Lidocaine suppresses ventricular arrhythmias arising in ischemic myocardium while having little effect on normal cardiac tissue. The pharmacological basis for this selectivity is:

• A Activation of acetylcholine-sensitive potassium currents in ventricular muscle
• B Selective accumulation in normal myocardium via the Na/K ATPase
• C Prolongation of the effective refractory period exclusively in healthy Purkinje fibers
• D Preferential binding to open and inactivated sodium channels, which accumulate in depolarized, frequently firing ischemic cells ✓

Explanation

Class IB drugs like lidocaine show use-dependence and state-dependence: they bind open and inactivated states of the sodium channel and dissociate rapidly from rested channels. Ischemic tissue is partially depolarized, fires more often, and spends more time with channels in blocked-favorable states, so lidocaine concentrates its effect there. Its rapid dissociation leaves normal tissue nearly untouched and shortens or barely changes the action potential duration, unlike class IA and IC agents. Options B, C and A describe mechanisms belonging to other drug classes entirely.

Reference: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

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