H H de Haan1, A J Gunn, P D Gluckman. 1. Research Centre for Developmental Medicine and Biology, School of Medicine, University of Auckland, New Zealand.
Abstract
OBJECTIVE: Brief repetitive total umbilical cord occlusions were used to induce fetal asphyxia and to evaluate the interrelationships with hypotension and fetal heart rate decelerations. STUDY DESIGN: In 21 chronically instrumented fetal lambs (gestational age 126.8 +/- 0.6 days), repetitive total umbilical cord occlusion was performed 1 out of 2.5 minutes (n = 7), 2 out of 5 minutes (n = 9), or not at all (shams, n = 5). Occlusions proceeded until fetal blood pressure was < 20 mm Hg or failed to recover to baseline before the next occlusion. RESULTS: At the nadir of asphyxia pH (mean +/- SEM) was 6.84 +/- 0.02, base excess 23.1 +/- 1.0 mmol/L, and lactate 14.2 +/- 0.4 mmol/L. Two fetuses died. The pattern of fetal heart rate decelerations remained relatively consistent throughout the experiments. In contrast, after an initial phase of sustained hypertension a progressive fall in trough blood pressure occurred after approximately 15 minutes of occlusion. The blood pressure recovery time in almost all fetuses lengthened abruptly near the end of the occlusion series, at a variable metabolic threshold. This was accompanied by a significant delay in fetal heart rate recovery in only five fetuses. CONCLUSIONS: Fetal compromise presented with the development of hypotension, without change in the pattern of fetal heart rate response. These data illustrate the limited diagnostic value of fetal heart rate monitoring to identify the development of cardiovascular compromise associated with severe decelerations in the previously healthy fetus.
OBJECTIVE: Brief repetitive total umbilical cord occlusions were used to induce fetal asphyxia and to evaluate the interrelationships with hypotension and fetal heart rate decelerations. STUDY DESIGN: In 21 chronically instrumented fetal lambs (gestational age 126.8 +/- 0.6 days), repetitive total umbilical cord occlusion was performed 1 out of 2.5 minutes (n = 7), 2 out of 5 minutes (n = 9), or not at all (shams, n = 5). Occlusions proceeded until fetal blood pressure was < 20 mm Hg or failed to recover to baseline before the next occlusion. RESULTS: At the nadir of asphyxia pH (mean +/- SEM) was 6.84 +/- 0.02, base excess 23.1 +/- 1.0 mmol/L, and lactate 14.2 +/- 0.4 mmol/L. Two fetuses died. The pattern of fetal heart rate decelerations remained relatively consistent throughout the experiments. In contrast, after an initial phase of sustained hypertension a progressive fall in trough blood pressure occurred after approximately 15 minutes of occlusion. The blood pressure recovery time in almost all fetuses lengthened abruptly near the end of the occlusion series, at a variable metabolic threshold. This was accompanied by a significant delay in fetal heart rate recovery in only five fetuses. CONCLUSIONS: Fetal compromise presented with the development of hypotension, without change in the pattern of fetal heart rate response. These data illustrate the limited diagnostic value of fetal heart rate monitoring to identify the development of cardiovascular compromise associated with severe decelerations in the previously healthy fetus.
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