Implementation of physiological interpretation of fetal heart rate changes: from scientific principles to frontline practice

Onset of uterine contractions which become progressively more frequent, intense and last for longer durations as the labor progresses is expected to cause a gradually evolving hypoxic stress to human fetuses. This is because of the repeated constriction of maternal spiral arterioles supplying the placental bed and compression of the umbilical cord as the labor advances. The majority of fetuses are able to mount physiological compensatory responses to protect their high priority central organs by maintaining aerobic metabolism. However, fetuses who are exposed to preexisting compromise such as chronic utero-placental insufficiency, chorioamnionitis or chronic fetal anemia and acidosis may not have sufficient reserves to withstand further hypoxic stress, leading to rapid decompensation and neurological injury or death. Physiological interpretation of fetal heart rate changes involves recognition of specific features of both hypoxic and non-hypoxic stresses on the cardiotocograph (CTG) and determining the fetal compensatory responses to ongoing stress. This approach which is based on the cardinal principle of individualization of care will enable frontline clinicians to differentiate features of compensation from decompensation. Timely interventions to improve intrauterine environment and/or to accomplish urgent birth will help avoid hypoxic ischemic encephalopathy (HIE) and its long term sequalae (cerebral palsy or learning difficulties) and perinatal deaths. Conversely, continuation of labor with careful observation in fetuses with compensated gradually evolving hypoxic stress will help avoid unnecessary intrapartum operative interventions. Emerging evidence suggests reduction in the rates of both HIE and emergency cesarean sections following the implementation of principles of physiological interpretation of CTG.