Labour physiology and CTG assessment

Intrapartum Monitoring, Postpartum Haemorrhage & Obstetric Emergencies

Intrapartum care requires continuous clinical vigilance to ensure maternal and fetal safety. Masterful management of labour stages, systematic cardiotocographic interpretation, structured resuscitation of postpartum haemorrhage, and rehearsed execution of emergency algorithms for shoulder dystocia and cord prolapse are fundamental competencies tested on the AMC examination.

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Stages and Physiology of Normal Labour

Normal labour is divided into three distinct physiological stages:

1. First Stage: From the onset of regular, painful uterine contractions leading to progressive effacement and dilatation of the cervix, terminating at complete dilatation ($10\text{ cm}$):
   • Latent Phase: Characterized by cervical effacement and slow dilatation up to $4\text{ to }5\text{ cm}$. Can last up to 20 hours in nulliparas and 14 hours in multiparas.

• Labour progress: Progress varies with stage, parity and circumstances. A fixed 1 cm/h expectation is not a universal diagnostic rule for arrest. Assess cervical change, contractions, membranes, position and maternal/fetal condition before augmentation or operative decisions.

1. Second Stage: From complete cervical dilatation ($10\text{ cm}$) to the birth of the baby:
   • Passive Phase: Full cervical dilatation prior to or in the absence of involuntary expulsive maternal pushing efforts (allowing passive descent of the fetal head to the pelvic floor).
   • Active Phase: Active maternal expulsive pushing with contractions. Expected duration is up to 2 hours in nulliparas (extended to 3 hours with epidural analgesia) and 1 hour in multiparas (extended to 2 hours with epidural). Delay beyond these limits warrants senior obstetric assessment for fetal malposition, cephalopelvic disproportion, or operative instrumental delivery.
2. Third Stage: From the delivery of the infant until the complete expulsion of the placenta and fetal membranes.
   • Active Management of Third Stage (Standard Australian Care): Reduces the incidence of primary postpartum haemorrhage by over 50%. Comprises three sequential interventions:
     1. Administration of a prophylactic uterotonic: Intramuscular oxytocin 10 IU administered with the delivery of the anterior shoulder or immediately following delivery of the infant.
     2. Deferred (delayed) cord clamping: Clamping the umbilical cord after 1 to 3 minutes, enhancing neonatal iron stores and reducing intraventricular haemorrhage in preterm infants (unless immediate neonatal resuscitation is required).
     3. Controlled cord traction (Brandt-Andrews manoeuvre): Applying gentle downward traction on the cord with one hand while the other hand applies counter-traction suprapubically upwards on the uterine body to prevent uterine inversion.

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Intrapartum Fetal Surveillance (RANZCOG CTG Guidelines)

The Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) provides explicit criteria for cardiotocography (CTG) interpretation. A systematic approach must evaluate five core parameters:

1. Contraction Pattern: Assessed over a 10-minute window. Normal frequency is $2\text{ to }5\text{ contractions per }10\text{ minutes}$. Uterine tachysystole is defined as $> 5\text{ contractions per }10\text{ minutes}$ over a 30-minute window, which risks compromising placental perfusion.
2. Baseline Fetal Heart Rate (BHR): Mean heart rate rounded to $5\text{ bpm}$ increments over 10 minutes:
   • Normal: $110\text{ to }160\text{ bpm}$.
   • Baseline Tachycardia ($> 160\text{ bpm}$): Caused by maternal pyrexia, intra-amniotic infection (chorioamnionitis), early fetal hypoxaemia, maternal dehydration, beta-agonist tocolytics, or maternal hyperthyroidism.
   • Baseline Bradycardia ($< 110\text{ bpm}$): Sustained rate $< 110\text{ bpm}$. Causes include maternal hypotension (e.g., post-epidural), rapid fetal descent, cord compression, uterine rupture, or congenital fetal heart block.
3. Baseline Variability: Fluctuations in the baseline rate reflecting autonomous autonomic regulation:
   • Normal variability: 6–25 bpm in the current RANZCOG classification. Reduced/absent variability is interpreted with duration, medication, sleep, gestation and other features.
   • Reduced Variability ($< 5\text{ bpm}$): Fetal sleep cycle (usually resolves within 40 minutes), central nervous system depressants (maternal opioids, magnesium sulfate), prematurity, or evolving fetal acidaemia.
   • Absent Variability: Undetectable fluctuations; highly pathological when accompanied by decelerations.
   • Increased (Saltatory) Variability ($> 25\text{ bpm}$): Acute transient fetal hypoxia or cord compression.
4. Accelerations: Transient increases in heart rate of $\ge 15\text{ bpm}$ above baseline lasting for $\ge 15\text{ seconds}$. Hallmark of an awake, non-acidaemic fetus.
5. Decelerations:
   • Early Decelerations: Symmetrical, gradual decrease and return of BHR where the nadir coincides precisely with the peak of the uterine contraction ("mirror image"). Mechanism: Increased intracranial pressure causing transient vagal stimulation from fetal head compression during contractions. Entirely physiological and benign; requires no intervention.
   • Variable Decelerations: Rapid drop to nadir in $< 30\text{ seconds}$, variable timing and shape relative to contractions, often with preceding and succeeding "shoulders" (accelerations). Mechanism: Umbilical cord compression. Uncomplicated variable decelerations are common; complicated variable decelerations (duration $> 60\text{ seconds}$, nadir $< 60\text{ bpm}$, loss of variability, or slow recovery) indicate significant fetal compromise.
   • Late Decelerations: Gradual decrease in BHR where the onset, nadir, and recovery occur delayed relative to the contraction, with the nadir occurring after the contraction peak, returning to baseline only after contraction completion. Mechanism: Uteroplacental insufficiency and transient hypoxaemia stimulating chemoreceptors. Always pathological; demands immediate intrauterine resuscitation and urgent delivery if persistent.
   • Prolonged deceleration: A fall persisting beyond 90 seconds warrants urgent assessment; duration, recovery, other CTG features and the clinical situation determine escalation. Persistent bradycardia is an emergency requiring preparation for expedited birth.

CTG Classification and Management

• CTG interpretation: Interpret baseline, variability and decelerations with the whole clinical picture. Absence of accelerations on an otherwise normal intrapartum trace does not alone establish fetal compromise. Compare maternal pulse and document changes over time.
  1. Oxytocin: Use the local PPH regimen with a slow IV dose and appropriate infusion. Rapid large boluses can cause hypotension; treatment is given with resuscitation and assessment of tone, trauma, tissue and coagulation.
  2. Stop oxytocin infusion immediately.
  3. Position mother in left lateral tilt to relieve aortocaval compression.
  4. Perform vaginal examination to exclude umbilical cord prolapse or rapid crowning.
  5. If non-reassuring pattern persists: obtain fetal scalp blood sampling for lactate ($< 4.2\text{ mmol/L}$ normal, $4.2\text{–}4.8\text{ mmol/L}$ borderline, $> 4.8\text{ mmol/L}$ indicates acidaemia requiring delivery) or expedite immediate Category 1 emergency delivery.

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Primary references (checked 7 October 2026): RANZCOG intrapartum surveillance; Queensland preterm birth guideline.