Lidocaine suppresses ventricular arrhythmias after acute myocardial infarction but is largely ineffective in atrial arrhythmias. The pharmacokinetic-pharmacodynamic property best explaining this selectivity is:
- A It accumulates preferentially in atrial tissue because of higher local blood flow
- B It shows rapid association and dissociation from open and inactivated sodium channels, states favored in depolarized ischemic ventricular tissue ✓
- C It binds avidly to resting channels, which are more abundant in ventricular muscle
- D It prolongs action potential duration selectively in Purkinje fibers
Correct answer: B. It shows rapid association and dissociation from open and inactivated sodium channels, states favored in depolarized ischemic ventricular tissue
Explanation
Lidocaine is a class IB agent with fast kinetics of binding to open and inactivated sodium channels. Ischemic ventricular cells are partially depolarized, spend more time in these channel states at higher firing rates, so lidocaine concentrates its block there while barely affecting normal atrial tissue. It shortens rather than prolongs APD in Purkinje fibers, eliminating option D, and its lack of resting-channel affinity distinguishes it from class IA drugs.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
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