BRADYCARDIA IN THE FETAL BABOON FOLLOWING PARACERVICAL-BLOCK ANESTHESIA

To define the causal relationship between the use of local anesthetics and fetal bradycardia, paracervical block anesthesia (PCB) with lidocaine or 2-chloroprocaine was induced on 52 occasions to 27 pregnant baboons. The dosages were comparable to those used clinically on the basis of maternal body weight. On 40 occasions PCB was induced with nonasphyxiated (normal) fetuses, 33% of which developed fetal bradycardia after PCB. Of these episodes of fetal bradycardia, 50% were accompanied by a decrease in PaO2 [arterial partial pressure of O2]. The other 12 fetuses had pHa < 7.25, and SaO2 [arterial O2 saturation] < 25%, and all exhibited bradycardia with further decreases in pHa and PaO2. A transient increase in uterine activity with a significant reduction in uterine blood flow occurred in 73% of the mothers after PCB. Peak concentrations of lidocaine of 2.3 .+-. 0.2 (SE) .mu.g/ml in the maternal blood and 0.8 .+-. 0.2 .mu.g/ml in the fetal blood were found at 8 min after PCB. These levels were far below those associated with myocardial toxicity. Apparently, fetal bradycardia subsequent to PCB is, in part, caused by a decrease in the O2 available to the fetus secondary to an increase in uterine activity and a reduction in uteroplacental perfusion. This manifestation may occur at drug concentrations in the mother and fetus that are far below toxic levels.