Dissecting the contributions of the peripheral chemoreflex and myocardial hypoxia to fetal heart rate decelerations in near-term fetal sheep.

The brief, repeated fetal hypoxaemia during labour can trigger intrapartum decelerations of the fetal heart rate (FHR) via the peripheral chemoreflex or the direct effects of myocardial hypoxia, but the relative contribution of these two mechanisms and how this balance changes with evolving fetal compromise remain unknown. In the present study, chronically instrumented near-term fetal sheep received surgical vagotomy (n = 8) or sham-vagotomy (control, n = 11) to disable the peripheral chemoreflex and unmask myocardial hypoxia. 1min complete umbilical cord occlusions (UCOs) were performed every 2.5min for 4h or until arterial pressure fell <20mmHg. Hypotension and severe acidaemia progressively developed after 65.7±7.2 UCOs in controls and 49.5±7.8 UCOs after vagotomy. Vagotomy was associated with faster development of metabolic acidaemia and faster impairment of arterial pressure during UCOs without impairing centralisation of blood flow or neurophysiological adaptation to UCOs. During the first half of the UCO series, before severe hypotension developed, vagotomy was associated with a marked increase in FHR during UCOs. After the onset of evolving severe hypotension, FHR fell faster in control fetuses during the first 20s of UCOs but FHR during the final 40s of UCOs progressively became similar between groups with no difference in the nadir of decelerations. In conclusion, FHR decelerations were initiated and sustained by the peripheral chemoreflex, at a time when fetuses were able to maintain arterial pressure. After the onset of evolving hypotension and acidaemia, the peripheral chemoreflex continued to initiate decelerations but myocardial hypoxia progressively became more important in sustaining and deepening decelerations. KEY POINTS: Brief repeated hypoxaemia during labour can trigger fetal heart rate decelerations by either the peripheral chemoreflex or myocardial hypoxia, but how this balance changes with fetal compromise is unknown. Reflex control of fetal heart rate was disabled by vagotomy to unmask the effects of myocardial hypoxia in chronically instrumented fetal sheep. Fetuses were then subjected to repeated brief hypoxaemia consistent with the rates of uterine contractions during labour. We show that the peripheral chemoreflex controls brief decelerations in their entirety at a time when fetuses were able to maintain normal or increased arterial pressure. The peripheral chemoreflex still initiated decelerations even after the onset of evolving hypotension and acidaemia, but myocardial hypoxia made an increasing contribution to sustain and deepen decelerations. Abstract figure legend We tested the relative contributions of the peripheral chemoreflex and myocardial hypoxia to intrapartum fetal heart rate decelerations by performing surgical vagotomy in fetal sheep to disable the peripheral chemoreflex and unmask myocardial hypoxia. These studies showed that the peripheral chemoreflex initiated and sustained decelerations in healthy fetuses. By contrast, after fetuses developed evolving cardiovascular compromise and were at risk of permanent brain injury, the peripheral chemoreflex initiated decelerations but myocardial hypoxia made an increasing contribution to sustain and deepen decelerations. This article is protected by copyright. All rights reserved.