In vivo electrophysiological effects of lidocaine in canine acute myocardial infarction.

Lidocaine was administered as a rapid intravenous bolus injection followed by a constant-rate intravenous infusion to nine dogs with 2-hour-old myocardial infarctions. Bipolar electrograms were recorded from and effective refractory periods were determined in the infarcted and normal zones of the heart. Intervals (Q-EG) were measured from the onset of the QRS complex in a standard electrocardiogram limb lead to the major deflection of the recorded electrograms from the normal and infarcted zones. QRS duration and serum lidocaine concentration were also determined. At serum concentrations considered to be therapeutic, lidocaine prolonged the Q-EG intervals in the infarcted zones of the heart 17-26% at peak effect (P less than 0.01), but it had no effect on the Q-EG intervals in the normal zone except for a slight (1.5%) prolongation shortly after the initial intravenous bolus injection. Lidocaine also had no effect on QRS duration. Similarly, lidocaine prolonged the effective refractory period of the infarcted zone 23% (P less than 0.01) at peak effect but had no effect on the effective refractory period of the normal zone. Prior to lidocaine administration, the mean effective refractory period of the normal zone was 26 msec longer than that of the infarcted zone, but at peak drug effect the disparity in refractoriness was reduced to 1 msec. The present study thus shows that lidocaine has different effects in infarcted and normal zones of the heart. In delaying activation and prolonging the effective refractory period of the infarcted zone of the heart, lidocaine has local anesthetic actions which might explain its effectiveness in curtailing ventricular arrhythmias after acute myocardial infarction.