胺碘酮致紫癜一例

1　临床资料患者女性 ,6 9岁 ,因冠心病、病态窦房结综合征于 2 0 0 1年 3月安装永久性人工心脏起搏器 (Sigma公司SSR2 0 3)。术后因持续性心房颤动 ,遵医嘱服用胺碘酮 [可达龙 ,杭州赛诺菲 圣德拉堡 民主制药有限公司生产 ,批号 (1999年 )国药准字XF2 0 13号 ]。按常规负荷量疗法服药 ,维持量为 0 .1g ,1次 d。口服胺碘酮后显效 ,偶有阵发性心房颤动发作 ,服药期间定期复查心电图、胸部X线、甲状腺激素、血常规等。同年 6月 3日 ,化验室检查 :红细胞 4.2 3× 10 1 2 L ,白细胞 5 .6 0× 10 9 L ,血小板 140× 10 9 L ,6月 2 2日 ,全身…     

胺碘酮致过敏性休克一例

患者女性,36岁,因室上性心动过速入院,给予胺碘酮静脉泵入,约3 min后出现面部潮红,视物模糊,心前区疼痛,伴皮肤苍白,出汗等症状,伴血压降低。改用普罗帕酮静脉滴注,约2 min,室上性心动过速终止。经补液等处理血压回升。约2 h后患者出现面部浮肿、全身散在皮疹伴瘙痒。考虑为胺碘酮所致休克。     

大剂量胺碘酮静脉注射在顽固性室性心动过速、心室颤动的临床应用

总结大剂量胺碘酮(Am)静脉注射治疗顽固室性心动过速(VT)和(或)心室颤动(VF)的用药经验.选择52例患者,男34例、女18例,年龄47.0±15.6(21～68)岁.对常规抗心律失常药物治疗无效,静脉注射负荷量Am,以3～5mg/kg稀释后10min内注入,随后以1.0～1.5mg/min泵入维持,若心律失常控制不满意,可每隔30min再注入75～150mg追加负荷量,同时口服Am,静脉用药平均7.5(6～12)天.第1个24hAm静脉用量为1865±272(I592～3120)mg,心律失常控制占56%(29/52),72h心律失常全部控制.1例96h后VT复发,追加Am负荷量后获控制,1例死于心源性休克.结论大剂量静脉注射Am对顽固VT和(或)VF安全有效,用药强调个体化.在用药过程中注意监测血压、心率、节律变化.预防心律失常复发需长期口服Am.     

过量口服胺碘酮致尖端扭转型室性心动过速1例

1　临床资料患者女性 ,6 7岁 ,农民 ,因反复头昏近三个月 ,伴胸闷、气促一月 ,晕厥二次于 2 0 0 0年 1月 2 7日转诊我院。既往高血压病史多年 ,未服用利尿剂。入院前因“心律失常 (频发室性期前收缩 )”在外院就诊 ,口服胺碘酮片 2 0 0 mg每日三次 ,连续服用至第 35天 ,在家休息时无明显诱因突发晕厥二次。急诊入院时一般情况尚可 ,神清 ,血压 12 0 / 80 mm Hg,心界不大 ,心率 5 3次 / min,律不齐 ,各瓣膜区未闻杂音 ,肺无罗音 ,腹部及神经系统未发现异常。实验室检查血钾 4 .0 mmol/ L ,血镁 0 .9m mol/ L,心肌酶未见异常 ;超声心动图示…     

静脉用胺碘酮致严重肝功能损害一例

胺碘酮是一个广谱的抗心律失常药物，临床上胺碘酮致严重肝功能损害较少见。现报道扩张性心肌病患者静脉用胺碘酮治疗室性心动过速(室速)所致严重肝功能损害，经联合护肝治疗后室速消失、肝功能恢复的1例病例。临床资料     

静注胺碘酮致窦性停搏5天一例报道

患者，男，66岁，因咳嗽、咳痰、胸闷、气短一周于2003年3月17日入院，既往有“肺结核”“乙肝”“糖尿病”“高血压性心脏病”，史10余年，血压最高160／110mmHg，问断服用药物治疗，入院查体：T：36．4℃，P：84次／分，R：24次／分，BP：145／80mmHg，神志清晰、精     

胺碘酮静脉注射治疗快速性心律失常20例临床观察

目的 探讨胺碘酮静脉给药治疗快速性心律失常的疗效及安全性。方法 20例难复性快速心律失常患者，予胺碘酮静脉注射液150mg溶于5％葡萄糖液20ml 15min内缓慢静脉注射，无效的间隔15min后重复1次，再以0．5—1mg／min维持静脉滴注，12例病人同时口服胺碘酮。结果 20例快速心律失常均被有效控制。结论 胺碘酮有较强的抗心律失常作用。它对房性、房室交界性、室性及预激综合征伴发的心律失常均有很好的疗效。     

胺碘酮致长间歇依赖型多形性室速1例

胺碘酮可引起QT间期延长 ,但诱发长间歇依赖型多形性室速 (VT)者很少 (<1 %) ,现将所见 1例报告如下。患者女 ,5 7岁。临床诊断冠心病 ,房颤。服用胺碘酮 1日 3次 ,每次 0 2。2 0 0 1年 3月 2 0日出院后自行间断服用。自诉 5月 7日起连续服用 6d ,每天 3次 ,每次 0 2 ,5月 1 4日出现心慌不适来院而描心电图 (见图 )。住院后停服胺碘酮 ,仅作对症处理后好转 ,房颤犹存 (图略 )。心电图分析 :图示aVF导联。P1 、P2 为窦性P波 ,外形稍有切迹 ,时限、电压正常。P -R间期 0 1 4s,下传QRS波呈“qR”型 (时限、振幅正常 )伴ST段水平延…     

静脉注射胺碘酮对冠心病快速型室上性心动过速的疗效

目的:观察静脉注射胺碘酮治疗冠心病快速型室上性心律失常(SVT)的疗效。方法:入选冠心脏病合并SVT患者,心动过速发作1～6h 79例,随机分为胺碘酮组(41例,脉注射胺碘酮150～450mg或改为静脉恒速泵注入),毛花甙C组(38例,静脉注射毛花甙C 0.4～1.0mg),观察其心率、QT间期变化及药物副作用。结果:两组心率均有明显控制,肢碘酮和毛花甙C组对STCA的有效率分别为92.6％与73.6％,胶碘酮疗效高于毛花甙C(P<0.01),QT间期及副作用差异无显著性意义。结论:胺碘酮对冠心病并SVT者的疗效显著高于毛花甙C。     

胺碘酮致起搏患者尖端扭转型室性心动过速一例

患者男性 ,81岁 ,1 994年因病窦综合征安置了VVI起搏器 ,起搏器工作正常。 2 0 0 2年 2月因心房颤动 (AF)使用胺碘酮治疗 ,48h后转复为窦性心律 ,此后AF复发 ,继续胺碘酮负荷治疗 ,出现晕厥症状 ,后证实为尖端扭转型室性心动过速 ,经停用胺碘酮 ,调高起搏节律治疗 ,症状稳定     

The use of oral amiodarone as a chronic treatment in a patient with prior fulminant hepatitis due to intravenous amiodarone

Acute hepatitis for intravenous amiodarone is an uncommon problem with scarce appearances in medical literature. Sometimes, it has postulated that the vehicle of the intravenous preparation and not the active principle is the possible cause of this complication. We report a patient with fulminating hepatitis and severe encephalopathy following the administration of intravenous amiodarone. We present also the clinical evolution of the patient after reintroduction of oral amiodarone. In the end, we make a review of the associated literature with our case.     

Distribution of amiodarone and desethylamiodarone in a patient with acute myocardial infarction after intravenous administration

The autopsy tissues concentration of amiodarone and desethylamiodarone of a man with acute myocardial infarction treated acutely with intravenous amiodarone is reported. Our data indicate that amiodarone is quickly distributed into all highly perfused tissues after intravenous administration with a high amiodarone/desethylamiodarone ratio. We also report here the autopsy case of a woman who died after 30 days of oral therapy with amiodarone. The increase in heart/plasma ratio of amiodarone and desethylamiodarone concentrations and the decrease in amiodarone/desethylamiodarone ratio after one month of therapy could explain the latency in the antiarrhythmic action of the drug.     

Torsade de pointes induced by intravenous and long-term oral amiodarone therapy in a patient with dilated cardiomyopathy

A 70-year-old woman with dilated cardiomyopathy and ventricular tachyarrhythmia was initially treated in 1990 with intravenous amiodarone (240 mg). She developed a junctional escape rhythm (48 beats/min) with QT prolongation (QT: 0.68 s) and 8 h later developed torsade de pointes (TdP). Because other antiarrhythmic drugs did not suppress the arrhythmia, oral amiodarone (100 mg/day) was started in 1995, 7 weeks before she presented with congestive heart failure. The QT prolongation (QTc: 0.64) increased after administration of dopamine, and TdP again developed. This case suggests that amiodarone induces proarrhythmias by different mechanisms when administered intravenously or orally.     

Hemodynamic effects of intravenous amiodarone

Amiodarone is a potent antiarrhythmic agent that is effective in controlling both atrial and ventricular arrhythmias. Recently, intravenous administration was demonstrated to be effective in the acute management of rhythm disorders and, in addition, appeared to shorten the loading period normally required for oral drug administration. This investigation examined the hemodynamic effects of amiodarone after both acute intravenous bolus and continuous intravenous administration. Patients with a left ventricular ejection fraction greater than 0.35 experienced improved cardiac performance due to both acute and chronic peripheral vasodilation. However, patients with a lower ejection fraction developed a 20% decrease in cardiac index and clinically significant elevation of right heart pressures after acute bolus administration; these changes were variably compensated for by peripheral vasodilation when the drug was administered intravenously over 3 to 5 days continuously. Therefore, intravenous amiodarone can result in significant impairment of left ventricular performance in patients with preexisting left ventricular dysfunction.     

Early hepatitis during intravenous amiodarone administration

Two patients with acute changes suggesting acute hepatitis after parenteral amiodarone administration are described. No other explanation for liver damage was found in these patients. Normalization of liver function in spite of continuation of drug infusion was observed.