A 72-year-old with severe aortic stenosis has a transvalvular gradient of 80 mmHg. His left ventricle has undergone concentric hypertrophy. The primary adaptive mechanism allowing maintenance of normal ejection fraction despite increased afterload is:
- A Increased sarcomere number in parallel reducing wall stress via Laplace's law ✓
- B Increased preload via Starling mechanism
- C Increased sarcomere number in series causing eccentric hypertrophy
- D Increased heart rate compensating for reduced stroke volume
Explanation
Concentric hypertrophy occurs in response to pressure overload (e.g., aortic stenosis or hypertension). By adding sarcomeres in parallel, wall thickness increases, and according to Laplace's law (wall stress = pressure × radius / 2 × thickness), increased wall thickness reduces systolic wall stress. This normalization of wall stress preserves contractile function and maintains ejection fraction despite the elevated afterload. Eccentric hypertrophy (sarcomeres in series, increasing chamber radius) occurs with volume overload and would worsen wall stress in pressure overload. Starling mechanism and heart rate compensation are secondary adaptive responses.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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