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Recent years have witnessed important advances in our understanding of the molecular and electrophysiologic mechanisms underlying the development of a variety of cardiac arrhythmias (Table 38–1) and conduction disturbances. Progress in our understanding of these phenomena has been fueled by innovative advances in our understanding of the genetic basis and predisposition for electrical dysfunction of the heart. These advances notwithstanding, our appreciation of the basis for many rhythm disturbances is incomplete. This chapter examines our present understanding of cellular, ionic, and molecular mechanisms responsible for cardiac arrhythmias, placing them in historical perspective whenever possible.

Table 38–1. Characteristics and Presumed Mechanisms of Cardiac Arrhythmia

Arrhythmic activity can be categorized as passive (eg, atrioventricular [AV] block) or active. The mechanisms responsible for active cardiac arrhythmias are generally divided into two major categories: (1) enhanced or abnormal impulse formation and (2) reentry (Fig. 38–1). Reentry occurs when a propagating impulse fails to die out after normal activation of the heart and persists to reexcite the heart after expiration of the refractory period. Evidence implicating reentry as a mechanism of cardiac arrhythmias stems back to the turn of century.1-3 Multichannel mapping studies documented that reentrant wavefronts may underlie the mechanisms of atrial4 and ventricular5 tachyarrhythmias. Phase 2 reentry,6 spiral waves of excitation,7 and fibrillatory conduction8 are interesting concepts of reentrant activity advanced to explain the development of extrasystolic activity and atrial as well as ventricular fibrillation (VF). Mechanisms responsible for abnormal impulse formation include enhanced automaticity and triggered activity. Automaticity can be further subdivided into normal and abnormal. Triggered activity consists of (1) early afterdepolarizations (EADs), (2) late-phase 3 EAD...

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