Atrioventricular Nodal and Sinoatrial Nodal Function in Humans

A constant intravenous infusion of phenylephrine (0.74±0.41 ,ug/kg/min) was given to 10 patients to cause a continuous augmentation in reflex vagal tone. After the infusion, the diastolic blood pressure increased from 76±7 to 89±11 mm Hg (p<0.01). The sinus cycle length and atrial-His (AH) interval were measured, and incremental atrial pacing was performed before and during phenylephrine infusion until atrioventricular (AV) nodal block was achieved. For each patient, the AV nodal function curve (i.e., the AH interval plotted as a function of the atrial pacing cycle length) was compared during both the control state and phenylephrine infusion; the AH intervals during each condition at chosen short (AHs) and long (AHL) cycle lengths were compared. The sinus cycle length increased during phenylephrine infusion from 941±294 to 1,115±347 msec (p=0.013). The AH interval during sinus rhythm was not significantly prolonged (77 versus 82 msec, p =NS). The shortest atrial pacing cycle length yielding 1:1 AV nodal conduction increased during phenylephrine infusion from 412±120 to 575+±211 msec (p<0.01). Of note, the degree of sinus cycle length prolongation did not correlate with the degree of prolongation in the shortest atrial pacing cycle length yielding 1:1 AV nodal conduction. The AV nodal function curve was shifted markedly to the right and only slightly upward. Thus, even though there was a significant increase in both AHL (from 84+±24 to 102+48 msec, p<0.05) and AHs (from 127 ±40 to 186±+66 msec, p<0.01), the mean increase in AHs was substantially greater (59 versus 18 msec,p< 0.01). We conclude that during baroreflex-induced enhanced vagal tone there is a significant depression of AV nodal conduction, primarily related to the stressed portion of the AV nodal function curve. Although baroreflex-induced changes in sinus automaticity and AV nodal conduction generally move in the same direction, the degree of negative dromotropic effects on AV nodal conduction cannot be predicted by the magnitude of change in sinus rate. (Circulation Research 1991;68:1614-1620)