Reynolds Joshua C, Judge Bryan S
Department of Emergency Medicine, Michigan State University College of Human Medicine, Grand Rapids, MI, USA; Spectrum Health Hospitals, Grand Rapids, MI, USA.
Department of Emergency Medicine, Michigan State University College of Human Medicine, Grand Rapids, MI, USA; Spectrum Health Hospitals, Grand Rapids, MI, USA; Grand Rapids Medical Education Partners Emergency Medicine Residency, Grand Rapids, MI, USA.
Am J Emerg Med. 2015 Oct;33(10):1542.e1-2. doi: 10.1016/j.ajem.2015.07.054. Epub 2015 Jul 29.
Flecainide 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.
氟卡尼是一种Ic类抗心律失常药物，用于预防和治疗快速性心律失常。氟卡尼毒性主要通过钠通道阻滞引起心血管和神经方面的影响。几乎没有证据支持特定的治疗方法，推荐的治疗方案是从其他钠通道阻滞剂的治疗方法推断而来的。传统上，这些治疗方法包括静脉输液、碳酸氢钠、血管加压药和心脏起搏。新的治疗方法包括静脉注射脂肪乳剂和静脉-动脉体外膜肺氧合（VA-ECMO）。一名24岁女性误服了她丈夫的氟卡尼，随后因严重休克和宽QRS波心动过缓被送往急诊科（ED）。尽管进行了积极的药物治疗，包括碳酸氢钠、血管加压药、心脏起搏和静脉注射脂肪乳剂，但她的病情仍恶化，出现了对标准复苏无效的无脉电活动（PEA）心脏骤停。在急诊科启动了静脉-动脉体外膜肺氧合，患者在重症监护病房仍处于昏迷和危重病状态。她的血流动力学和精神状态恢复了，但左腿出现了骨筋膜室综合征，需要进行筋膜切开术。她在住院第5天停止使用VA-ECMO，住院第6天拔管，住院第19天出院，神经功能恢复良好。静脉注射脂肪乳剂被认为可将致病药物隔离在血浆脂质“池”中，改变离子通道通透性，和/或改变心肌对脂肪酸的利用。静脉注射脂肪乳剂的证据质量一般较低。该患者使用静脉-动脉体外膜肺氧合来恢复器官灌注，并使药物进行自身代谢和清除。对于氟卡尼毒性继发的难治性休克和/或心脏骤停，应强烈考虑使用静脉-动脉体外膜肺氧合。
