胺碘酮静脉注射治疗快速性心律失常50例临床观察

胺碘酮是一种具有广泛、多种而独特电生理效应和药理作用的广谱抗心律失常药物，近年来广泛用于治疗快速性心律失常，特别是利多卡因、心律平等药物常规治疗剂量无效时，短时间内静脉大剂量注射胺碘酮往往有效。我院自2005年5月至2006年12月对50例快速心律失常住院患者在应用其他抗心律失常药物治疗无效时，采用胺碘酮静脉注射治疗，取得了满意疗效，现报告如下。     

静脉使用胺碘酮致过敏性休克3例

<正>胺碘酮是Ⅲ类抗心律失常药物,主要电生理效应是延长各心肌组织的动作电位及有效不应期,有利于消除返激动,同时具有轻度非竞争性的α及β肾上腺素受体阻断和轻度Ⅰ类与Ⅳ类抗心律失常药的特点,临床中较为常用。但由于其短期及长期的不良反应,导致胺碘酮的安全性一直受到关注。     

抗心律失常药物可引起心律失常

60年代以来,心律失常的发病机理及抗心律失常药物的作用等,取得了极大进展。多种新型抗心律失常药物被发现和合成。根据心律失常的电生理特性而选择治疗方案,是药物治疗心律失常取得重要进展的基础。但是,大量新型抗心律失常药物的问世,使临床治疗又遇到一些新问题,其中之一就是抗心律失常药物本身也可引起心律失常或使原有的心律失常加剧,而且这种不良反应随着抗心律失常药物的广泛应用更为普遍。乙胺碘呋酮(胺碘酮) 乙胺碘呋酮既能扩张冠状动脉,又兼有抗心绞痛及抗心律失常作用,而无明显的负性收缩能效应。它的主要电生理作用为延长房室结传导时间,延长心房、浦肯野(Purkinje)纤维和心室的动作电位时间,从而延长不应期。除能有效地治疗室上性和室性心动过速外,尚可治疗致命性室性心律失常,并有预仿效果。对预激综合     

胺碘酮对QTc离散度的影响

胺碘酮是目前较常用的抗心失常药物,其具有抗心律失常作用确切,致心律失常的发生率低,无明显负性肌力作用等优点,逐渐被许多临床医生所采用。胺碘酮的作用机理为延长心肌细胞动作电位时程,试用于各种室上性与室性快速性心律失常。近年来国内外有许多文章报道了胺碘酮的低?..     

胺碘酮治疗充血性心力衰竭伴室性心律失常临床疗效观察

44例充血性心力衰竭伴室性心律失常者,在常规抗心力衰竭治疗基础上,口服胺碘酮治疗2、8周后分析疗效及心功能改善情况。结果口服胺碘酮2周后总有效率为61.4%,8周后总有效率为86.4%。胺碘酮是一种广谱而安全的抗心律失常药物,对室性心律失常作用明确、安全,不良反应轻。     

1例胺碘酮引发尖端扭转性室速的护理体会

胺碘酮是Ⅲ类抗心律失常药物,能有效地治疗房性心律失常和室性心律失常,是一相对安全的药物,据报道胺碘酮基本不引发尖端扭转性室速[1].2005年3月,本院用胺碘酮治疗1例频发室速患者时,引发了尖端扭转性室速,经及时抢救及护理,病情转危为安.现将胺碘酮治疗的护理体会报告如下.     

静脉注射胺碘酮致严重不良反应2例临床护理

胺碘酮是目前临床应用最广泛的抗心律失常药物之一,它对多个离子通道均有阻断作用,同时具有Ⅰ、Ⅱ、Ⅲ及Ⅳ类抗心律失常的生理效应,抗心律失常疗效确切,也是目前唯一已证实的对于任何原因所导致的左室功能不良比较安全的药物[1].在缺血-再灌注损伤中,胺碘酮不仅是一种抗心律失常药物,还是一种心脏保护剂[2].静脉应用的主要不良反应为低血压、窦性心动过缓、房室传导阻滞、静脉炎等.近来,我科收治2例静脉注射胺碘酮致严重不良反应患者,经积极治疗与精心护理,取得满意效果.现报告如下.     

胺碘酮与甲状腺功能异常

正胺碘酮是当前最常用的广谱抗心律失常药物,其主体效应为阻断钾通道,延长心肌细胞动作电位时程的Ⅲ类抗心律失常药物,兼有不同程度的Ⅰ、Ⅱ及Ⅳ类抗心律失常药物效应,临床上广泛应用于室上性和室性心律失常的治疗。胺碘酮作为呋喃类结构的含碘化合物,长期应用可影响甲状腺激素代谢而诱发甲状腺功能异常,包括胺碘酮诱发甲状腺功能亢进症(AIT)和胺碘酮诱发甲状腺功能减退症(AIH),前者可分为两型:Ⅰ型AIT系血循环中高浓度碘致甲状腺激素合成增多:Ⅱ型AIT缘于甲状腺炎或甲状腺滤泡细胞破坏使甲状腺激素释放增多;部分患者表现为混     

胺碘酮治疗恶性室性心律失常病人的护理

胺碘酮属于Ⅲ类抗心律失常药 ,它兼有各类抗心律失常药物的某些特点 ,被视为一种广谱抗心律失常药 ,静脉给胺碘酮起效快速、无明显的血流动力学影响 ,且对利多卡因和普鲁卡因酰胺治疗无效的室性心动过速 (室速 )或心室纤颤 (室颤 )有效 ,对服用其他抗心律失常药物无效的恶性室速或室颤的控制率可达6 0 %～ 80 %[1] 。目前认为胺碘酮对于预防和控制致命性室速 ,特别是心肌梗死后发生的室速是最有效的药物之一 ,且胺碘酮具有对心脏的全面保护作用 ,可降低心功能衰竭病人心律失常相关死亡风险 ,并可改善心功能 ,目前临床应用日渐增加。我院IC…     

硫酸镁雷夫诺尔交替外敷治疗胺碘酮所致静脉炎的临床观察

胺碘酮属Ⅲ类抗心律失常药物,是一广谱而十分有效的抗心律失常药物,在防治危及生命的室性心律失常、心肌梗死后室性心律失常、心力衰竭中发生的室性心律失常、对猝死高危病人防治上应列为一线抗心律失常药物[1],现在我科广泛应用。但在临床静脉输注胺碘酮容易诱发静脉炎,这不仅     

Amiodarone: An emergency medicine perspective

Amiodarone is a highly efficacious antiarrhythmic agent for many cardiac arrhythmias, ranging from atrial fibrillation to malignant ventricular rhythm disturbances. Significant interest has developed in recent years with the publication of randomized controlled trials supporting the efficacy of amiodarone over placebo and lignocaine for improving survival to hospital in patients with shock‐resistant ventricular fibrillation. Amiodarone has complex pharmacological and pharmacokinetic properties. It has significant long‐term adverse effects, but short‐term administration of intravenous amiodarone is generally well tolerated. This article will explore issues related to the clinical use of amiodarone from an emergency medicine perspective.     

Serial electrophysiological studies in a young patient with recurrent ventricular fibrillation

A 28-year-old male with recurrent episodes of ventricular fibrillation, which were initiated by very early ventricular premature depolarizations with a normal QT interval, was subjected to three consecutive electrophysiological studies. During the first study, which was carried out to test the efficacy of amiodarone treatment, no ventricular arrhythmias could be induced. While on amiodarone therapy, the patient experienced another syncopal episode and therefore a second electrophysiological study was done. In that study, ventricular fibrillation was induced by ventricular stimulation. During the third study, which was carried out in order to evaluate the effect of the addition of quinidine to the ongoing amiodarone therapy, no more than three repetitive ventricular responses could be induced. The patient has been asymptomatic since the third study (fifteen months) with combined therapy of amiodarone and quinidine. The significance of the ability to induce ventricular fibrillation during an electrophysiological study is discussed as well as the value of such studies in determining the long-term efficacy of antiarrhythmic drug therapy.     

Isoproterenol as an adjunct for treatment of idiopathic ventricular fibrillation storm in a pregnant woman

Idiopathic ventricular fibrillation is a rare entity seen in a very small subset of patients presenting to the emergency department. Management of ventricular arrhythmias in pregnant women is similar to that in nonpregnant women, but special consideration is given to avoid adverse fetal effects when selecting antiarrhythmic agents. Electrical defibrillation is the intervention of choice in both pregnant and nonpregnant patients with ventricular fibrillation of all etiologies. This was not associated with any significant adverse effects for mother or fetus. Although lidocaine and sotalol are Food and Drug Administration category B antiarrhythmics used in pregnancy, Food and Drug Administration category C antiarrhythmics such as β-blockers and category D drugs such as amiodarone can be used as pharmacologic adjuncts to facilitate termination of recurrent ventricular fibrillation where other agents have failed. Isoproterenol has been used to terminate recurrent ventricular fibrillation in patients with Brugada syndrome and torsades de pointes resistant to magnesium therapy. This case report describes a previously healthy 32-year-old pregnant woman with recurrent idiopathic ventricular fibrillation that failed to respond to standard therapy including electrical defibrillation, intravenous lidocaine, metoprolol, and amiodarone but eventually terminated with isoproterenol infusion.     

Dronedarone: an overview

Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice. Until recently, a rhythm control strategy for AF has been limited by drug toxicity and side-effects, and landmark AF trials have shown that such a strategy is not superior to a rate control one. New antiarrhythmic drugs, free of undesired effects, would enhance the rhythm control strategy, with the possibility of sinus rhythm restoration and maintenance. One of the promising drugs recently approved for clinical use is dronedarone. This drug has amiodarone-like antiarrhythmic and electrophysiological properties, despite it having a modified structure and lacking an iodine moiety. Thus, dronedarone lacks amiodarone's organ toxicity (including adverse thyroid and pulmonary effects). The efficacy of dronedarone has been investigated in several clinical trials, proving its effect in the prevention of AF recurrence, rate control in paroxysmal/persistent and permanent AF, reduction of cardiovascular hospitalization or death from any cause, and others. Indirect comparisons with amiodarone, as well as one head-to-head study of the two drugs, indicate that the relative safety of dronedarone may be at a cost of its lower antiarrhythmic efficacy compared with amiodarone.     

Dronedarone for atrial fibrillation therapy

Dronedarone is a new benzofuran derivative that has been developed as an antiarrhythmic agent on the basis of the amiodarone molecular structure with the intent of maintaining the same pharmacological effects while reducing thyroid and pulmonary toxicity. The drug is a multichannel blocker with antiadrenergic properties: it reduces heart rate and prolongs the action potential duration. Dronedarone is primarily metabolized by cytochrome P450; its half-life is much shorter than that of amiodarone because of a lower lipophilicity. As a consequence, only 7 days are needed to reach steady-state plasma levels. It has been tested in clinical trials both for rate and rhythm control and, even if its antiarrhythmic efficacy seems to be somehow lower than that of amiodarone, dronedarone is less often discontinued due to adverse reactions or organic toxicity. For these reasons, dronedarone can be very useful in long-term treatment of atrial fibrillation, by reducing hospitalizations and mortality.     

Antiarrhythmic drugs for atrial fibrillation: focus on dronedarone

Patients with atrial fibrillation have an increased risk of stroke and heart failure, as well as impairment of their quality of life. Most trials have primarily focused on the prevention of stroke and heart failure, and the improvement of symptoms in these patients. More recently, a rate-control strategy has been reported to be a noninferior strategy compared with a rhythm-control strategy in atrial fibrillation patients. Many different classes of antiarrhythmic drugs have been used for rhythm control, with inconsistent results and adverse effects on mortality and morbidity. Of the available antiarrhythmic drugs, amiodarone is the single most effective drug in the prevention of atrial fibrillation recurrences and maintaining sinus rhythm; however, it is vastly limited by its various systemic side effects, especially those observed with long-term use. However, recent trial data from a new antiarrhythmic agent, dronedarone, suggest that this drug may be a safe alternative to amiodarone; however, its long-term efficacy and safety still require exploration.     

Pharmacological management of atrial fibrillation: an update

Therapy of atrial fibrillation remains difficult in many patients. There is increasing awareness that antiarrhythmic drug therapy instituted to maintain sinus rhythm after successful cardioversion of atrial fibrillation may pose a substantial risk to the patient. Therefore, results of prospective randomized trials are needed to allow a more evidence-based approach to the treatment of this common arrhythmia. Two recently published studies have shown superiority of amiodarone over conventional antiarrhythmic drugs in maintaining sinus rhythm. The largest such study published today, the Canadian Trial in Atrial Fibrillation (CTAF), has randomized 403 patients to amiodarone or to sotalol or propafenone. At the end of the observation period, amiodarone-treated patients were significantly more likely to remain in sinus rhythm than conventionally treated patients. A number of new antiarrhythmic drugs, mainly class III substances, are currently developed for the treatment of atrial fibrillation or atrial flutter. Ibutilide has recently been released for intravenous administration, attempting pharmacological cardioversion of atrial fibrillation/atrial flutter. It has been evaluated in a number of prospective trials, which showed a higher conversion rate in patients with atrial flutter. Dofetilide is another new compound developed mainly for maintenance of sinus rhythm after restoration of sinus rhythm. It has been evaluated in two prospective, randomized, placebo-controlled trials; moreover, analysis of the DIAMOND trials showed effectiveness of dofetilide in maintaining sinus rhythm in patients with depressed left ventricular function without increased mortality when compared with placebo. Finally, several ongoing studies compare the therapeutic strategy of controlling ventricular rate in atrial fibrillation compared with the strategy of maintaining sinus rhythm. These trials will help to optimize therapy in atrial fibrillation, the most commonly encountered arrhythmia.     

Antiarrhythmic therapy in patients with heart failure

In patients with severe chronic heart failure, many deaths are sudden due to life-threatening ventricular arrhythmias. Supraventricular arrhythmias such as paroxysmal or chronic atrial fibrillation may also cause serious complications in those patients due to acute loss of atrial contraction, pump failure during rapid ventricular response and embolic events. Two therapeutic strategies are currently available for therapy and prevention of malignant ventricular arrhythmias and subsequent sudden arrhythmic death: antiarrhythmic drug therapy and implantable defibrillators. However, selection of the most beneficial strategy for the individual patient to reduce the risk of sudden death remains a major challenge in cardiology. Betablockers exert a favorable antiarrhythmic action without increasing proarrhythmia, thus betablockers may serve as a basic medication in patients at risk for sudden death. However, the general use of antiarrhythmic drug therapy for symptomatic ventricular arrhythmias is not recommended, as these drugs have been shown to increase mortality in patients with severe congestive heart failure due to proarrhythmic or negative inotropic effects (e.g. class Ia antiarrhythmics). Even class III antiarrhythmic drugs such as amiodarone, which has been studied sufficiently in patients with left ventricular dysfunction, is not effective enough for significant reduction of cardiac mortality in patients with symptomatic ventricular arrhythmias and depressed ventricular function (e.g. EMIAT, CAMIAT). But as a positive result of available studies, amiodarone does not increase mortality in those patients. Dofetilide has also not been shown to prolong life significantly by suppressing malignant ventricular arrhythmias (DIAMOND-Study). In patients with symptomatic ventricular arrhythmias or aborted sudden death, ICD therapy has been proven to be superior to antiarrhythmic drug therapy in cardiac mortality reduction as a secondary prevention strategy (e.g. AVID, CASH, CIDS). For primary prevention of sudden arrhythmic death in high risk patients, 2 studies (MADIT, MUSST) have already demonstrated favorable results, decreasing mortality by ICD therapy in selected patient populations with partly-reduced ventricular function and unsustained but inducible ventricular tachycardias. This topic is, however, undergoing further evaluation by ongoing trials (e.g. MADIT II, SCD-HeFT). From available data, antiarrhythmic drug therapy in high risk patients is not justified on a routine basis, whereas ICD therapy as a secondary and perhaps primary prevention strategy will significantly reduce cardiac mortality in patients with severe heart failure. Sotalol, a class III antiarrhythmic agent, has recently been shown to reduce ICD-shock delivery which indicates that concomitant drug therapy in patients with an ICD device already implanted may be beneficial in terms of reducing ICD discharges due to ventricular and supraventricular tachycardias. In patients with paroxysmal atrial fibrillation and congestive heart failure, restitution of sinus rhythm is the primary therapeutic goal which can be safely achieved by amiodarone and dofetilide (DIAMOND). In the latter, continuous monitoring of the patient is mandatory because of increased risk of torsade de pointes arrhythmias during the first days of drug administration. In patients with chronic atrial fibrillation rate control and anticoagulation with warfarin is the primary therapeutic option, which can be achieved with either drug treatment (Digoxin, betablockers, amiodarone) or by His bundle ablation with subsequent pacemaker insertion.     

ANTIARRHYTHMIC THERAPY IN THE POST-INFARCTION SETTING: UPDATE FROM MAJOR AMIODARONE STUDIES

SUMMARY Many deaths among hospital survivors of acute myocardial infarction are due to sustained ventricular tachycardia and ventricular fibrillation. This has prompted the evaluation of prophylactic antiarrhythmic drugs and devices. Although it is widely agreed that antiarrhythmic treatment is useful, it is not certain which therapy provides optimal results. Increasing recognition of the efficacy of amiodarone has prompted the design of several trials of the drug. This paper focuses on primary prophylactic antiarryhthmic therapy in the post-infarction setting and particularly on recent amiodarone trials.     

Adverse Effects of Amiodarone

Amiodarone was introduced 30 years ago as an antianginal agent and subsequently has been used as an antiarrhythmic agent. This drug was initially used for patients with malignant ventricular arrhythmias; however, currently it is being used broadly for rate and rhythm control in patients with atrial fibrillation. At first, amiodarone was primarily used by cardiologists and today it is used throughout the medical profession. Amiodarone therapy can potentially result in a wide range of adverse effects. The majority of these adverse effects are dose related and reversible. The following is a review of the adverse effects and drug interactions of amiodarone along with recommendations for identification and management of these adverse effects.