The purpose of monitoring the fetus in labour is to try and identify those which might be at risk of hypoxic injury so that delivery can be expedited and potential problems prevented. This process of monitoring usually involves some form of fetal heart rate assessment, either with intermittent auscultation or by continuous electronic measurement (cardiotocography, CTG) and analysis of the fetal ECG waveform. Intermittent auscultation of the fetal heart is appropriate for monitoring fetal condition in low-risk labour, with electronic fetal monitoring being used either in high-risk labour or if concern is raised by intermittent auscultation in low-risk patients. The CTG is good at identifying the normal healthy fetus but there is a high false positive rate and many fetuses labelled as ‘distressed’ are actually not hypoxic. As a consequence, the rate of obstetric intervention may be increased in return for no neonatal benefit. Analysis of the ECG waveform in association with the CTG can improve its predictive ability for hypoxia.

Fetal oxygenation depends on a number of factors.

During a contraction, the intramural vessels supplying the placenta are constricted by the smooth muscle fibres of the uterus. Providing the contractions are not too long or too frequent, the placental blood supply has time to recover before the next contraction begins. In hyperstimulation, when the uterus is contracting too frequently, placental oxygenation may be impaired. In other circumstances, there may be placental hypoperfusion, for example following the distal sympathetic blockade and associated hypotension, which can occur with spinal or epidural anaesthesia.

A small, poorly-formed placenta is less capable of adequate oxygen transfer than a larger placenta. In this condition, the fetus may already be growth restricted prior to the onset of labour and therefore more susceptible to a hypoxic stress. In abruptio placentae, it is obvious that the resulting partial placental separation leaves a reduced surface area for vascular communication, and is therefore less efficient at oxygen exchange.

This is dependent on adequate fetal cardiac output. The fetus responds to hypoxic stress with peripheral vasoconstriction and redistribution of the blood to the heart and the brain. Prolonged vasoconstriction may lead to damage in other organs, particularly the gastrointestinal tract (necrotizing enterocolitis), the lungs (respiratory distress) and kidneys (acute renal failure).

Hypoxia also leads to anaerobic metabolism and acidosis. Acidosis is therefore a reflection of the degree of oxygenation, and this forms the basis of intrapartum fetal blood sampling.

Meconium (fetal stool) staining of the liquor is present in 15% of all deliveries at term and in about 40% at 42 weeks. The mechanism may be stimulation of the vagus (parasympathetic) nerves in utero causing the fetal gut to contract and the anal sphincter to relax. This often happens for no particular reason but it also may occur as a response to fetal hypoxia. While often not of clinical significance, the presence of meconium staining increases the likelihood that there is underlying fetal compromise. A normal cardiotocograph (CTG) provides reassurance, but an abnormal CTG becomes more significant in the presence of meconium and should lower the threshold for investigation or intervention.

As well as being a sign of fetal distress, meconium is found below the vocal cords postnatally in about one-third of cases in which it is present, and may give rise to the meconium aspiration syndrome. This is a form of neonatal pneumonitis. Clinical features range from mild neonatal tachypnoea to severe respiratory compromise. The incidence is probably unrelated to fetal hypoxia (and indeed the majority of babies with meconium aspiration syndrome are not acidotic at delivery) but the syndrome is more likely to be severe if there is associated hypoxia/acidosis. It is also more severe when the meconium is thick. There is no evidence to support early delivery in the absence of fetal distress, as it is likely that the aspiration occurs in utero rather than at delivery itself.

Meconium can be graded as follows:

Grade 1: good volume of liquor stained lightly with meconium

Grade 2: reasonable volume of liquor with heavy suspension of meconium

Grade 3: thick undiluted meconium of ‘pea-soup’ consistency.

The higher the grade, the more likely it is to be associated with metabolic acidosis and the meconium aspiration syndrome. It is appropriate to consider continuous electronic fetal heart rate recording if meconium is found to be present.

Assessment of the fetal heart rate can be used to provide some information about fetal well-being. In ‘low-risk’ labours, it is recommended to auscultate the fetal heart every 15 min before and after a contraction during the first stage of labour, and every 5 min between contractions in the second stage of labour. A baseline tachycardia or bradycardia, and the presence of decelerations are indications for further evaluation with continuous CTG monitoring. The heart can be auscultated using either a manual Pinard stethoscope or an electronic Doppler detector.

A cardiotocograph (CTG) provides a continuous printed record of the fetal heart rate and uterine contractions. The contractions are registered by a pressure monitor supported on the mother’s abdomen by an elastic belt, and the fetal heart rate is measured using either:

 an abdominal ultrasonic transmitter–receiver Doppler probe, which detects fetal cardiac movements and hence the heart rate, or

 a clip, known as a fetal scalp electrode (FSE), which is attached to the baby’s scalp and detects the R–R wave of the fetal ECG. It is usually used if the external abdominal monitoring is unsatisfactory.