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Our purpose was to evaluate the clinical validity of electronic fetal heart rate monitoring to detect fetal acidemia and to evaluate the prevalence of cerebral palsy in unselected low-risk pregnancies.We selected two secondary and two tertiary level institutions in which 10,030 infants were born. Among them, 5546 of the pregnancies were low-risk pregnancies by antepartum evaluation. The fetal heart rate patterns were interpreted according to the guidelines of the National Institute of Child Health and Human Development. The correlations between the fetal heart rate pattern and umbilical blood gases and the fetal heart rate pattern and cerebral palsy were studied. Spastic cerebral palsy was diagnosed ator =1 year by pediatric neurologists. Statistics included unpaired t test, contingency table with chi(2) and Fisher tests, and one-way analysis of variance with Bonferroni/Dunn test.On the basis of the severity of decelerations, frequency of decelerations, and decreased variability, umbilical pH, and Po(2) level were decreased accordingly, and incidence of pH7.1 was increased. Sensitivity and false-positive rate of nonreassuring fetal heart rate patterns for fetal acidemia were 63% and 89%. There were nine cerebral palsy cases: six of the cases were preexisting asphyxia before monitoring was initiated, two of the cases were cytomegaloviral infections, and one of the cases was a maternal amniotic fluid embolism.In low-risk pregnancies, intrapartum fetal heart rate monitoring was useful to detect fetal acidemia. Cerebral palsy caused by intrapartum asphyxia was restricted to unavoidable accidents under continuous fetal heart rate monitoring.

Objective: We sought to determine the effects of long-term hypoxemia on fetal cardiac output and flow distribution. Study Design: We exposed six pregnant sheep to high altitude (3820 m) hypoxia from 30 to 135 days' gestation (term 146 days). Ten to 14 days after surgery we determined fetal cardiac output and organ blood flows by means of the radiolabeled microsphere technique during a baseline period and also during an additional 30-minute period of more severe added acute hypoxemia. Results: Baseline maternal arterial Po 2 was 60.7 ± 1.7 torr and fell to 35.1 ± 3.0 torr during the added acute hypoxemia. Fetal arterial Po 2 decreased from 18.5 ± 1.1 to 11.4 ± 1.5 torr during added acute hypoxemia. Baseline fetal cardiac output was 351 ± 55 ml/min/kg, which was significantly lower than previously reported values in low-altitude fetuses. Blood flow to critical organs such as the heart and brain was maintained at levels found in low-altitude fetuses, but flow to the carcass was significantly lower (−49%) than the mean value reported in the literature for low-altitude fetuses. Oxygen delivery was also maintained at normal levels to the brain and heart but was reduced in the kidneys (−31%), gastrointestinal tract (51%), and carcass (−58%). During added acute hypoxemia cardiac output did not change significantly; however, blood flow to the brain, heart, and adrenal glands increased 112%, 135%, and 156% ( p Conclusion: We conclude that during long-term hypoxemia redistribution of fetal cardiac output is maintained favoring the brain and heart.