Influence of extracellular potassium levels on atrioventricular transmission

Dependence of transmission of excitation along atrial and A-V pathways on extracellular K + was studied in the isolated, Langendorff perfused, rabbit heart. It was found that atrial propagation velocity reaches a maximum at [K] 0 = 6 mm; slowing, presumably due to depolarization, ensues at higher [K] 0 . Propagation between upper His bundle and ventricles seems to behave in a similar way. Transmission across the A-V nodal area is markedly impaired at [K] 0 below 2 mm; A-V block is often observed. Higher [K] 0 levels shorten the A-V nodal transmission time; this speeding of transmission persists in [K] 0 levels high enough to cause impairment of propagation in atria. Furthermore, A-V nodal block caused by acetylcholine was shown to be abolished when [K] 0 is raised to an appropriate level. This antagonistic action is probably not due to release of catecholamines by the increased [K] 0 . A possible explanation for the [K] 0 dependence of A-V transmission is discussed in terms of the ionic hypothesis