阿司咪唑中毒致尖端扭转性室性心动过速一例

患者女性 ,5 0岁 ,因突发胸闷、心悸并晕厥 1次急诊入院 ,入院前 4ｈ误服大剂量阿司咪唑 (息斯敏 ,3ｍｇ× 85片 )2 5 5ｍｇ。入院时体格检查 :神志清醒 ,血压 12 0 /70ｍｍＨｇ(1ｍｍＨｇ =0 133ｋＰａ) ,心率 72次 /ｍｉｎ ,心电图示频发多源性室性早搏 (室早 )、ＱＴ间期延长 (0 6 4ｓ)、短阵多形室性心动过速 (室速 )。患者有慢性过敏性鼻炎病史 ,无心脏病史。入院后立即予以洗胃、利尿、吸氧、静脉注射利多卡因并维持静脉滴注以及补镁补钾治疗 ,心电监护示室性早搏明显减少 ,但ＱＴ间期长。入院后第 6ｈ患者小便时再发晕厥 1次 ,心电…     

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.     

洋地黄中毒致双向性室性心动过速1例

患者男,57岁。因反复胸闷、气急、双下肢浮肿4年余,加重1W,拟扩张性心肌病,慢性充血性心力衰竭,心功能Ⅲ级入院。近1年来服用地高辛0．25mg／qd。入院12导联同步心电图(图1)示：各导联未见明显P波,除aVR导联,各肢体导联可见QRS波呈两种形态和方向交替,Ⅰ、aVL导联分别为QS型与Rs型交替,Ⅱ、Ⅲ、aVF呈Rsr’型与rS型交替,     

多型性室性心动过速16例

本对１６例多形性室性心动过速（ＰＶＴ）行回顾性研究。观察了窦律时Ｔ波交替、ＱＴ间期延长、由室性期前收缩构成的联律问题的长短、房颤的心室率、抗心律失常药物与ＰＶＴ的关系。可见０ＰＶＴ重整后的危险性仍然存在。     

乌头中毒致多形室性心动过速1例

患者男性,73岁。因煮食附子汤后恶心、呕吐、腹泻、四肢麻痹、胸闷4h入院。查体：血压130／80mmHg,神清,对答切题。心率70次／分,律不齐,可闻早搏。心电图诊断：①窦性心律;②频发室性早搏伴短阵室性心动过速;③偶发房性早搏。给予洗胃、利尿、补液、护胃及利多卡因50mg静注后患者恢复窦性心律,胸闷、麻痹等症状好转。半小时后,心电监护示：阵发室性早搏二联律,再予利多卡因500mg维持静滴。翌日复查心电图正常。继续对症治疗与观察4d后治愈出院。     

洋地黄中毒致双向性室性心动过速2例

例1,男,80岁,于8年前即明确诊断为缺血性心脏病、永久性心房颤动(Af)、充血性心力衰竭(CHF).近6 d来心悸、胸闷加重,自服地高辛(0.25 mg,bid×5 d)、氢氯噻嗪等药物,于1 h前出现呼吸困难,不能平卧,于2005年5月26日17:10时急诊入院.体检:BP 100/70 mmHg(1 mmHg=0.133 kPa),神志恍惚,颈静脉怒张,双下肺湿啰音较多,心律尚齐,心音强弱不一,肝大肋下2横指,双下肢重度凹陷性水肿.     

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( )。     

心室起搏治疗窦性停搏并室性心动过速一例

患者女性，66岁，因抽搐、意识丧失3次入院。心电图示窦性停搏后出现常间歇，之后发生室性早搏二联律，继而出现室性心动过速。用较快起搏频率行右室心内膜临时起搏后室性早搏、室性心动过速消失。病情稳定后安装永久起搏器，病人痊愈出院。     

室性期前收缩长短周期现象诱发多形性室性心动过速1例

患者女性,14岁,因反复阵发性心悸伴晕厥半年来院就诊。体检:平卧位,T36.5℃,R21次/min,BP110/75mmHg,心界不大,心率84次/min,心律不齐,各瓣膜区未闻及病理性杂音。两肺无殊。腹软,肝脾未及。实验室检查:血常规、肝肾功能、血清电解质及心肌酶谱均正常。X线胸片示心影大小及形态均正常。超声心动描记术示各房室腔未见增大。临床诊断:晕厥待查。常规心电图(图略)示窦性心律,室性期前收缩。24h动态心电图(图1A)示:窦性P-P间期基本匀齐,为0.68s,Q-T间期0.36s,从第1个室性期前收缩QRS波群起始至下一窦性QRS波群起始间期为1.36s,已达窦性周…     

Polymorphic ventricular tachycardia

The case of a patient with torsade de pointes in the setting of congenital complete heart block is described. Lack of recognition of this polymorphic ventricular tachycardia resulted in therapy that potentiated the dysrhythmia. After correct recognition, and directed therapy, the patient responded appropriately. The clinical settings, recognition, and management options available for torsade de pointes are discussed to familiarize the emergency physician with this important and unique dysrhythmia.     

多形室性心动过速

多形室性心动过速(polymorphic ventricular tachycardia,PMVT)是以QRS波在形态和/或电轴方面发生频繁而快速改变为特征的频率超过100次/min的心室节律,其节律常不匀齐,可自发终止,亦可转化为心室颤动(室颤).     

Characteristics and prognosis of ventricular tachycardia induced by atrial fibrillation]

The aim of this study was to evaluate the clinical significance of ventricular tachycardia (VT) induced by atrial pacing. A group of 145 patients with spontaneous and induced VT was studied. Twenty-four VTs were induced by atrial stimulation (Group I) and 121 by ventricular stimulation (Group II). The underlying cardiac disease was comparable in the two groups (ejection fraction 32 +/- 14% versus 34 +/- 17%). Spontaneous bi-tachycardias, syncope and VT induced by exercise testing were more common in Group I. The prognosis was worse with 7 cardiac deaths in Group I versus 23 in Group II; recurrences of VT were commoner in group I. In this group, an electrophysiological (branch to branch or fascicular reentry) or clinical mechanism (ischaemia or poor haemodynamic status) could usually be demonstrated. Some cases of idiopathic VT were also observed in young patients. These results suggest that atrial stimulation should be performed routinely during electrophysiological studies of VT because the induction of VT by this method is not uncommon (16%). In addition, these cases of VT usually have a precise mechanism and a poor prognosis and, therefore, an appropriate treatment should be given.     

Polymorphic ventricular tachycardia induced by coronary vasospasm: a malignant case of variant angina

Variant angina is generally a benign disease with self limiting symptoms. But in some cases serious ventricular arrhythmias which can lead to death can be seen. In this paper we present a case of variant angina who subsequently developed polymorphic ventricular tachycardia and was treated successfully with long acting nitrate and calcium channel blockade therapy.     

Idiopathic verapamil-sensitive left ventricular tachycardia complicated by right ventricular outflow tract ventricular tachycardia and ventricular fibrillation.

Idiopathic ventricular tachycardias (VTs) are generally divided into those arising from the right ventricle and those arising from the left ventricle. There has been few reports of two morphologically distinct VT occurring in patients with no apparent structural heart disease. We report a patient with verapamil-sensitive left VT with a right bundle branch block pattern that spontaneously changed to VT with a left bundle branch block pattern. Ventricular fibrillation was induced by the application of programmed stimulation. Although it is unclear if our patient with pleomorphic VT has ventricular vulnerability, it is necessary to investigate further and follow him carefully.