A patient receiving moxifloxacin develops prolonged QTc on ECG. This adverse effect is most directly related to moxifloxacin's action on:

• A Inhibition of the rapid delayed rectifier potassium channel (hERG/IKr) ✓
• B Stimulation of cardiac beta-1 adrenergic receptors
• C Inhibition of cardiac sodium-calcium exchanger
• D Direct inhibition of cardiac DNA gyrase altering repolarization genes

Explanation

QTc prolongation by moxifloxacin (and other fluoroquinolones like levofloxacin to a lesser extent) results from blockade of the hERG cardiac potassium channel (IKr), which normally mediates rapid delayed rectifier current during cardiac repolarization. Inhibiting IKr delays repolarization, prolongs the QT interval, and predisposes to torsades de pointes. This is a class effect more pronounced with moxifloxacin than with ciprofloxacin.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.