Indications

For factors in high-risk pregnancies see Table 8.1.

Table 8.1 Factors involved in high-risk pregnancies

External monitoring

The FHR is derived from a Doppler ultrasound transducer that detects fetal heart movements and a pressure transducer that records the frequency and duration (but not strength) of uterine contractions. Both transducers are applied externally to the maternal abdominal wall.

Internal monitoring

The FHR is monitored via an electrode that is inserted transcervically to penetrate the fetal scalp and the frequency, duration and strength of uterine contractions are recorded via a fine intrauterine pressure catheter. Internal monitoring requires cervical dilatation and rupture of the membranes. Internal FHR monitoring provides a more accurate measurement of beat to beat and baseline variability than external monitoring.

A hybrid of internal measurement of fetal heart rate with external monitoring of contractions may be performed.

Physiological principles

The fetus requires an adequate supply of oxygen via the placenta and umbilical vein. Interruption of this blood supply may compromise a fetus without adequate reserve. Uterine contractions or cord compression may interrupt this blood supply. Fetal hypoxaemia may present itself as changes to the CTG tracing as discussed below.

Baseline FHR

The average FHR, excluding accelerations and decelerations, determined over a 5–10-minute period. Normal valves are 110–160 beats per minute (bpm).

Bradycardia

A baseline heart rate of less than 110 bpm (Fig. 8.2). A profound and sustained decrease in FHR is indicative of fetal distress.

Fig. 8.2 CTG of fetal bradycardia.

Tachycardia

A suspicious tachycardia is defined as being between 160 and 180 bpm, whereas a pathological recording is above 180 bpm. Fetal tachycardias may be associated with fetal distress, maternal pyrexia and/or intrauterine infection.

Baseline variability

This is the minor fluctuation in baseline fetal heart rate. It is measured by estimating the difference in beats per minute between the highest peak and lowest trough of fluctuation in a 1-minute segment of the trace. The normal baseline variability is >5 bpm between contractions. Decreased or absent variability (Fig. 8.3) reflects decreased fetal central nervous system activity (associated with fetal sleep cycles or maternal drug administration, e.g. opioid, magnesium, benzodiazepines). However sustained reduction in variability may indicate fetal hypoxaemia/acidosis.

Fig. 8.3 CTG of loss of variability.

Accelerations

This is defined as a transient increase in heart rate >15 bpm for at least 15 seconds. Accelerations are normal indicating fetal responsiveness. Two accelerations in 20 minutes is considered a reactive trace. The absence of accelerations with an otherwise normal CTG is of uncertain significance.

Decelerations

These may either be normal or pathological:

Fig. 8.4 CTGs of (A) early decelerations, (B) late decelerations and (C) variable decelerations.