On the Cause of Ventricular Asystole during Vagal Stimulation
In anesthetized dogs the vagus nerve was stimulated for 2 min; during the first minute the ventricles were driven at a rate higher than the control sinus rate; after discontinuation of the drive, the duration of asystole was prolonged. When the ventricles were driven at a rate lower than the sinus rate during vagal stimulation the subsequent asystole was shortened. Slowing sinus activity by graded vagal stimulation before maximal vagal stimulation led to a shorter asystole. Driving the ventricles at a rate higher than the sinus node rate before vagal stimulation resulted in longer asystole. In animals with chronic atrioventricular block, "overdriving" the ventricles resulted in subsequent temporary inhibition of ventricular pacemakers. In dogs with atrioventricular block, coronary sinus plasma potassium increased during the period of ventricular overdriving, and the magnitude of the rise was a function of the driving rate. These results support the concept that ventricular asystole results from the suppressive action of the fast rate imposed by the sinus node upon the slowly discharging ventricular pacemakers. Suppression of sinus node activity by the vagus reveals the rate-dependent inhibition of ventricular pacemakers. The mechanism of inhibition may be related to changes in ionic concentration gradients.
- rate-dependent pacemaker inhibition
- cardiac standstill
- sinus rate and ventricular pacemakers inhibition
- heart rate and potassium
- potassium and inhibition of ventricular pacemakers
- ventricular pacemakers
- ventricular escape
- anesthetized dogs
- Accepted December 26, 1966.
- © 1967 American Heart Association, Inc.