Abstract
The electrical effects of action potential collision were studied using a computer simulation of one-dimensional action potential propagation and tissue experiments from isolated cardiac Purkinje strands and papillary muscles. The effects of collision, when compared to normal one-way propagation, included quantitative changes in all of the measured indexes of action potential upstroke and repolarization. These changes can be attributed to spatiotemporal changes in the net membrane current. Parameter sensitivity and analytic techniques identified five factors which determine the collision-induced decrease in action potential area: conduction velocity, action potential height, cable radius, specific intracellular resistivity, and the specific membrane resistance during action potential repolarization. The simulations demonstrated that collision effects were independent of inhomogeneity in action potential duration, the spatial extent of the collision effects was greater than the passive space constant, and certain simulated abnormal conditions (e. g., discontinuous propagation, ischemic tissue) increased the magnitude of the collision effects. The tissue experiments supported the simulations regarding the changes in action potential configuration directly at and on each side of the collision site. Elevated [K+]0 increased the changes in action potential duration in both tissue preparations. In papillary muscles, collision effects in the transverse direction were confined to a narrower region than collision effects in the longitudinal direction with no difference in the peak magnitude of the changes. Action potential collision is a common occurrence in the heart.
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