A numerical study of cardiac arrhythmia and defibrillation validated by experiments
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Defibrillation is termination of arrhythmias by altering the transmembrane voltage through the delivery of electric shocks. Debates on the mechanisms behind defibrillations, however, have never ceased. More recent studies affirmed the contribution of inhomogeneities to depolarization in tissues during a defibrillation shock, stating the heterogeneities, such as vessels and bundles, which have different electrical conductivities than cardiac tissue, serve as virtual electrodes during an electric shock, creating excitations in tissues far away from the anode and cathode. Low energy anti-fibrillation pacing (LEAP) has been suggested as an alternative method to traditional defibrillation method, which applies a strong electric pulse to terminate the arrhythmia. LEAP delivers multiple low amplitude electric shocks through field electrodes close to, or inside the tissue. The main goal of this thesis is to investigate the mechanism of LEAP and to suggest ways to improve it. The main finding is that LEAP works by gradually synchronizing the electric activity to the same frequency through each additional shock. Because the tissue is synchronized to the same frequency, both depolarization and repolarization are synchronized and additional shocks will not restart arrhythmia. Modified Kuramoto phase diagrams showed that, during arrhythmias, phase is relatively evenly distributed, and once LEAP is applied, the phase over the domain is increasingly focused with each shock. To further quantify this synchronicity, we calculated the fraction of tissue excited (FTE) as a function of time. The FTE peak progressively increases to one with each pulse for successful LEAP and its derivative indicates how fast the tissue synchronizes. In contrast, during one-shock defibrillation, the FTE upstroke is much slower compared to LEAP, indicating that all cells are eventually excited but not at the same time. Therefore, the mechanism of one-shock defibrillation is not through synchronization but rather by resetting all cells to an excited state, which requires the use of stronger electrical shocks, as some cells are less excitable than the others due to the repolarization gradients during fibrillation. Numerical simulations in this study suggested some ways to improve LEAP by adjusting the pacing period as well as the shock timings. The success rate is higher when the pacing cycle length is close to the dominant period of the arrhythmia and when the first shock was applied at the downslope of the fraction of tissue excited (FTE) curve.