Clinical overview
The cardiotocograph (CTG) is the most widely used — and most widely misused — tool in intrapartum care. It records the fetal heart rate (FHR) against uterine activity, and is meant to be a screening test for fetal hypoxaemia developing in labour. Used well, it identifies the fetus that is decompensating in time to act. Used badly, it generates a torrent of false positives that drive unnecessary caesareans, while occasionally lulling clinicians into missing genuine deterioration. The competence that matters is not naming a deceleration but interpreting a whole trace in clinical context and converting that interpretation into a safe, timely decision.
Interpretation is therefore demanding: read the four features systematically, classify the trace, weigh it against the clinical picture (gestation, meconium, sepsis, growth restriction, oxytocin, stage of labour), decide on an action, and — critically — recognise when the CTG is no longer reassuring enough to wait. CTG never stands alone. It is one input alongside the partogram, the clinical risk assessment that selected the monitoring method (see Fetal monitoring methods), and your understanding of fetal oxygenation physiology (see Contractions fetal oxygenation). In South Africa, where intrapartum hypoxia and birth asphyxia remain a leading avoidable contributor to perinatal death in the Saving Mothers and Babies (NCCEMD/Perinatal Problem Identification Programme) data, disciplined CTG interpretation and timely escalation are core registrar competencies.
Core knowledge
Why the fetal heart rate tells us about oxygenation
The healthy fetal heart is driven by competing autonomic inputs. Sympathetic tone tends to raise the rate; parasympathetic (vagal) tone, maturing with gestation, lowers it and generates the beat-to-beat irregularity we see as variability. A well-oxygenated fetus with an intact, awake central nervous system produces a trace with normal baseline, normal variability and accelerations. Hypoxia and acidaemia blunt this autonomic richness: variability falls, accelerations disappear, and — depending on the mechanism — characteristic decelerations and baseline shifts emerge. The CTG is thus an indirect window onto cerebral oxygenation, and its features must always be read as a pattern over time, not as isolated events.
The physiological substrate matters because it explains the rules. Each contraction transiently reduces intervillous perfusion; a fetus with good reserve tolerates this, while one with reduced reserve (placental insufficiency, growth restriction — see Placental insufficiency response and Intrauterine growth restriction) decompensates. Cord compression triggers a vagal reflex (variable decelerations); head compression in the second stage does likewise; uteroplacental insufficiency produces the gradual, contraction-mirroring late deceleration that is the most ominous reflex pattern.
The four features
Every CTG is interpreted on four features, then classified. Define each precisely:
- Baseline rate — the mean FHR over ~5–10 minutes, excluding accelerations and decelerations. Standard normal teaching is 110–160 bpm. Below 110 is bradycardia; above 160 is tachycardia. Baseline tends to be at the higher end preterm.
- Variability — the bandwidth of beat-to-beat fluctuation around the baseline. Normal is conventionally 5–25 bpm. Reduced variability (<5 bpm) sustained over time is concerning; it may also reflect fetal sleep (usually <40 min) or maternal sedation/opioids. A sinusoidal pattern (smooth, regular oscillation, absent variability) is pathological and suggests severe anaemia or hypoxia.
- Accelerations — transient rises ≥15 bpm for ≥15 seconds (classic term threshold). Their presence is reassuring; their absence in an otherwise normal trace is of uncertain significance in labour.
- Decelerations — transient falls in FHR, classified by timing and shape:
- Early — shallow, symmetrical, mirror the contraction (nadir with peak); benign, vagal from head compression.
- Variable — abrupt drop and recovery, varying in timing/shape; usually cord compression. Concerning ("atypical/complicated") features classically include slow return to baseline, loss of variability within the deceleration, biphasic ("W") shape, and prolonged duration.
- Late — gradual onset, nadir after the contraction peak, gradual recovery; signify uteroplacental insufficiency and are the most worrying reflex pattern. Note the Nov 2025 NICE NG229 update: a late deceleration is now classed as a RED feature in its own right — regardless of duration or whether it is repetitive (the old "repetitive/periodic" qualifier was removed because late decelerations correlate with fetal hypoxia). So even an isolated late deceleration pushes the trace toward the pathological/urgent category and prompts escalation — do not wait for them to become repetitive.
- Prolonged — a fall lasting >2 minutes. Beyond ~3 minutes this is an acute event demanding immediate action.
Uterine activity
The "toco" half of the trace records frequency and (with intrauterine pressure catheters) strength of contractions. Tachysystole is >5 contractions in 10 minutes averaged over 30 minutes; it reduces the recovery time between contractions and is a frequent, correctable cause of an abnormal FHR — especially with oxytocin or prostaglandins. The NICE NG229 emphasis on tachysystole (>5 in 10) and contractions lasting >2 minutes as triggers for review reflects this: too-frequent contractions are a common, reversible driver of fetal compromise.