The effect of digitalis on refractoriness of the intact canine His-Purkinje system.

The effect of therapeutic doses of digitalis on functional (F), relative (R) and effective (E) refractory periods (RP) of the His-Purkinje system (HPS) was studied in 12 open-chested, innervated adult mongrel dogs (10-20 kg) during control and 15, 30 and 45-60 min after 0.016 mg/kg of intravenous ouabain. To determine the stability of the preparation and to assess time-dependent changes in His-Purkinje refractoriness, another six dogs (Group II) had similar studies, but without drug administration. In all dogs, the His bundle was paced by using the plunge wire technique at a predetermined cycle length (CL) and a premature stimulus (S2) to the His bundle was introduced at decreasing S1 S2 intervals. Following ouabain, in Group I dogs, at the longest Cls tested (458 +/- 125 msec; +/- SD) there was significant increase in the FRP (+4.34%; P less than 0.05), RRP (S2 V2 (+6.57%, P less than 0.05), RRP (Ab) (+6%, P less than 0.05) and ERP (52%, P less than 0.05) of the HPS. These significant changes were generally observed 30 minutes after drug administration. Changes in RPs were of greater magnitude at longer CLs (greater than 400 msec), but insignificant at shorter CLs (less than 400 msec). The H-V interval during sinus rhythm and the S1 V1 interval during His bundle pacing at all CLs did not change after ouabain. In Group II dogs there were no significant change in His-Purkinje refractoriness over 60 minutes. These findings suggest that therapeutic doses of digitalis 1) tend to increase refractoriness within the HPS to a very small degree, 2) have no appreciable effect on His-Purkinje conduction, and 3) affect CL-dependent changes in refractoriness. The His bundle extrastimulus method is useful in studying the HPS in the intact heart.

The 1,2,3,4 phenomenon. Atrioventricular nodal gap in the dog.

This study confirms the facility with which the so-called 1,2,3,4 phenomenon can be reproduced in intact dog hearts. When a series of three atrial premature beats (A2, A3, A4) were delivered following a constant A1-A1 drive, we demonstrated a narrow zone of A1-A3 and A1-A4 intervals in which A4 conducted to the ventricles in the presence of A3 but not in its absence. We used His bundle and multiple atrial electrograms to produce the phenomenon in nine of 16 dogs. Facilitation of conduction of A4 (1) occurred above the His bundle, (2) occurred within narrow ranges of A1-A3 and A1-A4 intervals, (3) required penetration of A3 into the atrioventricular (AV) node, (4) required critically long A2-H2 intervals, (5) always was associated with prolonged A4-H4 intervals, and (6) was limited by atrial refractoriness. An apparent or pseudo-1,2,3,4 phenomenon demostrated in five of 16 dogs occurred with (1) latency between S4 and A4, (2) a sinus nodal or atrial reentry beat, or (3) an atrial escape beat. In the absence of A3, A4 could be made to conduct by preexciting the ventricle in advance of V2. We found no evidence for dual AV nodal pathways. Our results suggest that the underlying mechanism for the 1,2,3,4 phenomenon is analogous to the phenomenon of the gap in AV conduction.