Physiological Changes During the 1st Stage of Labour

(Figure: Friedman's curve showing the latent and active phases of the first stage - Morgan & Mikhail's Clinical Anesthesiology)

I. Uterine Changes

• True labour begins when irregular Braxton Hicks contractions become coordinated, rhythmic, and progressive in strength and frequency.
• Early first stage (latent phase): contractions every 15-30 minutes, mild intensity (~25 mm Hg).
• As labour advances (active phase): contractions increase to every 3-5 minutes, with intensities of 25-60 mm Hg, and duration of 30-60 seconds.
• Contractions originate at the fundus and spread downward - the fundus and body contract strongly while the lower uterine segment remains relatively passive.
• Combined uterine and (later) abdominal muscular forces generate ~25 pounds of downward pressure per strong contraction on the fetus.
• Contractions are intermittent by necessity - continuous strong contractions would impede placental blood flow and cause fetal compromise. - Guyton & Hall Textbook of Medical Physiology

• The lower uterine segment (isthmus) progressively thins and stretches as labour advances.
• A physiological retraction ring (Bandl's ring) may be felt between the thicker upper segment and the thinner lower segment.

• Each contraction transiently reduces uteroplacental blood flow. Recovery occurs during the relaxation interval - this is why adequate inter-contraction intervals are physiologically essential.

II. Cervical Changes

• Preceded by cervical softening weeks before labour onset - mediated by inflammatory cells (neutrophil infiltration) and local cytokines causing collagen remodelling and water content increase.
• The cervix shortens (effaces) from a thick, closed tube ~3-4 cm long to a paper-thin, flush structure.
• In nulliparas: effacement precedes dilation. In multiparas: they may occur simultaneously.

• Latent phase: slow progressive effacement and minor dilation up to 4-6 cm over 6-12 hours (nullipara up to 20 hours is still considered normal). - Miller's Anesthesia
• Active phase: rapid dilation from 6 cm to 10 cm (or classically from 4 cm in older Friedman's model). Dilation rate in active phase should be at least 1-1.2 cm/hour in nulliparas and 1.5 cm/hour in multiparas.
• The full transition marks the end of the first stage. Typically, first stage lasts 8-12 hours in nulliparas and 5-8 hours in multiparas. - Morgan & Mikhail's Clinical Anesthesiology

III. Fetal Descent

• During the first stage, the presenting part (usually vertex) engages in and descends through the pelvis.
• The head acts as a wedge, progressively dilating the birth canal.
• Fetal station (level of presenting part relative to ischial spines) advances during the active phase.

IV. Membrane Changes

• The intact fetal membranes form a "forewaters" bag that transmits hydrostatic pressure evenly to help dilate the cervix.
• Membranes may rupture spontaneously (SROM) before or during the first stage - when this occurs, the amniotic fluid is lost and the fetal head directly presses on the cervix (more efficient pressure transmission).

V. Maternal Cardiovascular Changes

• Each uterine contraction displaces 300-500 mL of blood from the uterus into the central circulation, acting like an autotransfusion.
• Cardiac output rises approximately 45% above third-trimester baseline during active labour.
• Heart rate and blood pressure rise slightly with each painful contraction.
• The greatest cardiovascular strain occurs immediately after delivery (not during the first stage), when uterine involution relieves IVC compression and cardiac output rises 80% above third-trimester values. - Morgan & Mikhail's Clinical Anesthesiology

VI. Maternal Respiratory Changes

• Pain and anxiety during contractions cause maternal hyperventilation.
• Minute ventilation may increase by up to 300% during intense contractions.
• Oxygen consumption rises by ~60% above third-trimester values.
• Excessive hyperventilation can drive PaCO2 below 20 mm Hg, causing maternal and fetal hypoxaemia between contractions, reduced uterine blood flow, and fetal acidosis. - Morgan & Mikhail's Clinical Anesthesiology

VII. Pain Pathways During the First Stage

• Pain arises from myometrial hypoxia during contractions, progressive cervical dilation, and stretching of the lower uterine segment.
• The first stage produces predominantly visceral pain, carried by afferent fibres travelling with sympathetic nerves via the uterovaginal plexus -> inferior hypogastric plexus -> T10-L1 spinal roots.
• Latent phase: pain referred to T11-T12 dermatomes (lower abdomen, suprapubic).
• Active phase: pain expands to T10-L1 dermatomes, and is increasingly referred to the lumbosacral area, gluteal region, and thighs.
• Pain intensity correlates with cervical dilation and contraction frequency/intensity. Nulliparas typically experience greater first-stage pain than multiparas.
• At the end of the first stage, onset of perineal pain signals the beginning of fetal descent (transition to second stage). - Morgan & Mikhail's Clinical Anesthesiology

VIII. Hormonal and Biochemical Changes

• Oxytocin receptor upregulation: even though circulating oxytocin levels may not rise markedly at the onset of labour, the number of myometrial oxytocin receptors rapidly increases, sensitising the uterus.
• Prostaglandins (PGE2, PGF2α): synthesised by fetal membranes and decidual tissues, they enhance myometrial contractility and promote cervical ripening.
• Progesterone withdrawal (functional): reduced progesterone dominance allows pro-contractile pathways to predominate.
• Cortisol and fetal adrenal steroids: contribute to the initiation of labour signalling.
• Catecholamines: maternal stress and pain elevate adrenaline/noradrenaline, which can reduce uterine blood flow. - Morgan & Mikhail's Clinical Anesthesiology

IX. Prodromal Events Preceding True Labour (0-4 weeks before)

Summary Table: Latent vs Active Phase of First Stage