The functional role of structural complexities in the propagation of depolarization in the atrium of the dog. Cardiac conduction disturbances due to discontinuities of effective axial resistivity.

Abstract

Structural complexities produced by the inhomogeneous distribution of the connections between cells and between muscle bundles were previously of minor importance in the propagation of depolarization in cardiac muscle; conduction disturbances usually are attributed to changes in membrane properties along the course of the fibers. Marked effects of these connections on the velocity and the safety factor of propagation in atrial muscle under normal and abnormal conditions were observed. Within individual muscle bundles, intermittent connective tissue septa were associated with localized dissociation of excitation when propagation occurred in the transverse direction, but not when it occurred in the longitudinal direction. At sites where muscle bundles branch or join with other bundles, abrupt slowing of normal action potentials and changes in the shape of the extracellular waveform were observed. Such a junction in a computer simulation of propagation was studied, and the local delay of propagation and the change in the shape of the extracellular waveform could only be accounted for by an abrupt change in the effective axial resistivity in the direction of propagation. Under normal conditions enough depolarizing current is coupled across such discontinuities to maintain propagation. When the maximum membrane depolarizing current was reduced by increasing the extracellular K concentration or by premature stimulation, block occurred at these sites. Most known cardiac conduction disturbances considered to require longer refractory periods in the direction of propagation (e.g., local conduction delay, decremental conduction, block and reentry) can be produced by the effects on propagation of such discontinuities of effective axial resistivity. Models of propagation that ignore the inhomogeneous and multidimensional distribution of cell-to-cell connections produce incomplete, and sometimes incorrect, descriptions of normal and abnormal propagation in cardiac muscle.