The fetus receives its oxygen and nutrition through the umbilical cord (from the placenta) that floats in the amniotic fluid.  The placenta receives oxygen from the maternal blood. Uterine contractions of labour reduce or intermittently cut off the blood perfusion into the retroplacental area thus reducing the exchange of gases and essential nutrition to the fetus. Pregnancies known to be at high risk have continuous observation of the fetal heart rate (FHR) and uterine contractions i.e. cardiotocography (CTG) electronically (EFM). Electronic fetal monitoring by CTG is fraught with problems of high sensitivity but low specificity. Monitoring by CTG is by pattern recognition. This ends in unnecessary operative deliveries if interpreted without the understanding of the pathophysiology. At times the fetuses that are acidotic are missed. Fetal scalp blood sampling (FBS) increases the specificity and reduces un-necessary operative delivery rates. FBS is an intermittent measure and failure to get adequate samples is not uncommon. The value of FBS has been challenged.

The CTG at term should have a baseline rate between 110 to 160 bpm – however a rise in the baseline of a particular fetus of its own baseline within the normal range is of significance and may suggest hypoxia or infection. The presence of accelerations suggests a non acidotic fetus and is considered to reflect the integrity of the somatic nervous system. The baseline variability reflects the integrity of the autonomic nervous system (sympathetic and parasympathetic) and a normal baseline variability (BLV) of 5 to 25 beats reflect a small chance of acidosis. Reduction of BLV of < 5 bpm especially when associated with decelerations increases the chance of acidosis and the absence of variability with decelerations needs intervention in the form of changing position, hydration, stopping oxytocin, fetal scalp blood sampling or delivery of the fetus. The worsening pattern is reflected by the increase in baseline rate with catecholamine surge, absence of accelerations, increase in depth and duration of decelerations, reduction of time spent at the baseline rate and reduction and finally absent baseline variability (i.e. gradually developing hypoxia). With this progression and absent variability action should be to deliver the fetus unless spontaneous delivery is imminent or the situation of stress can be reduced or reversed. In the late first and second stage of labour at times the decelerations could last 90 to 120 seconds with the FHR being at the baseline rate for <60 seconds and mostly with salutatory variability (>25 bpm) reflecting hypoxia and over reaction by the autonomic nervous system. Intervention within 30 to 40 minutes is recommended to prevent sub-acute hypoxia leading to acidosis. A prolonged deceleration of <80 bpm is likely to lead to acidosis at a rate of 0.01 every minute and delivery within 15 minutes should help to avoid asphyxia. Some foetuses may be already partially compromised and present with absent or minimal baseline variability and shallow decelerations. They usually present a clinical history of meconium, infection, bleeding or absent fetal movements. These foetuses are best delivered early to avoid increasing hypoxia.