Aconitine poisoning causes potentially fatal arrhythmias. The primary electrophysiological mechanism responsible for the cardiac toxicity of aconitine is:

• A Blockade of voltage-gated sodium channels, similar to class I antiarrhythmics
• B Inhibition of Na-K ATPase, leading to intracellular sodium and calcium overload like cardiac glycosides
• C Activation of KATP channels causing membrane hyperpolarisation and conduction block
• D Persistent activation of voltage-gated sodium channels, preventing repolarisation and causing depolarisation block ✓

Explanation

Aconitine binds to voltage-gated sodium channels at the same site as veratridine (site 2), causing persistent channel opening and preventing inactivation. This continuous sodium influx leads to sustained depolarisation, muscle rigidity, and in the heart, ventricular tachycardia and ventricular fibrillation. Unlike class I antiarrhythmics which block channels, aconitine locks them open. Cardiac glycosides inhibit Na-K ATPase by a distinct mechanism. There is no KATP channel interaction.

Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.