The electrocardiogram

A wave appears on the ECG whenever a front of depolarisation or repolarisation moves through the myocardium; a wave is positive in a lead when the front moves toward the lead electrode. The P wave is atrial depolarisation. Atrial repolarisation is buried in the QRS. The PR interval, measured to the start of the QRS, includes the delay in the atrioventricular node that lets the atria empty before the ventricles contract; it lengthens in first-degree block. The QRS is ventricular depolarisation, which begins in the left side of the septum (the small q wave in left-sided leads), then sweeps the free walls from endocardium to epicardium; a narrow QRS means the bundle branches conducted normally. The ST segment corresponds to the plateau of the ventricular action potential, when there is no net current flow, and lies on the isoelectric line. The T wave is ventricular repolarisation; it is upright in most leads because the epicardium repolarises first, so the repolarisation front runs opposite to depolarisation but with reversed charge. The QT interval spans depolarisation and repolarisation and shortens with rate, so it is corrected (QTc). A small U wave after the T wave is sometimes seen and becomes prominent in hypokalaemia.

An electrode is a physical contact on the skin; a lead is a voltage measured between two points, so ten electrodes give twelve leads. The bipolar limb leads measure between two limbs: lead I from right arm (negative) to left arm (positive), lead II from right arm to left leg, lead III from left arm to left leg, and Einthoven law says that at any instant lead II equals lead I plus lead III. The augmented unipolar limb leads aVR, aVL and aVF measure each limb against the average of the other two and point at the right shoulder, the left shoulder and the feet. Together the six frontal-plane leads are spaced 30 degrees apart around the hexaxial reference system. The chest leads V1 to V6 are unipolar with a central terminal as reference and view the heart in the horizontal plane: V1 and V2 face the right ventricle and septum, V3 and V4 the anterior wall, V5 and V6 the lateral wall. Grouping the leads by territory is the basis of localising infarction: II, III and aVF are inferior leads, I, aVL, V5 and V6 lateral, V1 to V4 anteroseptal. The R wave grows from V1 to V6 as the electrode moves in front of the left ventricle.

Standard recording is 25 mm/s and 10 mm/mV, so one small square is 0.04 s and one large square 0.2 s. For a regular rhythm, rate equals 300 divided by the number of large squares between consecutive R waves, or 1500 divided by the number of small squares. For an irregular rhythm count the QRS complexes in 30 large squares (6 s) and multiply by ten. Sinus rhythm requires a P wave before every QRS, a QRS after every P, upright P waves in lead II and a constant PR interval. The mean electrical axis is the average direction of the QRS vector in the frontal plane. The quickest estimate uses leads I and aVF: both positive gives a normal axis (-30 to +90 degrees); lead I positive with aVF negative suggests left axis deviation, which is confirmed if lead II is also negative; lead I negative with aVF positive is right axis deviation. A more exact estimate takes the lead with the most isoelectric QRS and places the axis perpendicular to it, toward the leads with positive complexes. Right axis deviation appears with right ventricular hypertrophy and in tall thin people; left axis deviation with left ventricular hypertrophy, left anterior fascicular block and inferior infarction.

Electrical events lead mechanical ones by a short interval. The P wave precedes atrial contraction, which adds the last part of ventricular filling. The QRS precedes ventricular contraction, so the first heart sound falls just after the QRS, at the start of isovolumic contraction. The T wave falls at the end of ejection, and the second heart sound follows it as the semilunar valves close. Because it records only electrical activity, the ECG cannot measure contractility, stroke volume or the state of the valves; an apparently normal ECG can coexist with a failing pump and a chaotic ECG with reasonable output. Hypertrophy is inferred from voltage and axis, ischaemia and injury from ST and T changes, infarction from Q waves and evolving ST segments, electrolyte disturbance from T-wave shape (peaked in hyperkalaemia, flattened with U waves in hypokalaemia) and QT length (short with hypercalcaemia, long with hypocalcaemia). Drugs and rate change the QT, which is why it is corrected for rate before interpretation.