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1 Physiology, University of Auckland, Auckland, New Zealand
2 Physiology, University of Auckland, Auckland, New Zealand; Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand; Paediatrics, University of Auckland, Auckland, New Zealand
3 Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand
4 Liggins Institute, Faculty of Medicine and Health Science, University of Auckland, Auckland, New Zealand
5 Physiology, University of Auckland, Auckland, New Zealand; Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: l.bennet{at}auckland.ac.nz.
This study was undertaken to determine the mechanisms mediating changes in fetal heart rate variability (FHRV) during and after exposure to asphyxia in the premature fetus. Preterm fetal sheep at 0.6 gestation (91±1 days, term is 147 days) were exposed to either sham occlusion (n=10) or to complete umbilical cord occlusion for either 20 (n=7) or 30 minutes (n=10). Cord occlusion led to a transient increase in FHRV with abrupt body movements which resolved after 5 min. In the 30 min group there was a marked increase in FHRV in the final 10 min of occlusion, related to abnormal atrial activity. After reperfusion FHRV in both study groups was initially suppressed and progressively increased to baseline levels over the first four hours of recovery. In the 20 min group this improvement was associated with return of normal EEG activity and movements. In contrast, in the 30 min group the EEG was abnormal with epileptiform activity superimposed on a suppressed background which was associated with abnormal fetal movements. As the epileptiform activity resolved FHRV fell and became suppressed for the remainder of the study. Histological assessment after 72 h demonstrated severe brainstem injury in the 30 min group, but not in the 20 min group. In conclusion, during early recovery from asphyxia epileptiform activity and associated abnormal fetal movements related to evolving neural injury can cause a confounding transient increase in FHRV, which mimics the normal pattern of recovery. However, chronic suppression of FHRV was a strong predictor of severe brainstem injury.
This article has been cited by other articles:
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