Lidocaine suppresses ventricular arrhythmias after myocardial infarction but is largely ineffective against atrial arrhythmias. This tissue selectivity is best explained by its:
- A Selective blockade of the rapid delayed rectifier potassium current in Purkinje fibers
- B Preferential binding to channels in the open and inactivated states, which predominate in depolarized ischemic tissue ✓
- C Antagonism of muscarinic receptors unique to ventricular muscle
- D Enhancement of the slow inward calcium current in diseased myocytes
Correct answer: B. Preferential binding to channels in the open and inactivated states, which predominate in depolarized ischemic tissue
Explanation
Lidocaine is a class IB agent that binds sodium channels preferentially in their open and inactivated states. Ischemic and damaged ventricular tissue is relatively depolarized, with resting potentials shifted positive, so more channels reside in the inactivated state where lidocaine affinity is highest. Atrial action potentials are shorter and less inactivated-state dependent, explaining its ineffectiveness there. Potassium current blockade defines class III agents, and lidocaine does not alter calcium currents or cholinergic receptors.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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