Lidocaine suppresses ventricular arrhythmias arising in acutely ischaemic myocardium far more effectively than those arising in normal tissue. The pharmacological basis for this selectivity is:
- A Higher affinity for cardiac versus neuronal sodium channels
- B Selective uptake into ischaemic tissue via organic anion transporters
- C Preferential binding to open and inactivated sodium channels, which accumulate in depolarised ischaemic cells during rapid firing ✓
- D Inhibition of delayed rectifier potassium channels only in ischaemic zones
Correct answer: C. Preferential binding to open and inactivated sodium channels, which accumulate in depolarised ischaemic cells during rapid firing
Explanation
Ischaemic myocytes are partially depolarised, spend more time with sodium channels in open and inactivated states, and fire repetitively. Lidocaine binds preferentially to these channel states, showing strong frequency (use) dependence and little effect on normally polarised, slowly firing tissue. This explains its safety profile in normal conducting tissue and its value in ischaemia-driven ventricular ectopy. No transporter-based selectivity exists, and lidocaine does not block delayed rectifier potassium channels.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.