Lidocaine suppresses ventricular arrhythmias after myocardial infarction but is ineffective in atrial arrhythmias. The pharmacokinetic-pharmacodynamic reason for this tissue selectivity is:

• A Lidocaine accumulates only in ventricular myocytes because of selective uptake transporters
• B It is metabolized only by enzymes expressed in ventricular muscle
• C It selectively blocks atrial potassium channels
• D Its fast association and dissociation kinetics make block prominent in depolarized, frequently firing ischemic ventricular tissue but minimal in normally polarized atrial tissue ✓

Explanation

Lidocaine is a class Ib agent with rapid onset and offset of sodium channel block, giving strong use dependence. Ischemic ventricular cells are partially depolarized with reduced resting potential, which favors lidocaine binding, so block concentrates there. Atrial action potentials are shorter and normally polarized, so little block occurs, explaining its lack of efficacy in supraventricular arrhythmias.

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

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