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Andrew R. Houghton

and David Gray



March 2014 – chapter reviewed; no significant changes required.

Updated on 29 Oct 2015. The previous version of this content can be found here.
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date: 28 March 2017

The resting 12-lead ECG

The ECG has been recognized as a valuable diagnostic tool since the end of the 19th century. The normal ECG waveform consists of P, QRS, and T waves (and sometimes U waves)—P waves result from atrial depolarization, QRS complexes from ventricular depolarization, and T waves from ventricular repolarization. The standard 12-lead ECG utilizes 4 limb electrodes and 6 precordial electrodes to generate 12 leads or ‘views’ of the heart’s electrical activity. There are six limb leads (termed I, II, III, aVR, aVL, and aVF) and six precordial leads (termed V1, V2, V3, V4, V5, and V6). Supplementary ‘views’ can be obtained by using additional leads, such as V7, V8, and V9 to assess the posterior aspect of the heart and right-sided chest leads to look for a right ventricular myocardial infarction.

Assessment of the 12-lead ECG—this should be done in a methodical manner, working through each aspect in turn. Conventionally, the heart rate, rhythm and axis are assessed before inspection of each component of the waveform in turn—the P wave, PR interval, QRS complex, ST segment, T wave, QT interval, and U wave, with each component having its own range of normal attributes.

Myocardial hypertrophy—the ECG can be a specific but generally insensitive tool for detecting myocardial hypertrophy: (1) left ventricular hypertrophy can be assessed using a number of diagnostic criteria, including the Cornell criteria and the Romhilt–Estes scoring system; (2) right ventricular hypertrophy is indicated by a dominant R wave in lead V1 with right axis deviation; (3) left atrial hypertrophy is indicated by broad, bifid P waves; and (4) right atrial hypertrophy by tall P waves.

Conduction blocks—(1) left anterior hemiblock results from a block of conduction in the anterosuperior fascicle and is a cause of left axis deviation; (2) left posterior hemiblock results from a block of conduction in the posteroinferior fascicle and is a cause of right axis deviation; (3) left and right bundle branch blocks both cause broadening of the QRS complexes by prolonging ventricular depolarization, and both exhibit characteristic diagnostic features.

Ventricular pre-excitation—causes shortening of the PR interval and can result from Wolff–Parkinson–White-type pre-excitation, short PR-type pre-excitation, or Mahaim-type pre-excitation (for discussion of the 12-lead ECG in arrhythmia, see Chapter 16.4).

Acute coronary syndromes

The ECG is the most useful bedside triage tool in acute coronary syndromes, with utility in diagnosis, in location of the site of ischaemia/infarction, and as a prognostic indicator.

ST elevation myocardial infarction (STEMI)—the first indication of infarction on the ECG is usually ST segment elevation, which occurs within a few hours. The J point (the origin of the ST segment at its junction with the QRS complex) is elevated by 1 mm or more in two or more limb leads, or by 2 mm in two or more precordial leads. The ST segment returns to the baseline over the next 48 to 72 h, during which Q waves and symmetrically inverted T waves appear. Some patients develop left bundle branch block, either transiently or permanently. The ECG of a completed infarct shows new Q waves greater than 2 mm, R waves reduced in size or absent, and inverted T waves.

Non-ST-elevation myocardial infarction (NSTEMI)—ECG changes are more variable than in STEMI. The ECG may be normal on first presentation and remain unchanged throughout the acute admission; there may be transient ST segment depression indicative of myocardial ischaemia; in 20 to 30% the only change will be T wave inversion.

Difficulties in interpretation of the ECG in acute coronary syndromes—the ECG diagnosis of acute myocardial infarction can pose challenges in the setting of right ventricular infarction, atrial infarction, coronary artery spasm, reciprocal changes, ‘stuttering’ infarction, noninfarct ST-segment elevation, late presentation, left bundle branch block, prior infarction, pre-excitation, and T wave inversion.

Clinical decision-making—incorrect interpretation of an ECG can lead to inappropriate patient triage, either missing the opportunity to provide appropriate reperfusion therapy, or leading to inappropriate thrombolysis with attendant risk. Up to 12% of those with a high-risk ECG are missed on admission to the Emergency Department, yet pressure to provide treatment promptly to fulfil audit ‘targets’, e.g. door-to-needle time for thrombolysis, should not replace accuracy in diagnosis. It is sometimes better to wait a short while, control symptoms, give aspirin, and repeat the ECG than to make an incorrect diagnosis. It is easy to place too much reliance on minor changes on the ECG; it is gross changes of ST elevation or depression within the parameters above that should determine treatment.

Exercise ECG testing

Exercise ECG testing is better as an indicator of prognosis than as a diagnostic tool. The sensitivity of exercise ECG testing, the proportion with coronary disease correctly identified by the test, is 68% (range 23–100) and specificity, the proportion free of disease correctly identified by the test, is 77% (range 17–100). In multivessel disease, these figures are 81% (range 40–100) and 66% (range 17–100), respectively. This means that exercise testing frequently yields both false-positive results—incorrectly diagnosing disease when coronary arteries are normal or minimally diseased—and false-negative results—missing coronary disease when a flow-limiting, even critical left main stem, coronary stenosis is present.

Appearance of symptoms or ECG changes early in an exercise test is generally associated with more severe and extensive coronary disease and a poor prognosis. Changes within the first 3 min usually indicate severe coronary disease affecting the left main stem or the proximal segments of at least one major coronary artery. Multivessel coronary disease is more likely with ST segment down-sloping, delayed ST normalization after exercise, increased number of leads affected, and lower workload at which ECG changes appear.

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