A 50-year-old male on azithromycin for community-acquired pneumonia develops palpitations. ECG shows a prolonged QTc interval of 520 ms. Azithromycin causes QT prolongation primarily by:
- A Activating cardiac L-type calcium channels, increasing the plateau phase of the action potential
- B Blocking the cardiac hERG (IKr) potassium channel, prolonging cardiac repolarization ✓
- C Inhibiting the sodium-calcium exchanger in ventricular myocytes
- D Increasing early afterdepolarizations via beta-1 receptor sensitization
Correct answer: B. Blocking the cardiac hERG (IKr) potassium channel, prolonging cardiac repolarization
Explanation
Azithromycin (and other macrolides, particularly erythromycin) block the hERG (human ether-a-go-go related gene) cardiac potassium channel, which carries the rapid delayed rectifier potassium current (IKr) responsible for ventricular repolarization. Blockade of this channel delays repolarization, prolongs the QT interval, and can precipitate Torsades de Pointes (TdP), a potentially fatal ventricular arrhythmia. Risk is increased with concurrent QT-prolonging drugs, hypokalemia, hypomagnesemia, and structural heart disease.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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