Fetal heart rate (FHR) monitoring is now an established mode of fetal evaluation during labor, particularly in the mother whose fetus is at increased risk for asphyxial morbidity. Beat-to-beat FHR variability is becoming widely accepted as a most important prognostic indicator of a normoxic fetus. There is now evidence that a system of FHR interpretation which includes FHR varibility as well as FHR decelertions is less likely to falsely diagnose fetal compromise. Very little is known of the origin of the FHR variability, or the reason for its absence during severe fetal asphyxia. It is our hypothesis, supported by various clinical and physiological observations, that FHR variability depends on normal cerebral oxygen consumption. During fetal asphyxia, several fetal compensatory mechanisms come into play to ensure the maintenance of cerebral oxygen consumption. These include an increase in cerebral and myocardial blood flow to match their decreased arterio-venous oxygen difference, and shunting of blood flow away from non-vital organs. When these compensatory mechanisms fail, at severe degrees of asphyxia, cerebral and myocardial blood flows decrease, and we believe that FHR variability is lost. We plan to examine the relationship between FHR variability and cerebral oxygen consumption in sheep. Cerebral oxygen consumption will be measured by an application of the Fick principle, using radioactive microspheres to measure the blood flow under conditions of progressive asphyxia induced by uterine artery occlusion. FHR variability will be quantitated by indices already developed which can be calculated by computer processing of the fetal ECG. We believe that the resolution of the question of the physiologic significance of FHR variability is an important one for clinical obstetrics and will contribute to a more rational interpretation of FHR patterns, and improve the specificity of such interpretations.
