Electrophysiological control of ventricular rate during atrial fibrillation.

Thirteen anesthetized canine subjects (17-29 kg) were used to demonstrate that mild cervical left vagal stimulation could control ventricular rate effectively during atrial fibrillation (AF). Two studies are presented. The first study used six subjects to demonstrate the inverse relationship between (manually applied) left vagal stimulation and ventricular excitation (R wave) rate during AF. As left vagal stimulation frequency was increased, ventricular excitation rate decreased. In these studies, a left vagal stimulus frequency of 0-10 per second reduced the ventricular excitation rate from > 200/min to < 50/min. The decreasing ventricular excitation rate with increasing left vagal stimulation frequency was universal, occurring in all 26 trials with the six subjects. This fundamental principle was used to construct an automatic controller for use in the second study, in which seven subjects were used to demonstrate that ventricular rate can be brought to and maintained within a targeted range with the use of an automatic (closed-loop) controller. A 45-minute record of automatic ventricular rate control is presented. Similar records were obtained in all seven subjects.

Characterization of atrioventricular nodal response to electrical left vagal stimulation.

The dynamic effect of left vagal stimulation on atrioventricular conduction was studied in six isofluorane-anesthetized dogs ranging in weight from 22 to 29 kg. The cervical vagus nerve trunks were left intact and no beta-adrenergic blockade was produced so that any influences of the sympathetic nervous system and autonomic reflex activity could be observed. Atrial pacing was used to control the heart rate while single, short trains of left vagal stimulation were delivered and timed to occur at different instances during the cardiac cycle. The magnitude of the A-V delay depended on the instant of delivery of the train of vagal stimuli during the cardiac cycle. Vagal effect curves were constructed and fit to a mathematical equation which describes the pharmacokinetic behavior of a bolus injection of a drug whose onset time is of the same order as its half-life. The three parameters of this equation have physiologic significance and are related to nerve propagation time and synaptic delay, acetylcholine concentration rise, and the acetylcholineesterase mechanism. The maximum A-V delay occurred when the short train of left vagal stimuli was applied 200-300 ms after the atrial pacing stimulus and the total effect was virtually over by 800-1,000 ms.