Baker B W, Hughes S C, Shnider S M, Field D R, Rosen M A
Department of Anesthesia, University of California, San Francisco.
Anesthesiology. 1990 Jan;72(1):65-70. doi: 10.1097/00000542-199001000-00013.
The effects of maternal isoflurane-oxygen anesthesia (isoflurane, 1% inspired) were measured in eight pregnant ewes and their asphyxiated singleton fetuses. Stable fetal asphyxia, indicated by a stable fetal arterial pH of 7.1-7.2 units, was produced by maternal uterine artery occlusion. Maternal and fetal heart rates and blood pressures; maternal uterine artery flow; maternal arterial, fetal arterial, and sagittal sinus pH; and blood gas tensions were determined during an awake control period, during fetal asphyxia alone, and during fetal asphyxia plus isoflurane-oxygen. Measurements of representative fetal whole organ blood flows, cardiac output, and cerebral oxygen consumption were also made during each of the three experimental periods. During asphyxia alone regional and total brain, heart, and adrenal flows increased above control while flow to the spleen and carcass decreased. Similar responses were seen during asphyxia plus isoflurane-oxygen. Fetal arterial and sagittal sinus pH, base excess, po2, and oxygen saturation decreased, and hydrogen ion concentrations and pco2 increased during asphyxia alone and asphyxia plus isoflurane-oxygen. Cerebral oxygen consumption decreased significantly from control during asphyxia plus isoflurane-oxygen, whereas no significant changes occurred in cerebral oxygen delivery. These results support the conclusions that in the asphyxiated fetus: 1) acidosis is increased; 2) cardiac output is redistributed to vital organs; and 3) the balance of cerebral oxygen supply-to-demand is maintained during maternal isoflurane-oxygen anesthesia.
