Cardiotocograph (CTG) was introduced into clinical practice to promptly recognize the features of intrapartum fetal hypoxic stress, so that timely action could be taken to avoid hypoxic-ischaemic encephalopathy (HIE) and perinatal deaths. However, the current systematic evidence suggests that the introduction of CTG into clinical practice over 50 years has not resulted in improvement in the rates of cerebral palsy or perinatal deaths. This is because most fetuses are able to withstand intrapartum hypoxic stresses without sustaining damage, and if the features of fetal compensatory responses are erroneously considered as “pathological”, “Abnormal” or “Category III” CTG tracing, it would lead to an exponential increase in unnecessary operative interventions without any improvement in perinatal outcomes. Neonatal acidosis at birth, determined by the estimation of pH in the umbilical artery has been considered as a surrogate marker of poor perinatal outcome. This is because significant intrapartum fetal hypoxic stress which leads to fetal decompensation, would lead to the onset of anaerobic metabolism and production of lactic acid in fetal tissues and organs. Entry of lactic acid into the fetal systemic circulation may cause damage to fetal central organs resulting in organ damage and death, and this lactate may lower the pH in the umbilical artery. Understanding the different types of fetal hypoxia on the CTG trace may help practicing clinicians to predict the rate of fall in fetal pH, and therefore, predict the umbilical cord pH at birth. It is important to appreciate that non-hypoxic pathways of fetal compromise such as chorioamnionitis may not be associated with low umbilical arterial pH at birth. Fetal pathophysiological approach to CTG interpretation based on deeper understanding of types of intrapartum hypoxia and features of non-hypoxic pathways of injury may help avoid the onset of neonatal metabolic acidosis and improve perinatal outcomes.
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