A 68-year-old man with chronic heart failure develops worsening dyspnea. His PCWP is 28 mmHg and cardiac output is 3.1 L/min. The elevated PCWP primarily reflects dysfunction of which Frank-Starling mechanism component?
- A Impaired preload reduction via venodilation
- B Insufficient end-diastolic fiber stretch to augment stroke volume ✓
- C Excessive afterload reducing ejection fraction
- D Decreased myocardial oxygen consumption
Explanation
Elevated PCWP (>18 mmHg) indicates high left-sided filling pressures; in a failing heart, the Frank-Starling curve is depressed and flattened, so increasing preload (fiber stretch) no longer augments stroke volume but instead causes pulmonary congestion. The fundamental defect is impaired contractility such that increasing end-diastolic volume fails to translate into proportional stroke volume increase. Options A and D are compensatory responses rather than the primary mechanism; Option C (increased afterload) contributes but does not explain the elevated PCWP itself.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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