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Electrocardiography (ECG)

by Michael J. Shea, MD

The standard ECG provides 12 different vector views of the heart’s electrical activity as reflected by electrical potential differences between positive and negative electrodes placed on the limbs and chest wall. Six of these views are vertical (using frontal leads I, II, and III and limb leads aVR, aVL, and aVF), and 6 are horizontal (using precordial leads V 1 , V 2 , V 3 , V 4 , V 5 , and V 6 ). The 12-lead ECG is crucial for establishing many cardiac diagnoses, especially arrhythmias and myocardial ischemia (see Interpretation of Abnormal ECGs). It can also identify atrial enlargement, ventricular hypertrophy (see Criteria for ECG Diagnosis of Left Ventricular Hypertrophy), and conditions that predispose to syncope or sudden death (eg, Wolff-Parkinson-White syndrome, long QT syndrome, Brugada syndrome). A useful ECG tutorial is available from the University of Utah.

Interpretation of Abnormal ECGs

Abnormal Component


Possible Causes

P waves


Left or right atrial hypertrophy, atrial escape (ectopic) beats

P waves



P-P interval


Sinus arrhythmia

PR interval


First-degree atrioventricular block

PR interval


Mobitz type I atrioventricular block, multifocal atrial tachycardia

QRS complex



QT interval



QT interval


Hypercalcemia, hypermagnesemia, Graves disease, digoxin

ST segment


Myocardial ischemia; acute posterior MI; digoxin; ventricular hypertrophy; pulmonary embolism; left bundle branch block; right bundle branch block in leads V 1 V 3 and possibly in II, III, and aVF; hyperventilation; hypokalemia

ST segment


Myocardial ischemia, acute MI, left bundle branch block, acute pericarditis, left ventricular hypertrophy, hyperkalemia, pulmonary embolism, digoxin, normal variation (eg, athlete's heart), hypothermia

T wave


Hyperkalemia, acute MI, left bundle branch block, stroke, ventricular hypertrophy

T wave

Small, flattened, or inverted


U wave


Hypokalemia, hypomagnesemia, ischemia

Criteria for ECG Diagnosis of Left Ventricular Hypertrophy





R or S wave 20 mm in any limb lead


S wave in V 1 or V 2 30 mm


R wave in V 5 or V 6 30 mm


ST-T changes typical of LVH



No digitalis


Left atrial changes: P terminal wave in V 1 , amplitude 1 mm, and duration 0.04 sec


Left axis deviation 30°


QRS duration 90 msec


Interval between QRS and R-wave peak in V 5 or V 6 0.05 sec



V 1 S wave + V 5 or V 6 R wave 35 mm


aVL R wave 11 mm


Men: V 3 S wave + aVL R wave > 28 mm

Women: V 3 S wave + aVL R wave > 20 mm

LVH = left ventricular hypertrophy.

Standard ECG Components

By convention, the ECG tracing is divided into the P wave, PR interval, QRS complex, QT interval, ST segment, T wave, and U wave (see see Figure: ECG waves.).

ECG waves.


P wave

The P wave represents atrial depolarization. It is upright in most leads except aVR. It may be biphasic in leads II and V 1 ; the initial component represents right atrial activity, and the 2nd component represents left atrial activity.


PR interval


QRS complex

The QRS complex represents ventricular depolarization. The Q wave is the initial downward deflection; normal Q waves last < 0.05 sec in all leads except V 1-3 , in which any Q wave is considered abnormal, indicating past or current infarction. The R wave is the first upward deflection; criteria for normal height or size are not absolute, but taller R waves may be caused by ventricular hypertrophy. A 2nd upward deflection in a QRS complex is designated R. The S wave is the 2nd downward deflection if there is a Q wave and the first downward deflection if not. The QRS complex may be R alone, QS (no R), QR (no S), RS (no Q), or RSR, depending on the ECG lead, vector, and presence of heart disorders.

Normally, the QRS interval is 0.07 to 0.10 sec. An interval of 0.10 to 0.11 sec is considered incomplete bundle branch block or a nonspecific intraventricular conduction delay, depending on QRS morphology; 0.12 sec is considered complete bundle branch block or an intraventricular conduction delay. Normally, the QRS axis is 90° to −30°. An axis of −30° to −90° is considered left axis deviation and occurs in left anterior fascicular block (−60°) and inferior MI. An axis of 90° to 180° is considered right axis deviation; it occurs in any condition that increases pulmonary pressures and causes right ventricular hypertrophy (cor pulmonale, acute pulmonary embolism, pulmonary hypertension), and it sometimes occurs in right bundle branch block or left posterior fascicular block.

QT interval



where QT c is the corrected QT interval; R-R interval is the time between 2 QRS complexes. All intervals are recorded in seconds. QT c prolongation is strongly implicated in development of torsades de pointe ventricular tachycardia (see Long QT Syndrome and Torsades de Pointes Ventricular Tachycardia). QT c is often difficult to calculate because the end of the T wave is often unclear or followed by a U wave with which it merges. Numerous drugs are implicated in prolonging the QT interval (see ).

ST segment


ST segment elevation can be caused by

  • Early repolarization

  • Left ventricular hypertrophy

  • Myocardial ischemia and infarction

  • Left ventricular aneurysm

  • Pericarditis

  • Hyperkalemia

  • Hypothermia

  • Pulmonary embolism

ST segment depression can be caused by

  • Hypokalemia

  • Digoxin

  • Subendocardial ischemia

  • Reciprocal changes in acute MI

T wave


U wave


Specialized ECG Tests


Additional precordial leads

Additional precordial leads are used to help diagnose right ventricular and posterior wall MI.

Right-sided leads are placed across the right side of the chest to mirror standard left-sided leads. They are labeled V 1 R to V 6 R; sometimes only V 4 R is used, because it is the most sensitive for right ventricular MI.

Additional left-sided leads can be placed in the 5th intercostal space, with V 7 at the posterior axillary line, V 8 at the midscapular line, and V 9 at the left border of the spine. These leads are rarely used but may help diagnose a true posterior MI.

Esophageal lead


Signal averaging

Signal averaging of QRS waveforms creates a digital composite of several hundred cardiac cycles to detect high-frequency, low-amplitude potentials and microcurrents at the terminal part of the QRS complex. These findings represent areas of slow conduction through abnormal myocardium, indicating increased risk of reentrant ventricular tachycardia. Signal-averaged ECG is still largely a research technique but is occasionally used to assess risk of sudden cardiac death (eg, in post-MI patients without evidence of conduction delay, patients with myocardial ischemia and unexplained syncope, and those with nonischemic cardiomyopathy) and to assess efficacy of surgery to correct the arrhythmia. This technique may also be useful for assessing the proarrhythmic effects of antiarrhythmic drugs and for detecting rejection of heart transplants. Signal averaging of P waves is being studied as a way to identify patients at risk of atrial fibrillation.

Continuous ST-segment monitoring


QT dispersion


Heart rate variability

This measurement reflects the balance between sympathetic and parasympathetic (vagal) input to the heart. Decreased variability suggests decreased vagal input and increased sympathetic input, which predict increased risk of arrhythmias and mortality. The most common measure of variability is the mean of the standard deviations of all normal R-R intervals in a 24-h ECG recording. Heart rate variability is used primarily in research, but evidence suggests that it provides useful information about left ventricular dysfunction after MI, heart failure, and hypertrophic cardiomyopathy. Most Holter monitors have software that measures and analyzes heart rate variability.

Holter monitor


Event recorder


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