Differential effects of sympathetic activity on AV junctional automaticity and AV conduction

Abstract

Rapid ventricular response during episodes of supraventricular tachycardia are often followed, on abrupt cessation of the tachycardia, by prolonged pauses terminated by a sluggish and sometimes erratic escape of a supraventricular pacemaker. Such chronotropic-dromotropic paradoxes are readily reproduced in the animal laboratory following elimination of the sinus node and bilateral decentralization of the stellate ganglia and vagi. This study examined whether left stellate stimulation (0.5, 1, 2, 4, 8 and 16 Hz) or lack thereof differentially affected AV junctional automaticity and AV conduction. In the absence of any sympathetic neural activity (maximal sympathetic deficit), the AV junctional rate averaged a mere 22 +/- 2 percent of its peak performance, whereas under the same conditions, anterograde AV conduction averaged 73 +/- 5 percent and retrograde VA conduction 56 +/- 13 percent of their respective peak performances. On comparing the response curve (normalized responses) for AV junctional automaticity with that obtained for anterograde AV conduction the differences were significant at all frequencies between 0 and 4 Hz. Retrograde VA conduction (as assessed by the fastest ventricular pacing rate still conducted 1:1 to the atria) was always significantly less than anterograde AV conduction (as assessed by the fastest atrial pacing still conducted 1:1 to the ventricles). These results indicate that AV junctional automaticity is considerably more affected by sympathetic deficit than are either anterograde or retrograde AV conduction. In other words, AV junctional automaticity is far more dependent upon sympathetic input than AV conduction. While sympathetic influence is critical to the escape and maintenance of AV junctional automaticity both anterograde and retrograde AV conduction are remarkably resilient even under conditions of severe sympathetic deficit.

Heart Rate Variability Measures During Sinus Rhythm Predict Cycle Length Entropy During Atrial Fibrillation

“…However, the relative roles of sympathetic and vagal influences are likely different between them, given that the cellular mechanisms of autonomic regulation of sinoatrial automaticity are distinct from those affecting conduction velocity and refractoriness of nodal tissue. Indeed, these differential effects have been well demonstrated in animal models 22–25 . To the extent that both short‐term HRV parameters and entropy are determined by autonomics, these differences in sympathovagal balance between the SA node and the AV node act to weaken the correlations we studied here.…”