Mechanisms of clinical tachycardias.

Animal data suggest that cardiac arrhythmias can result from a variety of mechanisms. In clinical settings, arrhythmias that are easily initiated and terminated with programmed electrical stimulation are often designated as reentry tachycardias. However, proof of reentry is contingent upon demonstration of the entire circuit; this relation has been proposed for arrhythmias associated with large circuits, such as those seen in the Wolff-Parkinson-White syndrome. Reentry has also been proposed as the mechanism responsible for a variety of other tachycardias, including bundle branch and atrioventricular nodal reentry tachycardia, permanent junctional reentrant tachycardia, reentry tachycardia associated with nodoventricular Mahaim fibers and inducible atrial and ventricular tachycardia. Documentation of triggered rhythms as the mechanism responsible for clinical arrhythmias has been even more difficult. Examples of arrhythmias resulting from triggered activity may include those associated with digitalis toxicity arising from the atria, the atrioventricular junction or the ventricles. Clinical arrhythmias due to triggered activity in the absence of digitalis have also been described. Cardiac arrhythmias that cannot be induced by electrical stimulation are presumably due to normal or abnormal automaticity. Examples of normal automaticity in the human heart are sinus rhythm and junctional and idioventricular escape rhythms. Tachycardias by abnormal automaticity have seldom been investigated for the purpose of documenting the mechanism and therefore the limited data available make it difficult to draw any final conclusions.