As heart rate increases from 60 to 180 bpm, the duration of the ventricular action potential shortens markedly. Which mechanism primarily accounts for this rate-dependent shortening?

• A Increased intracellular Na+ activating the Na+/Ca2+ exchanger
• B Accumulation of extracellular K+ during rapid rates
• C Inactivation of L-type calcium channels and enhanced repolarizing K+ currents ✓
• D Reduced Na+/K+ ATPase activity causing depolarization block

Explanation

At faster heart rates, the action potential duration shortens because L-type calcium channels have less time to recover from inactivation (reducing inward plateau current), while delayed rectifier potassium currents (IKr, IKs) have less time to deactivate between beats, increasing outward current. This rate-dependent shortening is a fundamental property of ventricular myocardium and underlies the physiological QT shortening with tachycardia. Extracellular K+ accumulation is minor at physiological rates.

Reference: Ganong's Review of Medical Physiology, 26th ed.

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