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

Structural complexities produced by the inhomogeneous distribution of the connections between cells and between muscle bundles have previously been considered to be 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. However, the authors observed marked effects of these connections on the velocity and the safety factor of propagation in atrial muscle under normal and abnormal conditions. First, 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. Second, at sites where muscle bundles branch or join with other bundles, the authors observed abrupt slowing of normal action potentials and changes in the shape of the extracellular waveform. They also studied such a junction in a computer simulation of propagation and found that 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 discontinuity to maintain propagation. However, when the maximum membrane depolarizing current was reduced by increasing the extracellular potassium concentration or by premature stimulation, block occurred at these sites. The authors observed that 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. The results indicate that models of propagation that ignore the inhomogeneous and multidimensional distribution of cell-to-cell connections produce incomplete, and sometines incorrect, descriptions of normal and abnormal propagation in cardiac muscle.