Susceptibility to arrhythmias results from genetic abnormalities (most often affecting ion channels) and acquired structural heart disease. Susceptibility may be increased by electrolyte abnormalities, hormonal imbalances (thyrotoxicosis, hypercatecholamine states), hypoxia, drug effects (such as QT interval prolongation or changes in automaticity, conduction, and refractoriness), and myocardial ischemia. Most arrhythmias can be classified as (1) disorders of impulse formation or automaticity and (2) abnormalities of impulse conduction, (3) reentry, and (4) triggered activity.

Altered automaticity is the mechanism for sinus node arrest, many premature beats, and automatic rhythms as well as an initiating factor in reentry arrhythmias.

Abnormalities of impulse conduction can occur at the sinus or atrioventricular node, in the intraventricular conduction system, and within the atria or ventricles. These are responsible for sinoatrial exit block, for atrioventricular block at the node or below, and for establishing reentry circuits.

Reentry is the underlying mechanism for many arrhythmias, including premature beats, most paroxysmal supraventricular tachycardias, and atrial flutter. For reentry to occur, there must be an area of unidirectional block with an appropriate delay to allow repeat depolarization at the site of origin. Reentry is confirmed if the arrhythmia can be terminated by interruption of the circuit by a spontaneous or induced premature beat.

Triggered activity occurs when afterdepolarizations (abnormal electrical activity persisting after repolarization) reach the threshold level required to trigger a new depolarization. This may be the mechanism of ventricular tachycardia in the prolonged QT syndrome and in some cases of digitalis toxicity.

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Napolitano C et al: Genetics of ventricular tachycardia. Curr Opin Cardiol 2002;17:222.

Wall TS et al: Ventricular tachycardia in structurally normal hearts. Curr Cardiol Rep 2002;4:388.