Unmasking and Conversion of Gap Phenomenon in the Human Heart

Abstract

Two types of gap phenomena (types I and II ) have been described in human hearts and their electrophysiologic bases have been delineated. In both types of gap phenomena relatively early premature atrial impulses are blocked within some portion of the His-Purkinje system (HPS). By increasing the prematurity of the atrial depolarization, conduction to the ventricles resumes due to delay of the premature impulse with the atrioventricular node (A-VN) (type I gap) or within the proximal HPS (type II gap). Gap phenomena are not observed when the refractory period of the A-VN exceeds that of the HPS. Since atropine decreases refractoriness of the A-V node, its effect on the gap phenomena was studied in nine subjects. After administration of atropine (0.2-0.5 mg i.v.) type I gap was demonstrated in six subjects and type II gap in three subjects. When atropine shortened the functional and effective refractory period (ERP) of the A-V node, premature atrial impulses arrived at the HPS during its ERP. By a similar mechanism, type I gap was converted into type II gap in three subjects following atropine administration. Decreasing the basic atrial drive rate converted type II gap into type I (two subjects) and ultimately abolished both types of gap phenomena in all subjects. These results suggest that the gap penomenon may be functional in nature and may be readily manifested or abolished by varying the refractoriness of the A-V node relative to that of the HPS.