Intrapartum electronic fetal monitoring (EFM) is widely used throughout the developed and developing world. This practice is based on the understanding that fetal heart rate (FHR) is sensitive to hypoxia. During labour, the fetus may be exposed to acute hypoxia during uterine contractions or intrapartum insults, and has well‐established cardiovascular compensatory defence mechanisms, which ideally prevent hypoxic–ischaemic encephalopathy by maintaining perfusion pressure and substrate delivery to essential organs (Giussani et al. 1993). Failure of these compensatory mechanisms results in a progressively worsening metabolic acidosis. Development of severe acidaemia (pH < 7.05) is a key turning point after which fetuses are unable to maintain fetal cardiovascular defence mechanisms and cerebral perfusion, rendering them at risk of asphyxial brain injury (Gunn & Bennet, 2009). Therefore, intrapartum EFM aims to identify, via changes in FHR patterns, fetuses unable to initiate or maintain such compensatory adaptations in response to hypoxia, which become acidotic, and deliver them before they are at risk of asphyxia, severe acidosis, cardiovascular collapse, end organ damage or death.