Recovery of excitability of ventricular muscle was measured at numerous points in exposed dog ventricles at varying distances along six radial axes from a primary point of stimulation. Temporal dispersion of recovery of excitability at various points equidistant from the point of stimulation was minimal after a basic beat but was increased after an early premature beat. The degree of dispersion following a basic beat was increased by stimulation of the cardiac sympathetic nerves, administration of chloroform, ouabain intoxication, administration of higher doses of quinidine, myocardial ischemia, and hypothermia, but it was decreased by administration of sympathomimetic amines.

Effects of stimulation of the cardiac sympathetic nerves and intravenous administration of sympathomimetic amines on the multiple response or fibrillation threshold (VMRT) and on other properties of the dog ventricles were compared. Stimulation of the cardiac sympathetic nerves decreased the VMRT. Administration of sympathomimetic amines caused a brief decrease in the VMRT followed by a sustained increase. Temporal dispersion of recovery of excitability and the degree of ventricular vulnerability were closely related; the ventricle was more vulnerable to fibrillation when the dispersion was increased. The hyperkalemic effect of epinephrine was not responsible for the observed changes in ventricular vulnerability.

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Excessive delay and configurational change of ventricular responses to atrial premature beats, previously attributed to dissociation within the A-V node, were shown to be due to functional block of the right bundle branch. It was found that the refractory period (RP) of the right bundle branch often exceeded the functional refractory period (FRP) of the A-V node at slow heart rates, permitting an early premature atrial response to reach the ventricles before recovery of the right bundle. Vagal stimulation and rapid driving frequencies, by delaying the intranodal transit of the premature response, prevented the exposure of bundle branch block. Epinephrine in low doses sometimes facilitated its occurrence. Premature responses initiated in the His bundle in open heart preparations were commonly blocked in the right bundle under conditions in which atrial premature responses were normally propagated to the ventricles. Evidence was obtained in such preparations that the portion of the right bundle system beyond the site of the block was activated retrogradely from the left side. Under certain conditions the retrograde activation process returned to the His bundle and the atrium as an echo.