Susceptibility to arrhythmias may result from genetic abnormalities or acquired structural heart disease. Susceptibility may be increased by electrolyte abnormalities, hormonal imbalances (thyrotoxicosis, hypercatecholaminergic states), hypoxia, medication effects (such as QT interval prolongation or changes in automaticity, conduction, and refractoriness), and myocardial ischemia. Ongoing research has provided important information on the genetic basis of arrhythmias and knowledge in this arena is expanding rapidly. Most arrhythmias can be classified as (1) disorders of impulse formation or automaticity, (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 reentrant arrhythmias.
Abnormalities of impulse conduction or propagation can occur at the level of the sinus or AV node, in the intraventricular conduction system, and within the atria or ventricles. These are responsible for sinoatrial exit block, for AV block at the node or below, and for establishing reentry circuits.
Reentry is the underlying mechanism for many arrhythmias, including premature beats, many paroxysmal SVT, atrial flutter, and infarct-related ventricular tachycardia. 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.
Triggered activity occurs when after-depolarizations (abnormal electrical activity persisting after repolarization) reach the threshold level required to trigger a new depolarization. Triggered activity can be divided into two different categories: pause-dependent and catecholamine-dependent. Pause-dependent triggered activity is caused by early after-depolarizations (EADs) in phase 3 of the action potential. This is frequently the mechanism of polymorphic ventricular tachycardia. Catecholamine-dependent triggered activity is caused by delayed after-depolarizations (DADs) in phase 4 of the action potential. They may be seen in patients with digitalis toxicity, cardiac ischemia, or congenitally prolonged QT intervals. Increased sympathetic tone also plays a part in these arrhythmias. RV outflow tract ventricular tachycardia is attributed to this mechanism.