On the Mechanism of Idioventricular Pacemaker Suppression by Fast Drive

¹ Department of Physiology, State University of New York, Downstate Medical Center 450 Clarkson Avenue, Brooklyn, New York 11203

The role of vagal activity, potassium concentration, and temperature in overdrive suppression of ventricular pacemakers, was studied in anesthetized dogs with and without surgical atrioventricular block. The results were as follows. (1) Overdrive of an idioventricular pacemaker during vagal stimulation was followed by a second pause. (2) Hypothermia increased the duration of the vagal and overdrive pauses. (3) Coronary sinus plasma potassium concentration ([K]_cs) decreased with the onset of vagal stimulation and increased with overdrive during vagal stimulation. (4) The increase in [K]_cs during ventricular overdrive was greater in hypothermia than it was in normothermia when the same absolute rate of overdrive was used and was unchanged when the same relative rate of overdrive was used. (5) Hypothermia increased overdrive suppression more than can be accounted for by the decrease in spontaneous rate, (6) By predriving the ventricles and then overdriving them, the increase in [K]_cs was dissociated from the pause duration. It is concluded that during vagal stimulation ventricular arrest is due to the inhibition of idioventricular pacemakers by the sinus node by virtue of its faster rate and that changes in [K]_cs are due to rate changes and not to acetylcholine release. Overdrive suppression can be dissociated from an increase in extracellular potassium concentration. Its prolongation in hypothermia provides evidence for a metabolism-dependent mechanism.

Submitted on March 6, 1974
Accepted on July 31, 1974