Physiological Changes During the First Stage of Labour

1. Uterine Changes

• Throughout normal pregnancy, uterine contractions are irregular, incoordinate, and painless (Braxton Hicks). As term approaches they become more frequent, stronger, and coordinated.
• In active labour, contractions become regular, painful, progressive in frequency (every 2-3 min) and duration (45-60 sec), and coordinated (fundal dominance - contractions originate at the fundus and spread downward).
• Each contraction temporarily reduces uteroplacental blood flow, requiring adequate uterine relaxation between them for fetal oxygenation.

• The lower uterine segment progressively thins and stretches as the active upper segment thickens and contracts - this "polarity" draws the cervix upward.

2. Cervical Changes

• Begins in early pregnancy. Regulated alterations in fibrillar collagen processing and assembly progressively modify cervical architecture and reduce mechanical strength.
• Columnar glandular epithelial cells proliferate and secrete mucus, forming the mucus plug (operculum) that protects against ascending infection.

• Occurs 1-2 weeks before labour onset. Characterized by increased synthesis of hyaluronan, which increases tissue hydration and causes disorganization of collagen architecture, resulting in maximal decline in tensile strength.
• Local progesterone concentration falls; estrogen rises - this shift alters extracellular matrix composition.

• The cervix shortens from ~3-4 cm long to paper-thin as its substance is taken up into the lower uterine segment.
• In primiparae, effacement typically precedes dilation; in multiparae, dilation and effacement often occur simultaneously.
• Biochemical changes (increased hyaluronan synthesis, increased local progesterone metabolism), mechanical traction from contractions, and pressure from the fetal presenting part all drive effacement.

• Progressive opening of the external os from closed (0 cm) to full dilation (10 cm).
• Latent phase: Slow, from 0 to ~3-4 cm; mean duration ~6.4 hr (nulliparae), ~4.8 hr (multiparae).
• Active phase: Rapid dilation; minimum expected rate is ≥1.2 cm/hr (nulliparae) and ≥1.5 cm/hr (multiparae) by Friedman's criteria.
• Mean total first stage: ~11 hr (nulliparae), ~7.2 hr (multiparae) (Friedman, 1978).
• Prelabour cervical dilation averages 1.8 cm in nulliparae and 2.2 cm in multiparae in the last 3 days before onset (Hendricks et al., 1970).

3. Cardiovascular Changes

• Cardiac output rises by 12-31% during the first stage of labour, primarily due to a 22% increase in stroke volume with each contraction.
• Each uterine contraction transfers 300-500 mL of blood from the uterus into the general circulation, causing transient increases in venous return and blood pressure.
• Blood pressure may transiently increase during contractions; pain and anxiety further increase sympathetic tone.
• Laboring in the left lateral decubitus position and/or regional analgesia reduces - but does not abolish - this increment, since the autotransfusion effect from uterine contractions persists regardless of pain relief.
• By the second stage, cardiac output rises even further (~49%).
• Women with pre-existing cardiovascular compromise may decompensate during labour for these reasons.

4. Inflammatory / Immunological Changes

• Spontaneous labour at term is a physiological inflammatory process.
• Proinflammatory cytokines (IL-1β, IL-6, TNF-α, MCP-1/CCL2, IL-8/CXCL8) are released by uterine tissues.
• This triggers massive infiltration of neutrophils and monocytes into the cervix, myometrium, decidua, and fetal membranes.
• Monocytes differentiate into macrophages, producing an inflammatory environment that increases transcription of myometrial contraction-associated proteins (CAPs).
• Prostaglandins - key activators of the parturition pathway - are produced by these infiltrating immune cells and by decidua.
• Pattern recognition receptors (TLRs, NF-κB pathway) amplify the inflammatory cascade, feeding back to sustain contractions.

5. Hormonal Changes

• Progesterone withdrawal (functional, not absolute, in humans): the ratio of progesterone to estrogen shifts, reducing progesterone's myometrial-quiescence effects.
• Estrogen rises, upregulating oxytocin receptors, prostaglandin synthesis, and gap junction formation in myometrial cells.
• Oxytocin receptor density increases markedly at term; oxytocin drives coordinated contractions.
• Prostaglandins (PGE2, PGF2α) are key activators of the common pathway of parturition - they cause both myometrial contractions and cervical ripening.
• Relaxin (from corpus luteum) contributes to cervical remodeling.
• The fetal HPA axis activation and a rise in fetal cortisol contribute to the timing of parturition (better characterized in ruminants but relevant in humans).

6. Fetal Descent

• Descent of the fetal head begins well before the second stage.
• The rate of descent accelerates late in the first stage (as the active phase progresses and the head engages more deeply).
• Engagement, flexion, and internal rotation begin during the first stage.

7. Fetal Membranes and Amniotic Fluid

• The intact bag of waters (forewaters) transmits uterine pressure uniformly over the presenting part, aiding cervical dilation and protecting the umbilical cord.
• In many labours, the membranes rupture spontaneously toward the end of the first stage (or sometimes earlier); when this occurs, the fetal head acts as a direct dilating wedge.

8. Pain Mechanism

• First stage pain is primarily visceral - arising from uterine contractions and cervical dilation/effacement.
• Transmitted via T10-L1 nerve roots (lower thoracic and upper lumbar sympathetic afferents).
• Pain is crampy, diffuse, referred to the lower abdomen, groin, and back.