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Reentry and the development of cardiac arrhythmias

Philip J Podrid, MD, FACC
Section Editor
Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor
Brian C Downey, MD, FACC


Cardiac arrhythmias are generally produced by one of three mechanisms: enhanced automaticity, triggered activity, or reentry. Reentry, which occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after the refractory period has ended, is the electrophysiologic mechanism responsible for the majority of clinically important arrhythmias. Included among these arrhythmias are atrial fibrillation, atrial flutter, atrioventricular (AV) nodal reentry, AV reentry involving a bypass tract, ventricular tachycardia after myocardial infarction (MI) with the presence of left ventricular scar, and ventricular fibrillation.

The first demonstration of reentry in its simplest form (ie, the ring model) probably occurred in 1906 following the application of a stimulus to tissue from a jellyfish which initiated rhythmic contraction [1]. However, reentry was first conceived as a mechanism for arrhythmias in 1913 when it was recognized that reentrant tachycardias arise from circular electrical pathways, often initiated by a blocked impulse [2]. It was subsequently realized that reentry tachycardias may also be due to other mechanisms, including functional or leading circle circuits and abnormal electrical circuits caused by diseased myocardium.

The definition and characteristics of the different reentry circuits responsible for the most clinically significant arrhythmias are presented here, along with the electrophysiologic properties of these arrhythmias. The clinical presentation and management of the individual arrhythmias are discussed separately. (See "Management of new onset atrial fibrillation" and "Overview of atrial flutter" and "Atrioventricular nodal reentrant tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway" and "Sustained monomorphic ventricular tachycardia in patients with a prior myocardial infarction: Treatment and prognosis".)


Reentrant tachycardia (variously named reentrant excitation, reciprocating tachycardia, circus movement, and reciprocal or echo beats) is defined as a continuous repetitive propagation of an excitatory wave traveling in a circular path, returning to its site of origin to reactivate that site [1]. The one event crucial to the development of a reentrant tachycardia is the failure of a group of fibers to activate during a depolarization wave. The initiation of a reentrant arrhythmia also requires the presence of myocardial tissue with the following electrophysiologic properties (figure 1) [3-6]:

Adjacent tissue or pathways must have different electrophysiologic properties (conduction and refractoriness) and be joined proximally and distally, forming a circuit. These circuits may be fixed or stationary or may move within the myocardial substrate (as occurs with spiral waves).

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Literature review current through: Nov 2017. | This topic last updated: Apr 11, 2016.
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