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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.

A study of the transmission of early premature contractions between atria and ventricles and in the retrograde direction in the dog heart suggests the existence of two parallel A-V conduction pathways communicating with each other over one or more branches. The evidence is based on the excessive delay of very early premature responses in traversing the node, suggesting that a slowly conducting pathway recovers earlier than the normal "fast" pathway; on the echoing back to the chamber of origin of early premature responses; and on ventricular electrograms of "abnormal" configuration obtained during early premature responses. These observations and the hypothesis to which they lead provide a natural explanation for reciprocal rhythm and nodal paroxysmal tachycardia.