胺碘酮与利多卡因治疗心肺复苏过程中室性心律失常效果比较

目的 对比胺碘酮和利多卡因在治疗心肺复苏过程中出现的快速性室性心律失常的疗效。方法 心肺复苏过程中快速性心律失常患者57例。分别予胺碘酮（34例）及利多卡因（23例）治疗，持续心电监护观察其疗效。结果 胺碘酮组总有效率88．3％，利多卡因组总有效率60．8％，差异有显著性意义（P〈0．05）。结论 胺碘酮治疗心肺复苏过程中出现的快速性室性心律失常的疗效优于利多卡因。     

胺碘酮抢救心肺复苏中持续性恶性室性心律失常的应用

【目的】观察胺碘酮对心肺复苏过程中恶性室性心律失常的疗效。【方法】收集本院心肺复苏过程中出现的恶性室性心律失常患者66例,分别给予胺碘酮（n=38）和利多卡因（n=28）治疗,记录心律失常发生情况并判定疗效。【结果】胺碘酮治疗组显效20例（52．6％）,有效10例（26．3％）,无效8例（21．1％）,总有效率78．9％。利多卡因组显效7例（18．4％）,有效8例（28．6％）,无效13例（46．4％）,总有效率53．6％。两组有效率比较差异有显著性（P〈0．05）。【结论】胺碘酮治疗心肺复苏过程中恶性室性心律失常有良好的临床疗效。     

胺碘酮治疗心肺复苏过程中室性心律失常的疗效和安全性

目的:观察胺碘酮治疗心肺复苏过程中室性心律失常的疗效和安全性。方法:58例在心肺复苏过程中出现室性心律失常病人,首剂负荷剂量胺碘酮3～5mg/kg于10～15min内静脉注入,随后以0.5～1.5mg/min静脉泵入维持,若心律失常控制不满意,可间隔30min再静脉注射首剂负荷剂量,24h总量为1200～1500mg。结果:有效率为93.1%,副反应发生率为6.90%。结论:胺碘酮治疗心肺复苏过程中室性心律失常有效且安全。     

胺碘酮与利多卡因对急性乌头碱中毒所致快速性室性心律失常治疗效果的对比研究

目的 评价胺碘酮与利多卡因治疗急性乌头碱中毒所致快速性室性心律失常的疗效及安全性.方法 将130例患者分为胺碘酮治疗组68例,利多卡因治疗组62例,回顾比较两种药物对快速性室性心律失常的疗效、病死率和不良反应发生率.结果 在急性乌头碱中毒所致快速性室性心律失常的治疗中,胺碘酮组有效率97.05%(66/68),利多卡因组有效率75.81%(47/62),胺碘酮组优于利多卡因组,差异有统计学意义(P＜0.01).胺碘酮组发生不良反应7例,不良反应发生率10.29%;利多卡因组发生不良反应1例,不良反应发生率1.61%;利多卡因组不良反应发生率低于胺碘酮组,差异统计学意义(P<0.05).结论 胺碘酮是治疗急性乌头碱中毒所致快速性室性心律失常效果较好的药物,虽然不良反应发生率较高,但能通过合理使用预防,可以作为首选药物.     

胺碘酮对恶性室性心律失常治疗的疗效观察

目的 :观察胺碘酮对恶性室性心律失常治疗的疗效。方法 :对收入 CCU符合入选条件的 6 7例恶性室性心律失常患者随机分为 2组治疗。治疗组 32例 :部分病例采用胺碘酮转复 ;其余采用电转复 ,成功后用胺碘酮维持窦性心律 (窦律 )。对照组 35例 :应用利多卡因转复及维持窦律 ;利多卡因无效者改用胺碘酮治疗。结果 :治疗组转复成功率 83.33% (10 /12 ) ,维持窦律成功率 81.2 5 % (13/16 ) ,总有效率 78.12 % (2 5 /32 ) ,均明显高于对照组〔分别为 5 7.14 % (8/14 )、6 2 .2 5 % (10 /16 )和 5 4 .2 9% (18/35 )〕,且对照组中应用利多卡因转复及维持窦律失败的部分病例使用胺碘酮仍有效。结论 :胺碘酮是治疗恶性室性心律失常最有效的药物之一 ,特别是应用其它抗心律失常药物治疗无效的病例 ,应用胺碘酮可收到良好的治疗效果。     

胺碘酮治疗小儿室性心动过速疗效观察

目的 评价静脉应用胺碘酮对室性心动过速(VT)患儿的疗效及安全性.方法 42例急诊VT患者,随机分为两组,每组各21例,分别为观察组(胺碘酮)、对照组(利多卡因),观察组静脉应用胺碘酮急诊复率,对照组应用利多卡因急诊复律,观察两组复律成功率,评价安全性.结果 胺碘酮组复律成功率为80.9%,利多卡因组为38.09%,胺碘酮组明显高于利多卡因组(P<0.01).胺碘酮治疗前后血压比较,差异无统计学意义(P>0.05).2例静脉注射过程中出现血压偏低,无需特殊处理,无心动过缓出现,无QT间期延长.利多卡因组无明显不良反应.结论 静脉注射胺碘酮对儿童室性心动过速的即时疗效好,且较为安全,值得在基层医院推广.     

体外循环术后室性心律失常应用胺碘酮与利多卡因后血液动力学及临床疗效观察

目的 观察胺碘酮与利多卡因对体外循环术后室性心律失常的疗效及对血流动力学的影响.方法 体外循环术后并发室性心律失常患者87例,分为胺碘酮组(A组)42例和利多卡因组(L组)45例,分别予以胺碘酮及利多卡因治疗,持续心电监护,观察用药前后有创平均动脉压(MAP)、心率(HR)和中心静脉压(CVP)变化,比较临床疗效.结果 胺碘酮组总有效率92.86%,利多卡因组总有效率78.78%,差异有显著性意义(χ2=3.89,P<0.05);两组MAP、HR、CVP值比较,差异均无显著性意义(P>0.05).结论 胺碘酮治疗体外循环术后并发室性心律失常的有效率高于利多卡因,二者对血流动力学的影响差异小.     

门冬氨酸钾镁与胺碘酮联合治疗急性心肌梗死室性心律失常的疗效

目的:观察门冬氨酸钾镁与胺碘酮联合治疗急性心肌梗死(AMI)室性心律失常的作用。方法:观察128例AMI室性心律失常患者,在监护病房持续心电监护,将128例AMI患者分为治疗组(65例)(门冬氨酸钾镁与胺碘酮联合治疗)和对照组(63例),两组均给予扩冠脉、有溶栓适应证者行溶栓及对症治疗,治疗组予静滴门冬氨酸钾镁和胺碘酮治疗。对照组则静脉注射利多卡因治疗。结果:治疗组总有效率高于对照组(89%vs15%),室颤发生率和病死率较对照组低(P<0.05)。结论:门冬氨酸钾镁显著改善AMI患者的预后,可作为常规治疗用药;胺碘酮对心肌梗死急性期室性心律失常治疗安全、有效。     

胺碘酮联合美托洛尔治疗心力衰竭并室性心律失常疗效分析

目的：探讨胺碘酮联合小剂量美托洛尔治疗充血性心力衰竭（CHF）伴室性心律失常的有效性和安全性。方法：将62例CHF伴室性心律失常的患者随机分为胺碘酮联合美托洛尔组（治疗组32例）与美托洛尔组（对照组30例）,观察两组心律失常好转情况及心功能改善情况。结果：治疗组抗心律失常有效率及心功能改善情况均优于对照组（P〈0.05）。结论：胺碘酮联合小剂量美托洛尔治疗CHF并室性心律失常疗效好,使用安全,无明显副作用。     

胺碘酮分别联合比索洛尔、美托洛尔治疗收缩性心力衰竭合并室性心律失常的效果比较

目的比较胺碘酮分别联合比索洛尔、美托洛尔治疗收缩性心力衰竭合并室性心律失常的效果。方法选取2017年7月至2019年6月在我院治疗的106例合并室性心律失常的收缩性心力衰竭患者为研究对象,将其分为观察组与对照组,每组53例。观察组给予胺碘酮联合比索洛尔方案治疗;对照组给予胺碘酮联合美托洛尔方案治疗。比较两组心功能改善有效率、心律失常改善有效率。结果观察组患者的心功能改善有效率(92.45%比71.70%)、心律失常改善有效率(84.91%比67.92%)均明显高于对照组(P0.05)。结论胺碘酮与比索洛尔联合应用的临床疗效明显优于胺碘酮与美托洛尔联合应用的疗效,更具应用价值。     

Amiodarone and rural emergency medical services cardiac arrest patients: A cost analysis

Objective: Recent American Heart Association guidelines suggest amiodarone as an antiarrhythmic in refractory ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). The authors sought to assess the impact of amiodarone use on outcomes and cost associated with this practice in a rural emergency medical services (EMS) state. Methods: Statewide EMS records were reviewed for the calendar year 1999. Data reviewed included prehospital diagnosis, medications given by prehospital providers to patients with cardiac arrest, and procedures performed, including cardiopulmonary resuscitation (CPR) and defibrillation. Cost-benefit analysis assumed the cost of amiodarone treatment to be $137.65 per patient encounter. Absolute risk reduction (ARR) and number needed to treat (NNT) analysis utilized resuscitation rates published in the ARREST and ALIVE trials. Results: During the study period, EMS providers diagnosed 2,189 patients as having cardiac arrest. Five hundred thirty-five (24.4%) cardiac arrest patients were defibrillated. One hundred sixty patients (7.3%), including 15 who did not receive defibrillation, were given lidocaine during resuscitation efforts. The annual cost increase from current practice for a statewide amiodarone VF/VT protocol was $21,822.40 (10,572.87%). The initial cost to stock EMS vehicles for this protocol would be $50,115.52. The cost-benefit analysis yielded a potential for one additional patient survival to hospital discharge in Maine per 3.125 years of system-wide practice at a cost of $68,840.00. Conclusion: Based on current data, instituting amiodarone treatment for refractory VF and pulseless VT in a rural EMS setting requires the investment of substantial resources, relative to current treatment strategies, for any potential survival benefit. PREHOSPITAL EMERGENCY CARE 2002;6:291-294     

A MIODARONE AND R URAL E MERGENCY M EDICAL S ERVICES C ARDIAC A RREST P ATIENTS : A C OST A NALYSIS

Objective: Recent American Heart Association guidelines suggest amiodarone as an antiarrhythmic in refractory ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). The authors sought to assess the impact of amiodarone use on outcomes and cost associated with this practice in a rural emergency medical services (EMS) state. Methods: Statewide EMS records were reviewed for the calendar year 1999. Data reviewed included prehospital diagnosis, medications given by prehospital providers to patients with cardiac arrest, and procedures performed, including cardiopulmonary resuscitation (CPR) and defibrillation. Cost-benefit analysis assumed the cost of amiodarone treatment to be $137.65 per patient encounter. Absolute risk reduction (ARR) and number needed to treat (NNT) analysis utilized resuscitation rates published in the ARREST and ALIVE trials. Results: During the study period, EMS providers diagnosed 2,189 patients as having cardiac arrest. Five hundred thirty-five (24.4%) cardiac arrest patients were defibrillated. One hundred sixty patients (7.3%), including 15 who did not receive defibrillation, were given lidocaine during resuscitation efforts. The annual cost increase from current practice for a statewide amiodarone VF/VT protocol was $21,822.40 (10,572.87%). The initial cost to stock EMS vehicles for this protocol would be $50,115.52. The cost-benefit analysis yielded a potential for one additional patient survival to hospital discharge in Maine per 3.125 years of system-wide practice at a cost of $68,840.00. Conclusion: Based on current data, instituting amiodarone treatment for refractory VF and pulseless VT in a rural EMS setting requires the investment of substantial resources, relative to current treatment strategies, for any potential survival benefit.     

胺碘酮治疗充血性心衰合并无症状性室性心律失常52例分析

目的观察胺碘酮是否对室性心律失常有显著抑制作用并使左心室射血分数显著增加。方法采用双盲,安慰剂对照,其中52例充血性心力衰竭的患者,心脏扩大,室性早搏10次或以／小时,左心室射血分数在40％以下,随机分到胺碘酮治疗组（27例）或安慰剂组（25例）。主要终点为胺碘酮对左心室射血分数的影响及室性心律失常的抑制。结果胺碘酮明显更有效抑制室性心律失常,4周后左心室射血分数增加了8．8％。结论胺碘酮用于轻度到中度的心力衰竭患者时,药物耐受性好,可有效地抑制心律失常并改善心功能。     

Intravenous amiodarone in the treatment of refractory arrhythmias

Oral amiodarone's slow absorption handicaps rapid treatment of life-threatening arrhythmias. We used iv amiodarone to treat ten patients with hemodynamically significant atrial arrhythmias and life-threatening ventricular arrhythmias refractory to all conventional medical treatment. Arrhythmias were controlled in nine patients, five of whom became long-term survivors on oral amiodarone. Two patients died of cardiovascular collapse within 24 h of initiation of iv amiodarone. One other patient died postoperatively of cardiovascular collapse while on oral amiodarone, 2 wk after iv amiodarone. Another patient died of an unrelated cause 13 months after initiation of amiodarone. These results suggest that iv amiodarone is effective in controlling refractory atrial and ventricular arrhythmias and may shorten the latency period.     

Cumulative Effects of Amiodarone on Inducibility of Ventricular Tachycardia: Implications for Electrophysiological Testing

To determine whether the slow onset of action of amiodarone might result in a delayed effect on the inducibility of sustained ventricular arrhythmias, 45 patients with ischemic heart disease and inducible sustained monomorphic ventricular tachycardia were prospectively studied. Each patient had at least one initial repeat study on amiodarone and those with persistently inducible arrhythmias were rescheduled for further studies over the following 24 weeks. After 2-3 weeks of amiodarone therapy, nine patients no longer had inducible tachycardias, and tachycardia in another eight patients (18%) later became noninducible. Using life-table methods, analysis based on the results of the first re-study showed 18-month recurrence rates of 43% in the inducible vs 17% in the noninducible groups (p = 0.056). When the results of additional testing were then used to reclassify patients, the recurrence rates for these two groups were 50% and 17%, respectively (p = 0.004). Observation of blood pressure and level of consciousness during induced arrhythmias was also predictive of clinical tolerance in patients having recurrences; 16 of 19 patients experienced symptoms of similar severity to those produced during testing. We conclude: (1) early testing of amiodarone may result in misclassification of some patients as remaining inducible; (2) re-testing at a later time more accurately predicts tachycardia recurrence; (3) observation of hemodynamic response also provides important prognostic information.     

胺碘酮抗心律失常机制及急诊急救应用进展

心律失常是急诊常见急症,室性心动过速、心室颤动、心房颤动是心脏猝死的主要原因。尽管不断有新的抗心律失常药物问世,胺碘酮(乙胺碘呋酮,Amiodarone)由于药理学及电生理学机制的特殊性,在抗心律失常药物治疗领域具有不可替代的地位。随着医学实践的发展,其应用价值已被指南确立。特别是在院前急救及心肺复苏中使用,安全性高。1胺碘酮抗心律失常机制1.1胺碘酮具有多通道阻滞的药理与电生理作用20世纪90年代,心律失常抑制试验     

Predictive value of early electrophysiologic testing in determining long-term outcome with amiodarone treatment in patients with sustained ventricular tachycardia

This prospective study sought to determine whether programmed ventricular stimulation before hospital dismissal in patients who had received a loading dose of amiodarone would identify those at risk for recurrent ventricular arrhythmias. Between January 1985 and January 1989, 64 patients (55 men and 9 women; mean age, 64 years) with a history of sustained ventricular tachycardia (VT) or ventricular fibrillation were referred to our institution for electrophysiologic testing. Of these patients, 52 had coronary artery disease, 11 had dilated cardiomyopathy, and 1 had hypertrophic cardiomyopathy. Of the 64 patients, 47 had baseline tests while no drugs were administered and repeated electrophysiologic testing after 10 days of amiodarone loading (1.2 g/day). The other 17 patients had no baseline study because of instability of their arrhythmias but underwent electrophysiologic testing after amiodarone loading. Follow-up ranged from 7 to 1,536 days (mean, 652 days). During the follow-up period, recurrent arrhythmias were detected in 22 patients. Of the 64 patients, 14 had suppression of VT. Of 43 patients in whom the cycle lengths of VT were determined both at baseline and after amiodarone therapy, 20 had an increase of 100 ms or more, and 23 had no substantial change. The mean ejection fraction was 31%. Of a total of 16 deaths in the series, 8 were sudden. Suppression of VT during amiodarone therapy suggested a lower rate of fatal and nonfatal recurrent arrhythmias, but the difference was not statistically significant. An increase in the cycle length of VT did not predict an improved outcome. The age of the patient and the presence of a left ventricular aneurysm were slightly predictive of mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Normalization of peripheral thyroid hormone metabolism induced by successful chronic amiodarone treatment in patients with ventricular arrhythmias

Amiodarone, an antiarrhythmic agent, is also known to have important effects on the peripheral metabolism of thyroid hormones; the relationship between these two effects of the drug, however, is not well established. We tested the hypothesis that the antiarrhythmic effect of amiodarone might be mediated by its effect on the metabolism of thyroid hormones. Peripheral thyroid hormone metabolism was investigated using a double-tracer ([¹²⁵I]-T4 and [¹³¹I]-T3) procedure in 10 normal volunteers and 10 euthyroid patients with complex ventricular arrhythmias before and during 6 months‘ amiodarone treatment. The underlying cardiac disease was coronary artery disease in four cases, dilated cardiomyopathy in three and idiopathic arrhythmias in three. In all but one patient with complex ventricular arrhythmias amiodarone treatment resulted in a reduction of ≥ 80% of premature ventricular contractions and complete suppression of episodes of ventricular pairs or ventricular tachycardia. In all cases successful treatment with amiodarone was accompanied by normalization of all kinetic parameters: T4 to T3 conversion ratio and T3/T4 molar ratio of production decreased to mean values of 24.7 ± 17.5% and 0.35 ± 0.22% respectively, whereas T4 production rate increased (mean value 75.9 ± 30.0 nmol day^?1 m^?2). Our kinetic data indicate that long-term therapy with amiodarone, when effective in suppressing cardiac arrhythmias, also reduces peripheral T4 to T3 conversion, hence restoring the normal peripheral thyroid hormone metabolic pattern. In conclusion, our study confirms that the antiarrhythmic action of amiodarone may be (at least partially) mediated by its action on thyroid hormone metabolism, and may justify the hypothesis that an altered peripheral metabolism of thyroid hormones may play a role in the pathogenesis of complex ventricular arrhythmias.