Procaine Amide Against Re-Entrant Ventricular Arrhythmias
Lengthening R-V Intervals of Coupled Ventricular Premature Depolarizations as an Insight into the Mechanism of Action of Procaine Amide
Nine patients with coupled ventricular premature depolarizations (VPDs) were treated with intravenous procaine amide to abolish the arrhythmia. The effect of procaine amide on the electrocardiogram was carefully observed. Seven patients were treated with intermittent intravenous therapy-100 mg of procaine amide was injected every five minutes-and two were treated by constant intravenous infusion-200 µg/min/kg body weight; blood for plasma procaine amide concentration was obtained 4.5 to 5 min after each dose. As the cumulative dose of procaine amide increased, plasma drug concentration increased and the frequency of coupled VPDs progressively decreased. Moreover, in every patient an interesting electrocardiographic phenomenon was observed: as plasma drug concentration increased, the coupling interval progressively increased until the arrhythmia was completely abolished. A hypothesis for procaine amide's antiarrhythmic action is offered based on this new observation. This hypothesis suggests that procaine amide prolongs conduction in the depressed portion of a re-entrant pathway such that conduction is further delayed and block finally occurs, thereby terminating the arrhythmia.
- Plasma procaine amide concentration
- Antiarrhythmic drugs
- Two compartment drug model
- Computer analysis of arrhythmias
- Received February 23, 1973.
- Accepted July 13, 1973.
- © 1973 American Heart Association, Inc.