CENTRAL AND PERIPHERAL HEMODYNAMIC-CHANGES IN FETUSES WITH ABSENT END-DIASTOLIC VELOCITY IN UMBILICAL ARTERY - CORRELATION WITH COMPUTERIZED FETAL HEART-RATE PATTERN

OBJECTIVES: Our purpose was to study hemodynamic changes in peripheral and central blood vessels and to correlate these changes with the com puterized fetal heart rate pattern in fetuses with absent end-diastoli c velocity in the umbilical artery. STUDY DESIGN: Doppler studies of t he umbilical artery, the middle cerebral artery, and aortic and pulmon ic outflow, together with computerized fetal heart rate monitoring, we re performed every 2 to 4 days until delivery in 13 fetuses with absen t end-diastolic velocity in the umbilical artery. The pulsatility inde x was calculated from the flow velocity waveforms obtained from the um bilical and middle cerebral arteries. The velocity time integral (an i ndex of cardiac output) and the heart rate were calculated from the fl ow velocity waveforms obtained from the aortic and pulmonic outflow. R ESULTS: Two fetuses were delivered immediately after the first examina tion because of repetitive fetal heart rate decelerations. One fetus w as excluded from the study because of major malformations. Ten had thr ee to eight tests each. Six had a biphasic change of the middle cerebr al artery, which consisted of a decrease (p < 0.001) followed by an in crease in the pulsatility index (p < 0.05). When the middle cerebral a rtery lost its vasodilation, there was an increase in the middle cereb ral artery/umbilical artery pulsatility index ratio (p < 0.05). Left c ardiac output decreased (p < 0.05), resulting in an increase in the pu lmonary/aortic velocity time integral x heart rate ratio (p < 0.05). R educed fetal heart rate variation (< 30 msec) developed in all six fet uses, and they were delivered because of repetitive fetal heart rate d ecelerations. Four fetuses with only a decrease in the middle cerebral artery pulsatility index did not have reduced fetal heart rate variat ion or decelerations, the aortic velocity time integral x heart rate d idn't decrease, and the pulmonic/aortic velocity time integral x heart rate ratio didn't increase. These fetuses were delivered for reasons other than fetal distress. The middle cerebral artery pulsatility inde x correlated with the aortic velocity time integral x heart rate (r = -0.53, p < 0.0001), and the middle cerebral artery/umbilical artery pu lsatility index correlated with the pulmonic/aortic velocity time inte gral x heart rate (r = 0.56, p < 0.0001). CONCLUSION: Abnormal fetal h eart rate patterns occur in fetuses with absent end-diastolic velocity in the umbilical artery when the middle cerebral artery begins to los e its compensatory maximal dilation. The increase in the middle cerebr al artery pulsatility index is associated with a significant reduction in left ventricular output without significant changes in right ventr icular function. Thus it appears that a loss of autonomic reactivity o ccurs in the brain first and is followed within a few days by a simila r response in the heart, as shown by the decreased fetal heart rate va riation.