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Lead II
Lead II

An electrocardiogram (ECG or EKG, abbreviated from the German Elektrokardiogramm) is a graphic produced by an electrocardiograph, which records the electrical voltage in the heart in the form of a continuous strip graph. It is the prime tool in cardiac electrophysiology, and has a prime function in screening and diagnosis of cardiovascular diseases.


12-lead electrocardiogram (ECG) with ST-segment elevation in leads II, III and aVF, suggestive of an inferior acute myocardial infarction (AMI).
12-lead electrocardiogram (ECG) with ST-segment elevation in leads II, III and aVF, suggestive of an inferior acute myocardial infarction (AMI).

The ECG has a wide array of uses:

Lead placement

Lead I
Lead I

An ECG is constructed by measuring electrical potential between various points of the body using a galvanometer. Leads I, II and III are measured over the limbs: I is from the right to the left arm, II is from the right arm to the left leg and III is from the left arm to the left leg. From this, the imaginary point V is constructed, which is located centrally in the chest above the heart. The other nine leads are derived from potential between this point and the three limb leads (aVR, aVL and aVF) and the six precordial leads (V1-6).

Therefore, there are twelve leads in total. Each, by their nature, record information from particular parts of the heart:

  • The inferior leads (leads II, III and aVF) look at electrical activity from the vantage point of the inferior region (wall) of the heart. This is the apex of the left ventricle.
  • The lateral leads (I, aVL, V5 and V6) look at the electrical activity from the vantage point of the lateral wall of the heart, which is the lateral wall of the left ventricle.
  • The anterior leads, V1 through V6, and represent the anterior wall of the heart, or the frontal wall of the left ventricle.
  • aVR is rarely used for diagnostic information, but indicates if the ECG leads were placed correctly on the patient.

Understanding the usual and abnormal directions, or vectors, of depolarization and repolarization yields important diagnostic information. The right ventricle has very little muscle mass. It leaves only a small imprint on the ECG, making it more difficult to diagnose than changes in the left ventricle.

The leads measure the average electrical activity generated by the summation of the action potentials of the heart at a particular moment in time. For instance, during normal atrial systole, the summation of the electrical activity produces an electrical vector that is directed from the SA node towards the AV node, and spreads from the right atrium to the left atrium (since the SA node resides in the right atrium). This turns into the P wave on the EKG, which is upright in II, III, and aVF (since the general electrical activity is going towards those leads), and inverted in aVR (since it is going away from that lead).

The normal ECG

Drawing of the EKG, with labels of intervalsP=P wave, PR=PR segment, QRS=QRS complex, QT=QT interval, ST=ST segment, T=T wave.
Drawing of the EKG, with labels of intervals
P=P wave, PR=PR segment, QRS=QRS complex, QT=QT interval, ST=ST segment, T=T wave.
Electrocardiogram of a healthy man, 21 years old
Electrocardiogram of a healthy man, 21 years old

A typical ECG tracing of a normal heartbeat consists of a P wave, a QRS complex and a T wave. A small U wave is not normally visible.



The axis is the general direction of the electrical impulse through the heart. It is usually directed to the bottom left, although it can deviate to the right in very tall people and to the left in obesity. Extreme deviation is abnormal and indicates a bundle branch block, ventricular hypertrophy or (if to the right) pulmonary embolism. It also can diagnose dextrocardia or a reversal of the direction in which the heart faces, but this condition is very rare and often has already been diagnosed by something else(such as a chest x-ray).

P wave

The P wave is the electrical signature of the current that causes atrial contraction. Both the left and right atria contract simultaneously. Irregular or absent P waves may indicate arrhythmia. Its relationship to QRS complexes determines the presence of a heart block.


The QRS complex corresponds to the current that causes contraction of the left and right ventricles, which is much more forceful than that of the atria and involves more muscle mass, thus resulting in a greater ECG deflection.

The Q wave, when present, represents the small horizontal (left to right) current as the action potential travels through the interventricular septum. Very wide and deep Q waves do not have a septal origin, but indicate myocardial infarction.

The R and S waves indicate contraction of the myocardium. Abnormalities in the QRS complex may indicate bundle branch block (when wide), ventricular origin of tachycardia, ventricular hypertrophy or other ventricular abnormalities. The complexes are often small in pericarditis.

T wave

The T wave represents the repolarization of the ventricles. The QRS complex usually obscures the atrial repolarization wave so that it is not usually seen. Electrically, the cardiac muscle cells are like loaded springs. A small impulse sets them off, they depolarize and contract. Setting the spring up again is repolarization (more at action potential).

In most leads, the T wave is positive. Negative T waves can be signs of disease, although an inverted T wave is normal in V1 (and V2-3 in black people).

The ST segment connects the QRS complex and the T wave. It can be depressed in ischemia and elevated in myocardial infarction, and downslopes in digoxin use.

T wave abnormalities may indicate electrolyte disturbance, such as hyperkalemia.

ECG measures

QT interval

The QT interval is measured from the beginning of the QRS complex to the end of the T wave. The QT interval as well as the corrected QT interval are important in the diagnosis of long QT syndrome and short QT syndrome. The QT interval varies based on the heart rate, and various correction factors have been developed to correct the QT interval for the heart rate.

The most commonly used method for correcting the QT interval for rate is the one formulated by Bazett and published in 19201. Bazett's formula is QTc = \frac{QT}{\sqrt {RR} }, where QTc is the QT interval corrected for rate, and RR is the interval from the onset of one QRS complex to the onset of the next QRS complex, measured in seconds. However, this formula tends to not be accurate, and over-corrects at high heart rates and under-corrects at low heart rates.


ECG as done by Willem Einthoven
ECG as done by Willem Einthoven

In the 19th century it became clear that the heart generated electricity. The first to systematically approach the heart from an electrical point-of-view was Augustus Waller, working in St Mary's Hospital in Paddington, London. In 1911 he still saw little clinical application for his work. The breakthrough came when Willem Einthoven, working in Leiden, The Netherlands, invented the string galvanometer, which was much more precise than the capillary galvanometer that Waller used. Einthoven assigned the letters P, Q, R, S and T to the various deflections, and described the electrocardiographic features of a number of cardiovascular disorders. He was awarded the 1924 Nobel Prize for Physiology or Medicine for his discovery.

Representation in culture

The ECG has become so familiar to the general population that it is part of the logo of many medical organisations, representing the technical side of medicine vs. the Rod of Asclepius or caduceus, which are more traditional. Being an electrical representation, it signifies vitality and urgency.

In various television medical dramas, an isoelectric ECG (no cardiac electrical activity or flatline) is often used as a symbol of death or at least extreme medical peril. This is technically known as asystole, a form of cardiac arrest with a particularly bad prognosis.


  1. Bazett HC. An analysis of the time-relations of electrocardiograms. Heart 1920; 7:353-370
  2. Cooper JK. Electrocardiography 100 years ago. Origins, pioneers, and contributors. N Engl J Med 1986;315:461-4. PMID 3526152.

See also

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