Fetal heart rate variability changes during brief repeated umbilical cord occlusion in near term fetal sheep

• Published in: BJOG : an international journal of obstetrics and gynaecology Vol. 106; no. 7; pp. 664 - 671
• Main Authors: Westgate, Jenny A., Bennet, Laura, Gunn, Alistair J.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.07.1999
• Subjects: Acidosis - etiology; Animals; Blood Gas Analysis; Blood Pressure; Constriction; Female; Heart Rate, Fetal - physiology; Hydrogen-Ion Concentration; Pregnancy; Sheep; Umbilical Cord - blood supply
• ISSN: 1470-0328; 0306-5456; 1471-0528
• DOI: 10.1111/j.1471-0528.1999.tb08365.x

Objective To determine whether changes in fetal heart rate variation during repeated umbilical cord occlusions reflect evolving cardiovascular compromise in near term fetal sheep. Design 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. Sample Fourteen chronically instrumented fetal sheep, mean gestation 126.3 (2.6) days. Results 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. Conclusions 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.