A patient with severe aortic stenosis (AVA 0.7 cm²) has maintained normal stroke volume. Which Frank-Starling mechanism explains this preserved function, and what eventual failure mechanism supervenes?
- A Increased preload stretches sarcomeres toward optimal length, increasing cross-bridge formation; failure occurs when ventricular dilation reaches the descending limb of the Starling curve
- B Concentric LVH normalizes systolic wall stress (Laplace law), maintaining SV; failure occurs when hypertrophy becomes maladaptive — interstitial fibrosis, diastolic dysfunction, and ultimately systolic failure from reduced coronary reserve and energy depletion ✓
- C Tachycardia compensates for reduced SV per beat; failure occurs when heart rate can no longer increase
- D Baroreceptor-mediated RAAS activation increases contractility; failure occurs when RAAS is maximally activated
Explanation
In pressure overload (aortic stenosis), the LV initially compensates by concentric hypertrophy — parallel sarcomere addition thickens the wall. Per Laplace's law (wall stress = P×r / 2h), increased wall thickness (h) normalizes systolic stress despite high pressure (P), allowing maintained stroke volume with normal EF. Maladaptive consequences of excessive hypertrophy include: impaired diastolic filling (stiff ventricle → diastolic dysfunction), subendocardial ischemia (hypertrophied myocardium outgrows coronary supply), and fibrosis replacing cardiomyocytes → ultimately systolic dysfunction. Option A describes the eccentric (volume overload) compensation.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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