阿司咪唑中毒致多形室性心动过速、心室颤动一例

患者女性 ,5 0岁 ,因头晕、心悸入院。入院前 16ｈ内患者间断服用阿司咪唑 (息斯敏 ,西安杨森制药有限公司 )共35 0ｍｇ ,1ｈ后感头晕 ,恶心 ,2ｈ后症状加重并感阵发性心悸 ,气促 ,无晕厥。入院时血压 12 0 / 75ｍｍＨｇ (1ｍｍＨｇ =0 133ｋＰａ) ,心率 80次 /ｍｉｎ ,心律齐 ,无杂音。心电图示窦性心律 ,偶发室性早搏 (室早 ) ,ＱＴ间期延长为 0 6 0ｓ,急查电解质示血清钾 3 2ｍｍｏｌ/Ｌ ,临床诊断为阿司咪唑中毒。入院后立即洗胃 ,补钾 ,1ｈ后心电监护示频发多源室早 ,5ｍｉｎ后转为尖端扭转性室性心动过速 (Ｔｄｐ) ,继而转为心室颤…     

超剂量阿司咪唑致多形性室性心动过速

患者女性 ,2 1岁 ,12小时前睹气口服阿司咪唑 5 0片 ,发作性抽搐 2小时于 1995年 9月 12日来本院急诊。平时健康。体检 :T36 .5℃ ,R18次 /分 ,BP110 / 70 m m Hg;思睡状 ,口唇无发绀 ,双瞳孔 0 .4cm,等大等圆 ,对光反射敏感 ;双肺呼吸音清 ,未闻及罗音 ,HR80次 /分 ,心律不齐 ,有早搏 ,无心杂音 ;四肢肌力肌张力正常 ,病理征未引出。急诊心电图 (ECG) :窦性心律 ,多源性室性期前收缩 ,QTc0 .49秒。血 K+ 3 .5 mm ol/L ,Na+ 138m mol/ L ,CL- 10 2 m mol/ L。留观期 ,心电监测示 :短阵多形性室性心动过速 (VT) ,心室率 30 0次 /分 …     

阿司咪唑中毒致T波电交替及多形性室性心动过速1例

患者,女,24岁.因顿服阿司咪唑(息斯敏,西安杨森制药有限公司)共210 mg,1 h后出现头晕、恶心、心悸,于2006年3月20日18:20来院急诊.既往有过敏性鼻炎,否认心脏病史.     

鱼胆中毒致尖端扭转型室性心动过速1例

患者女性，25岁。因咳嗽咳痰口服草鱼胆2只后恶心呕吐、腹痛腹泻伴血尿及无尿2天人院。体检：BP120／90mmHg，神志清，巩膜无黄染。心率68次／min，心律齐，各瓣膜未闻及病理性杂音。右中肺可闻及湿哕音。腹平软，中上腹部压痛。神经系统检查阴性。实验室检查：血清K^ 、Na^ 、Cl^-、Ca^2 正常范围。血清GPT228U／L，GOT58U／L，LDH509U／L，BUN27．5mmol／L．Cr899umol／L。尿常规：红细胞( )，蛋白( )。     

伊布利特致尖端扭转性室性心动过速一例

患者女性，65岁，心悸1d于2004年11月1日13：30入院。既往史：冠心病病史4年；乳腺癌术后6个月，化疗3次。入院时查体：体温36．7℃，脉搏120次／min，呼吸18次／min，血压140／100mmHg（1mmHg=0．133kPa），神志清楚，双肺未闻及干湿哕音，右胸部见-20cm手术疤痕，心界叩诊略向左大，心率150次／min，心律绝对不规则，心音强弱不等，各瓣膜听诊区未闻及杂音。心电图示：心房颤动（房颤），心电轴左偏，室性早搏，T波改变，QTc=430ms（图1a）。患者人院后15：20给予富马酸伊布利特（河北联合制药股份有限公司生产，批号：040401）1mg，溶于0．9％氯化钠溶液20ml内10min静脉注射。15：30患者心电图示：房颤，心电轴左偏，室性早搏，短阵室性心动过速（室速），T波改变，QTc=470ms（图1b）。15：40富马酸伊布利特重复给药1次（同前）。15：50心电图示：窦性心律，心电轴左偏，P波改变，T波改变，QTc=500ms（图1C）。患者无不良主诉。16：30患者突然出现气短、抽搐和意识不清，心电监护显示尖端扭转性室速（图2）。立即给予150J同步直流电复律1次，转复为窦性心律，并给予利多卡因50mg静脉注射。血钾4．1mmol／L，血钠140．1mmol／L。此后至17：00给予利多卡因、硫酸镁、氯化钾持续静脉滴注，在此期间出现3次尖端扭转性室速，每次均以舒张晚期室性早搏诱发，均给予同步直流电复律转复，发作问期QTc为520～600ms（图1d）。18：00给予美托洛尔5mg溶于5％葡萄糖20ml中静脉推注。18：10美托洛尔重复给药1次（同前）。18：40给予美托洛尔50mg口服。在给予美托洛尔过程中患者血压、心率均在正常范围，无明显波动。19：00心电图示：窦性心律，QTc=540ms。     

索他洛尔致尖端扭转性室性心动过速一例

患者女性 ,47岁 ,因胸闷、心悸 2周入院。体格检查 :血压 130 /70ｍｍＨｇ(1ｍｍＨｇ =0 133ｋＰａ) ,神志清楚 ,口唇无紫绀 ,无颈静脉怒张 ,心率 83次 /ｍｉｎ ,心律不齐 ,可闻早搏3～ 5次 /ｍｉｎ ,未闻及心脏杂音 ,肝、脾未触及 ,双下肢无浮肿。实验室检查 :血清钾 4 6ｍｍｏｌ/Ｌ ,血清镁 0 95ｍｍｏｌ/Ｌ ,血清氯、钠、钙均正常。心电图示 :窦性心律 ,频发室性早搏 ,ＱＴｃ间期 0 44ｓ(图 1Ａ)。 2 4ｈ动态心电图示 :窦性心律 ,频发室性早搏 176 81次 /2 4ｈ。超声心动图示心脏各房室内径大小正常 ,左心室后壁及室间隔均不厚 ,左心…     

起搏器感知不良致尖端扭转性室性心动过速一例

患者男性 ,80岁。十二年前因“心房颤动伴Ⅲ度房室阻滞”在外院安置心脏ＶＶＩ起搏器 (ＣＰＩ,ＡＳＴＲＡＴ6)。 2 0 0 0年 2月 2日起反复出现头晕、胸闷。 2月 3日症状加重并多次出现短暂意识丧失伴四肢抽搐、小便失禁 ,每次持续约半分钟自行缓解。来院就诊后 ,又有类似发作 2次 ,每次发作时意识丧失 ,测血压为零 ,心电图示尖端扭转性室性心动过速(ＴＤＰ)、心室颤动 (简称室颤 ) ,起搏器感知不良 (见附图 )。给予 30 0Ｊ电击除颤 2次成功 ,其间ＴＤＰ发生时曾予利多卡因静脉推注无效。之后再次发生ＴＤＰ ,予静脉推注硫酸镁终止 ,并静脉滴…     

尖端扭转型室性心动过速的近代进展

尖端扭转型室性心动过速(Torsade de pointes,TdP)是一种介于室性心动过速(室速)和心室纤颤(室颤)之间的特殊类型的室速。近年来对TdP的命名、分类、发生机理及治疗均有新的认识。 一、概述 TdP早在50年前已被描述,但皆被误诊为室颤。Schwartz在1949年首先指出其发作的特点为短暂性,且可自行消失,因而称之为“短暂性室颤”。以后又由其     

变异型心绞痛致尖端扭转性室性心动过速1例

患者,女,40岁。主因头晕3年,胸闷、胸痛1个月,加重6d,于2006年4月5日入院。该患者3年前无诱因出现头晕、头痛,诊断为高血压,血压最高160/120mmHg(1mmHg=0.133kPa),口服北京降压0号、牛黄降压丸等药。1个月前出现活动后胸闷、胸痛,持续1~2min自行缓解,未诊治。6d前上述症状加重,休息时可出现胸闷、胸痛、出汗,多于凌晨发作,持续1~5min,含服速效救心丸好转,每日发作1~2次,无晕厥及意识障碍。否认糖尿病史、吸烟史及猝死家族史。否认奎尼丁、胺碘酮等用药史。体检:BP150/100mmHg。神志清楚。双肺呼吸音清。HR86次/min,律齐,未闻及杂音。腹…     

12例尖端扭转性室性心动过速临床分析

尖端扭转性室性心动过速(Torsades de pointes,Tdp)是一种恶性程度较高的多形性室性心动过速,临床并非少见,极易导致晕厥和心室颤动,严重威胁患者生命,正确及时识别和处理极为重要。本文回顾性分析12例TDP患者,分析其临床特征,以寻找影响其发作及终止的相关因素,目     

Torsade de pointe: Malignant cardiac arrhythmia induced by amantadine poisoning

A 37-year-old woman took 2.5 g of amantadine hydrochloride in a suicide attempt. Subsequently, cardiopulmonary arrest developed and was treated successfully. During the arrest and over the subsequent 48 hours, malignant tachyarrhythmlas were manifested by torsade de pointe and repeated episodes of ventricular fibrillation. Therapy with adrenergic agents such as isoproterenol and particularly dopamine seemed to exacerbate the ventricular tachyarrhythmias. The patient subsequently died of aspiration pneumonia and respiratory distress, and postmortem examination revealed a normal cardiovascular system. It appears that the dopaminergic activity of amantadine has potential for induction of malignant arrhythmias, particularly in the face of adrenergic agents such as dopamine and isoproterenol. This previously unreported observation needs to be considered in critically ill patients with amantadine toxicity.     

Torsade de pointes induced by N-acetylprocainamide

N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide. Initial evaluation with an intravenous infusion of NAPA indicated a favorable antiarrhythmic response. The QTC interval was prolonged, but the 2.4 ms/microgram per ml incremental QTC interval lengthening caused by NAPA was not greater than usual. During subsequent oral therapy with NAPA, torsade de pointes developed at plasma levels of this drug that appeared to be well tolerated during the initial evaluation.     

Torsade de pointes induced by ajmaline

Ajmaline, a reserpine derivative, is an effective class I antiarrhythmic agent. Herein we report two cases of ajmaline-induced abnormal QT prolongation accompanied by polymorphic ventricular tachycardia of the torsade de pointes type. Since ajmaline is increasingly used for the acute termination of wide complex tachycardia and as a diagnostic tool after syncope and in patients with idiopathic ventricular tachyarrhythmias, our observations suggest that caution should be exercised with regard to the effects of the drug on the QT interval and its potency to induce proarrhythmia of the torsade de pointes type.     

Torsade de pointes induced by citalopram and amiodarone

Long QT syndrome (LQTS) is a disorder of myocardial repolarization characterized by a prolonged QT interval on the electrocardiogram (ECG). This disorder is associated with an increased risk of torsade de pointes (TdP). We report a case of TdP induced by citalopram, a selective serotonin reuptake inhibitor (SSRI), taken in conjunction with amiodarone.     

Torsade de pointes induced by short-term oral amiodarone therapy.

Although amiodarone appears to have few pro-arrhythmic effects, torsade de pointes (TdP) has been observed during long-term drug administration, usually in conjunction with electrolyte disturbances, a change in drug dosage, or concomitant drug therapy. We report two cases of amiodarone-induced TdP shortly after administration of a low dose of oral amiodarone, in the absence of predisposing factors.     

Torsade de pointes induced by terfenadine in a patient with long QT syndrome

Torsade de pointes is a form of polymorphic ventricular tachycardia that is associated with prolongation of the QT interval. Although torsade de pointes is found in many clinical settings, it is mostly drug induced. Similar problems have been described with nonsedating H₁-receptor antagonists, such as astemizole and terfenadine. Terfenadine is a widely used antihistamine. The authors report a case of torsade de pointes in a patient with a possible congenital sporadic form of QT interval prolongation who was receiving a therapeutic dose of terfenadine.     

Torsade de pointes induced by hypocalcemia in a postoperative patient with thyrotoxicosis.

A 29-year-old woman with a long-term history of Graves' disease was admitted for thyroidectomy. Torsade de pointes occurred after the subtotal thyroidectomy. The level of her serum calcium was lower than normal. After administration of calcium gluconate intravenously, torsade de pointes disappeared and was no longer recorded. It is assumed that her torsade de pointes was caused by hypocalcemia as a complication of subtotal thyroidectomy.