Westgate J A, Bennet L, Gunn A J
Department of Obstetrics and Gynaecology, School of Medicine, University of Auckland, New Zealand.
Br J Obstet Gynaecol. 1999 Jul;106(7):664-71. doi: 10.1111/j.1471-0528.1999.tb08365.x.
To determine whether changes in fetal heart rate variation during repeated umbilical cord occlusions reflect evolving cardiovascular compromise in near term fetal sheep.
Fetal heart rate variation, fetal mean arterial pressure, electroencephalogram (EEG) and acid-base status were measured during one minute umbilical cord occlusions, repeated either every five minutes (1:5 group) or every 2.5 minutes (1:2.5 group) for four hours or until mean arterial pressure fell below 20 mmHg for two successive occlusions.
Fourteen chronically instrumented fetal sheep, mean gestation 126.3 (2.6) days.
Cord occlusion caused variable decelerations with initial sustained hypertension. In the 1:5 occlusion group mean arterial pressure remained elevated throughout, with little change in acid-base status (pH = 7.34 (0.07), base deficit = 1.3 (3.9) after 4 hours) and no significant change in fetal heart rate variation. In contrast, in the 1:2.5 group from the third occlusion there was progressive hypotension during occlusions, severe progressive metabolic acidaemia (pH 6.92 (0.1), base deficit 17.0 mmol/L (4.7) after the last occlusion) and marked EEG suppression (P < 0.01). Fetal heart rate variation increased with the onset of occlusions (P < 0.05) and then progressively fell with continued occlusions. During the last 30 minutes of occlusions, fetal heart rate variation was severely suppressed in four, but increased in two fetuses, while all six fetuses developed overshoot-instability of fetal heart rate and mean arterial pressure following each occlusion.
Acute progressive asphyxia was typically associated with an immediate, transient increase in fetal heart rate variation. Subsequently variation became suppressed in only two-thirds of fetuses during terminal acidaemia and hypotension. Fetal heart rate overshoot-instability may be a useful marker of fetal decompensation following variable decelerations.
确定在反复脐带闭塞期间胎儿心率变异性的变化是否反映近足月胎羊心血管功能逐渐受损。
在1分钟脐带闭塞期间测量胎儿心率变异性、胎儿平均动脉压、脑电图（EEG）和酸碱状态，每5分钟（1:5组）或每2.5分钟（1:2.5组）重复一次，持续4小时或直至平均动脉压连续两次闭塞低于20 mmHg。
14只长期植入仪器的胎羊，平均妊娠126.3（2.6）天。
脐带闭塞导致初始持续性高血压伴可变减速。在1:5闭塞组中，平均动脉压始终升高，酸碱状态变化不大（4小时后pH = 7.34（0.07），碱缺失 = 1.3（3.9）），胎儿心率变异性无显著变化。相比之下，在1:2.5组中，从第三次闭塞开始，闭塞期间出现进行性低血压、严重进行性代谢性酸血症（最后一次闭塞后pH 6.92（0.1），碱缺失17.0 mmol/L（4.7））和明显的脑电图抑制（P < 0.01）。胎儿心率变异性在闭塞开始时增加（P < 0.05），然后随着持续闭塞逐渐下降。在闭塞的最后30分钟内，4只胎儿的胎儿心率变异性严重受抑制，但2只胎儿增加，而所有6只胎儿在每次闭塞后均出现胎儿心率和平均动脉压的过冲-不稳定性。
急性进行性窒息通常与胎儿心率变异性立即、短暂增加有关。随后，在终末期酸血症和低血压期间，只有三分之二的胎儿变异性受到抑制。胎儿心率过冲-不稳定性可能是可变减速后胎儿失代偿的有用指标。
