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氟卡因中毒及碱化导致消除半衰期延长。

Flecainide poisoning and prolongation of elimination due to alkalinization.

机构信息

Division of Medical Toxicology, Department of Emergency Medicine, University of Iowa, Iowa City, IA, United States of America; Iowa Poison Control Center, Sioux City, IA, United States of America.

Department of Emergency Medicine, University of Iowa, Iowa City, IA, United States of America.

出版信息

Am J Emerg Med. 2022 Jun;56:394.e1-394.e4. doi: 10.1016/j.ajem.2022.03.006. Epub 2022 Mar 9.

DOI:10.1016/j.ajem.2022.03.006
PMID:35287973
Abstract

BACKGROUND

Flecainide is a 1C antidysrhythmic that is primarily used for ventricular tachycardia or premature ventricular contractions when other treatment is ineffective. It has a very narrow therapeutic window which may cause death in a double dose and requires inpatient initiation for cardiac monitoring. Despite established pharmacokinetic data from flecainide in therapeutic dosing, there is negligible data on flecainide toxicokinetics after an intentional overdose. Due to the inherent differences in pharmacokinetic and toxicokinetic principles, rarely can the peak effect or elimination half-life accurately be applied to the poisoned patient after an overdose. In overdose, flecainide can cause a variety of fatal dysrhythmias which may require sodium bicarbonate for stabilization but also may reduce the renal elimination of flecainide, meaning the life-saving treatment may prolong the time of toxicity.

CASE REPORT

We present a case of an acute ingestion of flecainide with a known time of ingestion and known amount of ingestion who experienced subsequent life-threatening effects which required endotracheal intubation, sodium bicarbonate, aggressive electrolyte repletion, and multiple days in an intensive care unit.

RESULTS

Serial serum and urine samples revealed a prolonged toxic serum concentration of flecainide.

CONCLUSION

These results demonstrate the change in elimination kinetics of flecainide in the setting of urinary alkalization which is evident through prolonged morphologic changes present on serial electrocardiograms.

摘要

背景

氟卡尼是一种 1C 抗心律失常药物,主要用于其他治疗无效的室性心动过速或室性早搏。它的治疗窗很窄,双倍剂量可能导致死亡,需要住院进行心脏监测。尽管氟卡尼在治疗剂量下有既定的药代动力学数据,但在故意过量后,关于氟卡尼毒代动力学的数据几乎可以忽略不计。由于药代动力学和毒代动力学原理的固有差异,很少能准确地将中毒患者的峰值效应或消除半衰期应用于过量后。在过量的情况下,氟卡尼会引起各种致命的心律失常,可能需要碳酸氢钠来稳定,但也可能减少氟卡尼的肾脏清除,这意味着救命治疗可能会延长毒性时间。

病例报告

我们报告了一例已知摄入时间和已知摄入量的急性氟卡尼摄入病例,该患者随后出现危及生命的效应,需要进行气管插管、碳酸氢钠、积极的电解质补充以及在重症监护病房多日治疗。

结果

连续的血清和尿液样本显示氟卡尼的毒性血清浓度延长。

结论

这些结果表明,在尿液碱化的情况下,氟卡尼的消除动力学发生了变化,这在连续心电图上呈现的形态学变化延长中得到了证实。

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