Background: Amiodarone is a class III antidysrhythmic first released for human use in 1962. As with other drugs in this class, amiodarone acts by blocking potassium channels thus prolonging the action potential. This, in turn, leads to a lengthening of depolarization of the atria and ventricles. The drug spread rapidly through US hospitals as it was touted as “always works, and no side effects,” by it’s pharmaceutical manufacturer (Bruen 2016).
Of course, nothing comes free and soon after the drug became widely used, a multitude of adverse effects became apparent. These included minor issues – sun sensitivity and corneal deposits – to major ones – thyroid dysfunction (hypo- and hyperthyroidism), pulmonary toxicity and liver damage. Additionally, the medication’s mechanism of action wasn’t clean and simple – amiodarone is no known to have sodium-channel blocking (Class I), beta-blocking (Class II) and calcium-channel blocking (Class IV) effects.
Despite the multitude of issues, the drug continued to be used extensively because of it’s purported benefits. The drug was most commonly applied in the Emergency Department (ED) for conversion of atrial fibrillation, conversion of stable ventricular tachycardia and in refractory VF/VT cardiac arrest.
This post dives into the three most common places amiodarone is employed in the ED: cardioverion of atrial fibrillation, cardioversion of VT and in refractory VF/VT cardiac arrest and demonstrates that superior evidence points to better options for management. Read more →