4.3.2 Paroxysmal tachycardias

 

Tachyarrhythmia may be divided into confusions of impulse propagation and disorders of impulse formation.

Disorders of impulse propagation (reentry) are generally considered to be the most common mechanism of sustained paroxysmal tachyarrhythmia. The requirements for initiating re-entry include electrophysiologic ununiformity (differences in conduction and/or refractoriness) in two or more regions of the heart connected with each other to form a potentially closed loop; unidirectional block in one pathway; slow conduction over an alternative pathway, allowing time for the initially blocked pathway to recover excitability; and re-excitation of the initially blocked pathway to complete a loop of activation. Repetitive circulation of the impulse over this loop can produce a sustained tachyarrhythmia. While anatomic obstacles may underlie reentry and provide an inexcitable center around which the impulse can circulate, they are not essential. Reentrant arrhythmias can be reproducibly initiated and terminated by premature complexes and rapid stimulation. The response of these arrhythmias to stimulation can help distinguish them from arrhythmias caused by triggered activity.

Disorders of impulse formation can be subdivided into tachyarrhythmias caused by enhanced automaticity and those caused by triggered activity. In addition to the sinus node, automatic pacemaker activity can be observed in specialized atrial fibers, fibers of the atrioventricular junction, and Purkinje fibers. Myocardial cells do not normally possess pacemaker activity. Enhancement of normal automaticity in latent pacemaker fibers or the development of abnormal automaticity due to partial depolarization of the resting membrane occurs as a consequence of a variety of pathophysiologic states, which include increased endogenous or exogenous catecholamines, electrolyte disturbances (hyperkalemia), hypoxia or ischemia,  mechanical effects (stretch), and drugs (digitalis, phenothiazines). Tachycardia caused by automaticity cannot be started or stopped by pacing.

Rhythms due to triggered activity are events that do not occur spontaneously but require a change in cardiac electrical frequency as a trigger. Triggered activity may be caused by early afterdepolarizations, which occur during phases 2 and 3 of the action potential, or delayed afterdepolarizations, which occur following completion of phase 3 of the action potential. Triggered activity has been observed in atrial, ventricular, and His-Purkinje tissue under conditions such as increased local catecholamine concentration, hyperkalemia, hypercalcemia, and digitalis intoxication (delayed afterdepolarizations) or during bradycardia, hypokalemia, or other situations prolonging action potential duration (early afterdepolarizations).

All of these conditions produce an accumulation of intracellular calcium. With increasing amplitude of the afterdepolarizations, threshold can be reached and repetitive activity produced. The exact role of triggered activity in spontaneous clinical arrhythmias is unknown, but tachyarrhythmias associated with digitalis intoxication, accelerated idioventricular rhythm in acute infarction and/or reperfusion, and exercise-induced ventricular tachycardia are believed to be caused by triggered activity due to delayed afterdepolarizations. «Torsade de pointes» («twisting of the points», polymorphic ventricular tachycardia associated with long QT intervals) may be caused by triggered activity due to early afterdepolarizations, although re-entry may also be operative.