Normal Labour — Comprehensive Exam-Ready Notes

1. DEFINITION

• Onset is clinically defined as painful, regular uterine contractions associated with cervical effacement and dilation
• Precise onset is often uncertain — the latent phase blurs into prelabour

2. PRELABOUR CHANGES

Nulliparas show greater effacement in prelabour; multiparas show greater dilation (Hendricks et al.). Mean cervical dilation in the last 3 days before labour: 1.8 cm nullipara / 2.2 cm multipara.

3. STAGES OF LABOUR

4. FIRST STAGE — FRIEDMAN CURVE

4a. Latent Phase

• Onset of contractions → beginning of active phase
• Little cervical dilation; major cervical changes are softening, effacement, and positioning
• Upper limits of normal:
  • Nullipara: < 20 hours
  • Multipara: < 14 hours
• Latent phase mean duration (Friedman data): ~6.4 hr nullipara / ~4.8 hr multipara

4b. Active Phase

• Begins at ~3–4 cm dilation (Friedman era) or ~6 cm (contemporary data — Zhang et al.)
• Rapid, near-linear cervical dilation
• Minimum rates (Friedman criteria):
  • Nullipara: ≥ 1.2 cm/hr
  • Multipara: ≥ 1.5 cm/hr
• Modern data (Zhang) show contemporary active phase begins later and progresses more slowly than Friedman described

Exam tip: Active phase arrest = no dilation for ≥ 2 hours in the active phase.

5. FETAL DESCENT

• Descent begins well before the second stage (often in late first stage)
• Rate of descent increases in late first stage and continues linearly into the second stage
• Maximum rate of descent (Friedman):
  • Nullipara: 3.3 ± 2.3 cm/hr
  • Multipara: 6.6 ± 4.4 cm/hr

• Negative = above spines (not engaged)
• Zero = at the level of spines (engaged)
• Positive = below spines

6. SECOND STAGE

• Full dilation → delivery of the infant
• Fetal head descent + rotation occur throughout this stage
• Historically limited to 2 hours; modern evidence does not support rigid time cutoffs when there is fetal well-being and progress

• If no serious FHR abnormalities, mother is well hydrated and comfortable, and there is any progress in descent/rotation → no mandatory operative delivery
• Prolonged second stage (epidural): Nullipara > 3 hr; Multipara > 2 hr — associated with increased chorioamnionitis, severe perineal lacerations, uterine atony, PPH
• Rouse et al.: 55% of women with second stage ≥ 3 hours still delivered vaginally

7. THIRD STAGE

• Delivery of infant → delivery of placenta
• Normal duration: < 30 minutes (typically 5–15 min)
• Signs of placental separation: fundal rise, cord lengthening, gush of blood, uterus becomes globular
• Active management (oxytocin + controlled cord traction) reduces PPH risk

8. UTERINE CONTRACTIONS IN ACTIVE LABOUR

Contractions 1–2 minutes apart may indicate increased intrauterine pressure — rule out abruptio placentae.

9. CARDINAL MOVEMENTS OF LABOUR (Second Stage)

1. Engagement — biparietal diameter at the pelvic inlet
2. Descent — throughout labour, most active in 2nd stage
3. Flexion — chin to chest; reduces presenting diameter
4. Internal rotation — occiput rotates to anterior (OA)
5. Extension — head delivers under pubic symphysis
6. External rotation (restitution) — shoulders align with AP diameter
7. Expulsion — delivery of shoulders and body

10. LABOUR ABNORMALITIES (High-Yield Exam Contrasts)

11. FETAL HEART RATE MONITORING

Baseline FHR

• Normal: 110–160 bpm
• Tachycardia: > 160 bpm; bradycardia: < 110 bpm

Variability

• Normal (moderate): 6–25 bpm fluctuation — most reassuring
• Absent/minimal variability: concerning for hypoxia or CNS depression

Accelerations

• Transient FHR rise ≥ 15 bpm above baseline lasting ≥ 15 seconds
• Reassuring; basis of reactive NST (≥ 2 accelerations)

Decelerations

Variable decelerations are the most common deceleration type, occurring in 50–80% of deliveries.

Causes of Fetal Bradycardia (exam list)

12. ANALGESIA IN LABOUR

13. QUICK-FIRE EXAM FACTS

• Labour is defined by painful contractions + cervical change (not contractions alone)
• Cervical dilation of 10 cm = full dilation = end of 1st stage
• Active phase begins at 6 cm by contemporary data (Zhang) vs. 3–4 cm (Friedman)
• Nullipara latent phase limit = 20 hr; multipara = 14 hr
• Active phase arrest = no dilation for ≥ 2 hours with adequate contractions
• Bloody show → labour typically within 3 days
• Normal contraction frequency in active labour = every 2–3 min
• Placenta should deliver within 30 minutes of birth (3rd stage)
• Most common deceleration = variable (cord compression)
• Late decelerations = uteroplacental insufficiency — never benign
• Mueller-Hillis maneuver = fundal pressure + vaginal exam to assess head descent (helps predict cephalopelvic proportion)

Pregnancy-Induced Hypertension: A Comprehensive Scholarly Review

1. Introduction

2. Classification

• Without severe features — BP 140–159/90–109 mmHg with proteinuria, without end-organ involvement
• With severe features — BP ≥ 160/110 mmHg, or evidence of renal, hepatic, neurological, or haematological compromise²

3. Epidemiology

• Nulliparity — the single greatest population-attributable fraction, accounting for 32.3% (95% CI: 27.4–37.0%) of cases²
• Extremes of reproductive age (adolescence and advanced maternal age)
• Prior preeclampsia
• Multiple gestation and molar pregnancy
• Chronic hypertension — 25% of such women develop superimposed preeclampsia²
• Pregestational diabetes mellitus — 20% overall risk; up to 70% in White's class F and R²
• Chronic renal disease
• Systemic lupus erythematosus and antiphospholipid syndrome
• Obesity and hypercholesterolaemia¹
• In vitro fertilisation and family history of preeclampsia²

4. Pathophysiology

4.1 The Placental Origin Hypothesis

Figure 1. In normal pregnancy (left), trophoblasts invade and dilate the spiral arteries into wide, low-resistance vessels. In preeclampsia (right), trophoblastic invasion is incomplete, leaving the arteries narrow and coiled with resultant placental ischaemia. — Guyton and Hall Textbook of Medical Physiology, p. 1041

4.2 Antiangiogenic Factors and Endothelial Dysfunction

• Soluble fms-like tyrosine kinase-1 (sFlt-1) — a circulating decoy receptor that sequesters and antagonises VEGF (vascular endothelial growth factor) and PlGF (placental growth factor), thereby impairing endothelial maintenance and nitric oxide production
• Soluble endoglin (sEng) — antagonises TGF-β signalling in endothelial cells, compounding vascular dysfunction

• Reduced production of vasodilators: prostacyclin (PGI₂) and prostaglandin E₂
• Increased production of the vasoconstrictor thromboxane A₂ (TXA₂)
• The net result is systemic vasoconstriction, hypertension, and platelet activation³

4.3 Vascular Reactivity and Angiotensin II Hypersensitivity

4.4 Inflammatory and Immunological Mechanisms

4.5 Haemodynamic Profile

1. Early phase: cardiac output is elevated and peripheral resistance begins to rise above normal
2. Established disease: cardiac output falls as peripheral resistance rises substantially, producing a paradoxically contracted intravascular volume (despite oedema)
3. Central venous pressures are typically normal; pulmonary capillary wedge pressure is variable

5. Systemic Consequences and Organ Pathology

5.1 Renal Effects

• Glomerular endotheliosis — pathognomonic histological lesion: swelling of glomerular endothelial cells with protein deposits in the basement membrane, narrowing the capillary lumen
• Decreased renal blood flow and GFR (contrary to the physiological increase of normal pregnancy)
• Proteinuria (> 300 mg/24 h), resulting from disruption of the glomerular filtration barrier
• Oliguria and, in severe cases, acute kidney injury

5.2 Hepatic Effects

• Hepatocellular necrosis and periportal haemorrhage from vasospasm
• Elevated liver transaminases (AST, ALT)
• Right upper quadrant or epigastric pain (hepatic capsule distension)
• Subcapsular haematoma and hepatic rupture — rare but catastrophic

5.3 Haematological Effects

• Thrombocytopenia — platelet consumption secondary to endothelial activation and microthrombi
• Microangiopathic haemolytic anaemia (MAHA) — fragmentation of erythrocytes across fibrin strands in small vessels
• In severe cases, disseminated intravascular coagulation (DIC)

5.4 Neurological Effects

• Severe headache, visual disturbances (scotomata, blurred vision), hyperreflexia
• Cerebral oedema and vasoconstriction
• Eclamptic seizures — generalised tonic-clonic; mechanism incompletely understood but involves posterior reversible encephalopathy (cerebral vasospasm and auto-regulatory breakthrough)
• Cortical blindness and intracranial haemorrhage in severe cases

5.5 Placental and Fetal Effects

• Placental infarction (ischaemic necrosis from chronic hypoperfusion)
• Retroplacental haemorrhage and abruption
• Increased syncytial epithelial knots on placental villi
• Acute atherosis — fibrinoid necrosis of decidual vessels with lipid-laden macrophage accumulation (the vascular hallmark on pathology)³
• Fetal growth restriction, oligohydramnios, fetal distress

6. HELLP Syndrome

• Microangiopathic haemolysis (elevated LDH, abnormal peripheral blood smear)
• AST and ALT > 70 U/L¹
• Platelet count < 100,000/μL¹

7. Diagnostic Criteria

• BP ≥ 140/90 mmHg on two occasions ≥ 4 hours apart, after 20 weeks gestation in a previously normotensive woman, plus
• Proteinuria > 300 mg/24 hours (or protein/creatinine ratio ≥ 0.3), or
• In the absence of proteinuria: thrombocytopenia (< 100,000/μL), renal insufficiency (creatinine > 1.1 mg/dL), impaired liver function (transaminases twice the upper limit of normal), pulmonary oedema, or new-onset headache unresponsive to analgesia²

• BP ≥ 160/110 mmHg on two occasions ≥ 4 hours apart
• Creatinine > 1.1 mg/dL or doubling of baseline
• Platelets < 100,000/μL
• Transaminases ≥ twice the upper limit of normal
• Pulmonary oedema
• New-onset headache or visual disturbances²

8. Management

8.1 General Principles

• Term (≥ 37 weeks) with any preeclampsia: prompt delivery
• Late preterm (34–36⁶⁄₇ weeks) with severe features: deliver
• Early preterm (< 34 weeks) without contraindications: expectant management with close surveillance to extend gestation and allow antenatal corticosteroid administration (betamethasone)

8.2 Antihypertensive Therapy

• Systolic BP > 160 mmHg or diastolic BP > 105 mmHg⁴

• Hydralazine 5–10 mg IV/IM, repeated at 20-minute intervals⁴
• Labetalol 20 mg IV, escalating to 40 mg at 10 min if BP uncontrolled⁴

• α-Methyldopa 250 mg twice daily — centrally acting α₂ agonist; established safety profile in pregnancy⁴
• Labetalol 100 mg twice daily — combined α₁/β-blocker⁴
• Nifedipine 30 mg once daily — calcium channel blocker; reasonable evidence of safety⁴

• ACE inhibitors and angiotensin receptor blockers — unequivocal adverse fetal effects (renal agenesis, fetal hypotension, oligohydramnios)⁴

8.3 Seizure Prevention and Treatment — Magnesium Sulphate

• Loading dose: 4–6 g IV over 15–20 minutes
• Maintenance: 1–2 g/hour IV infusion
• Monitor for toxicity: loss of deep tendon reflexes (first sign, at ~7 mEq/L), respiratory depression (> 10 mEq/L), cardiac arrest (> 15 mEq/L)
• Antidote: Calcium gluconate 1 g IV

8.4 Fetal Surveillance

• Serial growth ultrasound (every 3–4 weeks)
• Umbilical artery Doppler velocimetry — reversed end-diastolic flow is an indication for delivery regardless of gestational age²
• Non-stress testing (NST) and biophysical profile
• Continuous electronic fetal monitoring in labour

9. Prognosis and Long-Term Sequelae

• Women with a history of preeclampsia have a 2-fold increased lifetime risk of ischaemic heart disease, stroke, and hypertension
• The shared pathophysiology (endothelial dysfunction, inflammation, abnormal lipid metabolism) suggests that preeclampsia may unmask underlying susceptibility to vascular disease rather than simply cause it

10. Prevention

• Low-dose aspirin (81 mg/day, initiated between 12–28 weeks): reduces thromboxane synthesis preferentially over prostacyclin, restoring prostaglandin balance; recommended by USPSTF for women at high risk¹
• Calcium supplementation: reduces risk in populations with low dietary calcium intake
• Low-molecular-weight heparin in antiphospholipid syndrome
• There is no evidence that dietary salt restriction, bed rest, or vitamin C/E supplementation reduces incidence

11. Conclusion

Bibliography

1. Tintinalli JE, Ma OJ, Yealy DM, et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020. Chapter: "Preeclampsia and Eclampsia," pp. 2454–2470.
2. Resnik R, Lockwood CJ, Moore TR, et al. Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice. 8th ed. Elsevier; 2022. Chapter 45: "Preeclampsia and Eclampsia," pp. 1057–1120.
3. Kumar V, Abbas AK, Aster JC. Robbins & Kumar Basic Pathology. 11th ed. Elsevier; 2023. Chapter: "Preeclampsia/Eclampsia," pp. 701–702.
4. Brunton LL, Knollmann BC, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 14th ed. McGraw-Hill Education; 2023. Chapter: "Pregnancy-Induced Hypertension/Preeclampsia," pp. 95–104.
5. Hall JE, Hall ME. Guyton and Hall Textbook of Medical Physiology. 14th ed. Elsevier; 2021. Chapter 83: "Pregnancy and Lactation — Preeclampsia and Eclampsia," pp. 1040–1042.
6. Marx JA, Hockberger RS, Walls RM, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2023. Chapter: "Pregnancy-Induced Hypertension (Preeclampsia and Eclampsia)," pp. 4741–4776.