FACTORS DETERMINING THE PRODUCTION OF VENTRICULAR FIBRILLATION BY DIRECT CURRENTS (WITH A NOTE ON CHRONAXIE)

Abstract

Any type of stimulus above a certain critical value, introduced during the vulnerable period of late systole, causes fibrillation. In the case of direct currents, the effective excitant may be a brief rectilinear shock, probably not more than 0.04 sec. in duration or the closing or opening of more prolonged currents during this period of vulnerability. In the case of D.C. stimuli which exceed 0.05 or 0.06 sec., the factor which determines fibrillation in any specific instance depends upon the duration of the D.C. stimulus, upon the time that closure occurs with respect to the cycle, upon the character of the premature response evoked, upon the relation of opening to a normal or premature beat, etc. However, it can be demonstrated in many of these highly variable conditions, that a 2d effective stimulus, artificial or physiological, must strike during the vulnerable period of a premature systole in order to cause fibrillation. Such a concept harmonizes the apparent discrepancy that brief shocks of any form only cause fibrillation when they are applied during the vulnerable period, whereas D.C. shocks longer than 0.05 sec. may do so when they fall entirely in diastole, partly in systole and partly in diastole, or even when they extend over several beats. The chief secondary mechanisms by which shocks longer than 0.05 or 0.06 sec. become more potent fibrillation stimuli are fundamentally due to 2 well known peculiarities of such shocks: They are no longer unitary stimuli but are capable of exerting separate C and O effects, and they cause effects during persistence of the current which give rise to unpredictable spontaneous impulses either during the flow of the current or shortly after its cessation. In view of the greater tendency even of weak currents, 0.24-0.33 sec. in duration, to evoke spontaneous premature beats not related to C or O, the frequency of fibrillation by such currents in our series and the non-existence in the beating heart of any span of iso-excitability, the detn. of chronaxie of the ventricles by customary procedures lacks a sound physiological foundation.