Abstract

Halothane has become the preferred anesthetic agent during fetal surgery because it can be administered via maternal inhalation and it improves surgical exposure by relaxing the uterus. However, the effects of halothane anesthesia on fetal cardiovascular homeostasis during fetal surgery have not been documented. In 10 pregnant ewes, inhalation halothane anesthesia was administered and their fetuses were instrumented for cardiovascular evaluation. During a 1-hour period we evaluated the acute effects of halothane anesthesia on fetal hemodynamics, arterial blood gases, cardiac output, placental blood flow, total vascular resistance, systemic vascular resistance, and placental vascular resistance. Fetal cardiac output and placental blood flow were determined by the radiolabelled microsphere technique and resistances were calculated using pressure and flow data. These findings were compared to both the results we obtained in 15 fetal sheep anesthetized with the maternal administration of intravenous ketamine, and to the accepted values found in nonanesthetized, chronically instrumented fetal sheep. Our findings indicate that with halothane anesthesia during fetal surgery fetal cardiac output and placental blood flow significantly decrease, and total vascular resistance increases. Placental vascular resistance increases out of proportion to systemic vascular resistance, resulting in the shunting of blood away from the placenta. The combination of decreased cardiac output and increased shunting of blood away from the placenta causes depressed respiratory gas exchange. These findings are not present with other anesthetic agents. Halothane has significant negative effects on both the fetal heart and the peripheral vasculature which disrupt fetal cardiovascular homeostasis. Halothane is a poor anesthetic during fetal intervention.

View details for Web of Science ID A1993KY51400006

View details for PubMedID 8483067