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Palahniuk Richard J. MD; Doig, George A. MD; Johnson, Garry N. MD; Pash, Michael P. MD
Anesthesia & Analgesia: January 1980

Cerebrovascular autoregulation is lost during fetal asphyxia as cerebral vessels undergo compensatory vasodilation. In such a situation, maternal anesthetics, which decrease fetal arterial blood pressure and cardiac output, may further aggravate cerebral hypoxia. To examine this possibility, we prepared six pregnant ewes in such a manner as to be able to measure fetal regional cerebral blood flow in uteri during acidosis produced by partial umbilical cord compression both before and after 15 minutes of halothane anesthesia given to the mother.

Umbilical cord compression in the absence of anesthesia caused fetal metabolic and respiratory acidosis as evidenced by a decrease in arterial pH from 7.34 to 7.05; fetal arterial oxygen saturation simultaneously decreased from 29 to 17%. Halothane anesthesia administered to the mother of the acidotic fetus caused further aggravation of fetal acidosis (arterial pH 6.85) and oxygen desideration (10%) and the fetus became markedly hypotensive.

Blood flow to four cerebral areas increased 27 to 69% above control levels in the fetus during acidosis in the absence of maternal anesthesia but decreased to levels 30 to 42% below acidosis values when maternal anesthesia was combined with fetal acidosis. These data suggest that potent cardiovascular depressant anesthetics administered to the mother in the presence of fetal acidosis could decrease fetal cerebral oxygen delivery by interfering with fetal cardiovascular compensation during acidosis and reducing fetal cerebral blood flow.

Supported by grants from the Manitoba Medical Services Foundation and the Medical Research Council of Canada.

© 1980 International Anesthesia Research Society