Journal of Anaesthesia & Critical Care Case Reports

Vol 9 | Issue 2 | May-August 2023 | Page: 11-13 | Adam Lepkowsky, Angela Johnson, Alan Markowitz

DOI: https://doi.org/10.13107/jaccr.2023.v09i02.218

Author: Adam Lepkowsky [1], Angela Johnson [1], Alan Markowitz [2]

[1] University Hospitals Cleveland Medical Center, 11100 Euclid ave Cleveland, OH 44106.
[2] Harrington Heart & Vascular Institute, University Hospitals Cleveland Medical Center, 11100 Euclid ave Cleveland, OH 44106.

Address of Correspondence

Dr. Adam Lepkowsky
University Hospitals Cleveland Medical Center, 11100 Euclid ave Cleveland, OH 44106.
E-mail: adamlepkowsky@gmail.com

Abstract

Introduction: Propafenone is a class 1c antiarrhythmic that is used for the treatment of ventricular and supraventricular arrhythmias. Propafenone acts to block fast inward sodium channels in a rate dependent manner to prolong the QRS interval. The effect of acute propafenone toxicity mainly involve cardiovascular symptoms including hypotension, bradycardia, ventricular dysrhythmias, widening QRS, and heart block.
Case Presentation: A 67-year-old female presented to the ICU status post aortic valve replacement, ascending aorta replacement, and left atrial appendage clip. The patient was initiated on an amiodarone infusion for atrial fibrillation prophylaxis. She was restarted on home propafenone on post-operative day 2. On post-operative day 9 an EKG illustrated a wide complex tachycardia. Propafenone was immediately discontinued. On post-operative day 11 the patient converted to narrow complex atrial fibrillation with slowing of her heart rate consistent with the use dependent nature of 1c antiarrhythmics.
Conclusion: Cytochrome P450 inhibition caused by post-operative amiodarone administration was the likely cause of propafenone toxicity in this patient. This case demonstrates the importance of understanding the pharmacokinetics and pharmacodynamics of specific medications.
Keywords: Propafenone toxicity, Amiodarone, Cytochrome P450

References

[1] Funck-Brentano C, Kroemer HK, Lee JT, Roden DM. Propafenone. N Engl J Med. 1990 Feb 22;322(8):518-25.
[2] Bryson, H.M., Palmer, K.J., Langtry, H.D. et al. Propafenone. Drugs 45, 85–130 (1993).
[3] Harron, D.W.G., Brogden, R.N. Propafenone. Drugs 34, 617–647 (1987).
[4] Alsaad AA, Ortiz Gonzalez Y, Austin CO, Kusumoto F. Revisiting propafenone toxicity. BMJ Case Rep. 2017 Apr 26;2017:bcr2017219270.
[5] Ranger S, Talajic M, Lemery R, Roy D, Villemaire C, Nattel S. Kinetics of use-dependent ventricular conduction slowing by antiarrhythmic drugs in humans. Circulation. 1991 Jun;83(6):1987-94.
[6] Bhardwaj, B., Lazzara, R. and Stavrakis, S. (2014), Wide Complex Tachycardia in the Presence of Class I Antiarrhythmic Agents: A Diagnostic Challenge. Annals of Noninvasive Electrocardiology, 19: 289-292.
[7] Köppel C, Oberdisse U, Heinemeyer G. Clinical course and outcome in class IC antiarrhythmic overdose. J Toxicol Clin Toxicol. 1990;28(4):433-44.
[8] McDonald MG, Au NT, Rettie AE. P450-based drug-drug interactions of amiodarone and its metabolites: diversity of inhibitory mechanisms. Drug Metab Dispos 2015;43:1661–9.
[9] Latini, R., Tognoni, G. & Kates, R.E. Clinical Pharmacokinetics of Amiodarone. Clin Pharmacokinet 9, 136–156 (1984).

(Abstract Text HTML)     (Download PDF)