DISCUSSION

Bidirectional ventricular tachycardia is a rare ventricular dysrhythmia characterized by beat-to-beat variation in the QRS axis. The differential diagnosis for this dysrhythmia is limited to severe digitalis/digoxin toxicity,^{Reference Richter and Brugada1} familial catecholaminergic polymorphic ventricular tachycardia,^{Reference Femenia, Barbosa-Barros and Sampaio2} and herbal aconite poisoning.^{Reference Smith, Shah, Hunt and Herzog3} Importantly, if bidirectional ventricular tachycardia is recognized on ECG, digoxin toxicity should always be at the top of the differential diagnosis because it is this poisoning alone that has antidotal treatment. Consideration should be given to catecholaminergic polymorphic ventricular tachycardia and aconite toxicity as possible etiologies once digoxin toxicity has been ruled out.

Aconite (aconitum species) is a highly toxic plant that contains aconitine and related alkaloids. Aconite roots have been used in traditional Chinese medicine, only after processing, which reduces the toxic alkaloid content by up to 90%, for its analgesic, anti-inflammatory, and cardiotonic effects. Soaking and boiling during processing or decoction preparation will hydrolyze aconite alkaloids into less toxic and non-toxic derivatives. Inadequate processing, consumption of large amount, or ingestion of the raw plant will increase the risk of toxicity.^{Reference Chan4} Aconite poisoning is more common in East Asia. Recognition of this entity may pose a considerable challenge in both diagnosis and management, particularly in parts of the world where aconite use is less common.^{Reference Chan4} There are many different species of aconitum. In Europe and North America, aconite poisoning usually occurs after ingestion of aconitum napellus, commonly called monkshood, wolfsbane, or devil's helmet.^{Reference Chan4}

Ingestion of any part of the aconite plant or its extracts can cause cardiotoxicity, neurotoxicity, and gastrointestinal (GI) manifestations.^{Reference Chan4} Aconite binds to the open state of voltage-sensitive sodium channels and induces its persistent activation in the myocardium and the nervous system, rendering cells refractory to further excitation. Tachydysrhythmias occur predominantly because of triggered activity due to delayed and early after-depolarization within the cardiac myocytes.^{Reference Chan4}

Bidirectional ventricular tachycardia from aconite poisoning has been previously reported in North America.^{Reference Smith, Shah, Hunt and Herzog3} The clinical course has been characterized by refractory ventricular dysrhythmias often resolving after 24 hours, but, in some cases, complete recovery may be delayed beyond a week post-ingestion.^{Reference Coulson, Caparrotta and Thompson5} The mainstay of treatment is supportive care and management of ventricular dysrhythmias with standard Advanced Cardiac Life Support protocols. There is no antidote for aconite toxicity, but there have been anecdotal reports of successful restoration of sinus rhythm with anti-dysrhythmics, specifically those with sodium channel blocking properties: flecainide, lidocaine, procainamide, and amiodarone.^{Reference Coulson, Caparrotta and Thompson5} If ventricular dysrhythmias and hemodynamic compromise are refractory to medical management, early use of extracorporeal membrane oxygenation is recommended.^{Reference Chan4,Reference Coulson, Caparrotta and Thompson5} The aconitine alkaloids are rapidly absorbed from the GI tract and therefore GI decontamination, gastric lavage, or activated charcoal may only be considered in patients who present early to the ED with careful consideration of aspiration risk and airway protection. Enhanced elimination via extracorporeal techniques (e.g., hemodialysis) is unlikely to be effective in removing circulating aconitine due to its lipid solubility and large molecular size.^{Reference Chan4,Reference Coulson, Caparrotta and Thompson5}