Passive Propagation of Transmembrane Potential Induced by Intrinsic Capacitances of Myocardium Bioelectrolytes during Its Electrical Defibrillation

Abstract

External and implantable electric cardioverters/ defibrillators (ECD) are subject to continuous upgrading: the size and weight are reduced, whereas the energy transmitted to myocardium tissue is increased by optimization of the electric pulse shape; functional capacities for detection of the moment of exposure to electric pulse, documentation of the operating modes, and information exchange (including remote exchange) with medical personnel and patient (in portable models) are being improved [1, 3, 12]. Optimization of the medico-technical characteristics of modern ECDs and development of new models of ECDs are impossible without understanding the main bioelectrical characteristics of the process of defibrillation. However, in spite of extensive research in this field, there is still no acceptable unified theory of the mechanism (mechanisms) of defibrillation that can explain the majority of experimental findings. In particular, it is presently uncertain why a bipolar electric pulse is more effective for defibrillation [8]. Understanding of the mechanism of response of myocardium cells to external electrical effect of an electrode positioned at a distance significantly larger than several millimeters would provide a particularly deep insight into the mechanism of electrical defibrillation. On one hand, the mechanism of this response is due to passive propagation of transmembrane potential (TMP) deep into the myocardium during the exposure to the external electric pulse. This suggestion is supported by a large body of experimental findings. On the other hand, in accordance with theoretical models of electrophysical properties of myocardium, passive propagation of TMP during exposure to the external electric effect of an electrode positioned at a distance larger than several millimeters is impossible [10, 14]. This problem has been a subject of extensive research [10, 11]. Various theoretical models of passive propagation of TMP have been suggested to solve this problem. These models consider the conductive properties of the area of contact of myocyte cytoplasms, curvature of myocardium fibers, and heterogeneity of myocardial tissue at microscopic and macroscopic levels [5-7, 9-11, 13, 14, 17-19]. Nevertheless, the problem of determination of the predominant mechanism of defibrillation remains unsolved [10, 11]. The goal of this work was to describe the mechanism of passive propagation of TMP within the framework of bidomain description of the electrophysical properties of myocardium. According to this description, propagation of TMP is due to the intrinsic capacitances of bioelectrolytes [16]. This mechanism is due to the fact that both external and internal bioelectrolytes may have unbalanced (by absolute value) electric charges with respect to one another. In addition, these charges can sufficiently rapidly diffuse along bioelectrolytes, thereby contributing to the TMP due to electric induction. One of the advantages of this mechanism is that it is based on fundamental electrophysical properties of myocardium as a bidomain medium.