In refractory cases of ventricular arrhythmias and cardiogenic shock, it is most important to maintain systemic blood flow, blood pressure, and tissue oxygenation by the early use of cardiopulmonary bypass. Available clinical evidence suggests that amiodarone and flecainide are reasonable first-line treatment. Aconite-induced ventricular arrhythmias are often refractory to direct current cardioversion and antiarrhythmic drugs. Inotropic therapy is required if hypotension persists and atropine should be used to treat bradycardia. Management of aconite poisoning is supportive, including immediate attention to the vital functions and close monitoring of blood pressure and cardiac rhythm. The main causes of death are refractory ventricular arrhythmias and asystole and the overall in-hospital mortality is 5.5%. The gastrointestinal features include nausea, vomiting, abdominal pain, and diarrhea. The cardiovascular features include hypotension, chest pain, palpitations, bradycardia, sinus tachycardia, ventricular ectopics, ventricular tachycardia, and ventricular fibrillation. The neurological features can be sensory (paresthesia and numbness of face, perioral area, and the four limbs), motor (muscle weakness in the four limbs), or both. Patients present predominantly with a combination of neurological, cardiovascular, and gastrointestinal features. Aconitine, mesaconitine, and hypaconitine can induce strong contractions of the ileum through acetylcholine release from the postganglionic cholinergic nerves. Through its action on voltage-sensitive sodium channels in the axons, aconitine blocks neuromuscular transmission by decreasing the evoked quantal release of acetylcholine. It has hypotensive and bradycardic actions due to activation of the ventromedial nucleus of the hypothalamus. Aconitine has a positive inotropic effect by prolonging sodium influx during the action potential. The arrhythmogenic properties of aconitine are in part due to its cholinolytic (anticholinergic) effects mediated by the vagus nerve. The electrophysiological mechanism of arrhythmia induction is triggered activity due to delayed after-depolarization and early after-depolarization. Aconitine and mesaconitine bind with high affinity to the open state of the voltage-sensitive sodium channels at site 2, thereby causing a persistent activation of the sodium channels, which become refractory to excitation. The cardiotoxicity and neurotoxicity of aconitine and related alkaloids are due to their actions on the voltage-sensitive sodium channels of the cell membranes of excitable tissues, including the myocardium, nerves, and muscles.

Key articles with information on the use of aconite roots in traditional medicine, active (toxic) ingredients, mechanisms of toxicity, toxicokinetics of Aconitum alkaloids, and clinical features and management of aconite poisoning were reviewed. However, the use of a larger than recommended dose and inadequate processing increases the risk of poisoning.Ī Medline search (1963-February 2009) was conducted.

Soaking and boiling during processing or decoction preparation will hydrolyze aconite alkaloids into less toxic and non-toxic derivatives.

In traditional Chinese medicine, aconite roots are used only after processing to reduce the toxic alkaloid content. Severe aconite poisoning can occur after accidental ingestion of the wild plant or consumption of an herbal decoction made from aconite roots. The wild plant (especially the roots and root tubers) is extremely toxic. Aconitine and related alkaloids found in the Aconitum species are highly toxic cardiotoxins and neurotoxins.

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