Atrioventricular nodal conduction and refractoriness after intranodal collision from antegrade and retrograde impulses.

Publisher Website
Google Scholar
Abstract
Animal studies have suggest that spontaneous or programmed ventricular beats that occur simultaneously with atrial activation may facilitate atrioventricular (AV) nodal conduction during subsequent atrial impulses. This possibility has not been systematically studied in the human heart. In the present study the AV nodal conduction during a programmed atrial premature beat (S2) was analyzed. The S2 was delivered after a series of atrial drive beats (S1S1) of constant duration; this was termed stimulation method I. The results were compared with stimulation method II, which was ismilar to method I except that a single ventricular beat (Vs) was introduced simultaneously with the last S1. The longest and shortest possible paced atrial cycle lengths (CL) were scanned during both methods. Patients (26) were studied: 14 with a normal PR and normal intraventricular conduction (NIVC), 4 with 1st-degree AV nodal block and NIVC, 3 with a complete left bundle branch block (LBBB) pattern, 3 with a complete right bundle branch block (RBBB) pattern and 2 with an incomplete RBBB pattern. At the same S1S2 intervals, the AV nodal conduction times (S2H2 intervals) were consistently shorter with method II than with method I except in 3 patients, 2 with complete RBBB and 1 with complete LBBB. The magnitude of S2H2 shortening with method II was more pronounced at the shorter basic CL and shorter S1S2 intervals. During method I, the effective refractory period (ERP) of the AV node was measured in 13 patients, 8 with NIVC and 5 with preexisting bundle branch block. With method II, the ERP of the AV node shortened in all but 3 patients (1 with complete RBBB, 1 with incomplete RBBB and 1 with complete LBBB pattern), in whom this variable did not change. Apparently, intranodal collison from antegrade and retrograde impulses facilitates AV nodal conduction and shortens the ERP. The magnitude of this change is greater at shorter atrial CL and is probably related to deeper intranodal penetration of a Vs. The shortening in AV nodal conduction and refractoriness is not noted in patients with bundle branch block when retrograde conduction delay or block in the bundle branches coexists with the antegrade counterpart producing delayed or ineffective input ov Vs into the AV node.