Triggered Activity

Triggered activity occurs when after-depolarizations induced by a preceding action potential raise the resting membrane potential above the threshold value, leading to an additional action potential. After-depolarizations may be categorized as early, occurring during phase III of the action potential before achieving full repolarization, or delayed, occurring after full repolarization of the membrane. After-depolarizations may stimulate an isolated extrapropagated impulse or lead to sustained repetitive activity. The crucial difference between triggered activity and abnormal automaticity is that triggered activity depends on a preceding action potential and cannot be self-induced. After-depolarizations or triggered activity are often associated with excessive increases in intracel-lular [Ca++]. The potential for development of triggered activity is accentuated in the presence of an increase in extracellular [Ca++] that would increase the amount of ionized calcium entering the cell during depolarization. Furthermore, conditions or pharmacological interventions favoring prolongation of the plateau (phase 3) of the action potential and prolongation of the QT interval of the electrocardiogram would increase intracellular [Ca++] and the potential for proarrhythmia.

Early after-depolarizations are purported to be the mechanism giving rise to torsades de pointes. Conditions or drugs known to prolong the action potential, especially by interventions that decrease the outward potassium currents, facilitate development of torsades de pointes tachyarrhythmias. Early after-depolarizations may develop in association with hypokalemia, hypoxia, acidosis, and a wide range of pharmacological agents that interfere with outward currents or enhance inward currents. Antiarrhythmic agents, in particular sotalol, quinidine, and dofetilide, may give rise to after-depolarizations and torsades de pointes tachyarrhythmia in persons with underlying cardiac abnormalities or alterations in plasma electrolytes. Conditions leading to bradycardia also may facilitate development of torsades de pointes tachyarrhythmia.

Early after-depolarizations and the associated ventricular arrhythmia can be prevented or suppressed by the appropriate adjustment of plasma potassium and/or magnesium concentrations. Lidocaine or procainamide may be effective for termination of the arrhythmia.

Delayed after-depolarizations (Figure 16.4) may occur in the presence of a rapid heart rate, digitalis glyco-sides, hypokalemia, hypercalcemia and catecholamines. Each of these influences ultimately leads to an increase in intracellular ionized calcium that is known to activate an inward ionic current. The inward ionic current activates a nonselective channel that normally is involved with the transport of sodium but that under pathophys-iological conditions may permit the movement of sodium or potassium ions. Upon reaching threshold, the calcium-induced oscillatory potentials lead to the production of a sustained ventricular arrhythmia. Delayed after-depolarizations, in contrast to early after-depolarizations, are more likely to produce triggered tachy-arrhythmias during periods of short pacing cycle lengths (rapid heart rates). Exercise-induced ventricular tachycardia in persons without overt cardiac disease exemplifies such a situation. The electrophysiological abnormality is catecholamine dependent and calcium sensitive. The arrhythmia may respond to L-type calcium channel antagonists or inhibitors of the cardiac p-adrenoceptor. Each of these approaches would serve to reduce the tissue calcium concentration.

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