Postrepolarization refractoriness in ventricular cardiac cells: A simulation study

In this work, computer simulations have been used to investigate the mechanisms of postrepolarization refractoriness in cardiac tissue under ischemic conditions at the cellular level. For this purpose, the Luo-Rudy (phase II) model of the cardiac action potential has been used with the formulation of the ATP-sensitive K⁺ current by Ferrero et al being adopted. Cells were subject to simulated hyperkalemic and hypoxic conditions. Our results show that action potential duration (APD) progressively decreases with hyperkalemia, while effective refractory period (ERP) has a biphasic behavior with [K⁺]_o. The delay in the recovery from inactivation of the inward sodium current, as a consequence of diastolic depolarization, seems to be responsible for this phenomenon. Under ischemic conditions, this trend is maintained, though both APD and ERP values are significantly lowered.