• Joshua C Reynolds and Bryan S Judge.
• Department of Emergency Medicine, Michigan State University College of Human Medicine, Grand Rapids, MI, USA; Spectrum Health Hospitals, Grand Rapids, MI, USA.
• Am J Emerg Med. 2015 Oct 1;33(10):1542.e1-2.

AbstractFlecainide is a class Ic antidysrhythmic agent used to prevent and treat tachydysrhythmias. Flecainide toxicity primarily causes cardiovascular and neurologic effects through sodium-channel blockade. There is scant evidence to support specific management, and recommended therapies have been extrapolated from management of other sodium-channel blocking drugs. Traditionally, these therapies have consisted of intravenous fluids, sodium bicarbonate, vasopressors, and cardiac pacing. Novel therapies include intravenous fat emulsion and venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 24-year-old woman ingested her husband's flecainide and presented to the emergency department (ED) in profound shock with a wide complex bradydysrhythmia. Despite aggressive medical therapy including sodium bicarbonate, vasopressors, cardiac pacing, and intravenous fat emulsion, her condition deteriorated and she developed pulseless electrical activity (PEA) cardiac arrest refractory to standard resuscitation. Venoarterial extracorporeal membrane oxygenation was initiated in the ED, and the patient remained comatose and critically ill in the intensive care unit. Her hemodynamics and mental status recovered, but she had compartment syndrome in her left leg requiring fasciotomy. She was discontinued from VA-ECMO on hospital day 5, extubated on hospital day 6, and discharged home with excellent neurologic recovery on hospital day 19. Intravenous fat emulsion is thought to sequester the offending agent in a plasma lipid “sink,” alter ion channel permeability, and/or modify fatty acid utilization by the myocardium. The quality of evidence for intravenous fat emulsion is generally low. Venoarterial extracorporeal membrane oxygenation was used in this patient to restore organ perfusion and allow intrinsic drug metabolism and elimination. Venoarterial extracorporeal membrane oxygenation should be strongly considered for refractory shock and/or cardiac arrest secondary to flecainide toxicity.

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