Electrophysiologic Mechanisms for the Generation of Arrhythmias with Adrenergic Stimulation

It is universally accepted that adrenergic stimulation can generate tachyarrhythmias de novo and promote arrhythmogenesis in concert with other factors [1–4]. Adrenergic activity has been implicated in various types of rhythm disturbances, ranging from extrasystoles to life-threatening arrhythmias such as rapid ventricular tachycardia and ventricular fibrillation. The electrophysiologic bases for this potent arrhythmogenic activity are uncertain. The beta-adreneric effects of acceleration of the diastolic depolarization of pacemaker cells and reduction of the duration of the refractory period are most often identified as the arrhythmogenic actions. Such actions are coherent with arhythmogenesis, but it is implausible that such serious tachyarrhythmias as rapid ventricular tachycardia and ventricular fibrillation could be tied solely to these actions. The acceleration of subsidiary pacemakers in the ventricle would be expected to result in idioventricular tachycardias with moderately high rates. The shortening of refractory periods could promote the formation of reentrant circuits, but adrenergic abbreviation of refractoriness is usually a relatively small effect, in the order of 10–20 ms [5].