Concept of reentry versus automaticity

Abstract

Arrhythmias can result from abnormal impulse initiation or conduction. Abnormal initiation results from either automatlcity or triggered activity. Enhanced automaticity may be due to a normal automatic mechanism (a normal property of the sinus node and specialized conducting fibers) or to an abnormal mechanism such as automaticity in depolarized fibers. Triggered activity is caused by afterdepolarizations that occur either during repolarization (early afterdepolarization) or after repolarization is complete (delayed afterdepolarization). Triggered activity due to delayed afterdepolarizations is dependent on critical heart rates. Overdrive pacing may distinguish between normal and abnormal automaticity. Antiarrhythmic drugs can alter arrhythmias that result from abnormal impulse initiation. To suppress an arrhythmia resulting from abnormal impulse generation, a drug may (1) suppress the abnormal automatic mechanism, i.e., specific effect on ionic current; (2) suppress afterdepolarizations; (3) depress conduction in tissue surrounding automatic focus; or (4) modify refractory period of tissue in and around automatic focus. Abnormal impulse conduction results in reentrant excitation. Conditions necessary for reentry include a combination of unidirectional block and slowed conduction. A reentrant mechanism can be determined by an anatomically defined circuit or solely by the functional properties of the tissue (leading circle mechanism). Circus movement reentry around an anatomic obstacle may respond to antiarrhythmic drugs differently from reentry caused by a leading circle mechanism. Initiation and perpetuation of a reentry mechanism depends on a delicate interplay between conduction velocity and duration of the functional refractory period in the reentry circuit. Drugs can prevent a reentry mechanism by (1) eliminating premature beats that initiate the mechanism; (2) reducing the disparity in effective refractory periods; (3) improving conduction, thereby preventing unidirectional block; (4) further depressing conduction in a part of the circuit producing a bidirectional block; and (5) lengthening the functional refractory period in the tachycardia circuit more than the total circuit time. The effectiveness of drugs on reentry depends on the electrophysiologic substrate contributing to the reentrant mechanism. All of these mechanisms cause arrhythmias in the in situ canine heart and probably occur in humans. However, clinical pacing techniques are not sufficiently discriminating to distinguish between arrhythmic mechanisms. Ability to inltiate ventricular tachycardia with 1 or more premature beats is suggestive of reentry but does not rule out triggered automaticity. Demonstration of continuous fragmented electrical activity before the first beat of tachycardia and perpetuation of such activity during tachycardia provides more definitive evidence for a reentry mechanism.