The management of ventricular dysrhythmia in aconite poisoning

Abstract

Based on the evidence available from human case reports, flecainaide or amiodarone appear to be more associated with a return to sinus rhythm than lidocaine and/or cardioversion, although it is not established whether the administration of treatment caused reversion to normal sinus rhythm. The potential beneficial effects of amiodarone were not observed in animal studies. This may be due to intra-species differences between ion channels or relate to the wider cardiovascular toxicity of aconite that extends beyond arrhythmias. Prolonged cardiopulmonary resuscitation and cardiopulmonary bypass should be considered as an integral part of good clinical care as "time-buying" strategies to allow the body to excrete the toxic alkaloids. There may also be a role for mexiletine, procainamide and magnesium sulphate.

Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review

“…Because there is no specific antidote, supportive care based on blood pressure and cardiac rhythm can prevent refractory ventricular arrhythmias or asystole, which are the main causes of death during the first 24 h [18,22,25]. Understanding the interactions with electrolyte channels and cellular mechanisms relevant to the toxicology of Aconitum can contribute to the appropriate application of agents for aconite-related cardiotoxicity [25]. …”

“…Aconite alkaloids categorized as DDAs, especially aconitine and mesaconitine, exhibit a high affinity with site 2 of the alpha-subunit voltage-dependent sodium (Na + ) channels present on the cell membranes of excitable tissues, including most of the myocardium, nerves, and muscles [18,25]. The binding of these alkaloids promotes persistent opening of the Na + channel through suppressing conformational changes to the inactive state [25,26].…”

“…The binding of these alkaloids promotes persistent opening of the Na + channel through suppressing conformational changes to the inactive state [25,26]. Prolongation of the open state of Na + channels and late Na + current leads to an increase in intracellular Na + , with subsequent membrane depolarization and the duration of action potential, referred to as early afterdepolarization.…”

“…The increase in intracellular Na + favors an increase in intracellular Ca 2+ through the activation of the Ca 2+ /Na + bidirectional exchanger and the release of intracellular Ca 2+ stored in the sarcoplasmic reticulum [18,25,26]. Aconitine has also been shown to block the potassium channels responsible for rapid and ultra-rapid delayed rectifier currents, which can result in further prolongation of the action potential [15,25,27]. The effects on calcium and potassium develop delayed afterdepolarization during the refractory period.…”

“…The effects on calcium and potassium develop delayed afterdepolarization during the refractory period. Higher concentrations of aconitine suppress action potential transmission by continuous opening of the Na + channel, which reduces the release of acetylcholine at the axonal end terminus and the vagotonic effects at the myocardium [18,25]. The bradycardia and hypotensive manifestations can be explained by activation of the ventromedial nucleus of the hypothalamus associated with depression of the circulatory system and inhibition of L-type calcium channel currents that serve as a major driver of pacemaker monocytes [18,21,25,26,27].…”