Fetal heart rate monitoring in labor: from pattern recognition to fetal physiology.

Abstract

The journey of human labour involves hypoxic and mechanical stresses as a result of progressively increasing frequency, duration and strength of uterine contractions and resultant compression of umbilical cord. In addition, occlusion of the spiral arteries during myometrial contractions also leads to repetitive interruptions in the utero-placental circulation, predisposing a fetus to progressively worsening hypoxic stress as the labour progresses. The vast majority of fetuses are equipped with compensatory mechanisms to withstand these hypoxic and mechanical stresses. They emerge unharmed at birth. However, some fetuses may sustain an antenatal injury or experience a chronic utero-placental insufficiency prior to the onset of labour. These may impair the fetus to compensate for the ongoing hypoxic stress secondary to ongoing uterine contractions. Non-hypoxic pathways of neurological damage such as chorioamnionitis, fetal anaemia or an acute fetal hypovolemia may potentiate fetal neurological injury, especially if in the presence of a superimposed, additional hypoxic stress. The use of utero-tonic agents to induce or augment labour may increase the risk of hypoxic-ischaemic injury. Clinicians need to move away from "pattern recognition" guidelines ("Normal", "Suspicious", "Pathological"), and apply the knowledge of fetal physiology to differentiate fetal compensation from decompensation. Individualization of care is essential to optimize outcomes.