ab cof ecg

ABC OFCLINICAL ELECTRO-

CARDIOGRAPHY

FRANCIS MORRISJUNE EDHOUSE

WILLIAM J BRADYJOHN CAMM

BMJ Books

ABC OFCLINICAL ELECTROCARDIOGRAPHY

ABC OF CLINICAL ELECTROCARDIOGRAPHY

Edited by

FRANCIS MORRISConsultant in Emergency Medicine, Northern General Hospital, Sheffield

JUNE EDHOUSEConsultant in Emergency Medicine, Stepping Hill Hospital, Stockport

WILLIAM J BRADYAssociate Professor, Programme Director, and Vice Chair, Department of Emergency

Medicine, University of Virginia, Charlottesville, VA, USA

and

JOHN CAMMProfessor of Clinical Cardiology, St George’s Hospital Medical School, London

© BMJ Publishing Group 2003

All 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 DataA catalogue record for this book is available from the British Library

ISBN 0 7279 1536 3

Typeset by BMJ Electronic ProductionPrinted 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 rayWith permission from Sheila Terry/Science Photo Library

v

Contents

Contributors vi

Preface vii

1 Introduction. I—Leads, rate, rhythm, and cardiac axis 1Steve Meek, Francis Morris

2 Introduction. II—Basic terminology 5Steve Meek, Francis Morris

3 Bradycardias and atrioventricular conduction block 9David Da Costa, William J Brady, June Edhouse

4 Atrial arrhythmias 13Steve Goodacre, Richard Irons

5 Junctional tachycardias 17Demas Esberger, Sallyann Jones, Francis Morris

6 Broad complex tachycardia—Part I 21June Edhouse, Francis Morris

7 Broad complex tachycardia—Part II 25June Edhouse, Francis Morris

8 Acute myocardial infarction—Part I 29Francis Morris, William J Brady

9 Acute myocardial infarction—Part II 33June Edhouse, William J Brady, Francis Morris

10 Myocardial ischaemia 37Kevin Channer, Francis Morris

11 Exercise tolerance testing 41Jonathan Hill, Adam Timmis

12 Conditions affecting the right side of the heart 45Richard A Harrigan, Kevin Jones

13 Conditions affecting the left side of the heart 49June Edhouse, R K Thakur, Jihad M Khalil

14 Conditions not primarily affecting the heart 53Corey Slovis, Richard Jenkins

15 Paediatric electrocardiography 57Steve Goodacre, Karen McLeod

16 Cardiac arrest rhythms 61Robert French, Daniel DeBehnke, Stephen Hawes

17 Pacemakers and electrocardiography 66Richard Harper, Francis Morris

18 Pericarditis, myocarditis, drug effects, and congenital heart disease 70Chris A Ghammaghami, Jennifer H Lindsey

Index 75

William J BradyAssociate Professor, Programme Director, and Vice Chair,Department of Emergency Medicine, University of Virginia,Charlottesville, VA, USA

Kevin ChannerConsultant Cardiologist, Royal Hallamshire Hospital, Sheffield

David Da CostaConsultant Physician, Northern General Hospital, Sheffield

Daniel De BehnkeDepartment of Emergency Medicine, Medical College ofWisconsin, Milwaukee, WI, USA

June EdhouseConsultant in Emergency Medicine, Stepping Hill Hospital,Stockport

Demas EsbergerConsultant in Accident and Emergency Medicine, Queen’sMedical Centre, Nottingham

Robert FrenchDepartment of Emergency Medicine, Medical College ofWisconsin, Milwaukee, WI, USA

Chris A GhammaghamiAssistant Professor of Emergency and Internal Medicine,Director, Chest Pain Centre, Department of EmergencyMedicine, University of Virginia Health System, Charlottesville,VA, USA

Steve GoodacreHealth Services Research Fellow, Accident and EmergencyDepartment, Northern General Hospital, Sheffield

Richard HarperAssistant Professor, Department of Emergency Medicine,Oregon Health and Science University, Portland, Oregon, USA

Richard A HarriganAssociate Professor of Emergency Medicine, Temple UniversitySchool of Medicine, Associate Research Director, Division ofEmergency Medicine, Temple University Hospital, Philadelphia, PA, USA

Stephen HawesDepartment of Emergency Medicine, Wythenshaw Hospital,Manchester

Jonathan HillSpecialist Registrar in Cardiology, Barts and the London NHS Trust

Richard IronsConsultant in Accident and Emergency Medicine, Princess ofWales Hospital, Bridgend

Richard JenkinsSpecialist Registrar in General Medicine and Endocrinology,Northern General Hospital, Sheffield

Kevin JonesConsultant Chest Physician, Bolton Royal Hospital

Sallyann JonesSpecialist Registrar in Accident and Emergency Medicine,Queen’s Medical Centre, Nottingham

Jihad M KhalilThoracic and Cardiovascular Institute, Michigan StateUniversity, Lancing, MI, USA

Jennifer H LindseyFellow, Division of Cardiology, Department of Pediatrics,University of Virginia Health System, Charlottesville, VA, USA

Karen McLeodConsultant Paediatric Cardiologist, Royal Hospital forSick Children, Glasgow

Steve MeekConsultant in Emergency Medicine, Royal United Hospitals,Bath

Francis MorrisConsultant in Emergency Medicine, Northern GeneralHospital, Sheffield

Corey SlovisProfessor of Emergency Medicine and Medicine, VanderbiltUniversity Medical Center, Department of EmergencyMedicine, Nashville, TN, USA

R K ThakurProfessor of Medicine, Thoracic and Cardiovascular Institute,Michigan State University, Lancing, MI, USA

Adam TimmisConsultant Cardiologist, London Chest Hospital, Barts and theLondon NHS Trust

vi

Contributors

vii

Preface

To 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 MorrisSheffield 2002

1 Introduction. I—Leads, rate, rhythm, and cardiac axisSteve Meek, Francis Morris

Electrocardiography 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.These electrical changes are recorded via electrodes placed onthe limbs and chest wall and are transcribed on to graph paperto produce an electrocardiogram (commonly known as anECG).

The sinoatrial node acts as a natural pacemaker and initiatesatrial depolarisation. The impulse is propagated to theventricles by the atrioventricular node and spreads in acoordinated fashion throughout the ventricles via thespecialised conducting tissue of the His-Purkinje system. Thus,after delay in the atrioventricular mode, atrial contraction isfollowed by rapid and coordinated contraction of the ventricles.

The electrocardiogram is recorded on to standard papertravelling at a rate of 25 mm/s. The paper is divided into largesquares, each measuring 5 mm wide and equivalent to 0.2 s.Each large square is five small squares in width, and each smallsquare is 1 mm wide and equivalent to 0.04 s.

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 havehigh 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 electricalimpulse travelling directly towards the electrode produces anupright (“positive”) deflection relative to the isoelectric baseline,whereas an impulse moving directly away from an electrodeproduces a downward (“negative”) deflection relative to the

Throughout this article the duration ofwaveforms will be expressed as0.04 s = 1 mm = 1 small square

Sinoatrial nodeElectrically inertatrioventricularregion

Left bundle branch

Left anteriorhemifascicle

Left posteriorhemifascicle

Rightatrium

Leftatrium

Rightventricle

Leftventricle

Atrioventricular node

Right bundle branch

The His-Purkinje conduction system

V5

V5

Role of body habitus and disease on the amplitude of the QRS complex.Top: Low amplitude complexes in an obese woman with hypothyroidism.Bottom: High amplitude complexes in a hypertensive man

Speed : 25 mm/s Gain : 10 mm/mV

Standard calibration signal

1

baseline. 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.

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 V1and aVR look through the right atrium directly into the cavityof the left ventricle.

RateThe term tachycardia is used to describe a heart rate greaterthan 100 beats/min. A bradycardia is defined as a rate less than60 beats/min (or < 50 beats/min during sleep).

One large square of recording paper is equivalent to 0.2seconds; there are five large squares per second and 300 perminute. Thus when the rhythm is regular and the paper speedis 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.

Some countries use a paper speed of 50 mm/s as standard;the heart rate is calculated by dividing the number of largesquares 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-Rintervals, 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 becalculated from the rhythm strip (see next section). It takes one

Anatomical relations of leads in a standard 12 leadelectrocardiogramII, III, and aVF: inferior surface of the heartV1 to V4: anterior surfaceI, aVL, V5, and V6: lateral surfaceV1 and aVR: right atrium and cavity of left ventricle

Waveforms mentioned in this article (forexample, QRS complex, R wave, P wave)are explained in the next article

Wave of depolarisation

Wave of depolarisation. Shape of QRS complex in any lead depends onorientation of that lead to vector of depolarisation

II

I

aVF

aVLaVR

V1 V2 V3 V4

V5

V6

III

Vertical and horizontal perspective of the leads. The limb leads “view” theheart in the vertical plane and the chest leads in the horizontal plane

II

Regular rhythm: the R-R interval is two large squares. The rate is 150beats/min (300/2=150)

V1 V2V3

V4 V5V6

Position of the six chest electrodes for standard 12 leadelectrocardiography. V1: right sternal edge, 4th intercostalspace; V2: left sternal edge, 4th intercostal space; V3:between V2 and V4; V4: mid-clavicular line, 5th space; V5:anterior axillary line, horizontally in line with V4; V6:mid-axillary line, horizontally in line with V4

ABC of Clinical Electrocardiography

2

second 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.

RhythmTo 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 usedto record the rhythm strip.

The term “sinus rhythm” is used when the rhythm originatesin the sinus node and conducts to the ventricles.

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 duringinspiration.

Cardiac axisThe cardiac axis refers to the mean direction of the wave ofventricular depolarisation in the vertical plane, measured froma zero reference point. The zero reference point looks at theheart from the same viewpoint as lead I. An axis lying abovethis 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.

Cardinal features of sinus rhythmx The P wave is upright in leads I and IIx Each P wave is usually followed by a QRS complexx The heart rate is 60-99 beats/min

Normal findings in healthy individualsx Tall R wavesx Prominent U wavesx ST segment elevation (high-take off, benign early repolarisation)x Exaggerated sinus arrhythmiax Sinus bradycardiax Wandering atrial pacemakerx Wenckebach phenomenonx Junctional rhythmx 1st degree heart block

Conditions for which determination of the axis is helpful indiagnosisx Conduction defects—for example, left anterior hemiblockx Ventricular enlargement—for example, right ventricularhypertrophy

x Broad complex tachycardia—for example, bizarre axis suggestive ofventricular origin

x Congenital heart disease—for example, atrial septal defectsx Pre-excited conduction—for example, Wolff-Parkinson-Whitesyndrome

x Pulmonary embolus

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 here

I

II

aVL

0˚180˚

30˚150˚

-30˚-150˚

60˚120˚

-60˚-120˚

90˚

-90˚

aVR

aVF

III

Hexaxial diagram (projection of six leads in verticalplane) showing each lead’s view of the heart

Introduction. I—Leads, rate, rhythm, and cardiac axis

3

Several methods can be used to calculate the cardiac axis,though occasionally it can prove extremely difficult todetermine. The simplest method is by inspection of leads I, II,and III.

A more accurate estimate of the axis can be achieved if allsix 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 leadx With reference to the hexaxial diagram, inspect the QRScomplexes in the leads adjacent to the equiphasic lead. If thelead to the left side is positive, then the axis is 90° to theequiphasic lead towards the left. If the lead to the right side ispositive, then the axis is 90° to the equiphasic lead towards theright.

I

II

III

aVR

aVL

aVF

Determination of cardiac axis using the hexaxial diagram (see previouspage). Lead II (60°) is almost equiphasic and therefore the axis lies at 90° tothis lead (that is 150° to the right or −30° to the left). Examination of theadjacent leads (leads I and III) shows that lead I is positive. The cardiac axistherefore lies at about −30°

Calculating the cardiac axis

Normal axisRight axisdeviation

Left axisdeviation

Lead I Positive Negative PositiveLead II Positive Positive or

negativeNegative

Lead III Positive ornegative

Positive Negative


4

2 Introduction. II—Basic terminologySteve Meek, Francis Morris

This 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 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(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 andright arm electrodes), dextrocardia, or abnormal atrial rhythms.

The P wave in V1 is often biphasic. Early right atrial forcesare directed anteriorly, giving rise to an initial positivedeflection; these are followed by left atrial forces travellingposteriorly, 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 slightasynchrony 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 intervalAfter 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, thebundle of His and bundle branches, and the Purkinje fibres.

The PR interval is the time between the onset of atrialdepolarisation and the onset of ventricular depolarisation, and

Characteristics of the P wavex Positive in leads I and IIx Best seen in leads II and V1x Commonly biphasic in lead V1x < 3 small squares in durationx < 2.5 small squares in amplitude

P wave

Complex showing P wave highlighted

Sinoatrial node

Right atrium

Left atriumAtrioventricular node

Wave ofdepolarisation

Atrial depolarisation gives rise to the P wave

PR interval

PR segment

P

Q

S

T

U

R

Normal duration of PR interval is 0.12-0.20 s (three to five small squares)

I

II

P waves are usually more obvious in lead II than in lead I

5

it is measured from the beginning of the P wave to the firstdeflection of the QRS complex (see next section), whether thisbe a Q wave or an R wave. The normal duration of the PRinterval is three to five small squares (0.12-0.20 s).Abnormalities of the conducting system may lead totransmission delays, prolonging the PR interval.

QRS complexThe 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—forexample, 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 rightof the septum and thus registers an initial small positivedeflection (R wave) as the depolarisation wave travels towardsthis lead.

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 rightand left ventricles produces opposing electrical vectors, but theleft ventricle has the larger muscle mass and its depolarisationdominates the electrocardiogram.

In the precordial leads, QRS morphology changesdepending on whether the depolarisation forces are movingtowards or away from a lead. The forces generated by the freewall of the left ventricle predominate, and therefore in lead V1 asmall 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 equiphasicQRS complex is located over the transition zone; this liesbetween 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 oftensmaller 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 Rwaves > 30 mm are occasionally recorded in normal youngmale adults.

Nomenclature in QRS complexesQ wave: Any initial negative deflectionR wave: Any positive deflectionS wave: Any negative deflection after an R wave

Non-pathological Q waves are oftenpresent in leads I, III, aVL, V5, and V6

R wave

S waveQ wave

Composition of QRS complex

Sinoatrial node

Rightatrium

Leftatrium

Rightventricle


Leftventricle

Wave of depolarisation spreading throughout ventricles gives rise to QRScomplex

Transitional zone

V1 V2 V3 V4 V5 V6

Typical change in morphology of QRS complex from leads V1 to V6


6

ST 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 “TPsegment” 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 theST segment, and this is known as “high take-off.”

Non-pathological elevation of the ST segment is alsoassociated with benign early repolarisation (see article on acutemyocardial 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.

T 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 ishighly 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 ofhyperkalaemia.

The T wave shouldgenerally be at least 1/8but less than 2/3 of theamplitude of thecorresponding R wave;T wave amplitude rarelyexceeds 10 mm

ST segment TP segment

J point

The ST segment should be in the same horizontal plane as the TP segment;the J point is the point of inflection between the S wave and ST segment

V2 V4 V6

Change in ST segment morphology across the precordial leads

T wave

Complex showing T wave highlighted

V2

V3

Complexes in leads V2 and V3 showing high take-off

Introduction. II—Basic terminology

7

QT 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.

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 increasesslightly 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,leading 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.

V1

V2

V3

Obvious U waves in leads V1 to V3 in patient withhypokalaemia

aVL

QT interval

The QT interval is measured in leadaVL as this lead does not haveprominent U waves (diagram isscaled up)


8

3 Bradycardias and atrioventricular conduction blockDavid Da Costa, William J Brady, June Edhouse

By arbitrary definition, a bradycardia is a heart rate of < 60beats/min. A bradycardia may be a normal physiologicalphenomenon or result from a cardiac or non-cardiac disorder.

Sinus bradycardiaSinus 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.

The commonest pathological cause of sinus bradycardia isacute myocardial infarction. Sinus bradycardia is particularlyassociated with inferior myocardial infarction as the inferiormyocardial wall and the sinoatrial and atrioventricular nodesare usually all supplied by the right coronary artery.

Sick 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 nodebut is also associated with myocardial ischaemia, digoxin, andcardiac surgery.

The possible electrocardiographic features includepersistent sinus bradycardia, periods of sinoatrial block, sinusarrest, junctional or ventricular escape rhythms,tachycardia-bradycardia syndrome, paroxysmal atrial flutter, andatrial fibrillation. The commonest electrocardiographic featureis an inappropriate, persistent, and often severe sinusbradycardia.

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.

Many patients tolerate heart rates of40 beats/min surprisingly well, but atlower rates symptoms are likely toinclude dizziness, near syncope, syncope,ischaemic chest pain, Stokes-Adamsattacks, and hypoxic seizures

Pathological causes of sinus bradycardiax Acute myocardial infarctionx Drugs—for example, � blockers, digoxin, amiodaronex Obstructive jaundicex Raised intracranial pressurex Sick sinus syndromex Hypothermiax Hypothyroidism

Conditions associated with sinoatrial nodedysfunctionx Agex Idiopathic fibrosisx Ischaemia, including myocardial infarctionx High vagal tonex Myocarditisx Digoxin toxicity

Severe sinus bradycardia

Sinoatrial block (note the pause is twice the P-P interval)

Sinus arrest with pause of 4.4 s beforegeneration and conduction of ajunctional escape beat

9

Escape rhythms are the result of spontaneous activity from asubsidiary pacemaker, located in the atria, atrioventricularjunction, or ventricles. They take over when normal impulseformation or conduction fails and may be associated with anyprofound bradycardia.

Atrioventricular conduction blockAtrioventricular conduction can be delayed, intermittentlyblocked, or completely blocked—classified correspondingly asfirst, second, or third degree block.

First 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 PRinterval to > 0.2 s. A QRS complex follows each P wave, and thePR interval remains constant.

Second degree blockIn second degree block there is intermittent failure ofconduction between the atria and ventricles. Some P waves arenot followed by a QRS complex.

There are three types of second degree block. Mobitz type Iblock (Wenckebach phenomenon) is usually at the level of theatrioventricular node, producing intermittent failure oftransmission of the atrial impulse to the ventricles. The initialPR interval is normal but progressively lengthens with eachsuccessive beat until eventually atrioventricular transmission isblocked completely and the P wave is not followed by a QRScomplex. 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 atrioventricularblock, 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 relationto the QRS complexes and usually proceed at a faster rate.

A junctional escape beat has a normal QRS complex shapewith a rate of 40-60 beats/min. A ventricular escape rhythmhas broad complexes and is slow (15-40 beats/min)

Tachycardia-bradycardia syndromex Common in sick sinus syndromex Characterised by bursts of atrial tachycardia interspersed withperiods of bradycardia

x Paroxysmal atrial flutter or fibrillation may also occur, andcardioversion may be followed by a severe bradycardia

Causes of atrioventricular conduction blockx Myocardial ischaemia or infarctionx Degeneration of the His-Purkinje systemx Infection—for example, Lyme disease, diphtheriax Immunological disorders—for example, systemic lupuserythematosus

x Surgeryx Congenital disorders

V2

First degreeheart(atrioventricular)block

Mobitz type I block (Wenckebach phenomenon)

Mobitz type II block—a complication of an inferior myocardial infarction.The PR interval is identical before and after the P wave that is notconducted

Third 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 waves


10

A subsidiary pacemaker triggers ventricular contractions,though occasionally no escape rhythm occurs and asystolicarrest ensues. The rate and QRS morphology of the escaperhythm vary depending on the site of the pacemaker.

Bundle branch block and fascicularblockThe 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 ventricledepolarises in the normal way and thus the early part of theQRS complex appears normal. The wave of depolarisation thenspreads to the right ventricle through non-specialisedconducting tissue, with slow depolarisation of the right ventriclein a left to right direction. As left ventricular depolarisation iscomplete, the forces of right ventricular depolarisation areunopposed. Thus the later part of the QRS complex isabnormal; the right precordial leads have a prominent and lateR 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.

Left 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.

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.

Conditions associated with right bundle branch blockx Rheumatic heart diseasex Cor pulmonale/right ventricular hypertrophyx Myocarditis or cardiomyopathyx Ischaemic heart diseasex Degenerative disease of the conduction systemx Pulmonary embolusx Congenital heart disease—for example, in atrial septal defects

Diagnostic 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 directionto the dominant deflection of the QRS complex (appropriatediscordance)

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

Sinoatrial node

Rightatrium

Leftatrium

Rightventricle

Leftventricle


Right bundle branch block, showing the wave of depolarisation spreading tothe right ventricle through non-specialised conducting tissue

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Right bundle branch block

Diagnostic criteria for right bundle branch blockx 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 precordialleads

Bradycardias and atrioventricular conduction block

11

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 secondaryrepolarisation changes. ST segment depression and T waveinversion are seen in leads with a dominant R wave. ST segmentelevation and positive T waves are seen in leads with a dominantS wave. Thus there is discordance between the QRS complex andthe ST segment and T wave.

Fascicular blocksBlock 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.

Bifascicular block is the combination of right bundle branchblock and left anterior or posterior hemiblock. Theelectrocardiogram shows right bundle branch block with left orright axis deviation. Right bundle branch block with leftanterior 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.

Sinoatrial node

Rightatrium

Leftatrium

Rightventricle

Leftventricle


Left bundle branch block, showing depolarisation spreading from the rightto left ventricle

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Left bundle branch block

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Trifascicular block (right bundle branch block, left anterior hemiblock, andfirst degree heart block)


12

4 Atrial arrhythmiasSteve Goodacre, Richard Irons

In adults a tachycardia is any heart rate greater than 100 beatsper minute. Supraventricular tachycardias may be divided intotwo distinct groups depending on whether they arise from theatria or the atrioventricular junction. This article will considerthose arising from the atria: sinus tachycardia, atrial fibrillation,atrial flutter, and atrial tachycardia. Tachycardias arising fromre-entry circuits in the atrioventricular junction will beconsidered in the next article in the series.

Clinical 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.Coronary blood flow occurs during diastole, and as the heartrate increases diastole shortens. In the presence of coronaryatherosclerosis, blood flow may become critical andanginal-type chest pain may result. Similar chest pain, which isnot related to myocardial ischaemia, may also occur. Reducedcardiac performance produces symptoms of faintness orsyncope and leads to increased sympathetic stimulation, whichmay increase the heart rate further.

As a general rule the faster the ventricular rate, the morelikely the presence of symptoms—for example, chest pain,faintness, and breathlessness. Urgent treatment is needed forseverely symptomatic patients with a narrow complextachycardia.

Electrocardiographic featuresDifferentiation between different types of supraventriculartachycardia may be difficult, particularly when ventricular ratesexceed 150 beats/min.

Knowledge of the electrophysiology of these arrhythmiaswill 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 maybe of diagnostic value as slowing the ventricular rate allowsmore accurate visualisation of atrial activity. Such manoeuvreswill not usually stop the tachycardia, however, unless it is due tore-entry involving the atrioventricular node.

Sinus 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

Supraventricular tachycardiasFrom the atria or sinoatrial nodex Sinus tachycardiax Atrial fibrillationx Atrial flutterx Atrial tachycardia

From the atrioventricular nodex Atrioventricular re-entrant tachycardiax Atrioventricular nodal re-entrant tachycardia

Electrocardiographic characteristics of atrial arrhythmiasSinus tachycardiax P waves have normal morphologyx Atrial rate 100-200 beats/minx Regular ventricular rhythmx Ventricular rate 100-200 beats/minx One P wave precedes every QRS complex

Atrial tachycardiax Abnormal P wave morphologyx Atrial rate 100-250 beats/minx Ventricular rhythm usually regularx Variable ventricular rate

Atrial flutterx Undulating saw-toothed baseline F (flutter) wavesx Atrial rate 250-350 beats/minx Regular ventricular rhythmx Ventricular rate typically 150 beats/min (with 2:1 atrioventricularblock)

x 4:1 is also common (3:1 and 1:1 block uncommon)

Atrial fibrillationx P waves absent; oscillating baseline f (fibrillation) wavesx Atrial rate 350-600 beats/minx Irregular ventricular rhythmx Ventricular rate 100-180 beats/min

Electrocardiographic analysis shouldinclude measurement of the ventricularrate, assessment of the ventricularrhythm, identification of P, F, or f waves ,measurement of the atrial rate, andestablishment of the relation of P wavesto the ventricular complexes

Sinus tachycardia

13

the absence of an obvious underlying cause should promptconsideration of atrial flutter or atrial tachycardia.

Rarely the sinus tachycardia may be due to a re-entryphenomenon in the sinoatrial node. This is recognised byabrupt onset and termination, a very regular rate, and absenceof an underlying physiological stimulus. Theelectrocardiographic characteristics are otherwise identical. Therate is usually 130-140 beats/min, and vagal manoeuvres maybe successful in stopping the arrhythmia.

Atrial fibrillationThis is the most common sustained arrhythmia. Overallprevalence is 1% to 1.5%, but prevalence increases with age,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.

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 fibrillationis 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 variesbetween leads but may be so coarse that they are mistaken forflutter waves.

Conduction of atrial impulses to the ventricles is variableand unpredictable. Only a few of the impulses transmit throughthe 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

other 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, orpermanent. It may be precipitated by an atrial extrasystole orresult from degeneration of other supraventricular tachycardias,particularly atrial tachycardia and/or flutter.

Atrial flutterAtrial 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 theatrioventricular node. Typically 2:1 block (atrial rate to

Causes of sinus tachycardiaPhysiological—Exertion, anxiety, painPathological—Fever, anaemia, hypovolaemia, hypoxiaEndocrine—ThyrotoxicosisPharmacological—Adrenaline as a result of phaeochromocytoma;salbutamol; alcohol, caffeine

Causes of atrial fibrillationx Ischaemic heart diseasex Hypertensive heart diseasex Rheumatic heart diseasex Thyrotoxicosisx Alcohol misuse (acute orchronic)

x Cardiomyopathy (dilated orhypertrophic)

x Sick sinus syndromex Post-cardiac surgeryx Chronic pulmonary diseasex Idiopathic (lone)

Sinoatrial node

Right atrium


Atrial fibrillation is the result of multiple wavelets of depolarisation (shownby arrows) moving around the atria chaotically, rarely completing are-entrant circuit

Atrial fibrillation waves seen in lead V1

Rhythm strip in atrial fibrillation

Sinoatrial node

Right atrium


Atrial flutter is usually the result of a single re-entrant circuit in the rightatrium (top); atrial flutter showing obvious flutter waves (bottom)


14

ventricular 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 atrioventricularblock may allow identification of flutter waves.

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.

The ventricular rate depends on the degree ofatrioventricular block, but when 1:1 conduction occurs a rapidventricular response may result. Increasing the degree of blockwith carotid sinus massage or adenosine may aid the diagnosis.

There are four commonly recognised types of atrialtachycardia. Benign atrial tachycardia is a common arrhythmiain elderly people. It is paroxysmal in nature, has an atrial rate of80-140 beats/min and an abrupt onset and cessation, and isbrief in duration.

Types of atrial tachycardiax Benignx Incessant ectopicx Multifocalx Atrial tachycardia with block (digoxin toxicity)

Rhythm strip in atrial flutter (rate 150 beats/min)

Atrial flutter (rate 150 beats/min) with increasing block (flutter waves revealed after administration of adenosine)

Atrial flutter with variable block

Sinoatrial node

Right atrium


Atrial tachycardia is initiated by an ectopic atrial focus (the P wavemorphology therefore differs from that of sinus rhythm)

Atrial tachycardia with 2:1 block (note the inverted P waves)

Atrial arrhythmias

15

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. Itis 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.It is typically seen in association with chronic pulmonarydisease. Other causes include hypoxia or digoxin toxicity.

Atrial tachycardia with atrioventricular block is typicallyseen with digoxin toxicity. The ventricular rhythm is usuallyregular but may be irregular if atrioventricular block is variable.Although often referred to as “paroxysmal atrial tachycardiawith block” this arrhythmia is usually sustained.

Conditions associated with atrial tachycardiax Cardiomyopathyx Chronic obstructive pulmonary diseasex Ischaemic heart diseasex Rheumatic heart diseasex Sick sinus syndromex Digoxin toxicity

Multifocal atrial tachycardia

Atrial tachycardia with 2:1 block in patient with digoxin toxicity


16

5 Junctional tachycardiasDemas Esberger, Sallyann Jones, Francis Morris

Any tachyarrhythmia arising from the atria or theatrioventricular junction is a supraventricular tachycardia. Inclinical practice, however, the term supraventricular tachycardiais reserved for atrial tachycardias and arrhythmias arising fromthe region of the atrioventricular junction as a result of are-entry mechanism (junctional tachycardias). The mostcommon junctional tachycardias are atrioventricular nodalre-entrant tachycardia and atrioventricular re-entranttachycardia.

Atrioventricular nodal re-entranttachycardiaThis is the most common cause of paroxysmal regular narrowcomplex tachycardia. Affected individuals are usually young andhealthy with no organic heart disease.

MechanismIn atrioventricular nodal re-entrant tachycardia there are twofunctionally and anatomically different distinct pathways in theatrioventricular node, with different conduction velocities anddifferent 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 isconducted through the fast pathway and depolarises theventricles. 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 recoversfirst. An atrioventricular nodal re-entrant tachycardia is initiated,for 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 thenknown as permanent junctional re-entrant tachycardia and isrecognised by a long RP1 interval.

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.

Atrioventricularnode

His bundle

Slowpathway

Fastpathway

Mechanism of atrioventricular nodal re-entranttachycardia showing the slow and fast conduction routesand the final common pathway through the lower partof the atrioventricular node and bundle of His

Slowpathway

Fastpathway

Slowpathway

FastpathwayCircus

motion

Atrialbeatpremature

A premature atrial impulse finds the fast pathway refractory, allowingconduction only down the slow pathway (left). By the time the impulsereaches the His bundle, the fast pathway may have recovered, allowingretrograde conduction back up to the atria—the resultant “circus movement”gives rise to slow-fast atrioventricular nodal re-entrant tachycardia (right)

An atrioventricular nodal re-entrant tachycardia

17

In the relatively uncommon fast-slow atrioventricular nodalre-entrant tachycardia, atrial depolarisation lags behinddepolarisation of the ventricles, and inverted P waves mayfollow the T wave and precede the next QRS complex.

Clinical 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. Thefrequency of episodes can vary between several a day, or oneepisode in a lifetime. Most patients have only mild symptoms,such 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 ananatomically distinct atrioventricular connection. This accessoryconduction pathway allows the atrial impulse to bypass theatrioventricular 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 groovebetween the atria and ventricles, and in 10% of cases more thanone accessory pathway exists. The accessory pathway allows theformation of a re-entry circuit, which may give rise to either anarrow or a broad complex tachycardia, depending on whetherthe atrioventricular node or the accessory pathway is used forantegrade conduction.

Electrocardiographic 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 slowdepolarisation is then rapidly overtaken by depolarisationpropagated by the normal conduction system, and the rest ofthe QRS complex appears relatively normal.

Fast-slow atrioventricular nodal re-entranttachycardia is known as long RP1

tachycardia, and it may be difficult todistinguish from an atrial tachycardia

Symptoms are commonest in patientswith a very rapid heart rate andpre-existing heart disease

The commonest kind of atrioventricularre-entrant tachycardia occurs as part ofthe Wolff-Parkinson-White syndrome

Termination of atrioventricular nodal re-entrant tachycardia

Bundleof Kent

Early activationof the ventricle

In theWolff-Parkinson-Whitesyndrome the bundle ofKent provides a separateelectrical conduit betweenthe atria and the ventricles

In sinus rhythm conductionover the accessory pathwaygives rise to a short PRinterval and a delta wave


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Commonly, the accessory pathway is concealed—that is, it iscapable of conducting only in a retrograde fashion, fromventricles to atria. During sinus rhythm pre-excitation does notoccur and the electrocardiogram is normal.

Traditionally the Wolff-Parkinson-White syndrome has beenclassified into two types according to the electrocardiographicmorphology of the precordial leads. In type A, the delta waveand QRS complex are predominantly upright in the precordialleads. The dominant R wave in lead V1 may be misinterpretedas 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.

Mechanism 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.

Classification of Wolff-Parkinson-White syndromeType A (dominant R wave in V1 lead) may be confused with:x Right bundle branch blockx Right ventricular hypertrophyx Posterior myocardial infarction

Type B (negative QRS complex in V1 lead) may be confused with:x Left bundle branch blockx Anterior myocardial infarction

V1

Type A

V2 V3 V4 V5 V6

V3 V6V1 V4V2 V5

Type B

Wolff-Parkinson-White, type A and type B, characterised by morphology of the recording from leads V1 to V6

Mechanisms for orthodromic (left) and antidromic(right) atrioventricular re-entrant tachycardia

Orthodromic 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

Junctional tachycardias

19

Antidromic atrioventricular re-entrant tachycardia isrelatively uncommon, occurring in about 10% of patients withthe Wolff-Parkinson-White syndrome. The accessory pathwayallows antegrade conduction, and thus the impulse is conductedfrom the atria to the ventricles via the accessory pathway.Depolarisation is propagated through non-specialisedmyocardium, and the resulting QRS complex is broad andbizarre. The impulse then travels in a retrograde fashion via theatrioventricular node back to the atria.

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-Whitesyndrome the atrial impulses can be conducted via the accessorypathway, causing ventricular pre-excitation and producing broadQRS complexes with delta waves. Occasionally an impulse will beconducted 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.

Clinical 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.

Orthodromic atrioventricular re-entrant tachycardia occurswith antegrade conduction through the atrioventricularnode

Antidromic atrioventricular re-entrant tachycardia occurswith retrograde conduction through the atrioventricularnode

In some patients the accessory pathway allows very rapidconduction, and consequently very fast ventricular rates(in excess of 300 beats/min) may be seen, with theassociated risk of deterioration into ventricularfibrillation

Atrial fibrillation in theWolff-Parkinson-White syndrome


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6 Broad complex tachycardia—Part IJune Edhouse, Francis Morris

Broad complex tachycardias occur by various mechanisms andmay be ventricular or supraventricular in origin. In theemergency setting most broad complex tachycardias have aventricular origin. However, an arrhythmia arising from theatria or the atrioventricular junction will produce a broadcomplex if associated with ventricular pre-excitation or bundlebranch block. The causes of ventricular and supraventriculartachycardias are generally quite different, with widely differingprognoses. Most importantly, the treatment of a broad complextachycardia depends on the origin of the tachycardia. Thisarticle describes monomorphic ventricular tachycardias; otherventricular tachycardias and supraventricular tachycardias willbe 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.

Mechanisms of ventricular arrhythmiasThe mechanisms responsible for ventricular tachycardia includere-entry or increased myocardial automaticity. The tachycardiais 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

Varieties of broad complex tachycardiaVentricularRegularx Monomorphic ventricular tachycardiax Fascicular tachycardiax Right ventricular outflow tract tachycardiaIrregularx Torsades de pointes tachycardiax Polymorphic ventricular tachycardia

Supraventricularx Bundle branch block with aberrant conductionx Atrial tachycardia with pre-excitation

Ventricular tachycardia is described as“monomorphic” when the QRScomplexes have the same generalappearance, and “polymorphic” if there iswide beat to beat variation in QRSmorphology. Monomorphic ventriculartachycardia is the commonest form ofsustained ventricular tachycardia

The electrophysiology of a re-entry circuitwas described in last week’s article

Non-sustained ventricular tachycardia (top) and accelerated idioventricularrhythm (bottom)

PolymorphicMonomorphic

Monomorphic and polymorphic ventricular tachycardia

21

“macro” in scale and often occur in the zone of ischaemia orfibrosis surrounding damaged myocardium.

Ventricular tachycardia may result from direct damage tothe myocardium secondary to ischaemia or cardiomyopathy, orfrom the effects of myocarditis or drugs—for example, class 1antiarrhythmics (such as flecainide, quinidine, anddisopyramide). Monomorphic ventricular tachycardia usuallyoccurs after myocardial infarction and is a sign of extensivemyocardial damage; there is a high inhospital mortality, moreoften resulting from impaired ventricular function thanrecurrence of the arrhythmia.

Electrocardiographic 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 ofthe 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-Purkinjesystem, 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 thearrhythmia in some patients with ischaemic heart disease, andthe resulting complexes have a left bundle branch blockmorphology.

Rate and rhythmIn ventricular tachycardia the rate is normally 120-300beats/minute. The rhythm is regular or almost regular ( < 0.04 sbeat 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 axisIn a normal electrocardiogram the QRS axis in the meanfrontal plane is between − 30° and + 90°, with the axis mostcommonly lying at around 60°. With the onset of ventriculartachycardia 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 anextremely abnormal axis either to the left or right. When the

Triggered automaticity of a group of cellscan result from congenital or acquiredheart disease. Once initiated, thesetachycardias tend to accelerate but slowmarkedly before stopping

Ventricular tachycardia in a patient withchronic ischaemic heart disease isprobably caused by a re-entryphenomenon involving infarct scar tissue,and thus the arrhythmia tends to berecurrent

Ventricular tachycardia with very broad QRS complexes

Fascicular tachycardia with narrow QRS complexes

Sinoatrial node

Rightatrium

Leftatrium

Rightventricle


Ventricular tachycardia showing abnormal direction of wave ofdepolarisation, giving rise to bizarre axis

Axis changeAxis changeAxis change

Change in axis with onset of monomorphic ventricular tachycardia in leadaVR


22

QRS 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.

Direct evidence of independent atrial activityIn ventricular tachycardia, the sinus node continues to initiateatrial contraction. Since this atrial contraction is completelyindependent of ventricular activity, the resulting P waves aredissociated 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.

Although evidence of atrioventricular dissociation isdiagnostic for ventricular tachycardia, a lack of direct evidenceof independent P wave activity does not exclude the diagnosis.The situation may be complicated by artefacts that simulateP 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 adiagnosis 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 thoughthey 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 chestleads are either predominantly positive or predominantlynegative.

The presence of concordance suggests that the tachycardiahas a ventricular origin.

In some patients the atrioventricularnode allows retrograde conduction ofventricular impulses to the atria. Theresulting P waves are inverted and occurafter the QRS complex, usually with aconstant RP interval.

It is important to scrutinise the tracingsfrom all 12 leads of theelectrocardiogram, as P waves may beevident in some leads but not in others

Concordance can be eitherpositive or negative

Capture beat

Fusion beat

Atrioventricular dissociation in monomorphic ventricular tachycardia (note P waves, arrowed)

Broad complex tachycardia—Part I

23

Positive concordance probably indicates that the origin ofthe tachycardia lies on the posterior ventricular wall; the wave ofdepolarisation 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 V6

Positive concordance

V1 V2 V3

V4 V5 V6

Negative concordance: ventricular tachycardia in a 90 year old woman incongestive cardiac failure


24

7 Broad complex tachycardia—Part IIJune Edhouse, Francis Morris

This article continues the discussion, started last week, onventricular tachycardias and also examines how to determinewhether a broad complex tachycardia is ventricular orsupraventricular in origin.

Ventricular tachycardiasFascicular 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).Consequently, 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 tachycardiaoriginates from the posterior fascicle the frontal plane axis ofthe QRS complex is deviated to the left; when it originates fromthe anterior fascicle, right axis deviation is seen.

Right 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 terminatingor 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.

Torsades 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 recurunless the underlying cause is corrected. Occasionally it may beprolonged or degenerate into ventricular fibrillation. It isassociated with conditions that prolong the QT interval.

Transient prolongation of the QT interval is often seen inthe acute phase of myocardial infarction, and this may lead to

Torsades de pointes may be drug induced or secondary toelectrolyte disturbances

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Fascicular ventricular tachycardia (note the right bundle branch blockpattern and left axis deviation)

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Right ventricular outflow track tachycardia

Torsades de pointes

25

torsades de pointes. Ability to recognise torsades de pointes isimportant because its management is different from themanagement of other ventricular tachycardias.

Polymorphic ventricular tachycardiaPolymorphic ventricular tachycardia has the electrocardiographiccharacteristics of torsades de pointes but in sinus rhythm the QTinterval is normal. It is much less common than torsades depointes. If sustained, polymorphic ventricular tachycardia oftenleads to haemodynamic collapse. It can occur in acute myocardialinfarction and may deteriorate into ventricular fibrillation.Polymorphic ventricular tachycardia must be differentiated fromatrial fibrillation with pre-excitation, as both have the appearanceof an irregular broad complex tachycardia with variable QRSmorphology (see last week’s article).

Broad complex tachycardias ofsupraventricular originIn the presence of aberrant conduction or ventricularpre-excitation, any supraventricular tachycardia may present asa broad complex tachycardia and mimic ventricular tachycardia.

Atrial tachycardia with aberrant conductionAberrant conduction is defined as conduction through theatrioventricular node with delay or block, resulting in a broaderQRS complex. Aberrant conduction usually manifests as left orright bundle branch block, both of which have characteristicfeatures. The bundle branch block may predate the tachycardia,or it may be a rate related functional block, occurring whenatrial impulses arrive too rapidly for a bundle branch toconduct normally. When atrial fibrillation occurs with aberrantconduction and a rapid ventricular response, a totally irregularbroad complex tachycardia is produced.

Wolff-Parkinson-White syndromeBroad complex tachycardias may also occur in theWolff-Parkinson-White syndrome, either as an antidromicatrioventricular re-entrant tachycardia or in association withatrial flutter or fibrillation.

Causes of torsades de pointesDrugsx Antiarrhythmic drugs: classIa (disopyramide,procainamide, quinidine);class III (amiodarone,bretylium, sotalol)

x Antibacterials:erythromycin,fluoquinolones,trimethoprim

x Other drugs: terfenadine,cisapride, tricyclicantidepressants, haloperidol,lithium, phenothiazines,chloroquine, thioridazine

Electrolyte disturbancesx Hypokalaemiax Hypomagnesaemia

Congenital syndromesx Jervell and Lange-Nielsensyndrome

x Romano-Ward syndrome

Other causesx Ischaemic heart diseasex Myxoedemax Bradycardia due to sick sinussyndrome or complete heartblock

x Subarachnoid haemorrhage

Differentiation between ventricular tachycardia andsupraventricular tachycardia with bundle branch blockIf the tachycardia has a right bundle branch block morphology (apredominantly positive QRS complex in lead V1), a ventricular origin issuggested if there is:x QRS complex with duration > 0.14 sx Axis deviationx A QS wave or predominantly negative complex in lead V6x Concordance throughout the chest leads, with all deflectionspositive

x A single (R) or biphasic (QR or RS) R wave in lead V1x A triphasic R wave in lead V1, with the initial R wave taller than thesecondary R wave and an S wave that passes through the isoelectricline

If the tachycardia has a left bundle branch block morphology (apredominantly negative deflection in lead V1), a ventricular origin issuggested if there is:x Axis deviationx QRS complexes with duration > 0.16 sx A QS or predominantly negative deflection in lead V6x Concordance throughout the chest leads, with all deflectionsnegative

x An rS complex in lead V1

The Wolff-Parkinson-White syndrome isdiscussed in more detail in an earlierarticle, on junctional tachycardias

Polymorphic ventricular tachycardiadeteriorating into ventricularfibrillation

V6

Atrial fibrillation and left bundle branch block

I

Atrial flutter with left bundle branch block, giving rise tobroad complex tachycardia


26

Antidromic 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-Whitesyndrome the atrial impulses are conducted down the accessorypathway, which may allow rapid conduction and consequentlyvery fast ventricular rates.

The impulses conducted via the accessory pathway producebroad QRS complexes. Occasionally an impulse will beconducted via the atrioventricular node and produce a normalQRS complex or a fusion beat. The result is a completelyirregular and often rapid broad complex tachycardia with afairly constant QRS pattern, except for occasional normalcomplexes and fusion beats.

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 is90% predictive of ventricular tachycardia.

The symptoms associated with broad complex tachycardiadepend on the haemodynamic consequences of thearrhythmia—that is, they relate to the heart rate and theunderlying cardiac reserve rather than to the origin of thearrhythmia. It is wrong to assume that a patient with ventriculartachycardia 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 fusionbeats or captured beats. The duration of QRS complexes is alsoa key differentiating feature: those of > 0.14 s generally indicatea ventricular origin. Concordance throughout the chest leadsalso indicates ventricular tachycardia.

Drugs that block the atrioventricularnode—such as digoxin, verapamil, andadenosine—should be avoided as they canproduce an extremely rapid ventricularresponse

Danger of misdiagnosisx The safest option is to regard a broad complex tachycardia ofuncertain origin as ventricular tachycardia unless good evidencesuggests a supraventricular origin

x If a ventricular tachycardia is wrongly treated as supraventriculartachycardia, the consequences may be extremely serious

x Giving verapamil to a patient with ventricular tachycardia mayresult in hypotension, acceleration of the tachycardia, and death

In ventricular tachycardia the rhythm isregular or almost regular; if the rhythm isobviously irregular the most likelydiagnosis is atrial fibrillation with eitheraberrant conduction or pre-excitation

Antidromic atrioventricular re-entrant tachycardia,giving rise to broad complex tachycardia

Atrial fibrillation in patient withWolff-Parkinson-White syndrome(note irregularity of complexes)

Broad complex tachycardia—Part II

27

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.

Ventricular tachycardia and supraventricular tachycardiawith bundle branch block may produce similarelectrocardiograms. If a previous electrocardiogram shows abundle branch block pattern during sinus rhythm that is similarto or identical with that during the tachycardia, the origin of thetachycardia is likely to be supraventricular. But if the QRSmorphology changes during the tachycardia, a ventricularorigin 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.

Adenosine can also be used to blockconduction temporarily through theatrioventricular node to ascertain theorigin of a broad complex tachycardia,but failure to stop the tachycardia doesnot necessarily indicate a ventricularorigin

I II

V2 V3 V5V1 V4 V6

III aVLaVR aVF

Left axis deviation andright bundle branchblock in man withprevious inferiormyocardial infarction

V2 V3 V5V1 V4 V6

II III aVLI aVR aVF

Monomorphicventricular tachycardiain same patient,showing a shift of axisto right of >40° (notepositive concordance)


28

8 Acute myocardial infarction—Part IFrancis Morris, William J Brady

In the clinical assessment of chest pain, electrocardiographyis an essential adjunct to the clinical history and physicalexamination. A rapid and accurate diagnosis in patients withacute myocardial infarction is vital, as expeditious reperfusiontherapy can improve prognosis. The most frequently usedelectrocardiographic criterion for identifying acute myocardialinfarction is ST segment elevation in two or more anatomicallycontiguous 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 patientswith a proved acute myocardial infarction (on the basis ofclinical history and enzymatic markers) fail to develop STsegment elevation or depression. In most cases, however, serialelectrocardiograms show evolving changes that tend to followwell recognised patterns.

Hyperacute T wavesThe earliest signs of acute myocardial infarction are subtleand 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 theanterior 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 afterthe onset of the infarction and are followed by ST segmentchanges.

ST segment changesIn 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 normalconcavity. 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.

Indications for thrombolytic treatmentx ST elevation > 1 mm in two contiguous limb leads or > 2 mm intwo contiguous chest leads

x Posterior myocardial infarctionx Left bundle branch block

ST segment depression or enzymatic change are not indications forthrombolytic treatment

Sometimes the QRS complex, the ST segment, and theT wave fuse to form a single monophasic deflection, calleda giant R wave or “tombstone”

Normal

Peaked T wave

Degrees of STsegment elevation

Q wave formationand loss of R wave

T wave inversion

Sequence of changes seen during evolution of myocardial infarction

V2

V3

V5

V1 V4

V6

Hyperacute T waves

Anterior myocardial infarction with gross ST segment elevation (showing“tombstone” R waves)

V2 V3

V5

V1

V4 V6

29

Pathological Q wavesAs the acute myocardial infarction evolves, changes to the QRScomplex include loss of R wave height and the development ofpathological 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,though 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.

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 segmentand 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, andif 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 anacute 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.

Typically, the depressed ST segments tend to be horizontalor downsloping. The presence of reciprocal change isparticularly useful when there is doubt about the clinicalsignificance of ST segment elevation.

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Pathological Q waves in inferior and anterior leads

V2 V3

V5

V1

V4 V6

Long standing ST segment elevation and T wave inversion associated with aprevious anterior myocardial infarction (echocardiography showed a leftventricular aneurysm)

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

An inferolateral myocardial infarction withreciprocal changes in leads I, aVL, V1, and V2


30

Reciprocal change strongly indicates acute infarction, with asensitivity and positive predictive value of over 90%, though itsabsence 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 occuras 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 carriesa worse prognosis.

Localisation of site of infarctionThe distribution of changes recorded in acute myocardialinfarction 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 toinfarction. Anteroseptal infarcts are highly specific indicators ofdisease of the left anterior descending artery. Isolated inferiorinfarcts—changes in leads II, III, and aVF—are usually associatedwith disease in the right coronary or distal circumflex artery.Disease in the proximal circumflex artery is often associatedwith 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 bysigns of inferior infarction, associated with ST segmentelevation in lead V1. It is unusual for ST segment elevation inlead 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 STsegment elevation in right ventricular infarction may be shortlived.

Anatomical relationship of leadsInferior wall—Leads II, III, and aVFAnterior wall—Leads V1 to V4Lateral wall—Leads I, aVL, V5, and V6

Non-standard leadsRight ventricle—Right sided chest leads V1R to V6RPosterior wall—Leads V7 to V9

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Reciprocal changes: presence of widespread ST segment depression in theanterolateral leads strongly suggests that the subtle inferior ST segmentelevation is due to acute infarction

V3R

V4RV5R

V6R

V2R V1R

Placement of right sided chest leads

V2

V3

V5

V1 V4R

V6

II

III

aVL

I aVR

aVF

Acute inferior myocardial infarction withassociated right ventricular infarction

Acute myocardial infarction—Part I

31

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.

Posterior myocardial infarctionPosterior myocardial infarction refers to infarction of theposterobasal 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 outcomefor patients with posterior infarction.

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 leadsV1 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.

The diagnosis of rightventricular infarction isimportant as it may beassociated withhypotension. Treatmentwith nitrates or diureticsmay compound thehypotension, though thepatient may respond to afluid challenge

V2R

V3R

V5R

V1R V4R

V6R

II

III

aVL

I aVR

aVF

Acute inferior myocardial infarction with right ventricular involvement

V7 V8 V9

Scapula

Position of V7, V8, and V9on posterior chest wall

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Isolated posterior infarction with no associated inferior changes (note STsegment depression in leads V1 to V3)

V9

V8

ST segment elevation in posterior chest leads V8 and V9


32

9 Acute myocardial infarction—Part IIJune Edhouse, William J Brady, Francis Morris

This article describes the association of bundle branch blockwith acute myocardial infarction and the differential diagnosisof ST segment elevation.

Bundle 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 resultof 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 patientswith 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 branchblock is present, and many of the conventional diagnosticcriteria 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”between 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).

Recognition 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 specificindicators 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 acuteischaemia. Extreme ST segment elevation (>5 mm) in leads V1and V2 also suggests acute ischaemia. If doubt persists, serialelectrocardiograms may show evolving changes.

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Appropriate discordance in uncomplicated left bundle branch block (noteST elevation in leads V1 to V3)

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Acute myocardial infarction and left bundle branch block. Note that the STsegments are elevated in leads V5 and V6 (inappropriate concordance) andgrossly elevated (> 5 mm) in leads V2, V3, and V4; note also the ST segmentdepression in leads III and aVF

33

Right bundle branch blockRight bundle branch block is most commonly seen inassociation with coronary artery disease, but in many cases noorganic heart disease is present. Uncomplicated right bundlebranch block usually causes little ST segment displacement andneither causes nor masks Q waves. Thus it does not generallyinterfere with the diagnosis of acute myocardial infarction,though it may mask a posterior myocardial infarction.

Differential 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. Acorrect diagnosis has obvious advantages for the patient but isalso particularly important before the use of thrombolytictreatment so that unnecessary exposure to the risks ofthrombolytic drugs can be avoided.

The interpretation of ST segment elevation should alwaysbe made in the light of the clinical history and examinationfindings. There are often clues in the electrocardiogram todifferentiate the ST segment elevation of acute ischaemia fromother causes; for example, reciprocal changes (see last week’sarticle) may be present, which strongly indicate acute ischaemia.

The Brugada syndrome, which is familial,occurs particularly in young men and ischaracterised by right bundle branchblock and ST segment elevation in theright precordial leads. There is a highinstance of death as a result of ventriculartachyarrhythmias

Causes of ST segment elevationx Acute myocardial infarctionx “High take-off”x Benign early repolarisationx Left bundle branch blockx Left ventricular hypertrophyx Ventricular aneurysmx Coronary vasospasm/Printzmetal’s anginax Pericarditisx Brugada syndromex Subarachnoid haemorrhage

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

ST segment depression in precordial leads in 68 year old man with chest pain

A

B

C Inappropriate concordance in leadV1 in patient with left bundlebranch block (A); inappropriateconcordance in lead V6 in patientwith left bundle branch block (B);and exaggeration of appropriatediscordance in lead V1 in patientwith left bundle branch block (C)

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Development of left bundle branch block in sameman shortly after admission (note ST segmentdepression in lead V3; this is an example ofinappropriate concordance)


34

Serial electrocardiography or continuous ST segmentmonitoring is also useful as ischaemic ST segment elevationevolves 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.)

Benign early repolarisationA degree of ST segment elevation is often present in healthyindividuals, especially in young adults and in people of Africandescent. 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 itscharacteristic 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 infarctionThe 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 leftventricular aneurysm should be considered. Care should betaken 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 myocardialinfarction 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 injuredtissue 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 elevationThe 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. STsegment elevation or depression may be seen; a putative

V2 V3

V5

V1

V4 V6

Benign early repolarisation

V2 V3

V5

V1

V4 V6

Persistent ST segment elevation in anterior chest leads in association withleft ventricular aneurysm

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Acute pericarditis with widespread ST segment elevation and PR segmentdepression (see lead II)

Acute myocardial infarction—Part II

35

explanation 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 andare probably due to a combination of vasospasm andthrombosis.

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

ST segment elevation in leads V1 to V3 in patient with left ventricularhypertrophy

Reversible ST segment elevation associated withcoronary artery spasm


36

10 Myocardial ischaemiaKevin Channer, Francis Morris

In clinical practice electrocardiography is most often used toevaluate patients with suspected ischaemic heart disease. Wheninterpreted in the light of the clinical history,electrocardiograms 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 normalelectrocardiogram.

Myocardial ischaemia causes changes in the ST-T wave, butunlike a full thickness myocardial infarction it has no directeffects on the QRS complex (although ischaemia may give riseto bundle branch blocks, which prolongs the QRS complex).

When electrocardiographic abnormalities occur inassociation 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,or 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 forischaemia; they also occur in association with several otherdisease 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 inacute 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).

Electrocardiography is not sufficientlyspecific or sensitive to be used without apatient’s clinical history

Normal

Tall T wave

Biphasic T wave

Inverted T wave

Flat T wave T wave changes associated withischaemia

V2

V3

V5

V1 V4

V6

Tall T waves in myocardial ischaemia

Tall T waves in leads V2 and V3 in patient with recentinferoposterior myocardial infarction, indicatingposterior ischaemia

37

As there are other causes of abnormally tall T waves and nocommonly used criteria for the size of T waves, these changesare not always readily appreciated without comparison with aprevious electrocardiogram. Flattened T waves are often seen inpatients 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 inleads III, aVR, and V1 in association with a predominantlynegative QRS complex. T waves that are deep andsymmetrically inverted (arrowhead) strongly suggest myocardialischaemia.

In some patients with partial thickness ischaemia theT waves show a biphasic pattern. This occurs particularlyin 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.

ST 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 theST segment ends and the T wave starts. One of the first andmost subtle changes in the ST segment is flattening of thesegment, resulting in a more obvious angle between the STsegment and T wave.

Suggested criteria for size of T wavex 1/8 size of the R wavex < 2/3 size of the R wavex Height < 10 mm

T wave inversionx T wave inversion can be normalx It occurs in leads III, aVR, and V1 (and in V2, butonly in association with T wave inversion in leadV1)

V2

V3

V5

V1 V4

V6

Biphasic T waves in man aged 26 with unstable angina

A

C

B

D

ST changes with ischaemia showingnormal wave form (A); flattening ofST segment (B), making T wavemore obvious; horizontal (planar)ST segment depression (C); anddownsloping ST segmentdepression (D)

Subtle ST segment change in patient with ischaemic chest pain: when nopain is present (top) and when in pain (bottom)

Substantial ST segment depressionin patient with ischaemic chest pain

V2

V3

V5

V1 V4

V6

Arrowhead T wave inversion in patient with unstableangina


38

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 inassociation 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 segmentdepression 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 segmentmonitoring. 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 drugtreatment or revascularisation interventions.

ST 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 sameterritory may cause “normalisation” of the T waves (return to anupright position). Alternatively, further ischaemia may make theT wave inversion more pronounced.

Arrhythmias associated with acutemyocardial ischaemia or infarctionVentricular myocardial ischaemia may be arrhythmogenic, andextrasystoles 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

V2

V3

V5

V1 V4

V6

Widespread ST segment depression in patient withunstable angina

Non-ischaemic ST segment changes:in patient taking digoxin (top) andin patient with left ventricularhypertrophy (bottom)

Reversible ST segment changes in patient with chestpain; the ST segment elevation returns to normal as thechest pain settles

Normalisation of longstandinginverted T waves in patient withchest pain

Myocardial ischaemia

39

predicted the onset of ventricular fibrillation. Clinical trials haveclearly shown, however, that their suppression byantiarrhythmic drugs had no effect on the frequency ofsubsequent ventricular fibrillation.

Ventricular fibrillation is the commonest unheralded fatalarrhythmia in the first 24 hours of acute myocardial infarction.The prognosis depends almost entirely on the patient’sproximity to skilled medical help when the arrhythmia occurs.Cardiac arrest from ventricular fibrillation outside hospital isassociated with a long term survival of about 10%, comparedwith an initial survival of 90% when cardiac arrest occurs afteradmission to a coronary care unit. Studies have shown that thekey factor in prognosis is the speed with which electricaldefibrillation is delivered.

Heart 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 inferiorinfarction, the atrioventricular node’s arterial supply may becompromised resulting in various degrees of heart block.Atrioventricular block may be severe at first but usuallyimproves over subsequent days. Complete atrioventricular blockusually gives way to second degree and then first degree block.Although temporary transvenous cardiac pacing may benecessary for patients who are haemodynamicallycompromised, it is not mandatory in stable patients.

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).

Short runs of ventricular tachycardia area bad prognostic sign and shouldprobably be treated

Tachycardias of supraventricular origin,with the exception of atrial fibrillation,are uncommon after myocardialinfarction. Atrial fibrillation occurs inabout 10% of patients and is morecommon in those with heart failure,diabetes, and valvular heart disease. Itmay be transient or persistent and isoften a marker of haemodynamicinstability

When completeatrioventricular blockoccurs in association withacute anterior myocardialinfarction, transvenouscardiac pacing isrecommended

R on T, giving rise to ventricular fibrillation

Acute myocardial infarction with complete heart block


40

11 Exercise tolerance testingJonathan Hill, Adam Timmis

Exercise tolerance testing is an important diagnostic andprognostic tool for assessing patients with suspected or knownischaemic heart disease. During exercise, coronary blood flowmust 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 relevanceExercise tolerance testing (also known as exercise testing orexercise stress testing) is used routinely in evaluating patientswho present with chest pain, in patients who have chest pain onexertion, and in patients with known ischaemic heart disease.

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.

The 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 be4.8 METs (metabolic equivalents) during this stage. The speedand incline increase with each stage. A modified Bruce protocolis used for exercise testing within one week of myocardialinfarction.

Preparing the patient� Blockers should be discontinued the day before the test, anddixogin (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

ST segment depression (horizontal ordownsloping) is the most reliableindicator of exercise-induced ischaemia

Diagnostic indications for exercise testingx Assessment of chest pain in patients with intermediate probabilityfor coronary artery disease

x Arrhythmia provocationx Assessment of symptoms (for example, presyncope) occurringduring or after exercise

Workloadx Assessment of workload is measured by metabolic equivalents(METs)

x Workload is a reflection of oxygen consumption and hence energyuse

x 1 MET is 3.5 ml oxygen/kg per minute, which is the oxygenconsumption of an average individual at rest

x To carry out the activities of daily living an exercise intensity of atleast 5 METs is required

Patient exercising ontreadmill

Prognostic 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 dilatedcardiomyopathy or heart failure

x Assessment of treatment for arrhythmia

41

sitting and standing, are recorded as electrocardiographicchanges, particularly T wave inversion, may occur as the patientstands up to start walking on the treadmill. A short period ofelectrocardiographic recording during hyperventilation is alsovaluable for identifying changes resulting from hyperventilationrather than from coronary ischaemia.

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 ananxious patient relaxing. As the test progresses, however,systolic blood pressure should rise as exercise increases. A levelof up to 225 mm Hg is normal in adults, although athletes canhave higher levels. Diastolic blood pressure tends to fall slightly.The aim of the exercise is for the patient to achieve theirmaximum predicted heart rate.

SafetyIf patients are carefully selected for exercise testing, the rate ofserious complications (death or acute myocardial infarction) isabout 1 in 10 000 tests (0.01%). The incidence of ventriculartachycardia 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.Repolarisation 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 segmentduring exercise therefore slopes sharply upwards.

Maximum predicted heart ratex By convention, the maximum predicted heart rate is calculated as220 (210 for women) minus the patient’s age

x A satisfactory heart rate response is achieved on reaching 85% ofthe maximum predicted heart rate

x Attainment of maximum heart rate is a good prognostic sign

Contraindications for exercise testingx Acute myocardial infarction (within 4-6 days)x Unstable angina (rest pain in previous 48 hours)x Uncontrolled heart failurex Acute myocarditis or pericarditisx Acute systemic infectionx Deep vein thrombosisx Uncontrolled hypertension (systolic blood pressure > 220 mm Hg,diastolic > 120 mm Hg)

x Severe aortic stenosisx Severe hypertrophic obstructive cardiomyopathyx Untreated life threatening arrhythmiax Dissecting aneurysmx Recent aortic surgery

J point

Top: At rest. Bottom: Pathological ST segment depressionas measured 80 ms from J point

A B

C

Normal changes from rest (A), after three minutes’ exercise (B), and after six minutes’ exercise (C). Note the upsloping ST segments


42

By convention, ST segment depression is measured relativeto the isoelectric baseline (between the T and P waves) at 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.

Abnormal changes during exerciseThe standard criterion for an abnormal ST segment response ishorizontal (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 includeST 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.

A highly specific sign for ischaemia is inversion of theU wave. As U waves are often difficult to identify, especially athigh heart rates, this finding is not sensitive. The presence ofextrasystoles that have been induced by exercise is neithersensitive nor specific for coronary artery disease.

Stopping the testIn clinical practice, patients rarely exercise for the full duration(21 minutes) of the Bruce protocol. However, completion of9-12 minutes of exercise or reaching 85% of the maximum

Reasons for stopping a testElectrocardiographic criteriax Severe ST segment depression ( > 3 mm)x ST segment elevation > 1 mm in non-Q wave leadx Frequent ventricular extrasystoles (unless the test is to assessmentventricular arrhythmia)

x Onset of ventricular tachycardiax New atrial fibrillation or supraventricular tachycardiax Development of new bundle branch block (if the test is primarily todetect underlying coronary disease)

x New second or third degree heart blockx Cardiac arrest

Symptoms and signsx Patient requests stopping because of severe fatiguex Severe chest pain, dyspnoea, or dizzinessx Fall in systolic blood pressure ( > 20 mm Hg)x Rise in blood pressure (systolic > 300 mm Hg, diastolic

> 130 mm Hg)x Ataxia

A

B

C

D

E

Horizontal ST segment depression (A=at rest, B=after three minutes’exercise, C=after six minutes’ exercise) and downsloping ST segmentdepression (D=at rest, E=after six minutes’ exercise)

A B

T wave inversion in lead V5 at rest (A) andnormalisation of T waves with exercise (B)

Normal electrocardiographic changes during exercisex P wave increases in heightx R wave decreases in heightx J point becomes depressedx ST segment becomes sharply upslopingx Q-T interval shortensx T wave decreases in height

V2

V3

V4

V2

V3

V4

ST segments in leads V2 to V4 at rest (left) and after two minutes’ exercise(right) (note obvious ST elevation)

Exercise tolerance testing

43

predicted changes in heart rate is usually satisfactory. Anexercise test should end when diagnostic criteria have beenreached or when the patient’s symptoms and signs dictate.

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.

Interpreting the resultsDiagnostic testingAny abnormal electrocardiographic changes must beinterpreted in the light of the probability of coronary arterydisease and physiological response to exercise. A normal testresult or a result that indicates a low probability of coronaryartery disease is one in which 85% of the maximum predictedheart rate is achieved with a physiological response in bloodpressure and no associated ST segment depression.

A test that indicates a high probability of coronary arterydisease 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 revascularisationprocedure is contemplated; a less strenuous protocol is used.Testing provides prognostic information. Patients with lowexercise capacity and hypotension induced by exercise have apoor prognosis. Asymptomatic ST segment depression aftermyocardial infarction is associated with a more than 10-foldincrease in mortality compared with a normal exercise test.Conversely, patients who reach stage 3 of a modified Bruceprotocol with a blood pressure response of > 30 mmHg 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.

The most common reason for stopping anexercise test is fatigue and breathlessnessas a result of the unaccustomed exercise

Findings suggesting high probability of coronary arterydiseasex Horizontal ST segment depression of < 2 mmx Downsloping ST segment depressionx Early positive response within six minutesx Persistence of ST depression for more than six minutes intorecovery

x ST segment depression in five or more leadsx Exertional hypotension

Rationale for testingx Bayes’s theorem of diagnostic probability states that the predictivevalue of an abnormal exercise test will vary according to theprobability of coronary artery disease in the population understudy

x Exercise testing is therefore usually performed in patients with anmoderate probablility of coronary artery disease, rather than inthose with a very low or high probability

Rest Exercise Recovery

Marked ST changes in recovery but not during exercise


44

12 Conditions affecting the right side of the heartRichard A Harrigan, Kevin Jones

Many diseases of the right side of the heart are associated withelectrocardiographic abnormalities. Electrocardiography isneither a sensitive nor specific tool for diagnosing conditionssuch as right atrial enlargement, right ventricular hypertrophy,or pulmonary hypertension. However, an awareness of theelectrocardiographic abnormalities associated with theseconditions may support the patient’s clinical assessment andmay 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 Pwave. 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, andaVF is known as the P pulmonale.

The electrocardiographic changes suggesting right atrialenlargement often correlate poorly with the clinical andpathological findings. Right atrial enlargement is associatedwith 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 rightventricular 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.P pulmonale may appear transiently in patients with acutepulmonary embolism.

Right ventricular hypertrophyThe forces generated by right ventricular depolarisation aredirected rightwards and anteriorly and are almost completelymasked 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.

The electrocardiogram is a relatively insensitive indicator ofthe presence of right ventricular hypertrophy, and in mild casesof right ventricular hypertrophy the trace will be normal.

This article discusses right atrialenlargement, right ventricularhypertrophy, and theelectrocardiographic changes associatedwith chronic obstructive pulmonarydisease, pulmonary embolus, acute rightheart strain, and valvular heart disease

Diagnostic criteria for right ventricular hypertrophy(Provided the QRS duration is less than 0.12 s)x Right axis deviation of + 110° or morex Dominant R wave in lead V1x R wave in lead V1 >7 mm

Supporting criteriax ST segment depression and T wave inversion in leads V1 to V4x Deep S waves in leads V5, V6, I, and aVL

Right ventricular hypertrophy is associated withpulmonary hypertension, mitral stenosis, and, lesscommonly, conditions such as pulmonary stenosis andcongenital heart disease

II

III

aVF

Large P waves in leads II, III, and aVF (P pulmonale)

I

II

III

V1

V2

V3

Right ventricular hypertrophy secondary topulmonary stenosis (note the dominant Rwave in lead V1, presence of right atrialhypertrophy, right axis deviation, and Twave inversion in leads V1 to V3)

45

Lead V1 lies closest to the right ventricular myocardiumand is therefore best placed to detect the changes of rightventricular hypertrophy, and a dominant R wave in lead V1 isobserved. The increased rightward forces are reflected in thelimb leads, in the form of right axis deviation. Secondarychanges may be observed in the right precordial chest leads,where 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 witha range of conditions.

Chronic obstructive pulmonarydiseaseIn 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 thechest leads) shifts towards the left with persistence of an rSpattern as far as V5 or even V6. This may give rise to a“pseudoinfarct” pattern, with deep S waves in the rightprecordial leads simulating the appearance of the QS wavesand 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.

Cardiac arrhythmias may occur in patients with chronicobstructive pulmonary disease, particularly in association withan acute respiratory tract infection, respiratory failure, orpulmonary embolism. Arrhythmias are sometimes the result ofthe underlying disease process but may also occur as side effectsof the drugs used to treat the disease.

The arrhythmias are mostly supraventricular in origin andinclude atrial extrasystoles, atrial fibrillation or flutter, andmultifocal atrial tachycardia. Ventricular extrasystoles andventricular tachycardia may also occur.

Conditions associated with tall R wave in lead V1x Right ventricular hypertrophyx Posterior myocardial infarctionx Type A Wolff-Parkinson-White syndromex Right bundle branch block

A tall R wave in lead V1 is normal in children and young adults

Conditions associated with right axis deviationx Right ventricular hypertrophyx Left posterior hemiblockx Lateral myocardial infarctionx Acute right heart strain

Right axis deviation is normal in infants and children

About three quarters of patients withchronic obstructive pulmonary diseasehave electrocardiographic abnormalities.P pulmonale is often but not invariablypresent and may occur with or withoutclinical evidence of cor pulmonale

In chronic obstructive pulmonary disease theelectrocardiographic signs of right ventricularhypertrophy may be present, indicating the presence ofcor pulmonale

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Chronic obstructive pulmonary disease(note the P pulmonale, low amplitude QRScomplexes, and poor R wave progression)

Multifocal atrialtachycardia


46

Acute pulmonary embolismThe 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 theelectrocardiographic recording is also important as changesmay be transient. Patients who present with a small pulmonaryembolus are likely to have a normal electrocardiogram or atrace 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.T wave inversion in lead III may also be present, producing thewell known S1, Q3, T3 pattern.

Right ventricular dilatation may lead to right sidedconduction delays, which manifest as incomplete orcomplete right bundle branch block. There may be somerightward shift of the frontal plane QRS axis.Right atrial dilatation may lead to prominent P waves inthe inferior leads. Atrial arrhythmias including flutter andfibrillation are common, and T wave inversion in the rightprecordial leads may also occur

The S1, Q3, T3 pattern is seen in about12% of patients with a massive pulmonaryembolus

I

III

Sinus tachycardia and S1,Q3, T3 pattern in patientwith pulmonary embolus

II

III

aVRI

aVL

aVF

V1

V2

V3

V4

V5

V6

Preoperative electrocardiogram in otherwise healthy 38 year old man

II

III

aVRI

aVL

aVF

V1

V2

V3

V4

V5

V6 Acute pulmonaryembolism: 10 dayspostoperatively thesame patient developedacute dyspnoea andhypotension (note theT wave inversion in theright precordial leadsand lead III)

Conditions affecting the right side of the heart

47

Acute 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.Ventricular 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 dilatationmay also produce a strain pattern.

Right sided valvular problemsTricuspid stenosisTricuspid stenosis is a rare disorder and is usually associatedwith 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.

Tricuspid 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 andinclude incomplete right bundle branch block and atrialfibrillation.

Pulmonary stenosisPulmonary 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.

Electrocardiographic abnormalities found in acutepulmonary embolismx Sinus tachycardiax Atrial flutter or fibrillationx S1, Q3, T3 patternx Right bundle branch block (incomplete or complete)x T wave inversion in the right precordial leadsx P pulmonalex Right axis deviation

II

III

aVRI

aVL

aVF

V1

V2

V3

V4

V5

V6

S1, Q3, T3 pattern and right bundle branch block in patient withpulmonary embolus

V1

V2

V3

V4

V5

V6

Example of right heart strain: right ventricular hypertrophy withwidespread T wave inversion in chest leads

V1II

Biatrial abnormality


48

13 Conditions affecting the left side of the heartJune Edhouse, R K Thakur, Jihad M Khalil

Many cardiac and systemic illnesses can affect the left side of theheart. After a careful history and examination,electrocardiography and chest radiography are first lineinvestigations. Electrocardiography can provide supportiveevidence for conditions such as aortic stenosis, hypertension,and mitral stenosis. Recognition of the associatedelectrocardiographic abnormalities is important asmisinterpretation 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 travellingposteriorly, producing a later negative deflection. A largenegative deflection ( > 1 small square in area) suggests a leftatrial 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 apeak-to-peak interval of > 0.04 s suggests left atrialenlargement.

Any condition causing left ventricular hypertrophy mayproduce left atrial enlargement as a secondary phenomenon.Left atrial enlargement can occur in association with systemichypertension, aortic stenosis, mitral incompetence, andhypertrophic 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 criteriahave been suggested for the diagnosis of left ventricularhypertrophy, but none is universally accepted. Scoring systemsbased on these criteria have been developed, and although theyare highly specific diagnostic tools, poor sensitivity limits theiruse.

Electrocardiographic findingsThe electrocardiographic features of left ventricularhypertrophy are classified as either voltage criteria ornon-voltage criteria.

The electrocardiographic diagnosis of left ventricularhypertrophy is difficult in individuals aged under 40. Voltagecriteria lack specificity in this group because young people oftenhave high amplitude QRS complexes in the absence of leftventricular disease. Even when high amplitude QRS complexes

Conditions affecting left side of heart covered in this articlex Left atrial hypertrophyx Left ventricular hypertrophyx Valvular diseasex Cardiomyopathies (hypertrophic, dilated, restrictive)

Left ventricular hypertrophyVoltage criteriaLimb leadsx R wave in lead 1 plus S wave in lead III > 25 mmx R wave in lead aVL > 11 mmx R wave in lead aVF > 20 mmx S wave in lead aVR > 14 mmPrecordial leadsx R wave in leads V4, V5, or V6 > 26 mmx R wave in leads V5 or 6 plus S wave in lead V1 > 35 mmx Largest R wave plus largest S wave in precordial leads > 45 mm

Non-voltage criteriax Delayed ventricular activation time >0.05 s in leads V5 or V6 >0.05 sx ST segment depression and T wave inversion in the left precordialleads

The specificity of these criteria is age and sex dependent

Biphasic P wave in V1. The largenegative deflection indicates leftatrial abnormality (enlarged toshow detail)

P mitrale in lead II. P mitrale is aP wave that is abnormallynotched and wide and is usuallymost prominent in lead II; it iscommonly seen in associationwith mitral valve disease,particularly mitral stenosis(enlarged to show detail)

49

are 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.

The presence of these ST segment changes can causediagnostic difficulty in patients complaining of ischaemic-typechest 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 oldelectrocadiograms for comparison. Other non-voltage criteriaare common in left ventricular hypertrophy. Left atrialhypertrophy or prolonged atrial depolarisation and left axisdeviation are often present; and poor R wave progression iscommonly seen.

The electrocardiogram is abnormal in almost 50% ofpatients 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.

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Left ventricular hypertrophy in patient who had presented with chest painand was given thrombolytic therapy inappropriately because of the STsegment changes in V1 and V2

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Left ventricular hypertrophy without voltage criteria—in a man whopresented with heart failure secondary to severe aortic stenosis (gradient125 mm Hg). The ST segment changes are typical for left ventricularhypertrophy and there is evidence of left atrial enlargement. If the scoringsystem is used, these findings suggest left ventricular hypertrophy eventhough none of the R or S waves meets voltage criteria

Left ventricular hypertrophywith strain (note dominantR wave and repolarisationabnormality)

Scoring system for left ventricular hypertrophy (LVH)—suggested if points total >5Electrocardiographic feature No of pointsAmplitude (any of the following) 3x 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 LVHin the absence of digitalis 3

Left atrial involvement 3Left axis deviation 2QRS duration of >0.09 s 1Delayed ventricular activation time in leadsV5 and V6 of >0.05 s 1


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Valvular problemsA normal electrocardiogram virtually rules out the presence ofsevere aortic stenosis, except in congenital valve disease, wherethe trace may remain normal despite a substantial degree ofstenosis. Left ventricular hypertrophy is seen in about 75% ofpatients with severe aortic stenosis. Left atrial enlargement mayalso be seen in the electrocardiogram. Left axis deviation andleft bundle branch block may occur.

The cardiomyopathiesDiseases 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 maybe diverse.

Hypertrophic cardiomyopathyThis 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 wavesin the anterolateral or inferior chest leads, which may mimic theappearance of myocardial infarction. As the left ventriclebecomes increasingly less compliant, there is increasingresistance to atrial contraction, and signs of left atrialabnormality are commonly seen. Atrial fibrillation andsupraventricular tachycardias are common arrhythmias inpatients with hypertrophic cardiomyopathy. Ventriculartachycardias may also occur and are a cause of sudden death inthese patients.

Dilated cardiomyopathyMany patients with dilated cardiomyopathy have anatomical leftventricular hypertrophy, though the electrocardiographic signsof left ventricular hypertrophy are seen in only a third ofpatients. In some patients the signs of left ventricularhypertrophy may be masked as diffuse myocardial fibrosis canreduce the voltage of the QRS complexes. If right ventricularhypertrophy is also present the increased rightward forces ofdepolarisation may cancel out some of the leftward forces, againmasking the signs of left ventricular hypertrophy.

Signs of left atrial enlargement are common, and oftenthere is evidence of biatrial enlargement. Abnormal Q waves

Electrocardiographic features of valvular diseasex The electrocardiographic features of aortic regurgitation includethe features of left ventricular hypertrophy, often with the strainpattern

x Mitral stenosis is associated with left atrial abnormality or atrialfibrillation and right ventricular hypertrophy

x Mitral regurgitation is associated with atrial fibrillation, thoughagain the features of left atrial hypertrophy may be seen if thepatient is in sinus rhythm. Evidence of left ventricular hypertrophymay be seen

Common features of cardiomyopathyinclude electrical holes (Q waves),conduction defects (bundle branch blockand axis deviation), and arrhythmias

Main electrocardiographic changes associated withhypertrophic cardiomyopathyx Left ventricular hypertrophyx Left atrial enlargementx Abnormal inferior and anterior and/or lateral Q wavesx Bizarre QRS complexes masquerading, for example, aspre-excitation and bundle branch block

ECG changes in dilated cardiomyopathyx Left bundle branch blockx Left atrial enlargementx Abnormal Q waves in leads V1 to V4x Left ventricular hypertrophyx Arrhythmias—ventricular premature beats, ventricular tachycardia,atrial fibrillation

V4

aVLI

V1 V2 V3 V5 V6

II III aVR aVF

Abnormal Q waves in patient with hypertrophic cardiomyopathy

Conditions affecting the left side of the heart

51

may 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 cardiomyopathyRestrictive 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 myocardialinfiltration. Both supraventricular and ventricular arrhythmiasare common.

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.

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Dilated cardiomyopathy (note left ventricularhypertrophy pattern)

Electrocardiographic findings in restrictive cardiomyopathyx Low voltage QRS complexesx Conduction disturbancex Arrhythmias—supraventricular, ventricular

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Patient with restrictive cardiomyopathy due toamyloidosis (note the low voltage QRS complexes andthe right bundle branch block)


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14 Conditions not primarily affecting the heartCorey Slovis, Richard Jenkins

To function correctly, individual myocardial cells rely on normalconcentrations of biochemical parameters such as electrolytes,oxygen, hydrogen, glucose, and thyroid hormones, as well as anormal body temperature. Abnormalities of these and otherfactors affect the electrical activity of each myocardial cell andthus the surface electrocardiogram. Characteristicelectrocardiographic 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 onthe electrocardiogram. The most common changes associatedwith hyperkalaemia are tall, peaked T waves, reduced amplitudeand eventually loss of the P wave, and marked widening of theQRS complex.

The earliest changes associated with hyperkalaemia are tallT waves, best seen in leads II, III, and V2 to V4. Tall T waves areusually seen when the potassium concentration rises above5.5-6.5 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 theR 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.

The QRS complex will begin to widen with a potassiumconcentration of 7.0-8.0 mmol/l. Unlike right or left bundlebranch 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 theT wave and create a pattern resembling a sine wave—a“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.

It is important to recognise that someelectrocardiographic changes are due toconditions other than cardiac disease sothat appropriate treatment can be givenand unnecessary cardiac investigationavoided

Electrocardiographic features of hyperkalaemia

Serum potassium(mmol/l) Major change

5.5-6.5 Tall peaked T waves6.5-7.5 Loss of P waves7.0-8.0 Widening of QRS complexes8.0-10 Sine wave, ventricular arrhythmias, asystole

Tall peakedT wave

Loss ofP wave

Tall peakedT wave

Widened QRSwith tall T wave

Serial changes in hyperkalaemia

A B C

Serial 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)

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HypokalaemiaHypokalaemia may produce several electrocardiographicchanges, especially when there is total body depletion of bothpotassium and magnesium. The commonest changes aredecreased T wave amplitude, ST segment depression, andpresence of a U wave. Other findings, particularly in thepresence of coexistent hypomagnesaemia, include a prolongedQT 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 acommon finding in hypokalaemia. However, most cases of apresumed 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.

Patients with a potassium concentration below 2.5-3.0mmol/l often develop ventricular extrasystoles. Hypokalaemiamay also be associated with supraventricular arrhythmias, suchas paroxysmal atrial tachycardia, multifocal atrial tachycardia,atrial fibrillation, and atrial flutter.

HypothermiaHypothermia is present when the core temperature is less than35°C. As body temperature falls below normal, manycardiovascular and electrophysiological changes occur. Theearliest change seen in the electrocardiogram is an artefact dueto shivering, although some hypothermic patients haverelatively normal traces. The ability to shiver diminishes as bodytemperature falls, and shivering is uncommon below a coretemperature of 32°C.

As body temperature falls further, all metabolic andcardiovascular 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 beseen.

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 andsubarachnoid haemorrhage.

Electrocardiographic features of hypokalaemiax Broad, flat T wavesx ST depressionx QT interval prolongationx Ventricular arrhythmias (premature ventricular contractions,torsades de pointes, ventricular tachycardia, ventricular fibrillation)

Electrocardiographic features of hypothermiax Tremor artefact from shiveringx Atrial fibrillation with slow ventricular ratex J waves (Osborn waves)x Bradycardias, especially junctionalx Prolongation of PR, QRS, and QT intervalsx Premature ventricular beats, ventricular tachycardia, or ventricularfibrillation

x Asystole

ST depression A B

U wave

Flat T wave

Left: Diagram of electrocardiographic changes associated withhypokalaemia. Right: Electrocardiogram showing prominent U wave,potassium concentration 2.5 mmol/l (A) and massive U waves with STdepression and flat T waves, potassium concentration 1.6 mmol/l (B)

J wave

Sinus bradycardia, with a J wave, in a patient with hypothermia—coretemperature 29°C (note the shivering artefact)

A B

Broad complex tachycardia with a potassiumconcentration of 8.4 mmol/l (A); after treatment,narrower complexes with peaked T waves (B)


54

The J wave may even be a drug effect or, rarely, a normalvariant. The J wave is most commonly characterised by a“dome” or “hump” elevation in the terminal portion of the QRSdeflection and is best seen in the left chest leads. The size of theJ 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 andheart rate are early features in thyrotoxicosis. The mostcommon electrocardiographic changes seen in thyrotoxicosisare sinus tachycardia, an increased electrical amplitude of alldeflections, and atrial fibrillation.

About 50% of thyrotoxic patients have a resting pulse rateabove 100 beats/min. Atrial tachyarrhythmias are common asthe atria are very sensitive to the effects of triiodothyronine.Patients with thyroid storm may develop paroxysmalsupraventricular tachycardia with rates exceeding 200beats/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 mostcommon in elderly patients, men, those with a particularly highconcentration of thyroid hormone, and patients with left atrialenlargement or other intrinsic heart disease. Treatment of atrialfibrillation 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 1:1conduction, may also be seen.

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 numberof premature ventricular contractions.

HypothyroidismHypothyroidism causes slowing of the metabolic rate and affectsalmost all bodily functions, including heart rate andcontractility. It causes similar slowing of electrical conductionthroughout the heart.

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-existingheart disease may also develop increasing degrees of heartblock or bundle branch block (especially right bundle branchblock). Conduction abnormalities due to hypothyroidismresolve 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 ofdigitalis and are predisposed to all the arrhythmias associatedwith digitalis intoxication.

Ventricular arrhythmias are the most commonmechanism of death in hypothermia. They seem to bemore common during rewarming as the bodytemperature rises through the 28°-32°C range

Electrocardiographic features of thyrotoxicosisMost common findingsx Sinus tachycardiax Increased QRS voltagesx Atrial fibrillation

Other findingsx Supraventricular arrhythmias (premature atrial beats, paroxysmalsupraventricular tachycardia, multifocal atrial tachycardia, atrialflutter)

x Non-specific ST and T wave changesx Ventricular extrasystoles

Electrocardiographic features of hypothyroidismMost commonx Sinus bradycardiax Prolonged QT intervalx Flat or inverted T waves

Less commonx Heart blockx Low QRS voltagesx Intraventricular conduction defectsx Ventricular extrasystoles

Increasedvoltage

Atrialfibrillation

Rhythm strip

Left: Diagram of electrocardiographic changes associated with thyrotoxicosis.Right: Sinus tachycardia in patient with thyrotoxicosis

IncreasedPR

IncreasedQT

Low voltage

Inverted orflat T wave

Top: Diagram of electrocardiographic changes associated withhypothyroidism. Bottom: Bradycardia (note small QRS complexes andinverted T waves) in patient with hypothyroidism

Conditions not primarily affecting the heart

55

Uncommonly, patients may develop large pericardialeffusions, which give rise to electrical alternans (beat to beatvariation in QRS voltages). Myxoedema coma should always besuspected in patients with altered mental states who havebradycardia and low voltage QRS complexes ( < 1 mV) in allleads.

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,intravenous calcium may be dangerous in a patient who hasreceived 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.

Finally, artefacts due to shivering or tremor can obscureelectrocardiographic changes or simulate arrhythmias.

Non-specific T wave abnormalities are very common inhypothyroid patients. The T wave may be flattened orinverted in several leads. Unlike with most other causesof T wave abnormalities in hypothyroidism, associatedST changes are rarely seen

Short QT interval in patient with hypercalcaemia(calcium concentration 4 mmol/l)

Massive T wave inversion and QT prolongationassociated with subarachnoid haemorrhage

Electrocardiographic artefacts—“shivering artefact” inpatient with anterior myocardial infarction (top) andelectrical interference simulating tachycardia (bottom)


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15 Paediatric electrocardiographySteve Goodacre, Karen McLeod

General clinicians and junior paediatricians may have littleexperience of interpreting paediatric electrocardiograms.Although the basic principles of cardiac conduction anddepolarisation are the same as for adults, age related changes inthe anatomy and physiology of infants and children producenormal ranges for electrocardiographic features that differ fromadults and vary with age. Awareness of these differences is thekey to correct interpretation of paediatric electrocardiograms.

Recording the electrocardiogramTo obtain a satisfactory recording in young children requirespatience, and the parents may be helpful in providing a sourceof distraction. Limb electrodes may be placed in a moreproximal position to reduce movement artefacts. Standard adultelectrode positions are used but with the addition of either leadV3R or lead V4R to detect right ventricular or atrialhypertrophy. Standard paper speed (25 mm/s) and deflection(10 mm/mV) are used, although occasionally large QRScomplexes may require the gain to be halved.

Indications for electrocardiographyChest pain in children is rarely cardiac in origin and is oftenassociated with tenderness in the chest wall.Electrocardiography is not usually helpful in making adiagnosis, although a normal trace can be very reassuring to thefamily. 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.

Age 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 howthe 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 normalin 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 graduallyto lie between + 10° and + 100°.

The resting heart rate decreases from about 140 beats/minat birth to 120 beats/min at age 1 year, 100 at 5 years, and adultvalues by 10 years. The PR interval decreases from birth to age

Successful use of paediatric electrocardiographyx Be aware of age related differences in the indications forperforming electrocardiography, the normal ranges forelectrocardiographic variables, and the typical abnormalities ininfants and children

x Genuine abnormality is unusual; if abnormality is suspected, seek aspecialist opinion

Indications for paediatric electrocardiographyx Syncope or seizurex Exertional symptomsx Drug ingestionx Tachyarrhythmiax Bradyarrhythmiax Cyanotic episodesx Heart failurex Hypothermia

x Electrolyte disturbancex Kawasaki diseasex Rheumatic feverx Myocarditisx Myocardial contusionx Pericarditisx Post cardiac surgeryx Congenital heart defects

Paediatric electrocardiographic findings that may be normalx Heart rate > 100 beats/minx QRS axis > 90°x Right precordial T wave inversionx Dominant right precordial R wavesx Short PR and QT intervalsx Short P wave and short duration of QRS complexesx Inferior and lateral Q waves

I aVR V4R V4

II aVL V1 V5

III aVF V2 V6

Normal 12 lead electrocardiogram from 3 day old babyboy showing right axis deviation, dominant R wave inleads V4R and V1, and still predominantly upright Twave in V1. Persistence of upright T waves in rightprecordial leads beyond first week of life is sign of rightventricular hypertrophy

57

1 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.

Abnormal paediatricelectrocardiogramsDiagnosis of abnormality on a paediatric electrocardiogram willrequire knowledge of normal age related values, particularly forcriteria relating to right or left ventricular hypertrophy.

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 activationfrom a site other than the sinoatrial node.

Prolongation of the QRS complex may be due to bundlebranch block, ventricular hypertrophy, metabolic disturbances,or drugs.

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. Leftventricular hypertrophy may be indicated by deep Q waves inthe left precordial leads or the typical adult changes of lateralST depression and T wave inversion.

Normal values in paediatric electrocardiograms

Age

PRinterval

(ms)

QRSduration

(ms)

R wave (S wave)amplitude (mm)

Lead V1 Lead V6

Birth 80-160 < 75 5-26 (1-23) 0-12 (0-10)

6 months 70-150 < 75 3-20 (1-17) 6-22 (0-10)

1 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)

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Electrocardiogram from 12 year old (late childhood)(axis is now within normal “adult” range and R wave isno longer dominant in right precordial leads)

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Electrocardiogram from 13 year old boy with transposition of great arteriesand previous Mustard’s procedure. The right ventricle is the systemicventricle and the trace shows right ventricular hypertrophy with markedright axis deviation and a dominant R wave in the right precordial leads

II V4RV1III aVF

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


58

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 ofventricular arrhythmia and sudden cardiac death.

Q waves are normally present in leads II, III, aVF, V5, andV6. Q waves in other leads are rare and associated withdisease—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.

Abnormalities of rate and rhythmThe 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 quite

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Electrocardiogram from 11 year old girl with left ventricular hypertrophysecondary to systemic hypertension. There are tall voltages in the leftprecordial and limb leads with secondary ST depression and T waveinversion

Electrocardiogram from 9 year old boy showing marked sinus arrhythmia, a common finding in paediatric traces

Electrocardiogram from 3 year old girl with long QTsyndrome

Prolongation of QT interval in association with T wave alternans (notealternating upright and inverted T waves )

Paediatric electrocardiography

59

marked. Its relation to breathing—slowing on expiration andspeeding up on inspiration—allows diagnosis.

The approach to electrocardiographic diagnosis oftachyarrhythmias in children is similar to that used in adults.Most narrow complex tachycardias in children are due toatrioventricular re-entrant tachycardia secondary to anaccessory pathway. If the pathway conducts only retrogradely,the 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 otherwisenormal hearts.

Although all forms of ventricular tachycardia are rare, broadcomplex 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. Monomorphicventricular tachycardia may occur secondary to surgery forcongenital heart disease. Polymorphic ventricular tachycardia,or torsades de pointes, is associated with the long QTsyndrome.

Classification of atrioventricular block into first, second, andthird degree follows the same principles as for adults, althougha diagnosis of first degree heart block should take into accountthe variation of the PR interval with age. First degree heartblock and the Wenckebach phenomenon may be a normalfinding in otherwise healthy children. First or second degreeblock, however, can occur with rheumatic carditis, diphtheria,digoxin overdose, and congenital heart defects.

Extrasystolesx Atrial extrasystoles are very common and rarely associated withdisease

x Ventricular extrasystoles are also common and, in the context of thestructurally normal heart, are almost always benign

x Typically, atrial and ventricular extrasystoles are abolished byexercise

Aids for diagnosing tachycardias, such as atrioventriculardissociation and capture and fusion beats, are lesscommon in children than in adults

Complete atrioventricular blockx Complete atrioventricular block may be congenital or secondary tosurgery

x An association exists between congenital complete atrioventricularblock and maternal anti-La and anti-Ro antibodies, which arebelieved to cross the placenta and damage conduction tissue

Electrocardiogram showing atrial “flutter” in 14 year old girl with congenitalheart disease and previous atrial surgery (in neonates with atrial flutter, 1:1atrioventricular conduction is more common, which may make P waves anddiagnosis less evident)

Polymorphic ventricular tachycardia in 5 year old girl

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/min


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16 Cardiac arrest rhythmsRobert French, Daniel DeBehnke, Stephen Hawes

Successful resuscitation from cardiac arrest depends on promptrecognition and appropriate treatment of the arrest rhythm.Arrhythmias are frequent immediately before and after arrest;some are particularly serious because they may precipitatecardiac arrest—for example, ventricular tachycardia frequentlydeteriorates into fibrillation. Early recognition of sucharrhythmias 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 toproduce a detectable cardiac output. In ventricular fibrillationthe electrical activity is disorganised, and in asystole it is absentaltogether.

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.

Ventricular fibrillationMechanismsVentricular fibrillation probably begins in a localised area fromwhich waves of activation spread in all directions.

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.Although 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.

Cardiac arrest rhythmsx Ventricular fibrillationx Pulseless ventricular tachycardiax Pulseless electrical activity (electromechanicaldissociation)

x Asystole

Ventricular fibrillation is the commonestarrhythmia that causes sudden death outof hospital

Causes of ventricular fibrillationx Myocardial ischaemia/infarctionx Cardiomyopathyx Acidosisx Electrocutionx Drugs (for example—quinidine, digoxin, tricyclic antidepressants)x Electrolyte disturbance (for example—hypokalaemia)

Fine ventricular fibrillation

Coarse ventricular fibrillation

61

Potential pitfalls in diagnosisWhen the amplitude of the deflections is extremely low, fineventricular fibrillation can be mistaken for asystole. To avoid thismistake, check the “gain” (wave form amplitude) on theelectrocardiogram 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.

Electrocardiographic 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 vulnerableduring all phases of the cardiac cycle. T wave alternans, aregular beat to beat change in T wave amplitude, is also thoughtto predict ventricular fibrillation.

“Persistent movement artefact,” such asthat which occurs in a patient who isfitting, can simulate ventricular fibrillation

Movement artefact simulating ventricular fibrillation

T wave alternans

“R on T” phenomenongiving rise to ventricular fibrillation

Polymorphic ventriculartachycardia deteriorating into ventricularfibrillation


62

Pulseless 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 defibrillationbeing 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,or independent P wave activity.

Pulseless 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.Sometimes there is a bradycardia, with or without P waves, andoften with wide QRS complexes.

Clinical correlatesSuccessful treatment of pulseless electrical activity depends onwhether it is a primary cardiac event or is secondary to apotentially reversible disorder.

AsystoleMechanismsAsystole implies the absence of any cardiac electrical activity. Itresults from a failure of impulse formation in the pacemakertissue or from a failure of propagation to the

Potentially reversible causes of pulselesselectrical activityx Hypovolaemiax Cardiac tamponadex Tension pneumothoraxx Massive pulmonary embolismx Hyperkalaemia, hypokalaemia, and metabolicdisorders

x Hypothermiax Toxic disturbances—for example, overdoses of

� blockers, tricyclic antidepressants, or calciumchannel blockers

Capture beat in ventricular tachycardia

Fusion beat in ventricular tachycardia

Ventricular tachycardia with evidence of atrioventricular dissociation

Broad and slow rhythm in association with pulseless electrical activity

Narrow complex rhythm associated with pulseless electrical activity

Cardiac arrest rhythms

63

ventricles. 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 theelectrocardiogram 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.

Ventricular 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.

Bradycardias and conduction blocksThe term bradycardia refers to rates of < 60 beats/min, but arelative bradycardia exists when the rate is too slow for thehaemodynamic state of the patient. Some bradycardias mayprogress to asystole, and prophylactic transvenous pacing maybe needed. These include Mobitz type II block, complete heartblock with a wide QRS complex, symptomatic pauses lastingthree 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 of40-60 beats/min; the QRS morphology is normal, but invertedP waves may be apparent. Ventricular escape rhythms areusually slower (15-40 beats/min), with broad QRS complexesand no P waves.

“Peri-arrest” rhythms

x Arrhythmias are common immediately before and after arrest, andcardiac monitoring of patients at high risk is important

x These “peri-arrest” arrhythmias include bradycardias andconduction blocks, broad complex tachycardias, and narrowcomplex tachycardias

Escape rhythms represent a safety net preventing asystoleor extreme bradycardia; management should correct theunderlying rhythm abnormality

Asystole

Flat line artefact simulating asystole

Ventricular standstill

Top: Junctional escape rhythm. Bottom: Ventricular escape rhythm


64

Broad complex tachycardiasManagement of ventricular tachycardia precipitating cardiacarrest depends on the patient’s clinical state. However, sometypes of ventricular tachycardia warrant special mention.

Polymorphic ventricular tachycardiaIn polymorphic ventricular tachycardia, the QRS morphologyvaries from beat to beat. The rate is usually greater than200 beats/min. In sinus rhythm the QT interval is normal. Ifsustained, polymorphic ventricular tachycardia invariably leadsto haemodynamic collapse. It often occurs in association withacute myocardial infarction, and frequently deteriorates intoventricular fibrillation.

Torsades 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 isassociated with cardiac arrest or degenerates into ventricularfibrillation; both are managed by direct current cardioversion.

Ventricular tachyarrhythmias oftenprecipitate cardiac arrest, and they arecommon immediately after arrest

Polymorphic ventricular tachycardiarequires immediate direct currentcardioversion

Polymorphic ventricular tachycardia

Prolonged QT interval

Torsades de pointes

Cardiac arrest rhythms

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17 Pacemakers and electrocardiographyRichard Harper, Francis Morris

Since the placement of the first implantable electronicpacemaker in the 1950s, pacemakers have become increasinglycommon and complex. The first pacemakers were relativelysimple devices consisting of an oscillator, battery, and stimulusgenerator. They provided single chamber pacing at a singlefixed rate irrespective of the underlying rhythm. The secondgeneration 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 lifespan of about eight years and rarely malfunction.

In clinical practice a basic understanding ofelectrocardiography in patients with a pacemaker may behelpful in evaluating patients with syncope or near syncope(suggesting that the pacemaker may not be functioningnormally).

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 onbasic interpretation of electrocardiograms in the patients whohave a pacemaker.

Functions of pacemakersPacemakers can pace the ventricle or the atrium, or bothsequentially. Atrial or ventricular activity can be sensed, and thissensing may be used to trigger or inhibit pacer activity. Somepacemakers are rate adaptive.

The functions of a pacemaker are indicated by a genericcode accepted by the North American Society for Pacing andElectrophysiology 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 sinusnode dysfunction but intact cardiac conduction. This mode willsense 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.

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.

Modern pacemakers can sequentiallypace the right atrium or the ventricle, orboth, and adapt the discharge frequencyof the pacemaker to the patient’sphysiological needs

Indications for a permanent pacemakersystemx Sick sinus syndromex Complete heart blockx Mobitz-type II heart blockx Atrial tachycardia, and heart blockx Asystolex Carotid sinus hypersensitivity

Generic pacemaker code

Chamberpaced

Chambersensed

Responseto sensing

Ratemodulation*

Anti-tachycardiaAICDs

O=none O= none O= none O= none O= noneA = atrium A= atrium T= triggered R = rate

responsiveP = pacing

V = ventricle V = ventricle I = inhibited S = shockD = dualchamber

D = dualchamber

D = dual(T + I)

D = dual(P + S)

*This position may also be used to indicate the degree of programmability bythe codes P, M and C.AICD=Automatic implantable cardioverter defibrillator

Typical electrocardiogram produced by AAIpacing

Typical tracing produced by VVI pacing

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Dual 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 doesnot 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 importantbecause it determines the upper rate limit of the pacemaker.

Normal paced rhythmFor implanted pacemakers, the atrial lead is placed in the rightatrium and often in the appendage. A beat that is paced has aP wave of near normal appearance. The ventricular lead isplaced in the apex of the right ventricle. When the lead isstimulated it produces a wave of depolarisation that spreadsthrough the myocardium, bypassing the normal conductionsystem. The ventricles depolarise from right to left and fromapex to base. This usually produces an electrocardiogram withbroad 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 willconvert the pacer to asynchronous mode so that all sensing isdisabled. 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 thefunctioning of the pacemaker to be assessed. Removing themagnet will cause the pacemaker to revert to its programmedmode.

Pacemaker failureSeveral procedures are needed to assess a patient whosepacemaker may be malfunctioning: cardiac monitoring to assessrhythm disturbances; 12 lead electrocardiography to assess

Procedures to assess a possible pacemakermalfunctionx Cardiac monitoringx 12 lead electrocardiographyx Chest x ray examination

Typical tracing produced by DDD pacer

Defines lower rate unitBasic interval

Atrial

TARPDefines upper rate unit

AVI =PVARP =

TARP =

Atrioventricular intervalPostventricular atrial refractory periodTotal atrial refractory period

AVI PVARP

Total atrial refractory period

Top: Unipolar systems—note the large pacing spike.Bottom: Bipolar system in the same patient

Pacemakers and electrocardiography

67

pacer 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 orpersistently fails to sense the appropriate cardiac chamber, andtherefore the timing of the pacemaker stimulus isinappropriate. These mistimed pacemaker spikes may or maynot 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.

OversensingPacemakers 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. Thesensed signals are misinterpreted as spontaneous electrogramsfrom the appropriate cardiac chamber, and the result ispacemaker inhibition. This can lead to symptomaticbradycardia. The pacemaker system may need to be replaced ifthere are problems with the circuit, electrodes, or leads.

Failure 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 whenthe patient’s heart rate is below the pacer rate and nopacemaker activity is noted in the electrocardiogram.

Failure to captureFailure to capture should be easy to detect in theelectrocardiogram. Appropriately timed pacer spikes will bepresent, but the spikes fail to provide consistent capture. Thecommonest cause of loss of capture is dislodgment of thepacing electrode. Failure to capture may also result from leaddamage or pacemaker failure (rare).

Reprogramming the pacemaker mayeliminate the oversensing by adjustingamplifier sensitivity and refractoriness

Causes of failure to captureFailure of pacemakerx Battery failurex Circuit abnormalityx Inappropriate programmingx Problem with leadsx Lead dislodgmentx Cardiac perforationx Lead fracturex Insulation breakx Increased threshold

Failure to sense may be caused byfibrosis at the tip of the electrode,damage to the electrode or lead, ordislodgment of the lead

Loss of ventricular sensing. The first and thefifth complexes are ventricular paced beats.The second to fourth complexes are thepatient’s intrinsic rhythm, which have not beensensed, hence the inappropriately timedpacing spike

Loss of atrial pacing because ofoversensing preceding T wave.Ventricular pacing set at a low rate


68

Pacemaker mediated tachycardiasPacemaker mediated tachycardias are a result of interactionsbetween native cardiac activity and the pacemaker. In “endlessloop tachycardia,” a premature ventricular contraction isfollowed by retrograde atrial conduction. The pacemaker sensesthe retrograde atrial activity and a ventricular stimulus isgenerated. 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 syndromePacemaker syndrome refers to symptoms related to the use of apacemaker. When the atria and ventricles contract at the sametime the atrial contribution to ventricular filling is lost. It ispatients with ventricular pacemakers who are usually affectedby pacemaker syndrome. Ventricular pacing leads to retrogradeconduction 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.

Symptoms of pacemaker syndromex Patients usually present with non-specific symptoms and signs suchas dyspnoea, dizziness, fatigue, orthopnoea, and confusion

x Occasionally patients may complain of palpitations or pulsation inthe neck or abdomen

The most commonly reportedpacemaker mediated tachycardia is“endless loop tachycardia” which occursin patients with dual chamberpacemakers

VVI pacemaker with intermittentfailure to capture. Every secondpacemaker beat captures. The rest ofthe time, pacemaker spikes are seenbut not associated with capture

Pacemaker mediated tachycardia

Pacemaker syndrome: retrograde P waves are evident

Pacemakers and electrocardiography

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18 Pericarditis, myocarditis, drug effects, andcongenital heart diseaseChris A Ghammaghami, Jennifer H Lindsey

Pericarditis, 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.

PericarditisThe 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.

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.

MyocarditisThe 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 waveinversion, 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 ofantiarrhythmic drug actions can cause electrocardiographicchanges.

� Adrenergic receptor and non-dihydropyridine calciumchannel antagonists produce sinus bradycardia andatrioventricular block. Generally these drugs are safe and rarelycause severe bradycardia.

Digoxin and quinidine-like agents have narrowertherapeutic indices and can cause life threatening ventriculararrhythmias relatively often. Drugs which prolong the actionpotential duration (class Ia or class III) may cause torsades depointes. Powerful class I drugs (especially Ia or Ic) may causeQRS widening, bundle branch block, or completeatrioventricular block.

DigoxinDecades of clinical experience with digitalis compounds showthat nearly any arrhythmia can occur as a result of digoxin

Vaughan-Williams classificationClass I: Fast sodium channel blockersx 1a: quinidine, procainamide, disopyramidex 1b: lidocaine, phenytoin, mexilitene, tocainidex 1c: encainide, flecainide, propafenone

Class II: � adrenergic receptor antagonists(examples)x Propranolol, flecainide, propafenone

Class III: Potassium channel blockers (examples)x Bretylium, sotalol, amiodarone, ibutilide (notavailable in United Kingdom)

Class IV: Calcium channel blockers (examples)x Verapamil, diltiazem, nifedipine

V2

V3

V5

V1 V4

V6

II

III

aVL

I aVR

aVF

Pericarditis: note the ST elevation and PR segment depression

Pericarditis: details of the QRS complex in lead II (notethe PR segment depression)

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administration. At therapeutic levels QT duration is shortened,and the PR interval is moderately lengthened because ofincreased vagal tone. The “digoxin effect” refers to T waveinversion and downsloping ST segment depression. Thesefindings should not be interpreted as toxic effects. Excitatoryand inhibitory effects are responsible for the pro-arrhythmiccharacter of digoxin. A rhythm that is considered by some asnearly pathognomonic for digoxin intoxication, paroxysmalatrial tachycardia with variable atrioventricular nodalconduction (“PAT with block”), shows both types of effects.

Quinidine-like drugsThe class Ia antiarrhythmic effect is caused by the inhibition offast sodium channels. Many drugs (for example, disopyramide)share this effect to varying degrees and can share thepro-arrhythmic character of quinidine. Electrocardiographicindicators of toxic effects of quinidine include widening of theQRS complex, prolongation of the QT interval, andatrioventricular nodal blocks. The prolongation of the QTinterval 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.

Flecainide-like drugsFlecainide, propafenone, and moracizine can cause bundlebranch block. These drugs slow atrial tachycardias and can leadto a paradoxical increase of the ventricular response rate.Monomorphic ventricular tachycardia may also occur.

Congenital heart diseaseThe electrocardiographic findings associated with congenitallesions of the heart may be subtle, but generally they increase indirect proportion to the severity of the malformation’s impacton the patient’s physiology. Electrocardiographic abnormalitiesin children with heart murmurs should increase the clinician’s

Rhythm disturbances associated withdigoxin intoxicationx Sinus bradycardiax Sinoatrial blockx First, second, and third degree atrioventricularblock

x Atrial tachycardia (with or withoutatrioventricular block)

x Accelerated junctional rhythmx Junctional tachycardiax Ventricular tachycardia or fibrillation

Drugs causing prolongation of QT intervalAmiodarone, astemizole, bepridil, bretylium,cisapride, cocaine, tricyclic antidepressants,cyproheptadine, disopyramide, erythromycin,flecainide, thioridazine, pimozide, ibutilide,itraconazole, ketoconazole, phenothiazines,procainamide, propafenone, quinidine, quinine,sotalol, terfenadine, vasopressin

Differential diagnosis with selectedelectrocardiographic findings in congenitalheart diseaseAxis deviation or hypertrophyx Superior QRS axis: atrioventricular septaldefects, tricuspid atresia

x Left ventricular hypertrophy: aortic stenosis,hypertrophic cardiomyopathy

x Right ventricular hypertrophy: tetralogy of Fallot,severe pulmonary stenosis, secundumatrioventricular septal defect

x Combined ventricular hypertrophy: largeventricular septal defect, atrioventricular septaldefect

Digoxin effect

Atrial tachycardia with block

Prolonged QT interval (QTc 505 ms)

Polymorphic ventricular tachycardia in a patientwith quinidine intoxication

Pericarditis, myocarditis, drug effects, and congenital heart disease

71

suspicion 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 eitherbecause 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 appearrelatively 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:

x Ostium primum QRS axis: leftwards ( − 30° to − 90°)x Ostium secundum QRS axis: rightwards (0 to 180°), withmost being more than 100°

x Sinus venosus P wave axis: low atrial pacemaker.

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 arule 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.

I aVR V1

III aVF V3

V4

II aVL V2 V5

V6

Secundum atrial septal defect: note the right axis deviation and dominantR wave in lead V1

I aVR V1

III aVF V3

V4

II aVL V2 V5

V6

Primum atrial septal defect: note the left axis deviation (superior axis)

V1 V2 V3

V4 V5 V6

Ventricular septal defect: note that all leads are half standard calibration.The biventricular hypertrophy pattern is typical of a ventricular septal defect


72

Coarctation 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% ofasymptomatic 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 thetricuspid 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.

DextrocardiaDextrocardia 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 invertedP wave in lead I indicates dextrocardia.

Tricuspid 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.

I aVR V1

III aVF V3

V4

II aVL V2 V5

V6

Coarctation of the aorta in a 10 week old infant. The deep S wave seen inV1 reflecting striking left ventricular hypertrophy

I aVR V1

III aVF V3

V4

II aVL V2 V5

V6

Dextrocardia: note inverted P wave in lead I and poor R wave progression

I aVR V1

III aVF V3

V4

II aVL V2 V5

V6

Tricuspid atresia: note the left axis deviation and the right atrial enlargement

Pericarditis, myocarditis, drug effects, and congenital heart disease

73

Cyanotic 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, andprecordial 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 ventricularhypertrophy 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.

I aVR V1

III aVF V3

V4

II aVL V2 V5

V6

Congenitally corrected transposition of the great arteries: note the absenceof Q waves in lead 1, V5, and V6, which is characteristic of this lesion


74

75

atrial fibrillation 14defined 13diagnosis 27Wolff-Parkinson-White syndrome 20

atrial flutter 14–15defined 13paroxysmal atrial flutter 10

atrial refractory period 67atrial septal defects 72atrial tachycardias 15–16

aberrant conduction 26, 27with AV block 16benign paroxysmal 15conditions associated 16defined 13, 15–16incessant ectopic 16initiated by ectopic atrial focus 15multifocal 16, 46

atrioventricular dissociationmonomorphic ventricular tachycardias 22–4

clinical evidence 27ventricular tachycardias 22–4, 63

atrioventricular nodal re-entrant tachycardia 17–18

clinical presentation 18electrocardiogram findings 17–18mechanism 17termination 18

atrioventricular node 62:1 block 14, 16aberrant conduction 26block induction 15fast/slow pathways 17–18

atrioventricular (node) conduction block 10–12bundle branch block 11–12complete

acute myocardial infarction, transvenous cardiac pacing 40

paediatric electrocardiogram 60fascicular blocks 12first, second and third degree block 10–11induction 13left bundle branch block 11–12paediatric 60right bundle branch block 11tachycardia-bradycardia syndrome 10

atrioventricular re-entrant tachycardia 18–20antidromic 27paediatric 60Wolff-Parkinson-White syndrome 18–20

antidromic/orthodromic 20

Bayes’s theorem 44Bazett’s correction, QT interval 8bifascicular blocks 12body habitus effects 1

AAI pacing 66acute myocardial infarction 29–36

acute ischaemia 33antecedent, ST segment elevation 35appropriate concordance 33–4bundle branch block 33–4complete heart block 40evolution of electrocardiogram changes 29hyperacute T waves 29inappropriate concordance 33–4localisation of site of infarction 31—2

posterior 32right ventricular 31–2

pathological Q waves 30reciprocal ST segment depression 30–1sinus bradycardia 9ST segment changes 29

differential diagnosis 34–6elevation 34–6resolution of changes in T waves 30

treatment, indications for thrombolysis 29acute pericarditis, ST segment elevation 35acute pulmonary embolism 47–8acute right heart strain 48acyanotic lesions 72

atrial septal defects 72ventricular septal defects 72

adenosineAV block 28contraindications 20, 27

adenosine scintigraphy 42amyloidosis, restrictive cardiomyopathy 52anatomical relations, leads in standard 12 lead

electrocardiogram 2–3angina

ST segment elevation 36T wave inversion 38

antiphospholipid antibodies, congenital heart block 60arrhythmias see atrial arrhythmias; sinus arrhythmias;

ventricular arrhythmiasasystole 63–5

bradycardias and conduction blocks 64clinical correlates 64electrocardiogram features 64mechanisms 63–4peri-arrest rhythms 64polymorphic ventricular tachycardia 26, 65torsades de pointes 65ventricular standstill 64

atrial arrhythmias 13–16clinical relevance 13electrocardiogram characteristics and features 13sinus tachycardia 13–14supraventricular tachycardias, atrial/sinoatrial node 13see also atrial fibrillation; atrial tachycardia

atrial depolarisation, P wave 5

Index

Index

76

bradycardias 9–10defined 9relative 64sick sinus syndrome 9–10sinoatrial node dysfunction, associated conditions 9–10sinus bradycardia 9

broad complex tachycardias 21–8asystole, cardiac arrest rhythms 65management 28supraventricular origin 26–7

atrial tachycardia with aberrant conduction 26Wolff-Parkinson-White syndrome 26–7

terminology 21ventricular origin

with bundle branch block 26mechanisms 21–2

ventricular and supraventricular originclinical presentation 27differentiation 27–8electrocardiogram differences 27–8

ventricular tachycardia 25–6Brugada syndrome 34bundle branch block 33–4

differentiation from ventricular and supraventriculartachycardias 26, 28

bundle of His 1, 17fascicular tachycardias 25fast/slow pathways 17–18

bundle of Kent 18Wolff-Parkinson-White syndrome 18

capture beats 23cardiac arrest rhythms 61–5

asystole 63–5pulseless electrical activity 63pulseless ventricular tachycardia 63ventricular fibrillation 61–2

cardiac axis 3–4calculation 4determination of axis in diagnosis 3–4normal findings in healthy individuals 3sinus rhythm 3

cardiac rhythm assessment 3cardiomyopathies

dilated cardiomyopathy 51–2hypertrophic cardiomyopathy 51restrictive cardiomyopathy 52

carotid sinus massage 13, 28chronic obstructive pulmonary disease

right axis deviation 46tall R wave in lead V1 46

circumflex artery, occlusion 32coarctation of aorta 73congenital heart block, antiphospholipid antibodies 60congenital heart disease 71–4

acyanotic lesions 72coarctation of aorta 73congenitally corrected transposition of the great arteries 74cyanotic lesions 74dextrocardia 73differential diagnosis 71Ebstein’s anomaly 73tetralogy of Fallot 74tricuspid atresia 73Wolff-Parkinson-White syndrome 18–20, 26–7

congenitally corrected transposition of great arteries 74

coronary artery diseaseexercise tolerance testing 44left bundle branch block 11right ventricular myocardial infarction 32

cyanotic lesions 74

DDD pacer 67dextrocardia, P wave inversion 73digoxin 70–1

contraindications 20, 27, 40, 56intoxication 71rhythm disturbance 15, 71

dilated cardiomyopathy 51–2disopyramide, quinidine-like drugs 71driving groups, exercise tolerance testing 44drugs 70–1

Vaughan-Williams classification 70

Ebstein’s anomaly 73electrocardiogram 1

normal findings 3paediatric 57–8

paediatric 57–60escape beats 40escape rhythms 10, 64exercise tolerance testing 41–4

abnormal changes during exercise 43clinical relevance 41contraindications 42diagnostic indications 41interpreting results 44

coronary artery disease 44diagnostic and prognostic testing 44rationale for testing 44screening 44

limitations 42maximum predicted heart rate 42–3normal electrocardiogram changes during exercise 43normal trace during exercise 42occupational groups 44preparing the patient 41–2protocol 41safety 42stopping the test 43–4workload 41

fascicular blocks 12fascicular tachycardia 22, 25fast/slow pathways, atrioventricular node 17–18fits, persistent movement artefact 62flecainide-like drugs 63, 71fusion beats 23

heart ratecalculation 2–3

maximum predicted 42rulers 2–3

hemifascicular blocks 12hexaxial diagram 3His–Purkinje conduction system 1hypercalcaemia

QT interval 56U waves 8

hyperkalaemia 53T waves 7U waves 8

Index

77

hypertrophic cardiomyopathy 51hypoglycaemia 56hypokalaemia 54

Q waves 8U waves 8

hypothermia 54–5hypothyroidism 55–6

infarct scar tissueQ wave markers of necrosis 30re-entry circuits 22

intracranial haemorrhage, ST segment elevation 35–6ischaemic disease see myocardial ischaemia

J point see ST junctionJ waves (Osborn waves) 54–5junctional tachycardias 17–20

atrioventricular nodal re-entrant tachycardia 17–18atrioventricular re-entrant tachycardia 18–20Wolff-Parkinson-White syndrome 18–20see also supraventricular tachycardias

Katz-Wachtel phenomenon 72

leadsstandard 12 lead electrocardiogram 2–3

P waves 23right-sided in acute myocardial infarction 31

left atrial abnormality 49cardiomyopathy 51–2P waves 5

left bundle branch block 33–4left heart 49–52

cardiomyopathies 51–2left heart valvular problems 51–2left ventricular hypertrophy 49–50

electrocardiogram findings, scoring system 50left atrial abnormality 49

mitral stenosisP waves 5right ventricular hypertrophy 45–6

Mobitz type I/II block 10movement artefacts 62Mustard’s operation, transposition of great arteries,

electrocardiogram 58myocardial infarction see acute myocardial infarctionmyocardial ischaemia 37–40

arrhythmias associated with acute myocardial infarction or infarction 39–40

heart block 40re-entry circuits, infarct scar tissue 22ST segment depression 38–9ST segment elevation 39T wave changes 37–8

myocarditis 70

neonatal defects see congenital heart diseasenormal electrocardiogram 3

occupational groups, exercise tolerance testing 44Osborn waves 54–5

P wavesabsent 64atrial depolarisation 5

defined 5independent 27inversion 23, 73left atrial abnormality 5, 49mitral stenosis 5pacemaker syndrome 69standard 12 lead electrocardiogram 23Wolff-Parkinson-White syndrome 19

pacemakers 66–9clinical relevance 66failure 67–8

abnormalities of sensing 68capture 68–9pacing 68under and oversensing 68

functions 66–7AAI pacing 66dual chamber pacing 67VVI pacing 66

normal paced rhythm 67pacemaker syndrome 69pacemaker-mediated tachycardias 69

paediatric electrocardiography 57–60abnormal electrocardiogram 58–60

complete atrioventricular block 60extrasystoles 60normal values 58rate and rhythm 59–60

age related changes, normal cardiograms 57–8incessant ectopic atrial tachycardia 16indications 57recording electrocardiogram 57

paroxysmal atrial flutter 10peri-arrest rhythm 64pericarditis 70

differential diagnosis 35persistent movement artefact 62PR interval 5–6

sinus bradycardia 9premature atrial impulses 17Prinzmetal’s angina, ST segment elevation 36pseudoinfarct waves 46pulmonary embolism, acute 47–8pulmonary stenosis 48pulseless electrical activity 63

clinical correlates 63electrocardiogram features 63potentially reversible causes 63

pulseless ventricular tachycardia 61electrocardiogram features 63

Q waves 6hypertrophic cardiomyopathy 51marker of necrosis 30pathological, acute myocardial infarction 30

QRS complex 2–3, 6atrial septal defect and ventricular septal defect 72atrial tachycardia with aberrant conduction 26concordance, positive/negative 23–4depolarisation wave 2, 6hyperkalaemia 53Katz-Wachtel phenomenon 72paediatrics 57–8

QT interval 8hypercalcaemia 56long QT 60, 65

Index

78

paediatric 59–60prolongation 71

subarachnoid haemorrhage 56transient 25

quinidine-like drugs 71

R on T, ventricular fibrillation 62R waves 6

pseudo 17tall 46“tombstone” 29

R-R interval 2–3rate rulers 2–3re-entry circuits

infarct scar tissue 22right atrial 14sinoatrial node 14

renal failure, QRS complex, hyperkalaemia 53restrictive cardiomyopathy 52right atrial enlargement 45right atrial re-entry circuits 14right bundle branch block 28, 34right heart 45–8

acute pulmonary embolism 47–8acute right heart strain 48chronic obstructive pulmonary disease 46–7

right sided valvular problems 48pulmonary stenosis 48tricuspid regurgitation 48tricuspid stenosis 48

right ventricular dilatation 47right ventricular hypertrophy 45–6right ventricular myocardial infarction 31–2right ventricular outflow tract tachycardia 25right-sided chest leads in acute myocardial

infarction 31

S waves 6pseudo 17

shivering artefacts 56sick sinus syndrome 9–10sinoatrial block 9sinoatrial node 1

dysfunction, bradycardias associated 9–10P wave 5re-entry phenomena 14

sinus arrest 9sinus arrhythmia 3sinus bradycardia 9

hypothermia 54PR interval 9

sinus rhythm 3sinus tachycardia 13–14

causes 14embolism 47

defined 13paediatric 59–60

situs inversus 73ST junction 7ST segment 7

acute myocardial infarctionchanges 29reciprocal depression 30–1resolution of changes in ST segment and T waves 30

depressionangina 39

exercise 42–3left ventricular hypertrophy 49–50myocardial ischaemia 38–9

ST segment elevationacute myocardial infarction 34–6Brugada syndrome 34differential diagnosis 34–6

acute pericarditis 35antecedent acute myocardial infarction 35benign early repolarisation 35high take-off 35

myocardial ischaemia 39other causes 35–6paediatric 59

standard 12 lead electrocardiogram 2–3P waves 23paediatric 57–8right-sided in acute myocardial infarction 31

standard calibration signal 1standard rhythm strip 3subarachnoid haemorrhage

QT interval prolongation 56ST segment elevation 35–6

supraventricular tachycardiasatrial tachycardia with aberrant conduction 26broad complex tachycardias 26–7with bundle branch block, differentiation from

ventricular tachycardias 26, 28sources 13Wolff-Parkinson-White syndrome 26–7see also junctional tachycardias

systemic conditions, not primarily affecting the heart 53–6

T waves 7alternans 62criteria 38hyperacute, acute myocardial infarction 29inversion, angina 38, 39in ischaemia 37–8

tachycardia-bradycardia syndrome 10tachycardias

clinical relevance 13defined 13pacemaker-mediated tachycardias 69sinus tachycardia 13–14see also atrial; broad complex; junctional; supraventricular;

ventricularterminology 5–8tetralogy of Fallot 74thrombolysis, indications 29thyrotoxicosis 55“tombstone” R waves 29torsades de pointes 25–6, 65

causes 26transposition of great arteries

congenitally corrected 74electrocardiogram 58

transvenous cardiac pacing, acute myocardial infarction,complete atrioventricular (node) conduction block 40

tricuspid atresia 73tricuspid insufficiency, Ebstein’s anomaly 73tricuspid regurgitation 48tricuspid stenosis 48trifascicular blocks 12

U waves 8

Index

79

vagal stimulation 28valvular problems

left heart 51–2right heart 48

Vaughan-Williams classification of drugs 70ventricular arrhythmias, mechanisms 21–2ventricular escape rhythms 10, 64ventricular fibrillation 61–2

diagnosis, potential pitfalls 62features and predictors 61–2R on T 62

ventricular hypertrophyleft 49–50paediatric, diagnosis 58right 45–6right heart strain 48

ventricular pre-excitation 18ventricular septal defects 72ventricular standstill 64ventricular tachycardias 25–6

acute myocardial infarction 40atrioventricular dissociation 22–4, 63capture beats 23defined 21differentiation from supraventricular tachycardias with

bundle branch block 26fascicular tachycardia 25fusion beats 23mechanisms 21–2monomorphic 22–4

defined 21

duration and morphology of QRS complex 22frontal plane axis 22–3independent atrial activity 23–4

direct evidence 23indirect evidence 23–4

rate and rhythm 22polymorphic 26, 65, 71

defined 21see also torsades de pointes

positive/negative concordance, QRS complex 23–4prognosis 40right ventricular outflow tract 25torsades de pointes 25–6, 65

verapamil, contraindications 20, 27VVI pacing 66

waveforms 1–4wave of depolarisation 2

Wenckebach phenomenon 10paediatric 60

Wolff-Parkinson-White syndrome 18–20, 26atrial fibrillation 20atrioventricular re-entrant tachycardia

antidromic 20formation mechanism 19–20

bundle of Kent 18classification 19clinical presentation 20electrocardiogram features 18–19supraventricular tachycardias 26

workload, exercise tolerance testing 41

ab cof ecg

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