药物致Q-T间期延长的文献分析

近年来,临床实践有许多药物都会导致Q-T间期延长甚至尖端扭转型室性心律失常（TdP）。本文通过对1979年-2013年国内医药期刊公开报道的药物致Q-T间期延长的个案进行统计和分析,总结了56个病例的一般情况、引起Q-T间期延长的药物、发生时间及转归等,致Q-T间期延长药物中排在前三位的分别为抗心律失常药、抗微生物药、抗组胺药。大部分患者在用药后一个月内出现,停药及对症治疗后好转。临床医师应正确地认识药物致Q-T间期延长发生机制和易感因素,才能保证临床安全有效地使用药物。     

特发性Q-T间期延长综合征误诊分析

目的探讨特发性Q-T间期延长综合征误诊情况,提高对该病的认识和诊断。方法对本院于2010年2月~2013年2月收集的2例特发性Q-T间期延长综合征患者的临床诊断情况进行回顾性分析。结果有2例患者误诊为癫痫,通过吸痰、吸氧、镇静、倍他乐克等治疗后逐渐恢复正常。结论针对抽搐、昏厥等病因不明显患者应当进行心电图检查,可提高对特发性Q-T间期延长综合征诊断率,降低误诊情况,对其进行倍他乐克持续治疗可提高治愈率。     

Q-T间期延长综合征误诊为癫痫1例报告

1病例 患儿刘某,男性,10岁,间歇性晕厥、抽搐发作7年。患儿于3岁时开始常因劳累、＂上感＂、情绪激动而发作晕厥,抽搐,每次发作前20min左右即有胸痛、胸闷、心悸、烦躁等症状,每次持续约1min自行缓解;开始每年发作2～3次,以后逐渐频繁,近期每月发作1～2次,间歇期无任何症状。于当地医院诊断为＂癫痫＂,长期服用苯妥英钠和安定未见效果。近3d来因＂上感＂致晕厥、抽搐发作频繁,2～3次/d。于2011年8月6日来我院以＂癫痫＂在急诊科观察。     

继发性Q-T间期延长预后分析

目的分析继发性Q-T间期延长的预后。方法回顾性分析126例Q-T间期延长的临床资料。结果126例中,预后不良者42例,占33.3%,其中频发室性早搏3例,突然发生室性心动过速(室速)或心室纤颤(室颤)18例,猝死20例。继发性Q-T间期延长,出现T波形态改变的,提示有发生严重室性心律失常或猝死的危险。药物引起的QT间期延长者46例,导致严重的室性心律失常或室颤。4例在原发病引起Q-T间期延长情况下并发低钾,均发生严重心律失常;低钾合并低镁13例,均并发严重室性心律失常或猝死。结论Q-T间期延长患者易发生心律失常,引起严重的并发症,临床上应引起足够的重视。     

加替沙星注射液致Q-T间期延长

1名62岁女性,因患急性左心衰、肺部感染、2型糖尿病、糖尿病足,给予呋塞米、毛花苷丙静脉注射、加替沙星0.4g,1次/d静脉滴注。5d后,患者出现心动过缓,心电图示窦性心律,HR54次/min,QT间期0.56s,ST-T改变。立即停用加替沙星,给予对症治疗。7d后心电图示HR67次/min、QT间期0.36s。     

对特发性Q-T间期延长综合征的临床探讨

特发性Q-T间期延长综合征是复极延长为尖端扭转型心动过速是一种室性快速心律失常,可引起昏厥或死亡。心电图出现Q-T间隙延长,室性心律失常。其由电解质平衡紊乱,服用影响心室复极的药物等。还可能伴有先天性耳聋,其中最常见的是JerveII-Lange-NeiL-son综合征（常染色体隐性遗传性耳聋）、Romano-Wavcl综合征（常染色体显性遗传性耳聋）。患者有明显Q-T间期延长和形态异常,有发生尖端扭转型室性心动过速的危险并可致死亡。发病时常用β受体阻滞剂首选恢复左右星状神经结的平衡,对心跳暂停依赖性治疗以提高心率为主。除纠正病因外,对症治疗用异丙肾、阿托品或起搏治疗。而禁用Ia、Ic或Ⅲ类心律失常药物。     

患者口服抗心律失常药物胺碘酮致Q-T间期延长1例报告

1病历摘要 1.1临床资料患者霍亚兰,女性,71岁,汉族,已婚,农民,顺义区天竺镇楼台村。主因：“慢性咳嗽气喘50余年,加重3日。”经门诊于2013年12月3日以“慢性阻塞性肺疾病急性发作、冠状动脉性心脏病、陈旧性心梗、冠脉支架植入术后、高血压病、糖尿病”收入病房。     

莫沙比利合用利欧致Q-T间期延长1例

患者,女,73岁,因冠心病、心衰Ⅱ°、慢支急性发作伴感染、肺气肿、肺心病于2004年1月26日入住我科.BP120/90mmHg,HR 92bpm,心律齐,心尖区可闻及病理性S3,未闻及病理性杂音.ECG示窦性节律,ST-T改变,Q-T间期0.38S.血生化示肝功能正常,血尿素氮30.6mg/dl,血尿酸9.68mg/dl,血清钾正常,血清钠148.1mmol/L,血清氯109.2mmol/L.     

2例家族性Q-T间期延长综合征

例1：病人，女，63岁，退休工人，因阵发性晕厥反复发作曾5次住院。平时心电图检查：窦性心动过缓伴不齐，心率为54～65次／分，Q-T问期0.45～0.48秒。平时一般情况较好。第一次在外科行胆囊切除术，麻醉诱导期间出现晕厥，心电监护示：室性心动过速，经静脉推注利多卡因后恢复窦性心律。第二、三次均因受凉、劳累后出现晕厥、抽搐，急诊入院。心电监护示：室     

关于Q-T间期研究进展

目前医学界越来越重视Q—T间期改变，Q—T间期延长和Q—T间期离散度的变化，易致心律失常乃至心脏猝死。对其病因、发生机制、临床意义及治疗有了突破性进展。     

精神药物致肠梗阻临床分析

目的探讨住院精神疾病患者肠梗阻的原因及有关因素。方法对近10年来我院住院患者中21例患者发生的23次肠梗阻进行回顾分析。结果发生肠梗阻的患者中有20例次所服药物中有氯氮平(87％)。有2例为单一用氯丙嗪,1例为阿米替林。经停药或减药后,给予胃肠减压,纠正水电介质平衡,应用肠蠕动促进剂,多数病情均较快好转,有2例转院治疗。结论有较多的精神药物可以引起麻痹性肠梗阻,其中以氯氮平最为常见,与剂量无明显关系,可能个体对该药的敏感性有关。     

慢性肾衰患者心电图Q-T间期变化的探讨

本文对24例(45例次)慢性肾衰(CRF)患者的心电图进行分析,发现CRF患者出现Q—T间期延长者明显多于心、脑血管疾病。经分析Q—T间期变化与血清K~+有密切关系、与Na~+、Cl、Ca~(++)、Mg~(++)等无明显关系,似与尿毒症心肌病变有关。住院期间,Q—T间期延长组的病死率明显高于Q—T间期正常组。     

氟哌利多用于持续硬膜外镇痛对Q-T间期的影响

目的研究氟哌利多临床常用剂量术后持续硬膜外自控镇痛对QT间期的影响。方法30例ASAⅠ-Ⅱ级女性患者在连续硬膜外麻醉下行妇科手术,术后行持续硬膜外自控镇痛,随机分成三组,每组10例。三组术后均行持续硬膜外镇痛,镇痛药液总量100ml,内含吗啡4mg、0．5％布比卡因27ml和生理盐水73ml。对照组(C组)不加其他药物;氟哌利多1组(D5组)加氟哌利多5mg氟哌利多2组(D10组)加氟哌利多10mg。于术前与镇痛24、48h行体表12导联ECG检查,盲法测定并计算出平均QTc时间。结果三组患者术前QT间期无显著性差异,应用镇痛泵24、48h的QT间期与术前值亦无明显差异。结论临床剂量氟哌利多用于术后持续硬膜外自控镇痛中对QT间期无明显影响,初步提示氟哌利多用于术后持续硬膜外镇痛是安全的。     

Prolonged Q-T interval and severe tachyarrhythmias,common features of sotalol intoxication

Summary The findings in six patients admitted to hospital 0.5–4.5 h after the ingestion of an overdose of 2.4–8 g sotalol are described. In addition to bradycardia and hypotension, all patients had a considerably prolonged corrected Q-T interval, up to 172±8% of normal. Severe ventricular tachyarrhythmias occurred in five of the six patients, the risk was greatest up to 20 h after the ingestion of sotalol. The long Q-T interval returned to normal over 3 to 4 days, which is consistent with the long half-life of sotalol. In addition to its beta-blocking action, sotalol has marked electrophysiological properties of a Class III antiarrhythmic drugs, which are likely to be able to account for its observed effects. Special attention should be paid to the risk of severe ventricular arrhythmias in sotalol intoxications.     

Electrophysiologic interactions of antipsychotic drugs with central noradrenergic pathways

The pathway from the nucleus coeruleus to Purkinje neurons in rat cerebellar cortex was used to analyze effects of antipsychotic neuroleptic drugs on a central noradrenergic pathway. Fluphenazine and haloperidol produced a dose-dependent increase in Purkinje neuron spontaneous discharge. This effect was not seen in animals in which the noradrenergic input had been removed by the neurotoxin 6-hydroxydopamine. In contrast, the effects of neuroleptics were still present in animals which had received neonatal X-ray irradiation, which destroys intrinsic inhibitory and excitatory pathways in cerebellar cortex. Chlorpromazine produced the same increase in discharge rate, but was significantly less potent. -Flupenthixol was equipotent with fluphenazine, but -flupenthixol, a behaviorally inactive steroisomer, was without effect. The dose-response curves showed potencies similar to those in several animal behavioral paradigms. In addition, the rank order of potency was identical to that in clinical tests of antipsychotic activity. Three-week chronic administration of fluphenazine resulted in complete blockade of noradrenergic activity, with no further increase in Purkinje neurons spontaneous discharge rate by additional doses of drug. Thus, tolerance does not develop to the noradrenergic blocking effect of the neuroleptic. Taken together, this evidence suggests that antipsychotic neuroleptic drugs block noradrenergic neurotransmission in the CNS.     

Activation of midline thalamic nuclei by antipsychotic drugs

The thalamus has been proposed as a site which may be involved in the production of the syndrome of schizophrenia and the response of schizophrenic symptoms to treatment. These studies test whether, consistent with this hypothesis, the activation of thalamic nuclei is a shared property of neuroleptic antipsychotic drugs. Rats were given single doses of the typical high and low potency neuroleptics haloperidol (1 mg/kg) and chlorpromazine (20 mg/kg), the atypical neuroleptics thiroridazine (20 mg/kg) and clozapine (20 mg/kg), the specific dopamine antagonist raclopride (3 mg/kg), the mixed dopamine/serotonin antagonist risperidone (3 mg/kg) or drug-free vehicle. Increased expression of Fos-like protein was utilized as a marker of cellular activation. All drugs tested, including typical and atypical antipsychotic agents, led to similar effects on the midline thalamic paraventricular, centromedian and rhomboid nuclei and the nucleus reuniens. These results suggest that midline thalamic nuclei may participate in neural circuits mediating some of the shared effects of antipsychotic drugs. Received: 9 January 1997/Final verion: 13 June 1997     

2009年乌鲁木齐市第四人民医院住院患者抗精神病类药物使用分析

目的 了解乌鲁木齐市第四人民医院2009年抗精神病类药物的用药现状. 方法 以乌鲁木齐市第四人民医院2009年1～12月住院精神病患者处方为依据,从抗精神病药物的分类,精神病患者的年龄、性别、职业,单一用药、联合用药、药物的用法用量等方面,用药物利用指数（DUI）来分析抗精神病药物的应用情况. 结果 除了利培酮、碳酸锂、阿普唑仑的DUI＞1.0（分别为1.089、1.574、1.011）,其他均≤1.0. 结论 精神类药物在乌鲁木齐市第四人民医院临床使用基本合理,无滥用倾向.在用药选择上,患者的经济状况影响药物的选用,给患者用药时以单一用药为主,必要时辅以联合用药.     

Brain homovanillic acid: regional changes over time with antipsychotic drugs.

Acute administration of equivalent doses of either chlorpromazine, thioridazine, or clozapine, respectively, produced progressively smaller increases in brain homovanillic acid (HVA) in the rabbit; however, changes in HVA in three brain regions were of equal magnitude for a single dose of a given drug. Chronic administration of fluphenazine enanthate resulted in a decrease in HVA relative to acute treatment in caudate more than limbic regions. No differences between caudate and limbic regions were observed during daily chlorpromazine administration for 3 ro 8 days. Tolerance appeared to develop in approximately 1 week. Chronic treatment with clozapine produced no tolerance at one week but suggestive evidence of tolerance in caudate and limbic regions at two weeks. No tolerance was observed in the hypothalamus during chronic treatment with any drug used. Cisternal CSF HVA paralleled caudate HVA during acute and chronic treatments.     

Effects of antipsychotic drugs on operant responding after acute and repeated administration

RATIONALE: The current generation of atypical antipsychotic drugs represents an improvement over traditional ("typical") antipsychotics in many respects. However, a theoretical framework and adequate preclinical models have not yet been developed to predict or explain differences among the atypical antipsychotics, a necessary component of future development. OBJECTIVES: The purpose of the present set of experiments was to identify differences between the acute and subchronic effects of several atypical antipsychotic drugs and the typical antipsychotic haloperidol on operant responding in rats. METHODS: The effects of haloperidol and the atypical antipsychotics clozapine, olanzapine, risperidone, sertindole, quetiapine, remoxipride, and thioridazine were determined in rats trained to respond for food reward under a multiple fixed ratio 30/fixed interval 60 s schedule. A profile of the acute effects of each drug on response rates, response durations, and within-session effects were determined. Next, the dose of each drug that produced 75% suppression of response rates was administered for 16 consecutive days to determine whether or not tolerance would develop to the rate-suppressing effects of that dose. RESULTS: All drugs produced dose-related decreases in response rates. Only haloperidol and risperidone produced significant increases in response duration, while only haloperidol and remoxipride displayed within-session response decrements. Tolerance was evident for clozapine and to a lesser extent thioridazine. CONCLUSIONS: These results illustrate that the current generation of atypical antipsychotics are a heterogeneous group and that operant procedures may be useful for identifying differences preclinically. Specifically, clozapine appears to possess properties that distinguish it from other atypical antipsychotics, particularly after repeated dosing.