At a heart rate of 150 bpm, cardiac output is 9 L/min despite a stroke volume of only 60 mL. Which Frank-Starling mechanism best explains why stroke volume does not rise further despite increased contractile demand?

• A Increased afterload from peripheral vasoconstriction limits ejection fraction
• B Shortened diastole reduces ventricular filling time, lowering preload and end-diastolic volume ✓
• C Decreased myocardial O2 supply from tachycardia-induced hypoxia
• D Negative Anrep effect reduces intrinsic contractility at high rates

Explanation

At high heart rates, diastolic filling time is disproportionately shortened compared to systolic time. This reduces ventricular end-diastolic volume (preload), so the Frank-Starling mechanism operates on a lower point of the length-tension curve, limiting stroke volume. This rate-dependent preload reduction is the primary reason SV falls at extreme tachycardia. The Anrep effect is an adaptive increase in contractility, not a decrease; afterload changes occur but are secondary.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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