Dysrhythmias and ECG Abnormalities Associated with Amiodarone Toxicity
Dysrhythmias and ECG Abnormalities Associated with Amiodarone Toxicity
Amiodarone works by blocking potassium and calcium channels, affecting myocardial depolarization and repolarization. Amiodarone is typically used in the treatment of ventricular arrhythmias. The common indication for its use in the acute setting is atrial fibrillation with rapid ventricular response (Florek and Girzadas, 2021). Additionally, the drug has off label use in treating supraventricular tachyarrhythmias such as atrial fibrillation and preventing ventricular tachyarrhythmias in high-risk patients (Florek and Girzadas, 2021). Long term oral use is associated with adverse effects, including pulmonary, hematologic, cardiac, dermatological and ocular toxicities (Biancatelli, 2019). Further, the drug can cause epididymitis, neuromuscular disorders, thyroid disorders and psychiatric side effects.
Amiodarone has numerous cardiac and extracardiac effects. The ECG abnormalities seen with amiodarone toxicity include sinus bradycardia, Q.T prolongation and first-degree heart (A.V) block (Kumar and Singh, 2015). Bradycardia occurs due to amiodarone’s impairment of sinus beat formation and conduction, especially in patients with preexisting conduction disorders (Biancatelli et al.,2019). Amiodarone causes the prolongation of the action potential duration, which is reflected in the electrocardiogram. The most common side effect is severe sinus node dysfunction with marked sinus bradycardia (Bhatt, 2021). Coupled with Q.T prolongation, this side effect is prevalent among older adults. Studies have shown that amiodarone therapy in patients with structural heart disease and atrial fibrillation who are concomitantly treated with beta-blockers may have an increased risk of pro-arrhythmia (Schrickel et al.,2006). The drug also causes cardiogenic shock, hypersensitivity and adverse pulmonary toxicity.
Additionally, increased amiodarone toxicity leads to type one- and second-degree A.V block; other side effects are Torsades de Pointes and asystole; these side effects are, however, not common (Kumar and Singh, 2015). Lastly, hypotension may occur following intravenous administration of the drug, and in some cases, the hypotension may be refractory, resulting in death.
References
Bhatt, D. L. (2020). Opie’s Cardiovascular Drugs: A Companion to Braunwald’s Heart Disease. Elsevier Health Sciences.
Colunga Biancatelli, R. M., Congedo, V., Calvosa, L., Ciacciarelli, M., Polidoro, A., & Iuliano, L. (2019). Adverse reactions of Amiodarone. Journal of geriatric cardiology : JGC, 16(7), 552–566. https://doi.org/10.11909/j.issn.1671-5411.2019.07.004
Florek, J. B., & Girzadas, D. (2021). Amiodarone. In StatPearls [Internet]. StatPearls Publishing.
Pramod Kumar, V. S. (2015). Amiodarone Induced Variety of ECG Changes—A Beginners ECG Delight. Journal of Clinical & Experimental Cardiology, 06(07). https://doi.org/10.4172/2155-9880.1000391
Schrickel, J. W., Schwab, J. O., Yang, A., Bielik, H., Bitzen, A., Lüderitz, B., & Lewalter, T. (2006). Pro-arrhythmic effects of amiodarone and concomitant rate-control medication. Europace, 8(6), 403-407.