Weiner Z, Farmakides G, Schulman H, Penny B
Department of Obstetrics and Gynecology, Winthrop-University Hospital, Mineola, NY 11501.
Am J Obstet Gynecol. 1994 Feb;170(2):509-15. doi: 10.1016/s0002-9378(94)70219-5.
Our purpose was to study hemodynamic changes in peripheral and central blood vessels and to correlate these changes with the computerized fetal heart rate pattern in fetuses with absent end-diastolic velocity in the umbilical artery.
Doppler studies of the umbilical artery, the middle cerebral artery, and aortic and pulmonic outflow, together with computerized fetal heart rate monitoring, were performed every 2 to 4 days until delivery in 13 fetuses with absent end-diastolic velocity in the umbilical artery. The pulsatility index was calculated from the flow velocity waveforms obtained from the umbilical and middle cerebral arteries. The velocity time integral (an index of cardiac output) and the heart rate were calculated from the flow velocity waveforms obtained from the aortic and pulmonic outflow.
Two fetuses were delivered immediately after the first examination because of repetitive fetal heart rate decelerations. One fetus was excluded from the study because of major malformations. Ten had three to eight tests each. Six had a biphasic change of the middle cerebral artery, which consisted of a decrease (p < 0.001) followed by an increase in the pulsatility index (p < 0.05). When the middle cerebral artery lost its vasodilation, there was an increase in the middle cerebral artery/umbilical artery pulsatility index ratio (p < 0.05). Left cardiac output decreased (p < 0.05), resulting in an increase in the pulmonary/aortic velocity time integral x heart rate ratio (p < 0.05). Reduced fetal heart rate variation (< 30 msec) developed in all six fetuses, and they were delivered because of repetitive fetal heart rate decelerations. Four fetuses with only a decrease in the middle cerebral artery pulsatility index did not have reduced fetal heart rate variation or decelerations, the aortic velocity time integral x heart rate didn'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 index correlated with the aortic velocity time integral x heart rate (r = -0.53, p < 0.0001), and the middle cerebral artery/umbilical artery pulsatility index correlated with the pulmonic/aortic velocity time integral x heart rate (r = 0.56, p < 0.0001).
Abnormal fetal heart rate patterns occur in fetuses with absent end-diastolic velocity in the umbilical artery when the middle cerebral artery begins to lose its compensatory maximal dilation. The increase in the middle cerebral artery pulsatility index is associated with a significant reduction in left ventricular output without significant changes in right ventricular function. Thus it appears that a loss of autonomic reactivity occurs in the brain first and is followed within a few days by a similar response in the heart, as shown by the decreased fetal heart rate variation.
我们的目的是研究外周和中心血管的血流动力学变化，并将这些变化与脐动脉舒张末期血流速度消失的胎儿的计算机化胎心率模式相关联。
对13例脐动脉舒张末期血流速度消失的胎儿，每2至4天进行一次脐动脉、大脑中动脉、主动脉和肺动脉流出道的多普勒研究，同时进行计算机化胎心率监测，直至分娩。从脐动脉和大脑中动脉获得的血流速度波形计算搏动指数。从主动脉和肺动脉流出道获得的血流速度波形计算速度时间积分（心输出量指标）和心率。
2例胎儿在首次检查后因反复出现胎心率减速而立即分娩。1例胎儿因严重畸形被排除在研究之外。10例胎儿各进行了3至8次检查。6例大脑中动脉出现双相变化，即搏动指数先降低（p<0.001），随后升高（p<0.05）。当大脑中动脉失去血管舒张时，大脑中动脉/脐动脉搏动指数比值增加（p<0.05）。左心输出量降低（p<0.05），导致肺/主动脉速度时间积分×心率比值增加（p<0.05）。所有6例胎儿均出现胎心率变异减少（<30毫秒），并因反复出现胎心率减速而分娩。4例仅大脑中动脉搏动指数降低的胎儿未出现胎心率变异减少或减速，主动脉速度时间积分×心率未降低，肺/主动脉速度时间积分×心率比值未增加。这些胎儿因胎儿窘迫以外的原因分娩。大脑中动脉搏动指数与主动脉速度时间积分×心率相关（r=-0.53，p<0.0001），大脑中动脉/脐动脉搏动指数与肺/主动脉速度时间积分×心率相关（r=0.56，p<0.0001）。
当大脑中动脉开始失去代偿性最大舒张时，脐动脉舒张末期血流速度消失的胎儿会出现异常胎心率模式。大脑中动脉搏动指数的增加与左心室输出量显著降低相关，而右心室功能无显著变化。因此，似乎首先在大脑中出现自主反应性丧失，随后几天内心脏也出现类似反应，表现为胎心率变异减少。
