Abstract:
The physiology regulating fetal heart rate (FHR) patterns has always had a central role in the interpretation of intrapartum FHR patterns. In particular, the understanding of what regulates FHR decelerations and the concept that both hypoxic and non-hypoxic (and therefore benign) decelerations exist is central to the design of current classification systems. In this talk, I will firstly examine the recent experimental work utilising chronically instrumented fetal sheep from our lab that challenges whether the widely accepted non-hypoxic mechanisms (including the baroreflex secondary to umbilical cord occlusion) are physiologically capable of producing intrapartum decelerations. We instead propose that the vast majority of decelerations are mediated by a common mechanism, the peripheral chemoreflex secondary to brief fetal hypoxaemia during contractions with a secondary contribution from myocardial hypoxia in the setting of fetal compromise. I will additionally share our preliminary data which sheds light on the autonomic and behavioural regulators of fetal heart rate variability during labour, which may lead to novel biomarkers of fetal compromise. Secondly, I will briefly examine our recent work into preterm white matter injury after severe hypoxia. We have recently illustrated that chronic neuroinflammation is a critical pathological factor contributing to both diffuse and cystic patterns of white matter injury. This provides hope that even delayed anti-inflammatory treatments may improve neurodevelopmental outcomes in preterm infants.

Bio:
Christopher Lear is a developing clinician-scientist, working as a Senior Research Fellow at the Fetal Physiology and Neuroscience Group, University of Auckland, and as a Trainee Intern at Auckland City Hospital, New Zealand. His research interests include understanding how the fetus adapts to labour, how this is reflected in intrapartum fetal heart rate recordings and how this knowledge could be better used to find new biomarkers for fetal compromise. He additionally researches the neurobiology of hypoxic-ischaemic brain injury and aims to identify new neuroprotective and neuroreparative agents.