The management of ventricular dysrhythmia in aconite poisoning

• Published in: Clinical toxicology (Philadelphia, Pa.) Pa.), 2017-06, Vol.55 (5), p.313-321
• Main Authors: Coulson, James M., Caparrotta, Thomas M., Thompson, John P.
• Format: Article
• Language: English
• Subjects: Aconite; aconitine; Aconitum - chemistry; Aconitum - poisoning; amiodarone; Animals; Anti-Arrhythmia Agents - therapeutic use; Arrhythmias, Cardiac - chemically induced; Arrhythmias, Cardiac - drug therapy; Arrhythmias, Cardiac - physiopathology; Calcium - metabolism; Cardiopulmonary Bypass; Cardiopulmonary Resuscitation; Databases, Factual; direct cardioversion; Disease Models, Animal; dysrhythmia; Electric Countershock; flecainide; Heart Conduction System - drug effects; Heart Conduction System - physiopathology; Humans; lidocaine; Neurons - drug effects; Neurons - metabolism; Poisoning - etiology; Poisoning - physiopathology; prolonged cardio-pulmonary resuscitation; Sodium - metabolism; Sodium Channels - drug effects; Sodium Channels - metabolism; Toxicokinetics; Ventricular Fibrillation - chemically induced; Ventricular Fibrillation - drug therapy; Ventricular Fibrillation - physiopathology
• ISSN: 1556-3650; 1556-9519
• DOI: 10.1080/15563650.2017.1291944

Introduction: Aconite poisoning is relatively rare but is frequently complicated by ventricular dysrhythmias, which may be fatal. Molecular basis of aconite alkaloid ventricular arrhythmogenicity: Aconite exerts its toxic effects due to the presence of an admixture of alkaloids present in all parts of the plant. The major target of these aconite alkaloids is the fast voltage-gates sodium channel, where they cause persistent activation. This blockade of the channel in the activated state promotes automaticity within the ventricular myocardium and the generation of ventricular arrhythmias. Aconitine-induced arrhythmias: Aconite alkaloids are known to cause many different types of disturbance of heart rhythm. However, this focused review specifically looks at ventricular rhythm disturbances, namely ventricular ectopy, ventricular tachycardia, torsades des pointes and ventricular fibrillation. Objective: The objective of this review was to identify the outcome of anti-dysrhythmic strategies from animal studies and case reports in humans in order to guide the management of ventricular dysrhythmias in aconite poisoning in humans. Methods: A review of the literature in English was conducted in PubMed and Google Scholar from 1966 to July 2016 using the search terms "aconite/aconitine"; "aconite/aconitine + poisoning" and "aconite/aconitine + dysrhythmia". 168 human case-reports and case-series were identified by these searches, of which 103 were rejected if exposure to aconite did not result in ventricular dysrhythmias, if it was uncertain as to whether aconite had been ingested, if other agents were co-ingested, if there was insufficient information to determine the type of treatments administered or if there was insufficient information to determine outcome. Thus, 65 case reports of probable aconite poisoning that resulted in ventricular dysrhythmias were identified. Toxicokinetic data in aconite poisoning: Data were only available in three papers; the presence of ventricular rhythm disturbances directly correlated with the concentration of aconite alkaloids in the plasma. Management: 54 of 65 cases developed ventricular tachycardia, six developed torsades des pointes, 15 patients developed ventricular fibrillation, 10 developed ventricular ectopics and one developed a broad complex tachycardia not otherwise specified; each dysrhythmia was regarded as separate and patients may have had more than one dysrhythmia. 10 patients died, giving a mortality of 15%. In to