Maternal Physiological Changes in Pregnancy

Cardiovascular System

• Cardiac output: increases 30-50% by 28-32 weeks (peaks mid-third trimester); due to increased stroke volume (early pregnancy) and heart rate (+15-20 bpm)
• Systemic vascular resistance (SVR): decreases by 25-30% due to progesterone-mediated vasodilation and low-resistance uteroplacental circulation
• Blood pressure: falls in first and second trimester (nadir at 20-24 weeks), returns to pre-pregnancy levels by term
• Blood volume: increases by 40-50% (plasma volume rises more than red cell mass → physiological anaemia of pregnancy)
• Aortocaval compression: supine position after 20 weeks — gravid uterus compresses IVC and aorta → reduced venous return, hypotension, fetal compromise; managed with left lateral tilt

Respiratory System

• Tidal volume: increases 40% (progesterone-mediated central respiratory drive stimulation)
• Respiratory rate: unchanged
• Minute ventilation: increases 40% (due to increased tidal volume)
• Functional residual capacity (FRC): decreases 20% (elevated diaphragm)
• Oxygen consumption: increases 20%
• Arterial blood gases: respiratory alkalosis (PaCO2 ~4kPa/30mmHg; pH 7.44); compensated by renal bicarbonate excretion
• Clinical significance: pregnant women desaturate faster during intubation (reduced FRC + increased O2 consumption); pre-oxygenation is critical

Renal System

• Glomerular filtration rate (GFR): increases 50% by end of first trimester
• Renal plasma flow: increases 80%
• Serum creatinine: falls (normal in pregnancy ~50-70 umol/L; a "normal" non-pregnant creatinine may indicate renal impairment in pregnancy)
• Urea: falls
• Glycosuria: physiological — reduced tubular reabsorption threshold for glucose (does NOT indicate diabetes)
• Ureteric dilation: progesterone relaxation + mechanical compression by uterus (right > left); predisposes to UTI and pyelonephritis
• Proteinuria: up to 300mg/24h considered normal (above this = significant in pre-eclampsia context)

Haematological System

• Plasma volume: increases 50%
• Red cell mass: increases 20-30% → net result = physiological anaemia (Hb nadir at 28-32 weeks)
• White blood cells: leukocytosis (up to 15 × 10^9/L normal in pregnancy; up to 25 × 10^9/L in labour)
• Platelets: mild thrombocytopenia common (gestational thrombocytopenia >100 × 10^9/L is benign)
• Coagulation: hypercoagulable state — Factors VII, VIII, X, XII, fibrinogen increase; Protein S decreases; Protein C unchanged
• D-dimer: physiologically elevated — unreliable for VTE exclusion in pregnancy
• ESR: elevated (unreliable inflammatory marker in pregnancy)
• Iron requirements: increase 2-3 fold; folic acid requirements increase

Gastrointestinal System

• Lower oesophageal sphincter (LOS): tone decreased (progesterone) → gastro-oesophageal reflux
• Gastric emptying: delayed (particularly in labour) → increased aspiration risk with GA
• Gut motility: reduced → constipation
• Gallbladder: progesterone reduces motility → increased gallstone risk
• Liver function: alkaline phosphatase increases (placental isoenzyme); albumin decreases (dilutional); ALT/AST normally unchanged

Endocrine System

• hCG: produced by syncytiotrophoblast; peaks at 8-10 weeks; maintains corpus luteum; responsible for pregnancy nausea; structurally similar to TSH (can cause transient hyperthyroidism in first trimester)
• Human placental lactogen (hPL): anti-insulin, lipolytic; promotes maternal glucose availability for fetus; increases with gestational age
• Thyroid: TBG increases (oestrogen-driven) → total T4 increases but FREE T4 remains normal; TSH may decrease in first trimester (hCG cross-reactivity)
• Cortisol: total and free cortisol increase (CRH produced by placenta); but Cushing's features do not develop
• Prolactin: increases 10-fold; prepares breasts for lactation

Metabolic Changes

• First trimester: anabolic phase — fat storage, increased insulin sensitivity
• Second/third trimester: catabolic, diabetogenic — insulin resistance increases (hPL, cortisol, progesterone); ensures glucose availability for fetus
• Fasting state: accelerated starvation — rapid switch to ketogenesis; pregnant women develop ketosis faster
• Lipids: total cholesterol and triglycerides increase
• Calcium: total calcium decreases (dilutional), ionised calcium unchanged; increased intestinal absorption and renal reabsorption

Important Facts for MRCOG

• Cardiac output peaks at 28-32 weeks (+30-50%)
• Physiological anaemia: plasma volume rises more than red cell mass
• Respiratory alkalosis: PaCO2 ~30mmHg is normal in pregnancy
• GFR increases 50%; serum creatinine FALLS (a "normal" creatinine may be abnormal)
• Glycosuria is physiological — does not indicate diabetes
• Hypercoagulable state: increased factors + decreased Protein S
• D-dimer unreliable for VTE diagnosis in pregnancy
• Delayed gastric emptying + reduced LOS tone → aspiration risk with GA
• Diabetogenic state of late pregnancy: driven by hPL, cortisol, progesterone

Clinically reviewed by NHS obstetricians and gynaecologists

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