Shock-induced depolarization of refractory myocardium prevents wave-front propagation in defibrillation.
The elimination of most, if not all, propagating wave fronts of electrical activation by a shock constitutes a minimum prerequisite for successful defibrillation. However, the factors responsible for the prevention of postshock propagating activity are unknown. We investigated the determinants of this effect of defibrillation shocks in 23 Langendorff-perfused rabbit hearts by optically mapping cardiac cellular electrical activity by means of laser scanning. The optical action potentials obtained by this method were continuously recorded from 100 ventricular epicardial sites before, during, and after shock delivery during fibrillation. Analysis of activation maps showed that postshock propagating activity arose from areas depolarized by the shock. In 273 shock episodes, 898 sites at the border of shock-depolarized areas (BSDAs) from which wave-front propagation could have arisen were identified. The incidence of postshock propagation from BSDA sites was inversely related to refractoriness, as indexed by coupling interval (CI) or the optical takeoff potential (Vm). Specifically, there was a near-zero probability of postshock propagation if the shock caused depolarization at CIs < 50% of the fibrillation cycle length or from myocardium still depolarized to > or = 60% of the amplitude of a paced action potential (APA). Furthermore, incidences of wave-front propagation following shocks were consistently lower than the propagation incidences of naturally occurring unshocked fibrillation wave fronts, at comparable CIs and Vms. We conclude that the incidence of postshock wave-front propagation decreases with increasing refractoriness at the BSDA and that shock-induced depolarization of effectively refractory myocardium (ie, depolarized to > or = 60% APA) is required to guarantee the cessation of continued wave-front propagation in defibrillation.
Kwaku
K F
KF
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Dillon
S M
SM
D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004554:Electric Countershock; D004594:Electrophysiology; D005260:Female; D005711:Gallopamil / Q000494:pharmacology; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D011817:Rabbits; D012032:Refractory Period, Electrophysiological
D002121:Calcium Channel Blockers; D005711:Gallopamil