Lidocaine suppresses ventricular arrhythmias after myocardial infarction but has little effect on atrial arrhythmias. The pharmacologic basis for this atrial sparing is:
- A Lidocaine selectively accumulates in atrial nodal tissue
- B Lidocaine is inactivated by atrial acetylcholinesterase
- C It binds preferentially to the inactivated state of sodium channels, favored by the depolarized, frequently firing ischemic ventricular tissue, while atrial action potentials are too short to favor binding ✓
- D Atrial tissue lacks voltage-gated sodium channels entirely
Correct answer: C. It binds preferentially to the inactivated state of sodium channels, favored by the depolarized, frequently firing ischemic ventricular tissue, while atrial action potentials are too short to favor binding
Explanation
Class IB drugs like lidocaine show state-dependent (use-dependent) blockade, binding strongly to open and inactivated sodium channels. Ischemic ventricular cells are partially depolarized and fire repetitively, favoring drug access, whereas the short atrial action potential gives little time for channel occupancy. This underlies its selectivity for ventricular ectopy and its uselessness in atrial fibrillation. Atrial tissue certainly has sodium channels (option D is false), so the difference is kinetic, not structural.
Reference: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
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Written and medically reviewed by the StethoPrep medical team.