to exercise include EST elevation of > 1 mm, particularly in the absence of Q waves.This suggests severe coronary artery disease and is a sign ofpoor prognosis. T wave changes such as inversion andpseudo-normalisation (an inverted T wave that becomesupright) are non-specific changes. Horizontal ST segment depression (A=at rest, B=after three minutes’ V2 V2 exercise, C=after six minutes’ exercise) and downsloping ST segment depression (D=at rest, E=after six minutes’ exercise) V3 V3 A B T wave inversion in lead V5 at rest (A) and normalisation of T waves with exercise (B) Reasons for stopping a test V4 V4 Electrocardiographic criteria x Severe ST segment depression ( > 3 mm) x ST segment elevation > 1 mm in non-Q wave lead x Frequent ventricular extrasystoles (unless the test is to assessmentST segments in leads V2 to V4 at rest (left) and after two minutes’ exercise ventricular arrhythmia)(right) (note obvious ST elevation) x Onset of ventricular tachycardia x New atrial fibrillation or supraventricular tachycardia x Development of new bundle branch block (if the test is primarily to A highly specific sign for ischaemia is inversion of the detect underlying coronary disease)U wave. As U waves are often difficult to identify, especially at x New second or third degree heart blockhigh heart rates, this finding is not sensitive. The presence of x Cardiac arrestextrasystoles that have been induced by exercise is neither Symptoms and signssensitive nor specific for coronary artery disease. x Patient requests stopping because of severe fatigue x Severe chest pain, dyspnoea, or dizzinessStopping the test x Fall in systolic blood pressure ( > 20 mm Hg) x Rise in blood pressure (systolic > 300 mm Hg, diastolicIn clinical practice, patients rarely exercise for the full duration > 130 mm Hg)(21 minutes) of the Bruce protocol. However, completion of x Ataxia9-12 minutes of exercise or reaching 85% of the maximum 43
  • 51. ABC of Clinical Electrocardiographypredicted changes in heart rate is usually satisfactory. An The most common reason for stopping anexercise test should end when diagnostic criteria have been exercise test is fatigue and breathlessnessreached or when the patient’s symptoms and signs dictate. as a result of the unaccustomed exercise After the exercise has stopped, recording continues for upto 15 minutes. ST segment changes (or arrhythmias) may occurduring the recovery period that were not apparent duringexercise. Such changes generally carry the same significance asthose occurring during exercise. Rest Exercise RecoveryMarked ST changes in recovery but not during exerciseInterpreting the resultsDiagnostic testing Findings suggesting high probability of coronary arteryAny abnormal electrocardiographic changes must be diseaseinterpreted in the light of the probability of coronary artery x Horizontal ST segment depression of < 2 mmdisease and physiological response to exercise. A normal test x Downsloping ST segment depressionresult or a result that indicates a low probability of coronary x Early positive response within six minutesartery disease is one in which 85% of the maximum predicted x Persistence of ST depression for more than six minutes intoheart rate is achieved with a physiological response in blood recoverypressure and no associated ST segment depression. x ST segment depression in five or more leads A test that indicates a high probability of coronary artery x Exertional hypotensiondisease is one in which there is substantial ST depression at lowwork rate associated with typical angina-like pain and a drop inblood pressure. Deeper and more widespread ST depressiongenerally indicates more severe or extensive disease. False positive results are common in women, reflecting thelower incidence of coronary artery disease in this group.Prognostic testingExercise testing in patients who have just had a myocardialinfarction is indicated only in those in whom a revascularisation Rationale for testingprocedure is contemplated; a less strenuous protocol is used.Testing provides prognostic information. Patients with low x Bayes’s theorem of diagnostic probability states that the predictive value of an abnormal exercise test will vary according to theexercise capacity and hypotension induced by exercise have a probability of coronary artery disease in the population underpoor prognosis. Asymptomatic ST segment depression after studymyocardial infarction is associated with a more than 10-fold x Exercise testing is therefore usually performed in patients with anincrease in mortality compared with a normal exercise test. moderate probablility of coronary artery disease, rather than inConversely, patients who reach stage 3 of a modified Bruce those with a very low or high probabilityprotocol with a blood pressure response of > 30 mm Hg havean annual mortality of < 2%. Exercise testing can also addprognostic information in patients after percutaneoustransluminal coronary angiography or coronary artery bypassgraft.ScreeningExercise testing of asymptomatic patients is controversialbecause of the high false positive rate in such individuals.Angina remains the most reliable indicator of the need forfurther investigation. In certain asymptomatic groups with particular occupations(for example, pilots) there is a role for regular exercise testing,though more stringent criteria for an abnormal test result (suchas ST segment depression of > 2 mm) should be applied. In theUnited Kingdom, drivers of heavy goods vehicles and publicservice vehicles have to achieve test results clearly specified bythe Driver and Vehicle Licensing Agency before they areconsidered fit to drive.44
  • 52. 12 Conditions affecting the right side of the heartRichard A Harrigan, Kevin JonesMany diseases of the right side of the heart are associated withelectrocardiographic abnormalities. Electrocardiography is This article discusses right atrial enlargement, right ventricularneither a sensitive nor specific tool for diagnosing conditions hypertrophy, and thesuch as right atrial enlargement, right ventricular hypertrophy, electrocardiographic changes associatedor pulmonary hypertension. However, an awareness of the with chronic obstructive pulmonaryelectrocardiographic abnormalities associated with these disease, pulmonary embolus, acute rightconditions may support the patient’s clinical assessment and heart strain, and valvular heart diseasemay prevent the changes on the electrocardiogram from beingwrongly attributed to other conditions, such as ischaemia.Right atrial enlargementThe forces generated by right atrial depolarisation are directedanteriorly and inferiorly and produce the early part of the P IIwave. Right atrial hypertrophy or dilatation is thereforeassociated with tall P waves in the anterior and inferior leads,though the overall duration of the P wave is not usuallyprolonged. A tall P wave (height >2.5 mm) in leads II, III, and IIIaVF is known as the P pulmonale. The electrocardiographic changes suggesting right atrialenlargement often correlate poorly with the clinical andpathological findings. Right atrial enlargement is associated aVFwith chronic obstructive pulmonary disease, pulmonaryhypertension, and congenital heart disease—for example,pulmonary stenosis and tetralogy of Fallot. In practice, mostcases of right atrial enlargement are associated with right Large P waves in leads II, III, and aVF (P pulmonale)ventricular hypertrophy, and this may be reflected in theelectrocardiogram. The electrocardiographic features of rightatrial enlargement without coexisting right ventricularhypertrophy are seen in patients with tricuspid stenosis. Diagnostic criteria for right ventricular hypertrophyP pulmonale may appear transiently in patients with acutepulmonary embolism. (Provided the QRS duration is less than 0.12 s) x Right axis deviation of + 110° or more x Dominant R wave in lead V1 x R wave in lead V1 >7 mmRight ventricular hypertrophy Supporting criteriaThe forces generated by right ventricular depolarisation are x ST segment depression and T wave inversion in leads V1 to V4directed rightwards and anteriorly and are almost completely x Deep S waves in leads V5, V6, I, and aVLmasked by the dominant forces of left ventriculardepolarisation. In the presence of right ventricular hypertrophythe forces of depolarisation increase, and if the hypertrophy issevere these forces may dominate on the electrocardiogram. Right ventricular hypertrophy is associated with The electrocardiogram is a relatively insensitive indicator of pulmonary hypertension, mitral stenosis, and, lessthe presence of right ventricular hypertrophy, and in mild cases commonly, conditions such as pulmonary stenosis andof right ventricular hypertrophy the trace will be normal. congenital heart disease I V1 II V2 Right ventricular hypertrophy secondary to pulmonary stenosis (note the dominant R III V3 wave in lead V1, presence of right atrial hypertrophy, right axis deviation, and T wave inversion in leads V1 to V3) 45
  • 53. ABC of Clinical Electrocardiography Lead V1 lies closest to the right ventricular myocardium Conditions associated with tall R wave in lead V1and is therefore best placed to detect the changes of rightventricular hypertrophy, and a dominant R wave in lead V1 is x Right ventricular hypertrophy x Posterior myocardial infarctionobserved. The increased rightward forces are reflected in the x Type A Wolff-Parkinson-White syndromelimb leads, in the form of right axis deviation. Secondary x Right bundle branch blockchanges may be observed in the right precordial chest leads, A tall R wave in lead V1 is normal in children and young adultswhere ST segment depression and T wave inversion are seen. A dominant R wave in lead V1 can occur in otherconditions, but the absence of right axis deviation allows theseconditions to be differentiated from right ventricularhypertrophy. Isolated right axis deviation is also associated with Conditions associated with right axis deviationa range of conditions. x Right ventricular hypertrophy x Left posterior hemiblock x Lateral myocardial infarctionChronic obstructive pulmonary x Acute right heart straindisease Right axis deviation is normal in infants and childrenIn chronic obstructive pulmonary disease, hyperinflation of thelungs leads to depression of the diaphragm, and this isassociated with clockwise rotation of the heart along itslongitudinal axis. This clockwise rotation means that thetransitional zone (defined as the progression of rS to qR in the About three quarters of patients withchest leads) shifts towards the left with persistence of an rS chronic obstructive pulmonary diseasepattern as far as V5 or even V6. This may give rise to a have electrocardiographic abnormalities.“pseudoinfarct” pattern, with deep S waves in the right P pulmonale is often but not invariablyprecordial leads simulating the appearance of the QS waves present and may occur with or without clinical evidence of cor pulmonaleand poor R wave progression seen in anterior myocardialinfarction. The amplitude of the QRS complexes may be smallin patients with chronic obstructive pulmonary disease as thehyperinflated lungs are poor electrical conductors. I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 Chronic obstructive pulmonary disease (note the P pulmonale, low amplitude QRS complexes, and poor R wave progression) Cardiac arrhythmias may occur in patients with chronicobstructive pulmonary disease, particularly in association with In chronic obstructive pulmonary disease thean acute respiratory tract infection, respiratory failure, or electrocardiographic signs of right ventricularpulmonary embolism. Arrhythmias are sometimes the result of hypertrophy may be present, indicating the presence ofthe underlying disease process but may also occur as side effects cor pulmonaleof the drugs used to treat the disease. Multifocal atrial tachycardia The arrhythmias are mostly supraventricular in origin andinclude atrial extrasystoles, atrial fibrillation or flutter, andmultifocal atrial tachycardia. Ventricular extrasystoles andventricular tachycardia may also occur.46
  • 54. Conditions affecting the right side of the heartAcute pulmonary embolism IThe electrocardiographic features of acute pulmonaryembolism depend on the size of the embolus and itshaemodynamic effects and on the underlying cardiopulmonaryreserve of the patient. The timing and frequency of the IIIelectrocardiographic recording is also important as changesmay be transient. Patients who present with a small pulmonary Sinus tachycardia and S1,embolus are likely to have a normal electrocardiogram or a Q3, T3 pattern in patient with pulmonary embolustrace showing only sinus tachycardia. If the embolus is large and associated with pulmonaryartery obstruction, acute right ventricular dilatation may occur.This may produce an S wave in lead I and a Q wave in lead III. Right ventricular dilatation may lead to right sidedT wave inversion in lead III may also be present, producing the conduction delays, which manifest as incomplete orwell known S1, Q3, T3 pattern. complete right bundle branch block. There may be some rightward shift of the frontal plane QRS axis. Right atrial dilatation may lead to prominent P waves in The S1, Q3, T3 pattern is seen in about the inferior leads. Atrial arrhythmias including flutter and 12% of patients with a massive pulmonary fibrillation are common, and T wave inversion in the right embolus precordial leads may also occur I aVR V1 V4 II aVL V2 V5III aVF V3 V6Preoperative electrocardiogram in otherwise healthy 38 year old man I aVR V1 V4 II aVL V2 V5III aVF V3 V6 Acute pulmonary embolism: 10 days postoperatively the same patient developed acute dyspnoea and hypotension (note the T wave inversion in the right precordial leads and lead III) 47
  • 55. ABC of Clinical Electrocardiography I aVR V1 V4 Electrocardiographic abnormalities found in acute pulmonary embolism x Sinus tachycardia II aVL V2 V5 x Atrial flutter or fibrillation x S1, Q3, T3 pattern x Right bundle branch block (incomplete or complete) x T wave inversion in the right precordial leads x P pulmonale x Right axis deviation III aVF V3 V6S1, Q3, T3 pattern and right bundle branch block in patient withpulmonary embolusAcute right heart strainWhen the electrocardiogram shows features of right ventricularhypertrophy accompanied by ST segment depression andT wave inversion, a ventricular “strain” pattern is said to exist. V1 V4Ventricular strain is seen mainly in leads V1 and V2. Themechanism is unclear. A strain pattern is sometimes seen inacute massive pulmonary embolism but is also seen in patientswith right ventricular hypertrophy in the absence of anydetectable stress on the ventricle. Both pneumothorax andmassive pleural effusion with acute right ventricular dilatation V2 V5may also produce a strain pattern.Right sided valvular problemsTricuspid stenosisTricuspid stenosis is a rare disorder and is usually associated V3 V6with rheumatic heart disease. It appears in theelectrocardiogram as P pulmonale. It generally occurs inassociation with mitral valve disease, and therefore theelectrocardiogram often shows evidence of biatrialenlargement, indicated by a large biphasic P wave in lead V1with an initial positive deflection followed by a terminalnegative deflection. Example of right heart strain: right ventricular hypertrophy with widespread T wave inversion in chest leadsTricuspid regurgitationThe electrocardiogram is an unhelpful tool for diagnosingtricuspid regurgitation and generally shows the features of theunderlying cardiac disease. The electrocardiographicmanifestations of tricuspid regurgitation are non-specific and II V1include incomplete right bundle branch block and atrialfibrillation.Pulmonary stenosis Biatrial abnormalityPulmonary stenosis leads to pressure overload in the rightatrium and ventricle. The electrocardiogram may be completelynormal in the presence of mild pulmonary stenosis. Moresevere lesions are associated with electrocardiographic featuresof right atrial and ventricular hypertrophy, with tall P waves,marked right axis deviation, and a tall R wave in lead V1.48
  • 56. 13 Conditions affecting the left side of the heartJune Edhouse, R K Thakur, Jihad M KhalilMany cardiac and systemic illnesses can affect the left side of theheart. After a careful history and examination,electrocardiography and chest radiography are first line Conditions affecting left side of heart covered in this articleinvestigations. Electrocardiography can provide supportiveevidence for conditions such as aortic stenosis, hypertension, x Left atrial hypertrophy x Left ventricular hypertrophyand mitral stenosis. Recognition of the associated x Valvular diseaseelectrocardiographic abnormalities is important as x Cardiomyopathies (hypertrophic, dilated, restrictive)misinterpretation may lead to diagnostic error. This articledescribes the electrocardiographic changes associated with leftatrial hypertrophy, left ventricular hypertrophy, valvular disease,and cardiomyopathies.Left atrial abnormalityThe term left atrial abnormality is used to imply the presence ofatrial hypertrophy or dilatation, or both. Left atrialdepolarisation contributes to the middle and terminal portionsof the P wave. The changes of left atrial hypertrophy aretherefore seen in the late portion of the P wave. In addition, leftatrial depolarisation may be delayed, which may prolong theduration of the P wave. The P wave in lead V1 is often biphasic. Early right atrialforces are directed anteriorly giving rise to an initial positivedeflection; these are followed by left atrial forces travelling Biphasic P wave in V1. The large negative deflection indicates leftposteriorly, producing a later negative deflection. A large atrial abnormality (enlarged tonegative deflection ( > 1 small square in area) suggests a left show detail)atrial abnormality. Prolongation of P wave duration to greaterthan 0.12 s is often found in association with a left atrialabnormality. Normal P waves may be bifid, the minor notchprobably resulting from slight asynchrony between right andleft atrial depolarisation. However, a pronounced notch with a P mitrale in lead II. P mitrale is apeak-to-peak interval of > 0.04 s suggests left atrial P wave that is abnormallyenlargement. notched and wide and is usually most prominent in lead II; it is Any condition causing left ventricular hypertrophy may commonly seen in associationproduce left atrial enlargement as a secondary phenomenon. with mitral valve disease,Left atrial enlargement can occur in association with systemic particularly mitral stenosishypertension, aortic stenosis, mitral incompetence, and (enlarged to show detail)hypertrophic cardiomyopathy.Left ventricular hypertrophySystemic hypertension is the most common cause of leftventricular hypertrophy, but others include aortic stenosis andco-arctation of the aorta. Many electrocardiographic criteria Left ventricular hypertrophyhave been suggested for the diagnosis of left ventricular Voltage criteriahypertrophy, but none is universally accepted. Scoring systems Limb leadsbased on these criteria have been developed, and although they x R wave in lead 1 plus S wave in lead III > 25 mmare highly specific diagnostic tools, poor sensitivity limits their x R wave in lead aVL > 11 mmuse. x R wave in lead aVF > 20 mm x S wave in lead aVR > 14 mmElectrocardiographic findings Precordial leadsThe electrocardiographic features of left ventricular x R wave in leads V4, V5, or V6 > 26 mm x R wave in leads V5 or 6 plus S wave in lead V1 > 35 mmhypertrophy are classified as either voltage criteria or x Largest R wave plus largest S wave in precordial leads > 45 mmnon-voltage criteria. Non-voltage criteria The electrocardiographic diagnosis of left ventricular x Delayed ventricular activation time >0.05 s in leads V5 or V6 >0.05 shypertrophy is difficult in individuals aged under 40. Voltage x ST segment depression and T wave inversion in the left precordialcriteria lack specificity in this group because young people often leadshave high amplitude QRS complexes in the absence of left The specificity of these criteria is age and sex dependentventricular disease. Even when high amplitude QRS complexes 49
  • 57. ABC of Clinical Electrocardiographyare seen in association with non-voltage criteria—such as STsegment and T wave changes—a diagnosis cannot be made withconfidence. Typical repolarisation changes seen in leftventricular hypertrophy are ST segment depression and T waveinversion. This “strain” pattern is seen in the left precordialleads and is associated with reciprocal ST segment elevation inthe right precordial leads. I aVR V1 V4 II aVL V2 V5 Left ventricular hypertrophy with strain (note dominant R wave and repolarisation abnormality)The presence of these ST segment changes can causediagnostic difficulty in patients complaining of ischaemic-type III aVF V3 V6chest pain; failure to recognise the features of left ventricularhypertrophy can lead to the inappropriate administration ofthrombolytic therapy. Furthermore, in patients known to have left ventricularhypertrophy it can be difficult to diagnose confidently acuteischaemia on the basis of ST segment changes in the leftprecordial leads. It is an advantage to have old Left ventricular hypertrophy in patient who had presented with chest painelectrocadiograms for comparison. Other non-voltage criteria and was given thrombolytic therapy inappropriately because of the STare common in left ventricular hypertrophy. Left atrial segment changes in V1 and V2hypertrophy or prolonged atrial depolarisation and left axisdeviation are often present; and poor R wave progression iscommonly seen. The electrocardiogram is abnormal in almost 50% of I aVR V1 V4patients with hypertension, with minimal changes in 20% andobvious features of left ventricular hypertrophy in 30%. There isa linear correlation between the electrocardiographic changesand the severity and duration of the hypertension. Highamplitude QRS complexes are seen first, followed by thedevelopment of non-voltage criteria. The specificity of the electrocardiographic diagnosis of leftventricular hypertrophy is improved if a scoring system is used. II aVL V2 V5Scoring system for left ventricular hypertrophy (LVH)—suggested if points total >5Electrocardiographic feature No of pointsAmplitude (any of the following) 3 III aVF V3 V6x Largest R or S wave in limb leads >20 mmx S wave in leads V1 or V2 >30 mmx R wave in leads V5 or V6 >30 mmST-T wave segment changes typical for LVH in the absence of digitalis 3Left atrial involvement 3Left axis deviation 2 Left ventricular hypertrophy without voltage criteria—in a man whoQRS duration of >0.09 s 1 presented with heart failure secondary to severe aortic stenosis (gradientDelayed ventricular activation time in leads 125 mm Hg). The ST segment changes are typical for left ventricular V5 and V6 of >0.05 s 1 hypertrophy and there is evidence of left atrial enlargement. If the scoring system is used, these findings suggest left ventricular hypertrophy even though none of the R or S waves meets voltage criteria50
  • 58. Conditions affecting the left side of the heartValvular problemsA normal electrocardiogram virtually rules out the presence ofsevere aortic stenosis, except in congenital valve disease, where Electrocardiographic features of valvular diseasethe trace may remain normal despite a substantial degree of x The electrocardiographic features of aortic regurgitation includestenosis. Left ventricular hypertrophy is seen in about 75% of the features of left ventricular hypertrophy, often with the strain patternpatients with severe aortic stenosis. Left atrial enlargement may x Mitral stenosis is associated with left atrial abnormality or atrialalso be seen in the electrocardiogram. Left axis deviation and fibrillation and right ventricular hypertrophyleft bundle branch block may occur. x Mitral regurgitation is associated with atrial fibrillation, though again the features of left atrial hypertrophy may be seen if the patient is in sinus rhythm. Evidence of left ventricular hypertrophyThe cardiomyopathies may be seenDiseases of the myocardium are classified into three types onthe basis of their functional effects: hypertrophic (obstructed),dilated (congestive), or restrictive cardiomyopathy. Incardiomyopathy the myocardium is diffusely affected, andtherefore the resulting electrocardiographic abnormalities may Common features of cardiomyopathybe diverse. include electrical holes (Q waves), conduction defects (bundle branch blockHypertrophic cardiomyopathy and axis deviation), and arrhythmiasThis is characterised by marked myocardial thickeningpredominantly affecting the interventricular septum and/or theapex of the left ventricle. Electrocardiographic evidence of leftventricular hypertrophy is found in 50% of patients. Acharacteristic abnormality is the presence of abnormal Q waves Main electrocardiographic changes associated within the anterolateral or inferior chest leads, which may mimic the hypertrophic cardiomyopathyappearance of myocardial infarction. As the left ventricle x Left ventricular hypertrophybecomes increasingly less compliant, there is increasing x Left atrial enlargementresistance to atrial contraction, and signs of left atrial x Abnormal inferior and anterior and/or lateral Q wavesabnormality are commonly seen. Atrial fibrillation and x Bizarre QRS complexes masquerading, for example, assupraventricular tachycardias are common arrhythmias in pre-excitation and bundle branch blockpatients with hypertrophic cardiomyopathy. Ventriculartachycardias may also occur and are a cause of sudden death inthese patients. I II III aVR aVL aVF V1 V2 V3 V4 V5 V6Abnormal Q waves in patient with hypertrophic cardiomyopathyDilated cardiomyopathyMany patients with dilated cardiomyopathy have anatomical leftventricular hypertrophy, though the electrocardiographic signsof left ventricular hypertrophy are seen in only a third of ECG changes in dilated cardiomyopathypatients. In some patients the signs of left ventricular x Left bundle branch blockhypertrophy may be masked as diffuse myocardial fibrosis can x Left atrial enlargement x Abnormal Q waves in leads V1 to V4reduce the voltage of the QRS complexes. If right ventricular x Left ventricular hypertrophyhypertrophy is also present the increased rightward forces of x Arrhythmias—ventricular premature beats, ventricular tachycardia,depolarisation may cancel out some of the leftward forces, again atrial fibrillationmasking the signs of left ventricular hypertrophy. Signs of left atrial enlargement are common, and oftenthere is evidence of biatrial enlargement. Abnormal Q waves 51
  • 59. ABC of Clinical Electrocardiographymay be seen, though less commonly than in hypertrophiccardiomyopathy. Abnormal Q waves are most often seen inleads V1 to V4 and may mimic the appearance of a myocardialinfarction.Restrictive cardiomyopathy I aVR V1 V4Restrictive cardiomyopathy is the least common form ofcardiomyopathy and is the end result of several differentdiseases associated with myocardial infiltration—for example,amyloidosis, sarcoidosis, and haemochromatosis. The mostcommon electrocardiographic abnormality is the presence oflow voltage QRS complexes, probably due to myocardial II aVL V2 V5infiltration. Both supraventricular and ventricular arrhythmiasare common.Electrocardiographic findings in restrictive cardiomyopathyx Low voltage QRS complexesx Conduction disturbancex Arrhythmias—supraventricular, ventricular III aVF V3 V6 I aVR V1 V4 Dilated cardiomyopathy (note left ventricular hypertrophy pattern) II aVL V2 V5 III aVF V3 V6Patient with restrictive cardiomyopathy due toamyloidosis (note the low voltage QRS complexes andthe right bundle branch block)The box showing voltage criteria for left ventricular hypertrophy andthe box showing the scoring system are adapted from Chou T,Knilans TK. Electrocardiography in clinical practice. 4th ed. Philadelphia,PA: Saunders, 1996.52
  • 60. 14 Conditions not primarily affecting the heartCorey Slovis, Richard JenkinsTo function correctly, individual myocardial cells rely on normalconcentrations of biochemical parameters such as electrolytes, It is important to recognise that some electrocardiographic changes are due tooxygen, hydrogen, glucose, and thyroid hormones, as well as a conditions other than cardiac disease sonormal body temperature. Abnormalities of these and other that appropriate treatment can be givenfactors affect the electrical activity of each myocardial cell and and unnecessary cardiac investigationthus the surface electrocardiogram. Characteristic avoidedelectrocardiographic changes may provide useful diagnosticclues to the presence of metabolic abnormalities, the promptrecognition of which can be life saving.HyperkalaemiaIncreases in total body potassium may have dramatic effects on Electrocardiographic features of hyperkalaemiathe electrocardiogram. The most common changes associatedwith hyperkalaemia are tall, peaked T waves, reduced amplitude Serum potassiumand eventually loss of the P wave, and marked widening of the (mmol/l) Major changeQRS complex. 5.5-6.5 Tall peaked T waves The earliest changes associated with hyperkalaemia are tall 6.5-7.5 Loss of P wavesT waves, best seen in leads II, III, and V2 to V4. Tall T waves are 7.0-8.0 Widening of QRS complexesusually seen when the potassium concentration rises above 8.0-10 Sine wave, ventricular arrhythmias, asystole5.5-6.5 mmol/l. However, only about one in five hyperkalaemicpatients will have the classic tall, symmetrically narrow andpeaked T waves; the rest will merely have large amplitude Twaves. Hyperkalaemia should always be suspected when theamplitude of the T wave is greater than or equal to that of the Tall peaked T waveR wave in more than one lead. As the potassium concentration rises above 6.5-7.5 mmol/l,changes are seen in the PR interval and the P wave: the P wavewidens and flattens and the PR segment lengthens. As theconcentration rises, the P waves may disappear. Tall peaked The QRS complex will begin to widen with a potassium T wave Loss ofconcentration of 7.0-8.0 mmol/l. Unlike right or left bundle P wavebranch blocks, the QRS widening in hyperkalaemia affects allportions of the QRS complex and not just the terminal forces.As the QRS complex widens it may begin to merge with the Widened QRST wave and create a pattern resembling a sine wave—a with tall T wave“preterminal” rhythm. Death resulting from hyperkalaemia maybe due to asystole, ventricular fibrillation, or a wide pulselessidioventricular rhythm. Hyperkalaemia induced asystole is morelikely to be seen in patients who have had chronic, rather thanacute, hyperkalaemia. Serial changes in hyperkalaemia A B CSerial changes in patient with renal failure receiving treatment for hyperkalaemia. As potassium concentration drops, theelectrocardiogram changes: 9.3 mmol/l, very broad QRS complexes (A); 7.9 mmol/l, wide QRS complexes with peaked T waves andabsent P waves (B); 7.2 mmol/l, QRS complex continues to narrow and T waves diminish in size (C) 53
  • 61. ABC of Clinical Electrocardiography A B Broad complex tachycardia with a potassium concentration of 8.4 mmol/l (A); after treatment, narrower complexes with peaked T waves (B)HypokalaemiaHypokalaemia may produce several electrocardiographicchanges, especially when there is total body depletion of both Electrocardiographic features of hypokalaemiapotassium and magnesium. The commonest changes are x Broad, flat T wavesdecreased T wave amplitude, ST segment depression, and x ST depression x QT interval prolongationpresence of a U wave. Other findings, particularly in the x Ventricular arrhythmias (premature ventricular contractions,presence of coexistent hypomagnesaemia, include a prolonged torsades de pointes, ventricular tachycardia, ventricular fibrillation)QT interval, ventricular extrasystoles, and malignant ventriculararrhythmias such as ventricular tachycardia, torsades de pointes,and ventricular fibrillation. Electrocardiographic changes arenot common with mild to moderate hypokalaemia, and it isonly when serum concentrations are below 2.7 mmol/l thatchanges reliably appear. A prominent U wave in association with a small T wave areconsidered to be the classic electrocardiographic findings ofhypokalaemia. Many authors list a prolonged QT interval as a ST depression A Bcommon finding in hypokalaemia. However, most cases of a U wavepresumed prolongation of the QT interval are really QUintervals. Most hypokalaemic patients with true prolongation ofthe QT interval have coexisting hypomagnesaemia and are atrisk of ventricular arrhythmias, including torsades de pointes. Flat T wave Patients with a potassium concentration below 2.5-3.0mmol/l often develop ventricular extrasystoles. Hypokalaemia Left: Diagram of electrocardiographic changes associated with hypokalaemia. Right: Electrocardiogram showing prominent U wave,may also be associated with supraventricular arrhythmias, such potassium concentration 2.5 mmol/l (A) and massive U waves with STas paroxysmal atrial tachycardia, multifocal atrial tachycardia, depression and flat T waves, potassium concentration 1.6 mmol/l (B)atrial fibrillation, and atrial flutter.HypothermiaHypothermia is present when the core temperature is less than35°C. As body temperature falls below normal, many Electrocardiographic features of hypothermiacardiovascular and electrophysiological changes occur. The x Tremor artefact from shiveringearliest change seen in the electrocardiogram is an artefact due x Atrial fibrillation with slow ventricular rateto shivering, although some hypothermic patients have x J waves (Osborn waves)relatively normal traces. The ability to shiver diminishes as body x Bradycardias, especially junctionaltemperature falls, and shivering is uncommon below a core x Prolongation of PR, QRS, and QT intervals x Premature ventricular beats, ventricular tachycardia, or ventriculartemperature of 32°C. fibrillation As body temperature falls further, all metabolic and x Asystolecardiovascular processes slow progressively. Pacemaker (heartrate) and conduction velocity decline, resulting in bradycardia,heart block, and prolongation of the PR, QRS, and QTintervals. At core temperature below 32°C, regular andorganised atrial activation disappears and is replaced by varyingdegrees of slow, irregular, and disorganised activity. If coretemperature falls below 28°C, a junctional bradycardia may be J waveseen. The J wave (Osborn wave) is the most specificelectrocardiographic finding in hypothermia. It is considered bymany to be pathognomonic for hypothermia, but it may alsooccasionally be seen in hypercalcaemia and in central nervoussystem disorders, including massive head injury and Sinus bradycardia, with a J wave, in a patient with hypothermia—coresubarachnoid haemorrhage. temperature 29°C (note the shivering artefact)54
  • 62. Conditions not primarily affecting the heart The J wave may even be a drug effect or, rarely, a normal Ventricular arrhythmias are the most commonvariant. The J wave is most commonly characterised by a mechanism of death in hypothermia. They seem to be“dome” or “hump” elevation in the terminal portion of the QRS more common during rewarming as the bodydeflection and is best seen in the left chest leads. The size of the temperature rises through the 28°-32°C rangeJ wave often correlates with the severity of hypothermia( < 30°C) but the exact aetiology is not known.ThyrotoxicosisThe cardiovascular system is very sensitive to increased levels ofcirculating thyroid hormones. Increases in cardiac output and Electrocardiographic features of thyrotoxicosisheart rate are early features in thyrotoxicosis. The most Most common findingscommon electrocardiographic changes seen in thyrotoxicosis x Sinus tachycardia x Increased QRS voltagesare sinus tachycardia, an increased electrical amplitude of all x Atrial fibrillationdeflections, and atrial fibrillation. Other findings About 50% of thyrotoxic patients have a resting pulse rate x Supraventricular arrhythmias (premature atrial beats, paroxysmalabove 100 beats/min. Atrial tachyarrhythmias are common as supraventricular tachycardia, multifocal atrial tachycardia, atrialthe atria are very sensitive to the effects of triiodothyronine. flutter)Patients with thyroid storm may develop paroxysmal x Non-specific ST and T wave changessupraventricular tachycardia with rates exceeding 200 x Ventricular extrasystolesbeats/min. Elderly patients may develop ischaemic ST andT wave changes because of their tachycardias. Increased voltageis a common but non-specific electrocardiographic finding inhyperthyroidism, and is more commonly seen in youngerpatients. Atrial fibrillation is the most common sustained arrhythmiain thyrotoxicosis, occurring in about 20% of all cases. It is most Increased Rhythm strip voltagecommon in elderly patients, men, those with a particularly highconcentration of thyroid hormone, and patients with left atrialenlargement or other intrinsic heart disease. Treatment of atrial Atrial fibrillationfibrillation in thyrotoxicosis is difficult as the rhythm may berefractory to cardioversion. However, most cases revertspontaneously to sinus rhythm when euthyroid. Multifocal atrialtachycardia and atrial flutter with 2:1 conduction, and even 1:1 Left: Diagram of electrocardiographic changes associated with thyrotoxicosis.conduction, may also be seen. Right: Sinus tachycardia in patient with thyrotoxicosis Patients with thyrotoxicosis may have otherelectrocardiographic findings. Non-specific ST and T wavechanges are relatively common. Ventricular arrhythmias may beseen, though much less frequently than atrial arrhythmias.Thyrotoxic patients have two or three times the normal number Electrocardiographic features of hypothyroidismof premature ventricular contractions. Most common x Sinus bradycardia x Prolonged QT intervalHypothyroidism x Flat or inverted T wavesHypothyroidism causes slowing of the metabolic rate and affects Less common x Heart blockalmost all bodily functions, including heart rate and x Low QRS voltagescontractility. It causes similar slowing of electrical conduction x Intraventricular conduction defectsthroughout the heart. x Ventricular extrasystoles The most common electrocardiographic changes associatedwith hypothyroidism are sinus bradycardia, a prolonged QTinterval, and inverted or flat T waves. Most hypothyroid patientswill have a low to normal heart rate (about 50-70 beats/min).Patients with severe hypothyroidism and those with pre-existing Low voltageheart disease may also develop increasing degrees of heartblock or bundle branch block (especially right bundle branch Increased Increased Inverted orblock). Conduction abnormalities due to hypothyroidism PR QT flat T waveresolve with thyroid hormone therapy. Depolarisation, like all phases of the action potential, isslowed in hypothyroidism, and this results in a prolonged QTinterval. Torsades de pointes ventricular tachycardia has beenreported in hypothyroid patients and is related to prolongationof the QT interval, hypothyroidism induced electrolyteabnormalities, hypothermia, or hypoventilation. Hypothyroid patients are very sensitive to the effects of Top: Diagram of electrocardiographic changes associated withdigitalis and are predisposed to all the arrhythmias associated hypothyroidism. Bottom: Bradycardia (note small QRS complexes andwith digitalis intoxication. inverted T waves) in patient with hypothyroidism 55
  • 63. ABC of Clinical Electrocardiography Uncommonly, patients may develop large pericardial Non-specific T wave abnormalities are very common ineffusions, which give rise to electrical alternans (beat to beat hypothyroid patients. The T wave may be flattened orvariation in QRS voltages). Myxoedema coma should always be inverted in several leads. Unlike with most other causessuspected in patients with altered mental states who have of T wave abnormalities in hypothyroidism, associatedbradycardia and low voltage QRS complexes ( < 1 mV) in all ST changes are rarely seenleads.Other non-cardiac conditionsHypercalcaemia is associated with shortening of the QTinterval. At high calcium concentrations the duration of the Twave increases and the QT interval may then become normal.Digoxin may be harmful in hypercalcaemic patients and mayresult in tachyarrhythmias or bradyarrhythmias. Similarly, Short QT interval in patient with hypercalcaemiaintravenous calcium may be dangerous in a patient who has (calcium concentration 4 mmol/l)received digitalis. The QT prolongation seen in hypocalcaemiais primarily due to ST prolongation but is not thought to beclinical important. Hypoglycaemia is a common medical emergency, althoughit is not often recognised as having electrocardiographicsequelae. The electrocardiographic features include flattening ofthe T wave and QT prolongation. Acute electrocardiographic changes commonly accompanysevere subarachnoid haemorrhage. Typically these are STdepression or elevation and T wave inversion, although otherchanges, such as a prolonged QT interval, can also be seen. Massive T wave inversion and QT prolongation Finally, artefacts due to shivering or tremor can obscure associated with subarachnoid haemorrhageelectrocardiographic changes or simulate arrhythmias. Electrocardiographic artefacts—“shivering artefact” in patient with anterior myocardial infarction (top) and electrical interference simulating tachycardia (bottom)56
  • 64. 15 Paediatric electrocardiographySteve Goodacre, Karen McLeodGeneral clinicians and junior paediatricians may have little Successful use of paediatric electrocardiographyexperience of interpreting paediatric electrocardiograms.Although the basic principles of cardiac conduction and x Be aware of age related differences in the indications fordepolarisation are the same as for adults, age related changes in performing electrocardiography, the normal ranges for electrocardiographic variables, and the typical abnormalities inthe anatomy and physiology of infants and children produce infants and childrennormal ranges for electrocardiographic features that differ from x Genuine abnormality is unusual; if abnormality is suspected, seek aadults and vary with age. Awareness of these differences is the specialist opinionkey to correct interpretation of paediatric electrocardiograms.Recording the electrocardiogram Indications for paediatric electrocardiography x Syncope or seizure x Electrolyte disturbanceTo obtain a satisfactory recording in young children requires x Exertional symptoms x Kawasaki diseasepatience, and the parents may be helpful in providing a source x Drug ingestion x Rheumatic feverof distraction. Limb electrodes may be placed in a more x Tachyarrhythmia x Myocarditisproximal position to reduce movement artefacts. Standard adult x Bradyarrhythmia x Myocardial contusionelectrode positions are used but with the addition of either lead x Cyanotic episodes x PericarditisV3R or lead V4R to detect right ventricular or atrial x Heart failure x Post cardiac surgery x Hypothermia x Congenital heart defectshypertrophy. Standard paper speed (25 mm/s) and deflection(10 mm/mV) are used, although occasionally large QRScomplexes may require the gain to be halved. Paediatric electrocardiographic findings that may be normalIndications for electrocardiography x Heart rate > 100 beats/min x QRS axis > 90°Chest pain in children is rarely cardiac in origin and is often x Right precordial T wave inversionassociated with tenderness in the chest wall. x Dominant right precordial R wavesElectrocardiography is not usually helpful in making a x Short PR and QT intervals x Short P wave and short duration of QRS complexesdiagnosis, although a normal trace can be very reassuring to the x Inferior and lateral Q wavesfamily. Typical indications for paediatric electrocardiographyinclude syncope, exertional symptoms, tachyarrhythmias,bradyarrhythmias, and drug ingestion. Use ofelectrocardiography to evaluate congenital heart defects is aspecialist interest and will not be discussed here. I aVR V4R V4Age related changes in normalelectrocardiogramsFeatures that would be diagnosed as abnormal in an adult’selectrocardiogram may be normal, age related changes in apaediatric trace. The explanation for why this is so lies in how II aVL V1 V5the heart develops during infancy and childhood. At birth the right ventricle is larger than the left. Changes insystemic vascular resistance result in the left ventricle increasingin size until it is larger than the right ventricle by age 1 month.By age 6 months, the ratio of the right ventricle to the leftventricle is similar to that of an adult. Right axis deviation, largeprecordial R waves, and upright T waves are therefore normal III aVF V2 V6in the neonate. The T wave in lead V1 inverts by 7 days andtypically remains inverted until at least age 7 years. UprightT waves in the right precordial leads (V1 to V3) between ages7 days and 7 years are a potentially important abnormalityand usually indicate right ventricular hypertrophy. The QRS complex also reflects these changes. At birth, themean QRS axis lies between + 60° and + 160°, R waves areprominent in the right precordium, and S waves are prominentin the left precordium. By age 1 year, the axis changes gradually Normal 12 lead electrocardiogram from 3 day old babyto lie between + 10° and + 100°. boy showing right axis deviation, dominant R wave in leads V4R and V1, and still predominantly upright T The resting heart rate decreases from about 140 beats/min wave in V1. Persistence of upright T waves in rightat birth to 120 beats/min at age 1 year, 100 at 5 years, and adult precordial leads beyond first week of life is sign of rightvalues by 10 years. The PR interval decreases from birth to age ventricular hypertrophy 57
  • 65. ABC of Clinical Electrocardiography1 year and then gradually increases throughout childhood. TheP wave duration and the QRS duration also increase with age.The QT interval depends on heart rate and age, increasing withage while decreasing with heart rate. Q waves are normally seenin the inferior or lateral leads but signify disease if present inother leads. I aVR V1 V4Abnormal paediatricelectrocardiogramsDiagnosis of abnormality on a paediatric electrocardiogram willrequire knowledge of normal age related values, particularly forcriteria relating to right or left ventricular hypertrophy. II aVL V2 V5 P wave amplitude varies little with age and is best evaluatedfrom lead II, V1, or V4R. Wide P waves indicate left atrialhypertrophy, and P waves taller than 2.5 mm in lead II indicateright atrial hypertrophy. P waves showing an abnormal pattern,such as inversion in leads II or aVF, indicate atrial activation III aVF V3 V6from a site other than the sinoatrial node. II III aVF V1 V4R Electrocardiogram from 12 year old (late childhood) (axis is now within normal “adult” range and R wave is no longer dominant in right precordial leads)Electrocardiogram from 3 year old with restrictivecardiomyopathy and severe right and left atrialenlargement. Tall (>2.5 mm), wide P waves are clearlyseen in lead II, and P wave in V1 is markedly biphasic Prolongation of the QRS complex may be due to bundlebranch block, ventricular hypertrophy, metabolic disturbances,or drugs. I aVR V1 V4 Diagnosis of ventricular hypertrophy by “voltage criteria”will depend on age adjusted values for R wave and S waveamplitudes. However, several electrocardiographic features maybe useful in making a diagnosis. A qR complex or an rSR′pattern in lead V1, upright T waves in the right precordial leadsbetween ages 7 days and 7 years, marked right axis deviation(particularly associated with right atrial enlargement), andcomplete reversal of the adult precordial pattern of R and Swaves will all suggest right ventricular hypertrophy. Left II aVL V2 V5ventricular hypertrophy may be indicated by deep Q waves inthe left precordial leads or the typical adult changes of lateralST depression and T wave inversion. III aVF V3 V6Normal values in paediatric electrocardiograms R wave (S wave) PR QRS amplitude (mm) interval durationAge (ms) (ms) Lead V1 Lead V6Birth 80-160 < 75 5-26 (1-23) 0-12 (0-10) Electrocardiogram from 13 year old boy with transposition of great arteries and previous Mustard’s procedure. The right ventricle is the systemic6 months 70-150 < 75 3-20 (1-17) 6-22 (0-10) ventricle and the trace shows right ventricular hypertrophy with marked right axis deviation and a dominant R wave in the right precordial leads1 year 70-150 < 75 2-20 (1-20) 6-23 (0-7)5 years 80-160 < 80 1-16 (2-22) 8-25 (0-5)10 years 90-170 < 85 1-12 (3-25) 9-26 (0-4)58
  • 66. Paediatric electrocardiography The QT interval must be corrected for heart rate by dividingits value by the square root of the R-R interval. A corrected QTinterval exceeding 0.45 s should be considered prolonged, but itshould be noted that the QT interval is highly variable in thefirst three days of life. QT prolongation may be seen inassociation with hypokalaemia, hypocalcaemia, hypothermia,drug treatment, cerebral injury, and the congenital long QTsyndrome. Other features of the long QT syndrome includenotching of the T waves, abnormal U waves, relative bradycardiafor age, and T wave alternans. These children may be at risk of I aVR V1 V4ventricular arrhythmia and sudden cardiac death.Electrocardiogram from 3 year old girl with long QT II aVL V2 V5syndromeProlongation of QT interval in association with T wave alternans (notealternating upright and inverted T waves ) Q waves are normally present in leads II, III, aVF, V5, andV6. Q waves in other leads are rare and associated with III aVF V3 V6disease—for example, an anomalous left coronary artery, ormyocardial infarction secondary to Kawasaki syndrome,. ST segment elevation may be a normal finding in teenagersas a result of early repolarisation. It may also be seen inmyocardial infarction, myocarditis, or pericarditis. In addition to the changes seen in ventricular hypertrophy,T waves may be inverted as a result of myocardial disease(inflammation, infarction, or contusion). Flat T waves are seen inassociation with hypothyroidism. Abnormally tall T waves occurwith hyperkalaemia. Electrocardiogram from 11 year old girl with left ventricular hypertrophy secondary to systemic hypertension. There are tall voltages in the left precordial and limb leads with secondary ST depression and T waveAbnormalities of rate and rhythm inversionThe wide variation in children’s heart rate with age and activitymay lead to misinterpretation by those more used to adultelectrocardiography. Systemic illness must be considered in anychild presenting with an abnormal cardiac rate or rhythm. Sinustachycardia in babies and infants can result in rates of up to240 beats/min, and hypoxia, sepsis, acidosis, or intracraniallesions may cause bradycardia. Sinus arrhythmia is a commonfeature in children’s electrocardiograms and is often quiteElectrocardiogram from 9 year old boy showing marked sinus arrhythmia, a common finding in paediatric traces 59
  • 67. ABC of Clinical Electrocardiographymarked. Its relation to breathing—slowing on expiration and Extrasystolesspeeding up on inspiration—allows diagnosis. The approach to electrocardiographic diagnosis of x Atrial extrasystoles are very common and rarely associated with diseasetachyarrhythmias in children is similar to that used in adults. x Ventricular extrasystoles are also common and, in the context of theMost narrow complex tachycardias in children are due to structurally normal heart, are almost always benignatrioventricular re-entrant tachycardia secondary to an x Typically, atrial and ventricular extrasystoles are abolished byaccessory pathway. If the pathway conducts only retrogradely, exercisethe electrocardiogram in sinus rhythm will be normal and thepathway is said to be “concealed.” If the pathway conductsanterogradely in sinus rhythm, then the trace will show thetypical features of the Wolff-Parkinson-White syndrome. AVnodal re-entrant tachycardia is rare in infants but may be seenin later childhood and adolescence. Atrial flutter and fibrillation are rare in childhood and areusually associated with underlying structural heart disease orprevious cardiac surgery. Atrial flutter can present as anuncommon arrhythmia in neonates with apparently otherwise Electrocardiogram showing atrial “flutter” in 14 year old girl with congenital heart disease and previous atrial surgery (in neonates with atrial flutter, 1:1normal hearts. atrioventricular conduction is more common, which may make P waves and Although all forms of ventricular tachycardia are rare, broad diagnosis less evident)complex tachycardia should be considered to be ventriculartachycardia until proved otherwise. Bundle branch block(usually right bundle) often occurs after cardiac surgery, and aprevious electrocardiogram can be helpful. Monomorphic Aids for diagnosing tachycardias, such as atrioventricularventricular tachycardia may occur secondary to surgery for dissociation and capture and fusion beats, are lesscongenital heart disease. Polymorphic ventricular tachycardia, common in children than in adultsor torsades de pointes, is associated with the long QTsyndrome.Polymorphic ventricular tachycardia in 5 year old girl Classification of atrioventricular block into first, second, andthird degree follows the same principles as for adults, although Complete atrioventricular blocka diagnosis of first degree heart block should take into account x Complete atrioventricular block may be congenital or secondary tothe variation of the PR interval with age. First degree heart surgeryblock and the Wenckebach phenomenon may be a normal x An association exists between congenital complete atrioventricularfinding in otherwise healthy children. First or second degree block and maternal anti-La and anti-Ro antibodies, which areblock, however, can occur with rheumatic carditis, diphtheria, believed to cross the placenta and damage conduction tissuedigoxin overdose, and congenital heart defects.Electrocardiogram from 6 year old girl with congenital heart block secondary to maternal antiphospholipid antibodies; there is complete atrioventriculardissociation, and the ventricular escape rate is about 50 beats/min60
  • 68. 16 Cardiac arrest rhythmsRobert French, Daniel DeBehnke, Stephen HawesSuccessful resuscitation from cardiac arrest depends on promptrecognition and appropriate treatment of the arrest rhythm. Cardiac arrest rhythmsArrhythmias are frequent immediately before and after arrest; x Ventricular fibrillationsome are particularly serious because they may precipitate x Pulseless ventricular tachycardia x Pulseless electrical activity (electromechanicalcardiac arrest—for example, ventricular tachycardia frequently dissociation)deteriorates into fibrillation. Early recognition of such x Asystolearrhythmias is therefore vital, necessitating cardiac monitoringof vulnerable patients. The cardiac arrest rhythms are ventricular fibrillation,pulseless ventricular tachycardia, pulseless electrical activity(also termed electromechanical dissociation), and asystole. In pulseless ventricular tachycardia and electromechanicaldissociation, organised electrical activity is present but fails to Ventricular fibrillation is the commonestproduce a detectable cardiac output. In ventricular fibrillation arrhythmia that causes sudden death outthe electrical activity is disorganised, and in asystole it is absent of hospitalaltogether. Ventricular fibrillation is usually a primary cardiac event,and with early direct current cardioversion the prognosis isrelatively good. By contrast, asystole and electromechanicaldissociation have a poor prognosis, with survival dependent onthe presence of a treatable underlying condition. Causes of ventricular fibrillation x Myocardial ischaemia/infarctionVentricular fibrillation x Cardiomyopathy x AcidosisMechanisms x ElectrocutionVentricular fibrillation probably begins in a localised area from x Drugs (for example—quinidine, digoxin, tricyclic antidepressants)which waves of activation spread in all directions. x Electrolyte disturbance (for example—hypokalaemia) The individual myocardial cells contract in anuncoordinated, rapid fashion. Fibrillation seems to bemaintained by the continuous re-entry of waves of activation.Activation is initially rapid but slows as the myocardiumbecomes increasingly ischaemic.Electrocardiographic featuresThe chaotic myocardial activity is reflected in theelectrocardiogram, with rapid irregular deflections of varyingamplitude and morphology and no discernible QRS complexes.The deflection rate varies between 150 and 500 beats/min. Fine ventricular fibrillationAlthough the atria may continue to beat, no P waves are usuallydiscernible. Ventricular fibrillation may be termed “coarse” or“fine” depending on the amplitude of the deflections. Initially, ventricular fibrillation tends to be high amplitude(coarse) but later degenerates to fine ventricular fibrillation.Coarse ventricular fibrillation 61
  • 69. ABC of Clinical ElectrocardiographyPotential pitfalls in diagnosisWhen the amplitude of the deflections is extremely low, fine “Persistent movement artefact,” such asventricular fibrillation can be mistaken for asystole. To avoid this that which occurs in a patient who ismistake, check the “gain” (wave form amplitude) on the fitting, can simulate ventricular fibrillationelectrocardiogram machine in case it has been set at aninappropriately low level. In addition, check the trace from twoleads perpendicular to one another (for example, leads II andaVL) because occasionally a predominant ventricular fibrillationwave form vector may occur perpendicular to the sensingelectrode and appear as an almost flat line.Movement artefact simulating ventricular fibrillationElectrocardiographic predictorsAcute myocardial ischaemia or infarction, especially anteriorinfarction, is commonly associated with ventricular arrhythmias.Ventricular fibrillation is often preceded by episodes ofsustained or non-sustained ventricular tachycardia. Frequentpremature ventricular beats may herald the onset of ventricularfibrillation, especially if they occur when the myocardium is onlypartially repolarised (the “R on T” phenomenon), though in theischaemic myocardium the ventricles are probably vulnerable T wave alternansduring all phases of the cardiac cycle. T wave alternans, aregular beat to beat change in T wave amplitude, is also thoughtto predict ventricular fibrillation. “R on T” phenomenon giving rise to ventricular fibrillation Polymorphic ventricular tachycardia deteriorating into ventricular fibrillation62
  • 70. Cardiac arrest rhythmsPulseless ventricular tachycaridaVentricular tachycardias are the result of increased myocardialautomaticity or are secondary to a re-entry phenomenon. Theycan result from direct myocardial damage secondary toischaemia, cardiomyopathy, or myocarditis or be caused bydrugs—for example, class 1 antiarrhythmics such as flecainideand disopyramide. Pulseless ventricular tachycardia is managedin the same way as ventricular fibrillation, early defibrillation Capture beat in ventricular tachycardiabeing the mainstay of treatment.Electrocardiographic featuresIn a patient who is in the middle of a cardiac arrest 12 leadelectrocardiography is impractical; use a cardiac monitor todetermine the rhythm, and any broad complex tachycardiashould be assumed to be ventricular in origin. In ventricular tachycardia there is a broad complex, regulartachycardia with a rate of at least 120 beats/min. The diagnosisis confirmed if there is direct or indirect evidence ofatrioventricular dissociation, such as capture beat, fusion beat, Fusion beat in ventricular tachycardiaor independent P wave activity.Ventricular tachycardia with evidence of atrioventricular dissociationPulseless electrical activityIn pulseless electrical activity the heart continues to workelectrically but fails to provide a cardiac output sufficient toproduce a palpable pulse.Electrocardiographic features of pulseless electrical activityThe appearance of the electrocardiogram varies, but severalcommon patterns exist. There may be a normal sinus rhythm orsinus tachycardia, with discernible P waves and QRS complexes. Broad and slow rhythm in association with pulseless electrical activitySometimes there is a bradycardia, with or without P waves, andoften with wide QRS complexes.Narrow complex rhythm associated with pulseless electrical activityClinical correlates Potentially reversible causes of pulselessSuccessful treatment of pulseless electrical activity depends on electrical activitywhether it is a primary cardiac event or is secondary to a x Hypovolaemiapotentially reversible disorder. x Cardiac tamponade x Tension pneumothorax x Massive pulmonary embolismAsystole x Hyperkalaemia, hypokalaemia, and metabolic disordersMechanisms x HypothermiaAsystole implies the absence of any cardiac electrical activity. It x Toxic disturbances—for example, overdoses of blockers, tricyclic antidepressants, or calciumresults from a failure of impulse formation in the pacemaker channel blockerstissue or from a failure of propagation to the 63
  • 71. ABC of Clinical Electrocardiographyventricles. Ventricular and atrial asystole usually coexist.Asystole may be structurally mediated (for example, in acutemyocardial infarction), neurally mediated (for example, in aorticstenosis), or secondary to antiarrhythmic drugs.Electocardiographic features of asystoleIn asystole the electrocardiogram shows an almost flat line.Slight undulations are present because of baseline drift. Thereare several potential pitfalls in the diagnosis of asystole.A completely flat trace indicates that a monitoring lead hasbecome disconnected, so check that the leads are correctlyattached to the patient and the monitor. Check the Asystoleelectrocardiogram gain in case it has been set at aninappropriately low level. To eliminate the possibility ofmistaking fine ventricular fibrillation for asystole, check thetrace from two perpendicular leads.Clinical correlatesAsystole has the worst prognosis of all the arrest rhythms. Ifventricular fibrillation cannot be excluded confidently, make anattempt at defibrillation. Flat line artefact simulating asystoleVentricular standstillAtrial activity may continue for a short time after ventricularactivity has stopped and the electrocardiogram shows a flat lineinterrupted by only P waves. Conduction abnormalities that canherald ventricular standstill include trifascicular block and theoccurrence of alternating left and right bundle branch block.Ventricular standstillBradycardias and conduction blocksThe term bradycardia refers to rates of < 60 beats/min, but a “Peri-arrest” rhythmsrelative bradycardia exists when the rate is too slow for thehaemodynamic state of the patient. Some bradycardias may x Arrhythmias are common immediately before and after arrest, andprogress to asystole, and prophylactic transvenous pacing may cardiac monitoring of patients at high risk is important x These “peri-arrest” arrhythmias include bradycardias andbe needed. These include Mobitz type II block, complete heart conduction blocks, broad complex tachycardias, and narrowblock with a wide QRS complex, symptomatic pauses lasting complex tachycardiasthree seconds or more, and where there is a history of asystole. At low heart rates, escape beats may arise from subsidiarypacemaker tissue in the atrioventricular junction or ventricularmyocardium. A junctional escape rhythm usually has a rate of Escape rhythms represent a safety net preventing asystole40-60 beats/min; the QRS morphology is normal, but inverted or extreme bradycardia; management should correct theP waves may be apparent. Ventricular escape rhythms are underlying rhythm abnormalityusually slower (15-40 beats/min), with broad QRS complexesand no P waves.Top: Junctional escape rhythm. Bottom: Ventricular escape rhythm64
  • 72. Cardiac arrest rhythmsBroad complex tachycardiasManagement of ventricular tachycardia precipitating cardiacarrest depends on the patient’s clinical state. However, some Ventricular tachyarrhythmias often precipitate cardiac arrest, and they aretypes of ventricular tachycardia warrant special mention. common immediately after arrestPolymorphic ventricular tachycardiaIn polymorphic ventricular tachycardia, the QRS morphologyvaries from beat to beat. The rate is usually greater than Polymorphic ventricular tachycardia200 beats/min. In sinus rhythm the QT interval is normal. If requires immediate direct currentsustained, polymorphic ventricular tachycardia invariably leads cardioversionto haemodynamic collapse. It often occurs in association withacute myocardial infarction, and frequently deteriorates intoventricular fibrillation.Polymorphic ventricular tachycardiaTorsades de pointesTorsades de pointes is a type of polymorphic ventriculartachycardia in which the cardiac axis rotates over a sequence ofabout 5-20 beats, changing from one direction to the oppositedirection and back again. In sinus rhythm the QT interval isprolonged, and prominent U waves may be seen. Torsades de pointes tachycardia is not usually sustained butis recurrent, each bout lasting about 90 s. It may be druginduced, secondary to electrolyte disturbances, or associatedwith congenital syndromes with prolongation of the QTinterval. Its recognition is important because antiarrhythmicdrugs have a deleterious effect; management entails reversingthe underlying cause. Occasionally torsades de pointes is Prolonged QT intervalassociated with cardiac arrest or degenerates into ventricularfibrillation; both are managed by direct current cardioversion.Torsades de pointes 65
  • 73. 17 Pacemakers and electrocardiographyRichard Harper, Francis MorrisSince the placement of the first implantable electronicpacemaker in the 1950s, pacemakers have become increasingly Modern pacemakers can sequentiallycommon and complex. The first pacemakers were relatively pace the right atrium or the ventricle, orsimple devices consisting of an oscillator, battery, and stimulus both, and adapt the discharge frequencygenerator. They provided single chamber pacing at a single of the pacemaker to the patient’sfixed rate irrespective of the underlying rhythm. The second physiological needsgeneration of pacemaker had an amplifier and sensing circuit torecognise spontaneous cardiac activity and postpone pacingstimuli until a pause or bradycardia occurred.Clinical relevancePacemakers are implanted primarily for the treatment ofsymptomatic bradycardia. Modern units have an average life Indications for a permanent pacemakerspan of about eight years and rarely malfunction. system In clinical practice a basic understanding of x Sick sinus syndromeelectrocardiography in patients with a pacemaker may be x Complete heart blockhelpful in evaluating patients with syncope or near syncope x Mobitz-type II heart block x Atrial tachycardia, and heart block(suggesting that the pacemaker may not be functioning x Asystolenormally). x Carotid sinus hypersensitivity Troubleshooting potential pacemaker problems is a highlyspecialised area that needs a skilled technician to evaluatewhether the pacemaker is functioning correctly. This field isbeyond the scope of this chapter, which will concentrate on Generic pacemaker codebasic interpretation of electrocardiograms in the patients whohave a pacemaker. Anti- Chamber Chamber Response Rate tachycardia paced sensed to sensing modulation* AICDsFunctions of pacemakers O = none O = none O = none O = none O = none A = atrium A = atrium T = triggered R = rate P = pacingPacemakers can pace the ventricle or the atrium, or both responsivesequentially. Atrial or ventricular activity can be sensed, and this V = ventricle V = ventricle I = inhibited S = shocksensing may be used to trigger or inhibit pacer activity. Some D = dual D = dual D = dual D = dualpacemakers are rate adaptive. chamber chamber (T + I) (P + S) The functions of a pacemaker are indicated by a generic *This position may also be used to indicate the degree of programmability bycode accepted by the North American Society for Pacing and the codes P, M and C. AICD = Automatic implantable cardioverter defibrillatorElectrophysiology and the British Pacing and ElectrophysiologyGroup. It is a five letter code of which only the first four lettersare used commonly. The first letter identifies the chamberpaced, the second gives the chamber sensed, the third letterindicates the response to sensing, and the fourth identifies rateresponsiveness.AAI pacingAAI pacing is restricted to those patients with underlying sinus Typical electrocardiogram produced by AAInode dysfunction but intact cardiac conduction. This mode will pacingsense atrial activity and inhibit pacing if the patient’s heart rateremains above the preset target. At lower rates the pacerstimulates the atrium. Like all pacemakers, an AAI pacemakercan be rate adaptive (AAIR).VVI pacingVVI pacing is used in patients who do not have useful atrialfunction, including those with chronic atrial fibrillation or flutterand those with silent atria. Typical tracing produced by VVI pacing VVI pacing tracks only ventricular activity and paces theventricle if a QRS complex is not sensed within a predefinedinterval. VVI pacing may be used as a safety net in patients whoare unlikely to need more than occasional pacing.66
  • 74. Pacemakers and electrocardiographyDual chamber pacingDual chamber pacing has become more common asaccumulated evidence shows that sequential dual chamberpacing provides a better quality of life and improved functionalcapacity for patients. In DDD mode an atrial impulse isgenerated if the patient’s natural atrial activity fails to occurwithin a preset time period after the last atrial or ventricularevent. An atrial event (paced or sensed) begins theatrioventricular interval. If a spontaneous QRS complex does Typical tracing produced by DDD pacernot occur during the programmed atrioventricular interval, aventricular stimulus is generated. The ventricular stimulus, orsensed QRS complex, initiates a refractory period of the atrialamplifier known as the postventricular atrial refractory period.The combination of the atrioventricular interval and thepostventricular atrial refractory period form the total atrialrefractory period. The total atrial refractory period is important Atrial Defines lower rate unitbecause it determines the upper rate limit of the pacemaker. Basic intervalNormal paced rhythm AVI PVARPFor implanted pacemakers, the atrial lead is placed in the rightatrium and often in the appendage. A beat that is paced has a TARPP wave of near normal appearance. The ventricular lead is Defines upper rate unitplaced in the apex of the right ventricle. When the lead is AVI = Atrioventricular intervalstimulated it produces a wave of depolarisation that spreads PVARP = Postventricular atrial refractory periodthrough the myocardium, bypassing the normal conduction TARP = Total atrial refractory periodsystem. The ventricles depolarise from right to left and fromapex to base. This usually produces an electrocardiogram with Total atrial refractory periodbroad QRS complexes, a left bundle branch block pattern, andleft axis deviation. The QT interval is often prolonged and the Twaves are broad with a polarity opposite to that of the QRS. Pacing spikes in the electrocardiogram vary in size and areaffected by respiration. Unipolar systems common in the UnitedKingdom give rise to larger spikes than bipolar systems. Spikesfrom bipolar systems can be so small that they cannot be seen inthe electrocardiogram, especially when single leads are recorded. Pacemakers are normally programmed to pace at a rate of70 beats/min (lower rate limit). However, many pacemakersystems are programmed to initiate pacing only when theintrinsic (the patient’s own) heart rate drops as low as 50 or 60beats/min. Therefore, an electrocardiogram with no pacingspikes and with a spontaneous heart rate of 66 beats/min doesnot necessarily mean the pacemaker has malfunctioned. Heartrates above the lower rate limit will inhibit pacemaker activity,and therefore electrocardiography will not help in assessingwhether the pacemaker is functioning correctly. When thisoccurs carotid sinus massage can slow the intrinsic ratesufficiently to trigger pacemaker activity. Alternatively, placing a magnet over the pacemaker will Top: Unipolar systems—note the large pacing spike.convert the pacer to asynchronous mode so that all sensing is Bottom: Bipolar system in the same patientdisabled. Ventricular pacers operate in VOO mode, atrial pacersin AOO mode, and dual chamber pacers in DOO mode. Ifpacing suppresses the native rhythm, a completely pacedelectrocardiogram at a preset “magnet rate” will result. Manypacemakers have a preset “magnet rate” of 90-100 beats/min.This will usually suppress the native rhythm, allowing the Procedures to assess a possible pacemakerfunctioning of the pacemaker to be assessed. Removing the malfunctionmagnet will cause the pacemaker to revert to its programmed x Cardiac monitoringmode. x 12 lead electrocardiography x Chest x ray examinationPacemaker failureSeveral procedures are needed to assess a patient whosepacemaker may be malfunctioning: cardiac monitoring to assessrhythm disturbances; 12 lead electrocardiography to assess 67
  • 75. ABC of Clinical Electrocardiographypacer function; and chest x ray examination to check electrodeplacement and exclude lead fracture. A patient presenting withpacemaker failure will often have a recurrence of symptomaticbradycardia. If this is captured on a monitor, the diagnosis isconfirmed.Abnormalities of sensingUndersensingUndersensing occurs when the pacemaker intermittently or Failure to sense may be caused bypersistently fails to sense the appropriate cardiac chamber, and fibrosis at the tip of the electrode,therefore the timing of the pacemaker stimulus is damage to the electrode or lead, orinappropriate. These mistimed pacemaker spikes may or may dislodgment of the leadnot capture the heart, depending on their time ofoccurrence—for example, spikes occurring soon afterspontaneous activity will not capture the relevant chamberbecause it is still refractory. Loss of ventricular sensing. The first and the fifth complexes are ventricular paced beats. The second to fourth complexes are the patient’s intrinsic rhythm, which have not been sensed, hence the inappropriately timed pacing spikeOversensingPacemakers may sense electrograms evoked by the pacemakeritself, spontaneous T waves, or electrograms from anotherchamber, myopotentials, electromagnetic signals, radio signals,or spikes resulting from lead damage or circuit faults. The Reprogramming the pacemaker maysensed signals are misinterpreted as spontaneous electrograms eliminate the oversensing by adjustingfrom the appropriate cardiac chamber, and the result is amplifier sensitivity and refractorinesspacemaker inhibition. This can lead to symptomaticbradycardia. The pacemaker system may need to be replaced ifthere are problems with the circuit, electrodes, or leads. Loss of atrial pacing because of oversensing preceding T wave. Ventricular pacing set at a low rateFailure to paceFailure to pace is a common reason for pacemaker malfunctionand may be caused by failure of the pacemaker to provideoutput or failure of the pacemaker stimulus to capture. Failureof the pacemaker to provide output should be suspected when Causes of failure to capturethe patient’s heart rate is below the pacer rate and nopacemaker activity is noted in the electrocardiogram. Failure of pacemaker x Battery failure x Circuit abnormalityFailure to capture x Inappropriate programmingFailure to capture should be easy to detect in the x Problem with leadselectrocardiogram. Appropriately timed pacer spikes will be x Lead dislodgmentpresent, but the spikes fail to provide consistent capture. The x Cardiac perforationcommonest cause of loss of capture is dislodgment of the x Lead fracture x Insulation breakpacing electrode. Failure to capture may also result from lead x Increased thresholddamage or pacemaker failure (rare).68
  • 76. Pacemakers and electrocardiography VVI pacemaker with intermittent failure to capture. Every second pacemaker beat captures. The rest of the time, pacemaker spikes are seen but not associated with capturePacemaker mediated tachycardiasPacemaker mediated tachycardias are a result of interactions The most commonly reportedbetween native cardiac activity and the pacemaker. In “endless pacemaker mediated tachycardia isloop tachycardia,” a premature ventricular contraction is “endless loop tachycardia” which occursfollowed by retrograde atrial conduction. The pacemaker senses in patients with dual chamberthe retrograde atrial activity and a ventricular stimulus is pacemakersgenerated. If the retrograde conduction persists, a tachycardiaensues. The rate of this tachycardia will not exceed themaximum tracking rate of the pacemaker and is thereforeunlikely to result in instability. However, it is often highlysymptomatic. Appropriate reprogramming will usuallyeliminate endless loop tachycardia. Other premature ventricularcontractions include rapid ventricular pacing in response to thesensing of atrial tachycardias such as atrial fibrillation.Pacemaker mediated tachycardiaPacemaker syndromePacemaker syndrome refers to symptoms related to the use of a Symptoms of pacemaker syndromepacemaker. When the atria and ventricles contract at the sametime the atrial contribution to ventricular filling is lost. It is x Patients usually present with non-specific symptoms and signs such as dyspnoea, dizziness, fatigue, orthopnoea, and confusionpatients with ventricular pacemakers who are usually affected x Occasionally patients may complain of palpitations or pulsation inby pacemaker syndrome. Ventricular pacing leads to retrograde the neck or abdomenconduction to the atria. The atria contract against closedatrioventricular valves, and this results in pulmonary andsystemic venous distension, hypotension, and reduced cardiacoutput. The diagnosis is largely clinical but may be supportedby the presence of retrograde P waves in the electrocardiogram.Pacemaker syndrome: retrograde P waves are evident 69
  • 77. 18 Pericarditis, myocarditis, drug effects, andcongenital heart diseaseChris A Ghammaghami, Jennifer H LindseyPericarditis, myocarditis, drugs, and some congenital heartlesions all have various effects on the electrocardiogram thatcan help both in diagnosing a clinical syndrome andmonitoring disease progression or resolution. I aVR V1 V4PericarditisThe clinical presentation of pericarditis must be differentiatedfrom chest pain related to ischaemic heart disease. Although acareful history and physical examination help to distinguish thetwo diagnoses, the electrocardiographic changes of pericarditishave at least two characteristic features. II aVL V2 V5 Firstly, in pericarditis the ST segment elevation evolves overtime, is “saddle shaped” (concave upwards), widespread, and,with the exception of ST segment depression in lead aVR, is notassociated with reciprocal changes. Secondly, a common though subtle finding in pericarditis isthe presence of PR segment depression, which indicates atrialinvolvement in the inflammatory process. A reduction in QRSvoltage and, rarely, electrical alternans of the QRST complexcan be seen in patients developing a large pericardial effusion. III aVF V3 V6MyocarditisThe electrocardiographic findings in myocarditis are usuallymanifest in two distinct patterns: impairment of conduction,leading to atrioventricular, fascicular, or bundle branch blocks;and widespread ST and T wave changes. Diffuse T wave Pericarditis: note the ST elevation and PR segment depressioninversion, which may be associated with ST segment depression,is one of the most common findings. A resting sinus tachycardia can indicate early myocarditis.Later in the course of the disease, as ventricular function beginsto fail, serious arrhythmias are more common. Premature atrialand ventricular contractions can be followed by atrial fibrillationor flutter, and, in late stages, ventricular tachycardia andfibrillation.DrugsEach agent in the Vaughan-Williams classification of Pericarditis: details of the QRS complex in lead II (note the PR segment depression)antiarrhythmic drug actions can cause electrocardiographicchanges. Adrenergic receptor and non-dihydropyridine calciumchannel antagonists produce sinus bradycardia andatrioventricular block. Generally these drugs are safe and rarely Vaughan-Williams classificationcause severe bradycardia. Class I: Fast sodium channel blockers Digoxin and quinidine-like agents have narrower x 1a: quinidine, procainamide, disopyramide x 1b: lidocaine, phenytoin, mexilitene, tocainidetherapeutic indices and can cause life threatening ventricular x 1c: encainide, flecainide, propafenonearrhythmias relatively often. Drugs which prolong the action Class II: adrenergic receptor antagonistspotential duration (class Ia or class III) may cause torsades de (examples)pointes. Powerful class I drugs (especially Ia or Ic) may cause x Propranolol, flecainide, propafenoneQRS widening, bundle branch block, or complete Class III: Potassium channel blockers (examples)atrioventricular block. x Bretylium, sotalol, amiodarone, ibutilide (not available in United Kingdom)Digoxin Class IV: Calcium channel blockers (examples)Decades of clinical experience with digitalis compounds show x Verapamil, diltiazem, nifedipinethat nearly any arrhythmia can occur as a result of digoxin70
  • 78. Pericarditis, myocarditis, drug effects, and congenital heart diseaseadministration. At therapeutic levels QT duration is shortened, Rhythm disturbances associated withand the PR interval is moderately lengthened because of digoxin intoxicationincreased vagal tone. The “digoxin effect” refers to T waveinversion and downsloping ST segment depression. These x Sinus bradycardia x Sinoatrial blockfindings should not be interpreted as toxic effects. Excitatory x First, second, and third degree atrioventricularand inhibitory effects are responsible for the pro-arrhythmic blockcharacter of digoxin. A rhythm that is considered by some as x Atrial tachycardia (with or withoutnearly pathognomonic for digoxin intoxication, paroxysmal atrioventricular block)atrial tachycardia with variable atrioventricular nodal x Accelerated junctional rhythmconduction (“PAT with block”), shows both types of effects. x Junctional tachycardia x Ventricular tachycardia or fibrillationDigoxin effectAtrial tachycardia with blockQuinidine-like drugs Drugs causing prolongation of QT intervalThe class Ia antiarrhythmic effect is caused by the inhibition offast sodium channels. Many drugs (for example, disopyramide) Amiodarone, astemizole, bepridil, bretylium,share this effect to varying degrees and can share the cisapride, cocaine, tricyclic antidepressants, cyproheptadine, disopyramide, erythromycin,pro-arrhythmic character of quinidine. Electrocardiographic flecainide, thioridazine, pimozide, ibutilide,indicators of toxic effects of quinidine include widening of the itraconazole, ketoconazole, phenothiazines,QRS complex, prolongation of the QT interval, and procainamide, propafenone, quinidine, quinine,atrioventricular nodal blocks. The prolongation of the QT sotalol, terfenadine, vasopressininterval predisposes to the development of polymorphicventricular tachycardia. Slowing of atrial arrhythmia combinedwith improved atrioventricular conduction (anticholinergiceffect) can cause an increase in the ventricular rate response toatrial tachyarrhythmias. Prolonged QT interval (QTc 505 ms) Polymorphic ventricular tachycardia in a patient with quinidine intoxicationFlecainide-like drugs Differential diagnosis with selectedFlecainide, propafenone, and moracizine can cause bundle electrocardiographic findings in congenitalbranch block. These drugs slow atrial tachycardias and can lead heart diseaseto a paradoxical increase of the ventricular response rate.Monomorphic ventricular tachycardia may also occur. Axis deviation or hypertrophy x Superior QRS axis: atrioventricular septal defects, tricuspid atresia x Left ventricular hypertrophy: aortic stenosis,Congenital heart disease hypertrophic cardiomyopathy x Right ventricular hypertrophy: tetralogy of Fallot,The electrocardiographic findings associated with congenital severe pulmonary stenosis, secundumlesions of the heart may be subtle, but generally they increase in atrioventricular septal defectdirect proportion to the severity of the malformation’s impact x Combined ventricular hypertrophy: large ventricular septal defect, atrioventricular septalon the patient’s physiology. Electrocardiographic abnormalities defectin children with heart murmurs should increase the clinician’s 71
  • 79. ABC of Clinical Electrocardiographysuspicion of a structural lesion. Electrocardiography, however,has been replaced largely by echocardiography for diagnosingand monitoring congenital heart disease. Some congenitallesions are discussed below; others are not included either I aVR V1 V4because they are associated with relatively normalelectrocardiograms or because the disease is rare.Acyanotic lesionsAtrial septal defectsAn atrial septal defect results from incomplete closure of theatrial septum in utero. The electrocardiogram may appear II aVL V2 V5relatively normal, with normal P waves in most cases. PRinterval prolongation and first degree heart block may occur inup to 20% of cases, but higher grade atrioventricular blocks areuncommon. QRS complexes may show some right ventricularconduction delay denoted by an rsR1 in V1, but this may also bea normal variant. Associated mitral valve clefts can occur,leading to mitral regurgitation and, if severe, left ventricularhypertrophy. The QRS axis can help to differentiate the twopredominant types of atrial septal defect in the following way: III aVF V3 V6x Ostium primum QRS axis: leftwards ( − 30° to − 90°)x Ostium secundum QRS axis: rightwards (0 to 180°), with most being more than 100°x Sinus venosus P wave axis: low atrial pacemaker. Secundum atrial septal defect: note the right axis deviation and dominant R wave in lead V1 I aVR V1 V4 V1 V2 V3 II aVL V2 V5 III aVF V3 V6 V4 V5 V6Primum atrial septal defect: note the left axis deviation (superior axis)Ventricular septal defectsVentricular septal defects are the most common cardiac defectsat birth. Small ventricular septal defects close spontaneously in50-70% of cases during childhood. Generally these are notassociated with any electrocardiographic abnormalities. As a Ventricular septal defect: note that all leads are half standard calibration. The biventricular hypertrophy pattern is typical of a ventricular septal defectrule the degree of the electrocardiographic abnormality isdirectly proportional to the haemodynamic effect on ventricularfunction. A medium sized ventricular septal defect can exhibitleft ventricular hypertrophy and left atrial enlargement. A largeventricular septal defect results in biventricular hypertrophyand equiphasic QRS complexes in the mid-precordium knownas the Katz-Wachtel phenomenon.72
  • 80. Pericarditis, myocarditis, drug effects, and congenital heart diseaseCoarctation of the aortaCoarctation of the aorta results in left ventricular hypertrophyin 50-60% of asymptomatic children and adults. The strainpattern of lateral T wave inversions is seen in about only 20% of I aVR V1 V4asymptomatic children and adults. ST-T wave abnormalities inthe lateral precordial leads are not associated with simplecoarctation and imply additional cardiac disease—for example,left ventricular outflow obstruction. Generally left atrialabnormalities are not seen unless mitral regurgitation develops.Ebstein’s anomalyEbstein’s anomaly is the downward displacement of the II aVL V2 V5tricuspid valve into the right ventricle causing “atrialisation” ofthe upper segment of the right ventricle. Tricuspid insufficiencyis common, leading to dilation of the right atria, which isindicated by tall peaked P waves in lead II and the anterior leadsV1-2. The conduction system itself may be altered by thisanomaly, leading to right bundle branch block (complete orincomplete) in 75-80% of patients, a widened QRS complex, orwidened PR interval prolongation, or both the latter.Additionally, there is an association with theWolff-Parkinson-White syndrome in up to 25% of cases. III aVF V3 V6DextrocardiaDextrocardia is the presence of the heart in the right side of thechest. It can occur alone or in association with situs inversus(complete inversion of the abdominal organs). Examination of the electrocardiogram in situs inversus willshow two obvious abnormalities: loss of the normal precordialR wave progression (prominent right and diminished left lateralprecordial forces) and presence of inverted P-QRS-T waves inlead I. If the electrocardiogram has been recorded correctly, andthe patient is in sinus rhythm, the presence of an inverted Coarctation of the aorta in a 10 week old infant. The deep S wave seen inP wave in lead I indicates dextrocardia. V1 reflecting striking left ventricular hypertrophy I aVR V1 V4 I aVR V1 V4 II aVL V2 V5 II aVL V2 V5 III aVF V3 V6Dextrocardia: note inverted P wave in lead I and poor R wave progression III aVF V3 V6Tricuspid atresiaAn atrial septal defect must be present to allow for anycirculation in the presence of tricuspid atresia. The typicalelectrocardiographic changes associated with atrial septaldefects are seen as well as left axis deviation. Right atrialenlargement occurs and is indicated by tall P waves in leads I, II,and V1. Often there is an associated ventricular septal defect.Occasionally PR interval prolongation occurs and a “pseudopre-excitation” delta wave (not caused by an actual accessorypathway) is seen. Tricuspid atresia: note the left axis deviation and the right atrial enlargement 73
  • 81. ABC of Clinical ElectrocardiographyCyanotic lesionsAt birth the normal infant’s electrocardiogram will show a rightventricular predominance. Over the first month of life the leftventricle becomes more prominent than the right, and I aVR V1 V4precordial voltage and QRS axis reflect this change. In thecyanotic lesions of the heart, this right sided dominance oftenpersists because there is an increase in pulmonary pressure andresultant hypertrophy of the right ventricle relative to the left.Tetralogy of FallotThere are no specific electrocardiographic signs for diagnosingtetralogy of Fallot. Right axis deviation and right ventricular II aVL V2 V5hypertrophy are common, however, so their absence should putthe diagnosis of Fallot’s tetralogy into question. The presence ofa left axis deviation in a patient with a known Fallot’s tetralogysuggests a complete atrioventricular canal.Congenitally corrected transposition of the great arteriesIn congenitally corrected transposition of the great arteries,Q waves will be absent in the left precordial leads andprominent in the right. As many as a third of these patients willdevelop a congenital third degree atrioventricular nodal block. III aVF V3 V6 Congenitally corrected transposition of the great arteries: note the absence of Q waves in lead 1, V5, and V6, which is characteristic of this lesion74
  • 82. IndexAAI pacing 66 atrial fibrillation 14acute myocardial infarction 29–36 defined 13 acute ischaemia 33 diagnosis 27 antecedent, ST segment elevation 35 Wolff-Parkinson-White syndrome 20 appropriate concordance 33–4 atrial flutter 14–15 bundle branch block 33–4 defined 13 complete heart block 40 paroxysmal atrial flutter 10 evolution of electrocardiogram changes 29 atrial refractory period 67 hyperacute T waves 29 atrial septal defects 72 inappropriate concordance 33–4 atrial tachycardias 15–16 localisation of site of infarction 31—2 aberrant conduction 26, 27 posterior 32 with AV block 16 right ventricular 31–2 benign paroxysmal 15 pathological Q waves 30 conditions associated 16 reciprocal ST segment depression 30–1 defined 13, 15–16 sinus bradycardia 9 incessant ectopic 16 ST segment changes 29 initiated by ectopic atrial focus 15 differential diagnosis 34–6 multifocal 16, 46 elevation 34–6 atrioventricular dissociation resolution of changes in T waves 30 monomorphic ventricular tachycardias 22–4 treatment, indications for thrombolysis 29 clinical evidence 27acute pericarditis, ST segment elevation 35 ventricular tachycardias 22–4, 63acute pulmonary embolism 47–8 atrioventricular nodal re-entrant tachycardiaacute right heart strain 48 17–18acyanotic lesions 72 clinical presentation 18 atrial septal defects 72 electrocardiogram findings 17–18 ventricular septal defects 72 mechanism 17adenosine termination 18 AV block 28 atrioventricular node 6 contraindications 20, 27 2:1 block 14, 16adenosine scintigraphy 42 aberrant conduction 26amyloidosis, restrictive cardiomyopathy 52 block induction 15anatomical relations, leads in standard 12 lead fast/slow pathways 17–18 electrocardiogram 2–3 atrioventricular (node) conduction block 10–12angina bundle branch block 11–12 ST segment elevation 36 complete T wave inversion 38 acute myocardial infarction, transvenous cardiacantiphospholipid antibodies, congenital heart block 60 pacing 40arrhythmias see atrial arrhythmias; sinus arrhythmias; paediatric electrocardiogram 60 ventricular arrhythmias fascicular blocks 12asystole 63–5 first, second and third degree block 10–11 bradycardias and conduction blocks 64 induction 13 clinical correlates 64 left bundle branch block 11–12 electrocardiogram features 64 paediatric 60 mechanisms 63–4 right bundle branch block 11 peri-arrest rhythms 64 tachycardia-bradycardia syndrome 10 polymorphic ventricular tachycardia 26, 65 atrioventricular re-entrant tachycardia 18–20 torsades de pointes 65 antidromic 27 ventricular standstill 64 paediatric 60atrial arrhythmias 13–16 Wolff-Parkinson-White syndrome 18–20 clinical relevance 13 antidromic/orthodromic 20 electrocardiogram characteristics and features 13 sinus tachycardia 13–14 Bayes’s theorem 44 supraventricular tachycardias, atrial/sinoatrial node 13 Bazett’s correction, QT interval 8 see also atrial fibrillation; atrial tachycardia bifascicular blocks 12atrial depolarisation, P wave 5 body habitus effects 1 75
  • 83. Indexbradycardias 9–10 coronary artery disease defined 9 exercise tolerance testing 44 relative 64 left bundle branch block 11 sick sinus syndrome 9–10 right ventricular myocardial infarction 32 sinoatrial node dysfunction, associated conditions 9–10 cyanotic lesions 74 sinus bradycardia 9broad complex tachycardias 21–8 DDD pacer 67 asystole, cardiac arrest rhythms 65 dextrocardia, P wave inversion 73 management 28 digoxin 70–1 supraventricular origin 26–7 contraindications 20, 27, 40, 56 atrial tachycardia with aberrant conduction 26 intoxication 71 Wolff-Parkinson-White syndrome 26–7 rhythm disturbance 15, 71 terminology 21 dilated cardiomyopathy 51–2 ventricular origin disopyramide, quinidine-like drugs 71 with bundle branch block 26 driving groups, exercise tolerance testing 44 mechanisms 21–2 drugs 70–1 ventricular and supraventricular origin Vaughan-Williams classification 70 clinical presentation 27 differentiation 27–8 Ebstein’s anomaly 73 electrocardiogram differences 27–8 electrocardiogram 1 ventricular tachycardia 25–6 normal findings 3Brugada syndrome 34 paediatric 57–8bundle branch block 33–4 paediatric 57–60 differentiation from ventricular and supraventricular escape beats 40 tachycardias 26, 28 escape rhythms 10, 64bundle of His 1, 17 exercise tolerance testing 41–4 fascicular tachycardias 25 abnormal changes during exercise 43 fast/slow pathways 17–18 clinical relevance 41bundle of Kent 18 contraindications 42 Wolff-Parkinson-White syndrome 18 diagnostic indications 41 interpreting results 44capture beats 23 coronary artery disease 44cardiac arrest rhythms 61–5 diagnostic and prognostic testing 44 asystole 63–5 rationale for testing 44 pulseless electrical activity 63 screening 44 pulseless ventricular tachycardia 63 limitations 42 ventricular fibrillation 61–2 maximum predicted heart rate 42–3cardiac axis 3–4 normal electrocardiogram changes during exercise 43 calculation 4 normal trace during exercise 42 determination of axis in diagnosis 3–4 occupational groups 44 normal findings in healthy individuals 3 preparing the patient 41–2 sinus rhythm 3 protocol 41cardiac rhythm assessment 3 safety 42cardiomyopathies stopping the test 43–4 dilated cardiomyopathy 51–2 workload 41 hypertrophic cardiomyopathy 51 restrictive cardiomyopathy 52 fascicular blocks 12carotid sinus massage 13, 28 fascicular tachycardia 22, 25chronic obstructive pulmonary disease fast/slow pathways, atrioventricular node 17–18 right axis deviation 46 fits, persistent movement artefact 62 tall R wave in lead V1 46 flecainide-like drugs 63, 71circumflex artery, occlusion 32 fusion beats 23coarctation of aorta 73congenital heart block, antiphospholipid antibodies 60 heart ratecongenital heart disease 71–4 calculation 2–3 acyanotic lesions 72 maximum predicted 42 coarctation of aorta 73 rulers 2–3 congenitally corrected transposition of the great arteries 74 hemifascicular blocks 12 cyanotic lesions 74 hexaxial diagram 3 dextrocardia 73 His–Purkinje conduction system 1 differential diagnosis 71 hypercalcaemia Ebstein’s anomaly 73 QT interval 56 tetralogy of Fallot 74 U waves 8 tricuspid atresia 73 hyperkalaemia 53 Wolff-Parkinson-White syndrome 18–20, 26–7 T waves 7congenitally corrected transposition of great arteries 74 U waves 876
  • 84. Indexhypertrophic cardiomyopathy 51 defined 5hypoglycaemia 56 independent 27hypokalaemia 54 inversion 23, 73 Q waves 8 left atrial abnormality 5, 49 U waves 8 mitral stenosis 5hypothermia 54–5 pacemaker syndrome 69hypothyroidism 55–6 standard 12 lead electrocardiogram 23 Wolff-Parkinson-White syndrome 19infarct scar tissue pacemakers 66–9 Q wave markers of necrosis 30 clinical relevance 66 re-entry circuits 22 failure 67–8intracranial haemorrhage, ST segment elevation 35–6 abnormalities of sensing 68ischaemic disease see myocardial ischaemia capture 68–9 pacing 68J point see ST junction under and oversensing 68J waves (Osborn waves) 54–5 functions 66–7junctional tachycardias 17–20 AAI pacing 66 atrioventricular nodal re-entrant tachycardia 17–18 dual chamber pacing 67 atrioventricular re-entrant tachycardia 18–20 VVI pacing 66 Wolff-Parkinson-White syndrome 18–20 normal paced rhythm 67 see also supraventricular tachycardias pacemaker syndrome 69 pacemaker-mediated tachycardias 69Katz-Wachtel phenomenon 72 paediatric electrocardiography 57–60 abnormal electrocardiogram 58–60leads complete atrioventricular block 60 standard 12 lead electrocardiogram 2–3 extrasystoles 60 P waves 23 normal values 58 right-sided in acute myocardial infarction 31 rate and rhythm 59–60left atrial abnormality 49 age related changes, normal cardiograms 57–8 cardiomyopathy 51–2 incessant ectopic atrial tachycardia 16 P waves 5 indications 57left bundle branch block 33–4 recording electrocardiogram 57left heart 49–52 paroxysmal atrial flutter 10 cardiomyopathies 51–2 peri-arrest rhythm 64left heart valvular problems 51–2 pericarditis 70left ventricular hypertrophy 49–50 differential diagnosis 35 electrocardiogram findings, scoring system 50 persistent movement artefact 62 left atrial abnormality 49 PR interval 5–6 sinus bradycardia 9mitral stenosis premature atrial impulses 17 P waves 5 Prinzmetal’s angina, ST segment elevation 36 right ventricular hypertrophy 45–6 pseudoinfarct waves 46Mobitz type I/II block 10 pulmonary embolism, acute 47–8movement artefacts 62 pulmonary stenosis 48Mustard’s operation, transposition of great arteries, pulseless electrical activity 63 electrocardiogram 58 clinical correlates 63myocardial infarction see acute myocardial infarction electrocardiogram features 63myocardial ischaemia 37–40 potentially reversible causes 63 arrhythmias associated with acute myocardial infarction pulseless ventricular tachycardia 61 or infarction 39–40 electrocardiogram features 63 heart block 40 re-entry circuits, infarct scar tissue 22 Q waves 6 ST segment depression 38–9 hypertrophic cardiomyopathy 51 ST segment elevation 39 marker of necrosis 30 T wave changes 37–8 pathological, acute myocardial infarction 30myocarditis 70 QRS complex 2–3, 6 atrial septal defect and ventricular septal defect 72neonatal defects see congenital heart disease atrial tachycardia with aberrant conduction 26normal electrocardiogram 3 concordance, positive/negative 23–4 depolarisation wave 2, 6occupational groups, exercise tolerance testing 44 hyperkalaemia 53Osborn waves 54–5 Katz-Wachtel phenomenon 72 paediatrics 57–8P waves QT interval 8 absent 64 hypercalcaemia 56 atrial depolarisation 5 long QT 60, 65 77
  • 85. Index paediatric 59–60 exercise 42–3 prolongation 71 left ventricular hypertrophy 49–50 subarachnoid haemorrhage 56 myocardial ischaemia 38–9 transient 25 ST segment elevationquinidine-like drugs 71 acute myocardial infarction 34–6 Brugada syndrome 34R on T, ventricular fibrillation 62 differential diagnosis 34–6R waves 6 acute pericarditis 35 pseudo 17 antecedent acute myocardial infarction 35 tall 46 benign early repolarisation 35 “tombstone” 29 high take-off 35R-R interval 2–3 myocardial ischaemia 39rate rulers 2–3 other causes 35–6re-entry circuits paediatric 59 infarct scar tissue 22 standard 12 lead electrocardiogram 2–3 right atrial 14 P waves 23 sinoatrial node 14 paediatric 57–8renal failure, QRS complex, hyperkalaemia 53 right-sided in acute myocardial infarction 31restrictive cardiomyopathy 52 standard calibration signal 1right atrial enlargement 45 standard rhythm strip 3right atrial re-entry circuits 14 subarachnoid haemorrhageright bundle branch block 28, 34 QT interval prolongation 56right heart 45–8 ST segment elevation 35–6 acute pulmonary embolism 47–8 supraventricular tachycardias acute right heart strain 48 atrial tachycardia with aberrant conduction 26 chronic obstructive pulmonary disease 46–7 broad complex tachycardias 26–7right sided valvular problems 48 with bundle branch block, differentiation from pulmonary stenosis 48 ventricular tachycardias 26, 28 tricuspid regurgitation 48 sources 13 tricuspid stenosis 48 Wolff-Parkinson-White syndrome 26–7right ventricular dilatation 47 see also junctional tachycardiasright ventricular hypertrophy 45–6 systemic conditions, not primarily affecting the heart 53–6right ventricular myocardial infarction 31–2right ventricular outflow tract tachycardia 25 T waves 7right-sided chest leads in acute myocardial alternans 62 infarction 31 criteria 38 hyperacute, acute myocardial infarction 29S waves 6 inversion, angina 38, 39 pseudo 17 in ischaemia 37–8shivering artefacts 56 tachycardia-bradycardia syndrome 10sick sinus syndrome 9–10 tachycardiassinoatrial block 9 clinical relevance 13sinoatrial node 1 defined 13 dysfunction, bradycardias associated 9–10 pacemaker-mediated tachycardias 69 P wave 5 sinus tachycardia 13–14 re-entry phenomena 14 see also atrial; broad complex; junctional; supraventricular;sinus arrest 9 ventricularsinus arrhythmia 3 terminology 5–8sinus bradycardia 9 tetralogy of Fallot 74 hypothermia 54 thrombolysis, indications 29 PR interval 9 thyrotoxicosis 55sinus rhythm 3 “tombstone” R waves 29sinus tachycardia 13–14 torsades de pointes 25–6, 65 causes 14 causes 26 embolism 47 transposition of great arteries defined 13 congenitally corrected 74 paediatric 59–60 electrocardiogram 58situs inversus 73 transvenous cardiac pacing, acute myocardial infarction,ST junction 7 complete atrioventricular (node) conduction block 40ST segment 7 tricuspid atresia 73 acute myocardial infarction tricuspid insufficiency, Ebstein’s anomaly 73 changes 29 tricuspid regurgitation 48 reciprocal depression 30–1 tricuspid stenosis 48 resolution of changes in ST segment and T waves 30 trifascicular blocks 12 depression angina 39 U waves 878
  • 86. Indexvagal stimulation 28 duration and morphology of QRS complex 22valvular problems frontal plane axis 22–3 left heart 51–2 independent atrial activity 23–4 right heart 48 direct evidence 23Vaughan-Williams classification of drugs 70 indirect evidence 23–4ventricular arrhythmias, mechanisms 21–2 rate and rhythm 22ventricular escape rhythms 10, 64 polymorphic 26, 65, 71ventricular fibrillation 61–2 defined 21 diagnosis, potential pitfalls 62 see also torsades de pointes features and predictors 61–2 positive/negative concordance, QRS complex 23–4 R on T 62 prognosis 40ventricular hypertrophy right ventricular outflow tract 25 left 49–50 torsades de pointes 25–6, 65 paediatric, diagnosis 58 verapamil, contraindications 20, 27 right 45–6 VVI pacing 66 right heart strain 48ventricular pre-excitation 18 waveforms 1–4ventricular septal defects 72 wave of depolarisation 2ventricular standstill 64 Wenckebach phenomenon 10ventricular tachycardias 25–6 paediatric 60 acute myocardial infarction 40 Wolff-Parkinson-White syndrome 18–20, 26 atrioventricular dissociation 22–4, 63 atrial fibrillation 20 capture beats 23 atrioventricular re-entrant tachycardia defined 21 antidromic 20 differentiation from supraventricular tachycardias with formation mechanism 19–20 bundle branch block 26 bundle of Kent 18 fascicular tachycardia 25 classification 19 fusion beats 23 clinical presentation 20 mechanisms 21–2 electrocardiogram features 18–19 monomorphic 22–4 supraventricular tachycardias 26 defined 21 workload, exercise tolerance testing 41 79

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