- Journal List
- BMJ
- v.324(7341); 2002 Apr 6
- PMC1122768
As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsem*nt of, or agreement with, the contents by NLM or the National Institutes of Health.
Learn more: PMC Disclaimer | PMC Copyright Notice
BMJ. 2002 Apr 6; 324(7341): 831–834.
PMCID: PMC1122768
PMID: 11934778
ABC of clinical electrocardiography
Francis Morris and William J Brady
Copyright and License information PMC Disclaimer
In the clinicalassessment of chest pain, electrocardiography is an essentialadjunct to the clinical history and physical examination. A rapid andaccurate diagnosis in patients with acute myocardial infarction isvital, as expeditious reperfusion therapy can improve prognosis. Themost frequently used electrocardiographic criterion for identifyingacute myocardial infarction is ST segment elevation in two or moreanatomically contiguous leads. The ST segment elevation associated withan evolving myocardial infarction is often readily identifiable, but aknowledge of the common “pseudo” infarct patterns is essential toavoid the unnecessary use of thrombolytic treatment.
Indications for thrombolytic treatment
ST elevation >1 mm in two contiguous limbleads or >2 mm in two contiguous chest leads
Posterior myocardial infarction
Left bundle branch block
ST segment depression or enzymatic change arenot indications for thrombolytic treatment
In the early stages of acute myocardial infarction theelectrocardiogram may be normal or near normal; less than half ofpatients with acute myocardial infarction have clear diagnostic changeson their first trace. About 10% of patients with a proved acutemyocardial infarction (on the basis of clinical history and enzymaticmarkers) fail to develop ST segment elevation or depression. In mostcases, however, serial electrocardiograms show evolving changes thattend to follow well recognised patterns.
Hyperacute T waves
The earliest signs of acutemyocardial infarction are subtle and include increased T waveamplitude over the affected area. T waves become more prominent,symmetrical, and pointed (“hyperacute”). Hyperacute T waves aremost evident in the anterior chest leads and are more readily visiblewhen an old electrocardiogram is available for comparison. Thesechanges in T waves are usually present for only five to 30 minutesafter the onset of the infarction and are followed by ST segmentchanges.
ST segment changes
In practice, ST segment elevation is often theearliest recognised sign of acute myocardial infarction and is usuallyevident within hours of the onset of symptoms. Initially the ST segmentmay straighten, with loss of the ST-T wave angle . Then the T wavebecomes broad and the ST segment elevates, losing its normal concavity.As further elevation occurs, the ST segment tends to become convexupwards. The degree of ST segment elevation varies between subtlechanges of <1 mm to gross elevation of >10mm.
Sometimesthe QRS complex, the ST segment, and the T wave fuse to form asingle monophasic deflection, called a giant R wave or“tombstone”
Pathological Q waves
As the acute myocardial infarctionevolves, changes to the QRS complex include loss of R wave height andthe development of pathological Q waves.
Both of these changes develop as a result of the loss ofviable myocardium beneath the recording electrode, and the Q wavesare the only firm electrocardiographic evidence of myocardial necrosis.Q waves may develop within one to two hours of the onset of symptoms ofacute myocardial infarction, though often they take 12 hours andoccasionally up to 24 hours to appear. The presence of pathological Qwaves, 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, the patientmay still benefit from thrombolysis or direct intervention.
When there is extensive myocardial infarction, Q waves act asa permanent marker of necrosis. With more localised infarction the scartissue may contract during the healing process, reducing the size ofthe electrically inert area and causing the disappearance of the Qwaves.
Resolution of changes in ST segment and T waves
As the infarct evolves, the STsegment elevation diminishes and the T waves begin to invert. The STsegment elevation associated with an inferior myocardial infarction maytake up to two weeks to resolve. ST segment elevation associated withanterior myocardial infarction may persist for even longer, and if aleft ventricular aneurysm develops it may persist indefinitely. T waveinversion may also persist for many months and occasionally remains asa permanent sign of infarction.
Reciprocal ST segment depression
ST segment depression in leads remote from the site ofan acute infarct is known as reciprocal change and is a highlysensitive indicator of acute myocardial infarction. Reciprocal changesare seen in up to 70% of inferior and 30% of anterior infarctions.
Typically, the depressed ST segments tend to be horizontal ordownsloping. The presence of reciprocal change is particularly usefulwhen there is doubt about the clinical significance of ST segmentelevation.
Reciprocal change strongly indicates acuteinfarction, with a sensitivity and positive predictive value of over90%, though its absence does not rule out the diagnosis.
The pathogenesis of reciprocal change is uncertain. Reciprocalchanges are most frequently seen when the infarct is large, and theymay reflect an extension of the infarct or occur as a result ofcoexisting remote ischaemia. Alternatively, it may be a benignelectrical phenomenon. The positive potentials that are recorded byelectrodes facing the area of acute injury are projected as negativedeflections in leads opposite the injured area, thus producing a“mirror image” change. Extensive reciprocal ST segment depressionin remote regions often indicates widespread arterial disease andconsequently carries a worse prognosis.
Localisation of site of infarction
The distribution of changes recordedin acute myocardial infarction allows the area of infarction to belocalised, thus indicating the site of arterial disease. Proximalarterial occlusions tend to produce the most widespreadelectrocardiographic abnormalities. The anterior and inferior aspectsof the heart are the areas most commonly subject to infarction.Anteroseptal infarcts are highly specific indicators of disease of theleft anterior descending artery. Isolated inferior infarcts—changes inleads II, III, and aVF—are usually associated with disease in theright coronary or distal circumflex artery. Disease in the proximalcircumflex artery is often associated with a lateral infarctpattern—that is, in leads I, aVL, V5, and V6.
Anatomical relationship of leads
Inferior wall—Leads II, III, and aVF
Anterior wall—Leads V1 to V4
Lateral wall—Leads I, aVL, V5, and V6
Non-standard leads
Right ventricle—Right sided chest leads V1R toV6R
Posterior wall—Leads V7 toV9
Right ventricular infarction
Right ventricular infarction is oftenoverlooked, as standard 12 lead electrocardiography is not aparticularly sensitive indicator of right ventricular damage. Rightventricular infarction is associated with 40% of inferior infarctions.It may also complicate some anterior infarctions but rarely occurs asan isolated phenomenon. On the standard 12 lead electrocardiogram rightventricular infarction is indicated by signs of inferior infarction,associated with ST segment elevation in lead V1. It is unusual for STsegment elevation in lead 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 is leadV4R (an electrode is placed over the right fifth intercostal space inthe mid-clavicular line). Lead V4R should be recorded as soon aspossible in all patients with inferior infarction, as ST segmentelevation in right ventricular infarction may be shortlived.
Thediagnosis of right ventricular infarction is important as it may beassociated with hypotension. Treatment with nitrates or diuretics maycompound the hypotension, though the patient may respond to a fluidchallenge
Right ventricularinfarction usually results from occlusion of the right coronaryartery proximal to the right ventricular marginal branches, hence itsassociation with inferior infarction. Less commonly, right ventricularinfarction is associated with occlusion of the circumflex artery, andif this vessel is dominant there may be an associated inferolateralwall infarction.
Posterior myocardial infarction
Posterior myocardial infarction refers to infarction of theposterobasal wall of the left ventricle. The diagnosis is often missedas the standard 12 lead electrocardiography does not include posteriorleads. Early detection is important as expeditious thrombolytictreatment may improve the outcome for patients with posteriorinfarction.
The changes of posterior myocardial infarction are seenindirectly in the anterior precordial leads. Leads V1 to V3 face theendocardial surface of the posterior wall of the left ventricle. Asthese leads record from the opposite side of the heart instead ofdirectly over the infarct, the changes of posterior infarction arereversed in these leads. The R waves increase in size, becoming broaderand dominant, and are associated with ST depression and upright Twaves. This contrasts with the Q waves, ST segment elevation, and Twave inversion seen in acute anterior myocardial infarction. Ischaemiaof the anterior wall of the left ventricle also produces ST segmentdepression in leads V1 to V3, and this must be differentiated fromposterior myocardial infarction. The use of posterior leads V7 to V9will show ST segment elevation in patients with posterior infarction.These additional leads therefore provide valuable information, and theyhelp in identfying the patients who may benefitfrom urgent reperfusion therapy.
Figure
Sequence of changes seen during evolution of myocardialinfarction
Figure
Hyperacute T waves
Figure
Anterior myocardial infarction with gross ST segment elevation(showing “tombstone” R waves)
Figure
Pathological Q waves in inferior and anterior leads
Figure
Long standing ST segment elevation and T wave inversionassociated with a previous anterior myocardial infarction(echocardiography showed a left ventricular aneurysm)
Figure
An inferolateral myocardial infarction with reciprocal changesin leads I, aVL, V1, and V2
Figure
Reciprocal changes: presence of widespread ST segment depressionin the anterolateral leads strongly suggests that the subtle inferiorST segment elevation is due to acute infarction
Figure
Placement of right sided chest leads
Figure
Acute inferior myocardial infarction with associated rightventricular infarction
Figure
Acute inferior myocardial infarction with right ventricularinvolvement
Figure
Position of V7, V8, and V9 on posterior chest wall
Figure
Isolated posterior infarction with no associated inferiorchanges (note ST segment depression in leads V1 to V3)
Figure
ST segment elevation in posterior chest leads V8 and V9
Footnotes
The ABC of clinical electrocardiography isedited by Francis Morris, consultant in emergency medicine at theNorthern General Hospital, Sheffield; June Edhouse, consultant inemergency medicine, Stepping Hill Hospital, Stockport; William J Brady,associate professor, programme director, and vice chair, department ofemergency medicine, University of Virginia, Charlottesville, VA, USA;and John Camm, professor of clinical cardiology, St George's HospitalMedical School, London. The series will be published as a book in thesummer.
Articles from The BMJ are provided here courtesy of BMJ Publishing Group