Reflections of the Role of Adrenergic Mechanisms in Ventricular Arrhythmias

Abstract

Electrophysiological and pathological data presented in Chapter III of this book show that surviving myocardial cells at the margins, endothelial or epicardial surfaces of an infarcted area may be of etiological importance in the development of arrhythmias. Alterations in their rates and pathways of depolarization and repolarization and of their effective refractory periods are important factors in generating ventricular arrhythmias. In abnormal myocardium, enhanced automaticity and/or myocardial conduction abnormalities produce depolarizing selfperpetuating rapid circuits with reentry of waves of depolarization producing contractions. Waves of depolarization arising from a single (or a few) abnormal site(s) result in one or more ventricular extrasystoles. Ventricular tachycardia is a sustained rapid series of such ventricular contractions; ejection of ventricular contents maintains, to some extent, the circulation of blood. Ventricular tachycardia may degenerate into ventricular fibrillation. Indeed, it appears from the results reported by Dr. Scherlag that a short series of three to four ventricular tachycardia-like beats (triplets or quadruplets) often initiates ventricular fibrillation. In ventricular fibrillation, chaotic multifocal depolarization waves make effective ventricular contraction impossible; there is complete disruption of cardiac function, failure of ventricular ejection of blood, and sudden death.