ELECTROPORATION AND SHOCK-INDUCED TRANSMEMBRANE POTENTIAL IN A CARDIAC FIBER DURING DEFIBRILLATION STRENGTH SHOCKS

Experimental studies have shown that the magnitude of the shock-induce d transmembrane potential (V-m) saturates with increasing electric fie ld strength. This study uses a mathematical model to investigate the e ffects of electroporation and membrane kinetics on V-m in a cardiac fi ber. The model consists of the core conductor equation for a one-dimen sional fiber, where excitability is represented by the Luo-Rudy dynami c model (1994-1995) and electroporation is described by a membrane con ductance that increases exponentially with V-m squared. For shocks del ivered during the plateau of an action potential, the model reproduces the experimentally observed saturation of V-m with a root mean square error of 4.27% and a correlation coefficient of 0.9992. For shocks de livered during diastole, the saturation of V-m is qualitatively reprod uced even when the sodium and calcium channels are inactivated. Quanti tative replication of the response to diastolic shocks is hindered by the choice of electroporation parameters (optimized for shocks deliver ed during the plateau) and differences in the membrane kinetics betwee n model and experiment. The complex behavior of V-m during large shock s is due to a combination of electroporation, electrotonus, propagatio n, and active membrane kinetics. The modeling results imply that the e xperimentally observed saturation of V-m is due to electroporation of the lipid bilayer. (C) 1998 Biomedical Engineering Society.