Magnesium in Aconitine‐Induced Electrical Storm—Mechanism Yes, Mandate No

Aconitine poisoning produces lethal ventricular arrhythmias through persistent activation of cardiac sodium channels. We critically comment on a recent case report describing 28 biphasic shocks for aconitine-induced electrical storm, addressing three fundamental questions. First, we demonstrate that verapamil is contraindicated as it worsens hypotension and reflex sympathetic activation without antagonizing sodium channel toxicity. Second, we review the evidence for magnesium sulfate: while basic science and observational data support its mechanistic role as a calcium antagonist and sodium channel modulator, Class IC antiarrhythmics (flecainide) demonstrate superior conversion rates (86% vs. 22% for magnesium monotherapy). Magnesium should be viewed as an evidence-based adjunct, not mandated first-line therapy. Third, we identify critical monitoring gaps including dynamic electrolyte assessment, ionized calcium repletion, and toxin quantification that must be addressed in future cases. We propose a practical, evidence-based algorithm emphasizing: (1) first-line flecainide 2 mg/kg IV, (2) magnesium sulfate adjunct targeting serum levels of 1.5-2.0 mmol/L, (3) aggressive calcium repletion to > 1.00 mmol/L, (4) early high-flux hemoperfusion within 6 h, and (5) VA-ECMO for refractory cases. Verapamil, diltiazem, and β-blockers as sole agents should be explicitly avoided.