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Can We Learn about Ventricular Fibrillation in Man by Studying Animal Models of Defibrillation?

Ventricular fibrillation (VF), regardless of proximate cause or ultimate mechanism, is the “final common pathway” of sudden cardiac death, a scourge of the modern world that claims more than 450,000 lives per year in the United States.1 The chaotic and seemingly random nature of VF, as well as the short period of time that this condition can be tolerated in the intact animal, has led to the effort to try to understand VF by analyzing attempts to terminate it by electrical defibrillation. A large body of data, often obtained in idealized animal models and with extremely complicated technologies, has led to several competing hypotheses. Initially it was thought that defibrillation could succeed only if the applied shock was sufficiently strong to terminate all electrical activity.2 Subsequently, it was presented that shock-induced termination of fibrillatory activity in most, but not necessarily all, of the ventricle could result in successful defibrillation.3,4 This concept, the “critical mass” hypothesis, states that remaining postshock fibrillatory activity extinguishes because it is contained in too small a mass of ventricular myocardium to sustain fibrillation. This is similar to our concept of atrial fibrillation, as understood in the light of the multiple wavelet hypothesis: if an insufficient number of simultaneous wavelets exist, wavefront collision and extinction may lead to VF termination on a more or less statistical basis. Testing and refinement of these classic models of VF and defibrillation awaited the development of computer-assisted electrical mapping. The first challenge to the critical mass hypothesis, the upper limit of vulnerability (ULV) hypothesis, is based on the following concepts.5,6 A shock that does not result in successful defibrillation [even shocks well below the defibrillation threshold (DFT)] does terminate all fibrillatory activity, resulting in an “isoelectric interval” that may last for more than 50 msec. Afterward, slower and more uniform activation originates from areas of low-voltage gradients, which can result in refibrillation. This concept was appealing in that it unified the process of failed defibrillation with the relatively recent but secure understanding of induction of VF with shocks delivered in sinus rhythm during the vulnerable period (critical point reentry, upper limit of vulnerability).7 High-voltage shocks, on the other hand, prevent the development of critical point reentry in sinus rhythm and, according to this hypothesis, prevent refibrillation following defibrillation of VF. Support for this hypothesis included detailed epicardial electrical mapping in animal models that demon-