[Mechanisms of electrical defibrillation].

Ventricular fibrillation has been described as a "chaotic, random, asynchronous electrical activity of the ventricles due to repetitive reentrant excitation and/or rapid focal discharge". Reentrant and non-reentrant mechanisms are responsible for the initiation of ventricular fibrillation. After fibrillation has been induced, it is thought that multiple, disorganized, wandering wavelets follow constantly changing reentrant pathways. Electrical defibrillation is the only valid therapeutic approach for ventricular fibrillation. A successful defibrillation shock must be of sufficient strength to stop fibrillation but must not be so strong that damage to the myocardium occurs. The clinical use of the implantable cardioverter/defibrillator device has significantly stimulated research in the field of cardiac defibrillation. In order to develop more efficient shock waveforms and electrode configurations for smaller, and also longer lasting devices, we need a better understanding of the basic mechanisms of defibrillation. The development of computerized electrical mapping systems, capable of recording before, during and after a defibrillation shock, optical recording systems and microelectrodes, for action potential recording before and after the shock application and mathematical models have contributed much to the understanding of defibrillation mechanisms.An electrical shock hits the cardiac cells in different phases of their action potential. This results in 1) direct activation, 2) a "graded response", or 3) no effect. "Graded response" produces prolongation of the action potential and prolongs refractoriness without giving rise to a propagated activation front. Refractory period prolongation in an area that is still refractory at the time of the shock is critical for successful defibrillation. Mapping studies have shown that for successful defibrillation with monophasic shocks a minimal potential gradient of 5-7 V/cm is necessary (the exact value depends on the waveform and the orientation of the cells with respect to the electric field).Several hypotheses have been developed in order to explain the mechanisms that underlie successful defibrillation shocks. This paper will discuss the various theories. The "upper limit of vulnerability" hypothesis for defibrillation states that a successful defibrillation shock must stop existing activation fronts by directly exciting or by prolonging refractoriness just in front of the upcoming activation fronts and must not give rise to new activation fronts at the border of the directly excited area. Shocks slightly weaker then necessary to defibrillate stop fibrillation activation fronts, but give rise to new activation fronts that reinitiate fibrillation. These new activation fronts arise at a "critical point," where a critical shock potential gradient interferes with a critical degree of tissue refractoriness. Mappping studies support the "upper limit of vulnerability" hypothesis of defibrillation but not all defibrillation failures, however, can be explained by this hypothesis.Clinical data and experimental results have shown that biphasic shocks may have lower defibrillation thresholds than monophasic shocks. The advantage of defibrillation with a biphasic waveform is not yet clearly understood. We discuss some possible reasons why some biphasic waveforms have lower defibrillation thresholds than monophasic waveforms.