Ventricular fibrillation due to single, localized induction and condenser shocks applied during the vulnerable phase of ventricular systole
31 Jan 1940-American Journal of Physiology (American Physiological Society)-Vol. 128, Iss: 3, pp 500-505
TL;DR: It is shown that in order to produce premature contractions by shocks applied during systole it was necessary to utilize very strong break shocks, and in the zeal to elicit such contractions ventricular fibrillation all too often terminated the experiment.
Abstract: It is generally believed that in order to induce ventricular fibrillation by electric currents they must not only have a minimal intensity but must act for a fair interval of time (ca, several seconds). Indeed, the variation in duration of a current has been used as a criterion of the sensitivity of the heart (1). In 1934 King (2) and in 1936, Ferris, King, Spence and Williams (3) reported that shocks as short as 0.03 second are effective in fibrillating the ventricles provided they are applied during the occurrence of the T wave, which they interpreted as the partial refractory phase. Previous to this, de Boer (4) had shown that a process similar to fibrillation in mammalian hearts can be induced in the frog’s ventricle by induction shocks applied near the end of the systole, but he believed only during a hypodynamic state. Andrus, Carter and Wheeler (5) found that an induction shock similarly introduced into normal auricles of dogs caused auricular fibrillation. During 1923-24 the senior author (6) in studying the response of the dog’s ventricles to strong induction shocks demonstrated that the mammalian ventricle is not refractory to stimuli for a considerable, though apparently variable, interval of systole (last 0.03-0.09 sec. of systole). In order to produce premature contractions by shocks applied during systole it was necessary to utilize very strong break shocks, and in the zeal to elicit such contractions ventricular fibrillation all too often terminated the experiment. A survey of many records has shown that this was due to single shocks and that all were delivered somewhere during the non-refractory phase of ventricular systole. In view of the importance of observations that a very brief shock is capable of inducing fibrillation even when the exciting current traverses only a small area of the ventricle, it seemed important
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TL;DR: The results show that the large dispersion of repolarization facilitates the development of a conduction delay necessary to induce sustained arrhythmia by an early premature stimulus applied at the site with a short MAP.
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790 citations
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