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Effects of lidocaine on blood pressure, heart rate, electrocortical activity, pH, and blood gases were studied in chronically catheterized sheep fetuses in utero. Lidocaine infused at a constant rate of less than I mg. · min. −1 · Kg. −1 into a fetal femoral vein did not cause changes in fetal blood pressure, heart rate, pH, or blood gases. Infusion rates above 1 mg. · min. −1 · Kg. −1 caused sudden, phasic increases in blood pressure in the majority of the fetuses. The heart rate increased in association with each phasic increase in blood pressure. In some fetuses the heart rate decelerated after the initial acceleration. Fetal electrocortical recordings showed that each phasic change in blood pressure and heart rate was secondary to epileptiform activity. The concentration of lidocaine in fetal arterial blood was 11.6 ± 3.8 μg per milliliter when the first phasic increase in blood pressure occurred. Tracheal pressure recordings showed deep fetal breathing movements with each epileptiform activity. It is concluded that lidocaine causes convulsions in the fetal sheep and that the cardiovascular changes are due to central stimulation during these convulsions. In newborn lambs lidocaine produced similar epileptiform activity associated with tonic-clonic convulsions and cardiovascular changes. Fetal arterial pH was not affected until the phasic changes occurred, after which the pH fell rapidly in the majority of the fetuses. In three paralyzed fetuses the pH also decreased at the onset of phasic increases in blood pressure. This indicated that muscular activtiy was not the main cause of the acidemia during fetal epileptiform activity. Bolus injections of lidocaine in doses of 3.0 to 22.2 mg. per kilogram of fetal weight caused an immediate decrease in blood pressure and heart rate. These changes were related to the dose of lidocaine. The convulsive dose of lidocaine as a bolus injection ranged from 8.0 to 22.2 mg. per kilogram.

In 16 patients with intraventricular conduction delay (IVCD) and cardiac arrhythmias, procaine amide (PA) was infused intravenously at rates of 30-40 mg/min until a maximum dose of 750-1,000 mg was administered. His bundle electrograms and plasma PA levels were obtained every 5 min during infusion and for 25 min thereafter. The mean peak PA level (10.2 ± 3.4 µg/ml) was achieved at the end of infusion. Mean control A-V nodal conduction times (A-H: 99.5 ± 34 msec) and A-H at peak PA levels (90 ± 15.3) did not differ significantly. However, the mean infranodal conduction time (H-Q) at peak PA (68.1 ± 14.8 msec) was significantly higher than control measurements (57.6 ± 13 msec) ( P < 0.001), with a mean percent increase of 18% (11 msec), and maximal prolongation of H-Q occurred at peak PA blood levels. There was no statistically significant correlation between maximum absolute or percent change in H-Q and control H-Q, control QRS duration, or peak PA levels. One patient with sinus bradycardia had further decreases in rate and a junctional rhythm after PA. Intravenous administration of PA appears safe and effective for patients with IVCD in terms of arrhythmia control and absence of high degree A-V block, ventricular ectopic beats, or standstill, but caution should be used in treating patients with sinus bradycardia.