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Physiological Changes in Pregnancy: Cardiac, Hematological, Pulmonological, and Renal

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1. CARDIOVASCULAR (CARDIAC) CHANGES

Summary of Changes

Causes & Pathophysiology

• Begins as early as week 6 of gestation
• Results from combined increases in stroke volume (+30%) and heart rate (+20%)
• Driven by increased metabolic demands of the mother and fetus
• Twin pregnancies increase CO a further 10–15%
• During labor and immediately postpartum, CO surges an additional 60–80% due to catecholamine release, relief of IVC compression, uterine contraction autotransfusion, and blood loss

• A primary, early change appearing in the first trimester; nadir in mid-second trimester
• Caused by: (1) progesterone and estrogen causing smooth muscle relaxation; (2) development of a low-resistance uteroplacental circulation; (3) vasodilatory prostaglandins
• Results in a drop of BP by 5–10 mmHg until the third trimester, when BP returns to near baseline

• Approximately +10 bpm above pre-pregnancy baseline
• Mediated by increased sympathetic tone and hormonal changes to maintain CO

• Cardiac chambers enlarge; myocardial hypertrophy is often seen on echocardiography
• Elevation of the diaphragm by the gravid uterus shifts the heart's position, producing:
  • Appearance of cardiomegaly on CXR
  • Left axis deviation and T-wave changes on ECG
  • Grade I–II systolic ejection flow murmur (due to increased flow)
  • Exaggerated splitting of S1
  • Audible S3 in some patients
  • Occasional small asymptomatic pericardial effusion

• After week 20, the gravid uterus compresses the inferior vena cava in the supine position
• ~5% of women develop frank supine hypotension syndrome (pallor, sweating, nausea, hypotension)
• Aortic compression also reduces uteroplacental blood flow
• Chronic partial caval compression → venous stasis, edema, phlebitis, and distension of epidural veins

• Pulmonary vascular resistance falls ~30%, preventing rises in pulmonary artery pressure despite increased CO

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2. HEMATOLOGICAL CHANGES

Causes & Pathophysiology

• Total blood volume increases by 1,000–1,500 mL by term (reaches ~90 mL/kg)
• Driven by estrogen-stimulated activation of the renin-angiotensin-aldosterone system → sodium and water retention
• Serves to: meet increased metabolic demands; protect against hemorrhage at delivery (average loss: 200–500 mL vaginal, 800–1,000 mL cesarean); reduce blood viscosity

• Plasma volume rises disproportionately (+55%) vs. red cell mass (+45%) → dilutional anemia
• Hemoglobin typically stays >11 g/dL
• The P50 for hemoglobin increases from 27 → 30 mmHg (rightward shift of the oxyhemoglobin dissociation curve), enhancing O₂ delivery to tissues and compensating for the drop in Hb
• Elevated 2,3-DPG levels drive this rightward shift
• Combined with increased CO, overall oxygen delivery to tissues is maintained

• Platelet count falls ~10% due to plasma volume expansion and increased platelet consumption (gestational thrombocytopenia)
• Rarely clinically significant in healthy pregnancies

• Clotting factors increase by +30–250%: Factors I (fibrinogen), VII, VIII, IX, X, XII all rise markedly
• Protein S (anticoagulant) decreases; acquired resistance to activated Protein C develops
• Combined with venous stasis from IVC compression → Virchow's triad is partially fulfilled
• Purpose: prepares for hemostasis at delivery
• Risk: markedly increased risk of venous thromboembolism (DVT, PE) during pregnancy and postpartum

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3. PULMONARY (RESPIRATORY) CHANGES

Causes & Pathophysiology

• Progesterone (rises up to 20× normal by term) directly stimulates the respiratory center in the medulla, increasing sensitivity to CO₂
• Result: tidal volume rises +40%, respiratory rate +15% → minute ventilation +50% by term
• PaCO₂ falls to 28–32 mmHg — a respiratory alkalosis; compensated by renal excretion of HCO₃⁻ (falls ~15%), maintaining near-normal pH
• PaO₂ rises slightly from hyperventilation
• Maternal alkalosis creates a favorable gradient for CO₂ diffusion from fetus → mother across the placenta

• Rises +20–50% by term due to increased maternal metabolic rate, fetal demands, and increased cardiac work
• The rightward shift of the O₂ dissociation curve (elevated 2,3-DPG, P50 30 mmHg) facilitates O₂ offloading to tissues

• Falls up to 20% at term; returns to normal within 48 hours of delivery
• Caused by upward displacement of the diaphragm by the enlarging uterus, compressing the lungs and reducing expiratory reserve volume
• The diaphragm itself retains full excursion; the chest compensates with increased anteroposterior diameter
• Vital capacity and closing capacity are minimally affected

• Rapid O₂ desaturation during apnea → preoxygenation is mandatory before general anesthesia
• In supine position at term, closing volume may exceed FRC → atelectasis and V/Q mismatch
• The decrease in FRC + increase in minute ventilation also accelerates uptake of inhalational anesthetics

• Caused by progesterone-mediated bronchodilation (relaxes bronchial smooth muscle)
• Flow-volume loops are unaffected

• Mucosal engorgement of the respiratory tract (due to estrogen-induced capillary congestion) → friable, edematous airways prone to trauma, bleeding, and obstruction during intubation
• CXR shows prominent pulmonary vascular markings (due to increased pulmonary blood volume) and elevated diaphragm

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4. RENAL CHANGES

Causes & Pathophysiology

• Begins early in pregnancy, paralleling the increase in cardiac output
• Driven by: (1) increased CO delivering more blood to kidneys; (2) renal vasodilation from progesterone, relaxin, and prostacyclin reducing renal afferent arteriolar resistance; (3) activation of the RAAS increasing renal perfusion pressure
• GFR rises ~50% by the end of the first trimester

• Direct consequence of increased GFR — creatinine is cleared more rapidly
• Normal pregnancy values: serum Cr ~0.5 mg/dL, BUN ~9 mg/dL
• A "normal" creatinine of 1.0 mg/dL in a pregnant woman actually indicates significant renal dysfunction

• Decreased renal tubular threshold for glucose and amino acids relative to the elevated filtered load
• Results in physiological glycosuria (1–10 g/day) and proteinuria (<300 mg/day)
• Does NOT indicate diabetes or renal disease unless thresholds are exceeded

• Drops by 8–10 mOsm/kg due to dilutional effects of plasma volume expansion and resetting of the osmoreceptor threshold (likely mediated by relaxin and hCG)
• Serum sodium falls slightly but remains within reference range

• The ureters and renal pelvis dilate (physiological hydroureter/hydronephrosis), particularly on the right side, due to: (1) progesterone-mediated smooth muscle relaxation; (2) mechanical compression by the gravid uterus
• This dilation predisposes to urinary stasis and ascending UTI/pyelonephritis

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Integrating Summary

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