Effect of Different Currents and Extracellular Potassium Ion Concentration on Anodal Excitation of Cardiac Tissue

Abstract

Background:In order to understand defibrillation completely and thereby to design better defibrillators, we need to understand fibrillation and the effect of electrical stimulation on cardiac tissue. We address this issue by studying anodal excitation applied to the refractory tissue and by measuring the refractoriness of the cardiac tissue through the strength-Interval (SI) curve. The anodal SI curve contains a in which the S2 threshold increases as the interval increases. Our goal is to find the mechanism of the dip and to determine how calcium currents, sodium calcium exchange (NCX) current and elevated extracellular potassium ion concentration, [K]e, influences the dip in the anodal strength-interval curve.Methods and Results:Computer simulations of unipolar stimulation were performed using the bidomain model, with membrane kinetics governed by the Luo-Rudy model. The SI curve is determined by applying a threshold stimulus at different time intervals after a previous action potential. The dip disappears with no NCX current, but is present with 50% and 75% reduction of normal NCX current. The calcium induced calcium release (CICR) current and/or calcium uptake current are not responsible for the dip in the anodal SI curve. High [K]e results in the disappearance of the dip in the anodal SI curve because the tissue remained refractory after the transmembrane potential returned to its resting state.Conclusions:Neither NCX nor calcium current is responsible for the dip in the anodal SI curve. It is due to the electrotonic interaction between regions of depolarization and hyperpolarization following the S2 stimulus. The dominance of the electrotonic mechanism emphasizes the importance of the spatial distribution of virtual electrodes during excitation, which ultimately clarifies tissue-shock interactions and optimizes advanced defibrillation protocols.