A 26-year-old woman with known mitral stenosis (valve area 1.2 cm²) becomes pregnant. At 28 weeks, she develops dyspnea at rest, orthopnea, and a chest X-ray shows pulmonary venous congestion. She is in sinus rhythm. What is the underlying pathophysiology explaining why pregnancy particularly decompensates mitral stenosis at this gestational age?

• A Increased heart rate (physiological tachycardia of pregnancy) reduces diastolic filling time and raises left atrial pressure across the fixed stenotic valve ✓
• B Decrease in serum albumin in third trimester reduces plasma oncotic pressure causing pulmonary edema
• C Physiological hemodilution causes right heart dilatation, causing paradoxical shift of interventricular septum that worsens left ventricular filling
• D Elevated progesterone increases pulmonary vascular resistance in the third trimester

Explanation

Mitral stenosis (MS) is the most common rheumatic valvular disease in pregnancy in India. Pregnancy increases cardiac output by 40–50% (beginning in first trimester, peaking at 28–32 weeks), heart rate rises by 10–20 bpm, and blood volume increases 40–50%. In MS, the stenotic valve creates a fixed obstruction to left atrial outflow. The higher physiological heart rate of pregnancy (up to 90–100 bpm) critically shortens diastolic filling time—the period when blood crosses the mitral valve—raising mean left atrial pressure, causing pulmonary venous hypertension and pulmonary edema. This explains why MS decompensation peaks at 28–32 weeks (maximum hemodynamic load). Management includes diuretics, rate control (beta-blockers), and possibly percutaneous balloon mitral valvotomy if valve anatomy is suitable.

Reference: Williams Obstetrics, 26th ed.

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Written and medically reviewed by the StethoPrep medical team.