The peripheral chemoreflex: indefatigable guardian of fetal physiological adaptation to labour

The fetus is consistently exposed to repeated periods of impaired oxygen (hypoxaemia) and nutrient supply in labour. This is balanced by the healthy fetus's remarkable anaerobic tolerance and impressive ability to mount protective adaptations to hypoxaemia. The most important mediator of fetal adaptations to brief repeated hypoxaemia is the peripheral chemoreflex, a rapid reflex response to acute falls in arterial oxygen tension. The overwhelming majority of fetuses are able to respond to repeated uterine contractions without developing hypotension or hypoxic–ischaemic injury. In contrast, fetuses who are either exposed to severe hypoxaemia, for example during uterine hyperstimulation, or enter labour with reduced anaerobic reserve (e.g. as shown by severe fetal growth restriction) are at increased risk of developing intermittent hypotension and cerebral hypoperfusion. It is remarkable to note that when fetuses develop hypotension during such repeated severe hypoxaemia, it is not mediated by impaired reflex adaptation, but by failure to maintain combined ventricular output, likely due to a combination of exhaustion of myocardial glycogen and evolving myocardial injury. The chemoreflex is suppressed by relatively long periods of severe hypoxaemia of 1.5–2 min, longer than the typical contraction. Even in this setting, the peripheral chemoreflex is consistently reactivated between contractions. These findings demonstrate that the peripheral chemoreflex is an indefatigable guardian of fetal adaptation to labour. The slippery slope during labour. Labour is naturally associated with repeated periods of impaired gaseous exchange and therefore intermittent hypoxaemia. The fetus responds by protective activation of the peripheral chemoreflex to firstly reduce heart rate (intrapartum decelerations) in order to reduce myocardial oxygen usage and secondly to promote peripheral vasoconstriction to centralise blood flow to the heart, brain and adrenal glands. The healthy fetus is therefore at low risk of developing hypotension thanks to these robust defences. This tolerance is nonetheless finite, and brief, repeated but severe hypoxaemia ultimately depletes fetal anaerobic reserves (primarily related to myocardial glycogen levels), resulting in progressive loss of myocardial contractility. Despite continued peripheral chemoreflex activation and effective peripheral vasoconstriction, reduced combined ventricular output results in evolving hypotension. Hypotension and s