In one line
The cardiotocograph is a screening test for fetal hypoxia with high sensitivity and dismal specificity; the consultant skill is not pattern-spotting but distinguishing the fetus that is compensating from the one that is decompensating, acting on reversible causes first, and confirming or refuting suspected acidaemia before an irreversible decision — because continuous CTG halves neonatal seizures but does nothing for cerebral palsy or mortality while sharply raising the caesarean rate.
Mechanism & pathophysiology
The fetal heart rate is a window onto the autonomic nervous system, and the autonomic nervous system reports on cerebral oxygenation. Everything the trace shows — the baseline, the variability, the shape and timing of decelerations — is a readout of how the fetal brainstem is being perfused, which is why a CTG can warn of hypoxia before the tissue is injured and why it cannot tell you that injury has already occurred.
Oxygen reaches the fetus by a delivery chain that can fail at any link: maternal arterial oxygen content, uteroplacental blood flow through the spiral arteries, transfer across the placental villous membrane, umbilical venous return, and fetal cardiac output. Labour stresses every link. Each contraction transiently occludes the spiral arteries and interrupts intervillous perfusion, so the fetus must withstand repeated 60–90-second ischaemic insults and recover in the gaps between them. A healthy term fetus has the reserve to do this many hundreds of times; a growth-restricted, post-dates, or acidotic fetus does not.
When oxygen delivery falls, the response unfolds as a sequence, and reading where a fetus sits on that sequence is the whole of intrapartum interpretation:
- Hypoxaemia — reduced oxygen in the blood, no tissue effect yet. The fetus mounts a chemoreceptor- and catecholamine-mediated response: peripheral vasoconstriction, redistribution of cardiac output to brain, heart and adrenals, and a rise in baseline rate. Decelerations may appear but variability is preserved. This is compensation, and it can continue for hours without harm.
- Hypoxia — oxygen lack now reaches the tissues. Anaerobic glycolysis in peripheral beds generates lactate; a respiratory (CO₂-driven) acidosis is buffered, but as redistribution is sustained the picture shifts.
- Metabolic acidaemia — once anaerobic metabolism in the central organs cannot be offset, fixed acid accumulates, the base deficit climbs, and myocardial function and central nervous control begin to fail. Variability is lost, the baseline may fall, and decelerations deepen and stop recovering. This is decompensation, and it is the state that precedes hypoxic-ischaemic injury.
The individual features map onto this physiology:
- Baseline (normal 110–160 bpm) is set by the balance of sympathetic and parasympathetic tone. A rising baseline is an early catecholamine-driven sign; tachycardia (>160 for >10 min) accompanies maternal pyrexia (the commonest cause), early hypoxaemia, beta-agonists and fetal tachyarrhythmia. Bradycardia (<110 for >10 min) is most ominous as a terminal sign of profound hypoxia but also occurs with maternal hypothermia, beta-blockade and heart block.
- Variability (normal 5–25 bpm) is the most informative single feature because it requires an intact, oxygenated brainstem oscillating sympathetic against parasympathetic output beat to beat. Reduced variability (<5 bpm for >50 min, or >3 min within a deceleration) reflects central depression — from acidosis, but equally from fetal sleep, opioids and magnesium sulphate, which is why isolated reduced variability is interpreted cautiously and in context. Variability that is preserved despite decelerations is the single most reassuring finding on a worrying trace: a fetus that can still oscillate its rate is still compensating.
- Accelerations denote a neurologically responsive, non-acidotic fetus; their absence in labour is of uncertain significance and is not, on its own, pathological.
- Decelerations are where mechanism and management converge:
- Early decelerations are shallow, symmetrical, and mirror the contraction; they are vagally mediated by head compression and carry no hypoxic meaning.
- Variable decelerations are abrupt (onset to nadir <30 s), vary in size and shape, and reflect a baroreceptor response to cord compression. The majority of intrapartum decelerations are variable, and most are benign. They acquire significance when they evolve "atypical" features — slow recovery, loss of variability within the deceleration, a combined U-shaped component, or duration beyond 3 minutes — signalling an emerging chemoreceptor (hypoxic) element.
- Late decelerations are smooth, U-shaped, begin after the contraction peak and return to baseline after the contraction ends; they are chemoreceptor-mediated and indicate that contraction-associated hypoxaemia is reaching the chemoreceptors. Repetitive late decelerations with reduced variability are the classic decompensation pattern.
- Prolonged decelerations (>3 min) demand the operator at the bedside: below 80 bpm with reduced variability they carry a chemoreceptor component and frequently accompany acute events.
The distinction between respiratory and metabolic acidosis is not academic, because it separates a fetus that will recover within minutes of birth from one that has sustained a tissue insult. A respiratory acidosis is pure CO₂ retention from a brief interruption of gas exchange — a low pH with a high pCO₂ and a near-normal base deficit — and it corrects rapidly once the cord is cut and the lungs aerate. A metabolic acidosis reflects accumulated fixed acid from anaerobic metabolism — a low pH with a raised base deficit (the threshold of concern is a base deficit ≥12 mmol/L) — and it is the type associated with hypoxic-ischaemic injury. The CTG tracks the trajectory between these states: a fetus with preserved variability and recovering decelerations is buffering a respiratory load; a fetus with absent variability and non-recovering late decelerations is building the metabolic deficit that confirmation at delivery (paired cord gases) will later quantify. This is why a worrying trace is interrogated during labour with a test of acid–base status rather than left to declare itself, and why the cord gases drawn at birth are the retrospective check on whether the intrapartum read was right.
The corollary that governs everything downstream: the CTG detects the physiological state, not the outcome. A fetus can sit in stable compensation indefinitely and a normal trace is genuinely reassuring; but suspicious and pathological traces have a very high false-positive rate for actual acidaemia, because the same pattern is produced by a fetus that will be perfectly well and by one that is decompensating. That asymmetry — excellent at confirming health, poor at confirming harm — is the reason every intervention that follows is aimed at reversing a cause and confirming the suspicion, not at delivering on the trace alone.
Assessment
Interpretation is a structured read of five features against a stated risk context, then a category, then a search for cause — never a category in isolation.
- Establish the risk context first. Continuous CTG is indicated where the risk of hypoxia is raised: intrapartum risk factors include meconium-stained liquor, antepartum or intrapartum bleeding, maternal pyrexia or sepsis, oxytocin augmentation, suspected growth restriction or oligohydramnios, prematurity, post-dates, hypertensive disease, diabetes, previous caesarean, and a multiple pregnancy. The same trace means different things in a low-risk multipara and a growth-restricted post-dates primigravida; the denominator changes the index of suspicion.
- Read the four basic features, then classify. Baseline, variability, accelerations and decelerations are each judged over a 10-minute window against the contraction pattern, and the trace is then categorised. Re-evaluate at least every 30 minutes, and continuously when abnormal — the signal changes through labour.
- Tachysystole and the contractions. Excessive uterine activity (>5 contractions in 10 minutes over two successive 10-minute periods) is the commonest reversible driver of an abnormal trace, because it shortens the recovery interval the fetus needs between perfusion insults. Always read the toco channel alongside the rate.
- Exclude the maternal heart rate masquerading as the fetal. Doppler external monitoring can double-count or lock onto the maternal pulse, especially in the second stage; an apparent "acceleration with every push" is the giveaway. Where any doubt exists, palpate the maternal pulse against the trace, or move to a fetal scalp electrode — a recurring and preventable medico-legal trap is a reassuring trace that was, in fact, recording a well mother over a dying fetus.
- Sinusoidal versus pseudosinusoidal. A true sinusoidal pattern — regular, smooth, undulating, 5–15 bpm amplitude, 3–5 cycles/min, lasting >30 min with absent accelerations — is pathological and points to fetal anaemia (rhesus alloimmunisation, fetomaternal haemorrhage, twin-to-twin transfusion, ruptured vasa praevia) or severe acute hypoxia, and triggers urgent action. The pseudosinusoidal pattern is jagged, transient (typically <30 min), often follows maternal opioids or fetal mouthing, and is benign; the discriminator is the smoothness and the duration.
Categorisation — what the classification actually means
The international systems share one three-tier architecture — normal / suspicious / pathological — built from the same four features. The point of the category is not to label but to set the tempo of response: a normal trace needs nothing, a suspicious trace needs a search for and correction of reversible causes plus closer observation, and a pathological trace needs immediate action on reversible causes and a decision about expediting delivery if it does not recover.