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氟卡尼毒性导致起搏器延迟和间歇性夺获失败。

Flecainide Toxicity Resulting in Pacemaker Latency and Intermittent Failure to Capture.

作者信息

Suffredini John M, Rutland Joshua, Akpunonu Peter, Baum Regan, Catanzaro John, Elayi Claude S

机构信息

Department of Internal Medicine, University of Kentucky, Lexington, KY, USA.

Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, USA.

出版信息

Am J Case Rep. 2019 Aug 30;20:1279-1283. doi: 10.12659/AJCR.916370.

DOI:10.12659/AJCR.916370
PMID:31467262
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6735620/
Abstract

BACKGROUND Flecainide is a class Ic antiarrhythmic agent used in the treatment of supraventricular and ventricular arrhythmias. It is associated with a potent adverse effect profile; however, the effects of flecainide toxicity in the setting of a pacemaker have not been well described. We describe a unique case of flecainide toxicity secondary to acute kidney injury in the setting of a dual-chamber pacemaker, resulting in ventricular capture latency and intermittent failure to capture. CASE REPORT The patient was a 91-year-old female with a history of atrial fibrillation maintained in sinus rhythm on flecainide, who presented complaining of purple visual disturbances and syncope. She was found to be hypotensive and bradycardic, with a heart rate between 30 to 40 beats per minute. Lab work was notable for creatinine at 2.12 mg/dL. A 12-lead ECG demonstrated atrial and ventricular pacing with severely widened QRS complex and a significant latency between the pacemaker ventricular spike and the ventricular capture. The pacemaker was interrogated, revealing a significant increase in ventricular threshold from 0.75 V at 0.5 ms at baseline to 5.0 V at 1 ms to obtain consistent capture. After multiple boluses of IV sodium bicarbonate, the QRS acutely narrowed, latency interval improved, and consistent pacing capture was achieved. The flecainide level drawn on arrival was 3.09 mcg/mL. CONCLUSIONS Flecainide increases the ventricular capture threshold for pacemakers. Toxicity in these patients may present with pacemaker ventricular capture latency or failure to capture.

摘要

背景

氟卡尼是一种Ic类抗心律失常药物,用于治疗室上性和室性心律失常。它具有一系列强效不良反应;然而,在起搏器植入情况下氟卡尼毒性的影响尚未得到充分描述。我们描述了一例独特的病例,在双腔起搏器植入情况下,急性肾损伤继发氟卡尼毒性,导致心室夺获延迟和间歇性夺获失败。

病例报告

患者为一名91岁女性,有房颤病史,服用氟卡尼维持窦性心律,因出现紫色视觉障碍和晕厥前来就诊。检查发现她血压低、心动过缓,心率每分钟30至40次。实验室检查显示肌酐为2.12mg/dL。12导联心电图显示心房和心室起搏,QRS波群严重增宽,起搏器心室脉冲与心室夺获之间有明显延迟。对起搏器进行问询,结果显示心室阈值从基线时0.5毫秒的0.75V显著增加到1毫秒时的5.0V才能获得稳定夺获。静脉注射多次碳酸氢钠后,QRS波群急性变窄,延迟间期改善,实现了稳定的起搏夺获。入院时测得的氟卡尼水平为每毫升3.09微克。

结论

氟卡尼会提高起搏器的心室夺获阈值。这些患者的毒性可能表现为起搏器心室夺获延迟或夺获失败。

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BMJ Case Rep. 2015 Aug 18;2015:bcr2015210598. doi: 10.1136/bcr-2015-210598.
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Narrow therapeutic index drugs: a clinical pharmacological consideration to flecainide.窄治疗指数药物:对氟卡尼的临床药理学考量
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