The role of cardiac tissue structure in defibrillation
Description
Although defibrillation of the heart is a commonly used life-saving procedure, the mechanisms by which strong electrical shocks terminate episodes of fibrillation remain largely unknown. This study presents an inquiry into the mechanisms for defibrillation. It regards defibrillation as occurring in two stages. First, the applied electrical shock induces changes in transmembrane potential, or virtual electrode polarization (VEP), and second, the VEP affects the time course of action potentials at the myocyte level Regarding the first stage, the interaction between applied electric fields, cardiac tissue structure, and shock-induced VEP is examined. It is demonstrated that: (1) Fiber architecture plays a significant role in shock-induced VEP for both uniform and non-uniform electric field shocks. (2) Electric shocks induce VEP in the depth of the myocardium large enough in both magnitude and extent to significantly affect underlying conduction patterns. (3) The shock-induced change in cardiac tissue structure---electroporation of the cellular membrane---alters the shape and increases the magnitude of shock-induced VEP In the second part of this research, post-shock arrhythmogenesis is examined. It is demonstrated that: (1) In the absence of electrotonic interaction, monophasic shock-induced changes in transmembrane potential either prolong or shorten the action potential duration, depending on shock strength, coupling interval, and shock polarity. Biphasic shocks do not deexcite the action potential as readily as monophasic shocks, and they can excite tissue at rest regardless of polarity. (2) In a two-dimensional model with non-uniform fiber curvature, it is demonstrated that the success of monophasic shocks depends on the amount of time excited tissue remains refractory compared to the amount of time it takes for shock-induced excitable gaps to be consumed. (3) In the culmination of this research, the above mentioned mechanisms are observed in an anatomically accurate model of the (three-dimensional) rabbit ventricles complete with fiber architecture These findings elucidate the mechanisms at work during the defibrillation process. Cardiac tissue structure plays a critical role in the shock-induced VEP throughout the heart. The perturbed or 'reprogrammed' time course of action potentials converts the pre-shock fibrillatory conduction pattern into a new conduction pattern, which in the case of a successful defibrillation shock, annihilates all reentrant conduction