扭转点室性心动过速,QT间期和精神药物

W. Victor, MD R. Vieweg, MD Christopher S. Nicholson
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引用次数: 7

摘要

扭转点(扭转点)室性心动过速是一种罕见但可能危及生命的心律失常。QRS复合体的正弦形态非常不寻常,并将这种节律障碍归入多形性室性心动过速的范畴。浦肯野纤维动作电位的第2或第3期去极化后早期是最常用于解释心电图QT间期延长和随后的点扭转的机制。IA类抗心律失常药物如奎尼丁和较新的3型抗心律失常药物是诱发这种心律失常最常见的药物。许多精神药物,特别是三环抗抑郁药和标准抗精神病药物,具有类似奎尼丁的性质,并与点扭转有关。在抗精神病药物中,硫吡嗪和氟哌啶醇——特别是静脉注射大剂量氟哌啶醇——可导致多达1%的病例出现多态性室性心动过速。选择性血清素再摄取抑制剂(SSRIs)和奈法唑酮通过药物-药物相互作用可产生扭转点。临床上,椎体扭转患者通常无症状或仅出现轻微的晕厥前症状。然而,明显的晕厥可能是这种心动过速的一部分。偶尔,多形性室性心动过速退化为心室颤动,这可能是致命的。点扭转性室性心动过速的危险因素包括冠状动脉疾病、心肌疾病、瓣膜性心脏病、基线QT间期延长、心传导障碍、心源性慢性心律失常以及电解质和代谢障碍。识别和停用致病药物或逆转和纠正易感条件仍然是治疗点扭转性室性心动过速的基石。由于点扭转性室性心动过速的治疗不同于单型性室性心动过速的治疗,区分单型和多型性室性心动过速是非常重要的。精神科医生应该熟悉多形性室性心动过速的危险因素、病因和病理生理学。这样的努力将最好地保护精神科医生和他们的病人免受这种节律障碍的困扰。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Torsade de Pointes ventricular tachycardia, QT interval, and psychotropic drugs

Torsade de pointes (“twisting of the points”) ventricular tachycardia is a rare, but potentially life-threatening, cardiac arrhythmia. The sinusoidal morphology of the QRS complexes is very unusual and places this rhythm disturbance in the category of polymorphic ventricular tachycardia. Early afterdepolarization during phases 2 or 3 of the Purkinje fiber action potential is the mechanism most commonly used to explain electrocardiographic QT interval prolongation and subsequent torsade de pointes.

Type IA class antiarrhythmic drugs like quinidine and the newer type 3 antiarrhythmic drugs constitute the most common agents inducing this arrhythmia. Many psychotropic drugs, particularly tricyclic antidepressants and standard antipsychotic drugs, have quinidine-like properties and have been associated with torsade de pointes. Of the antipsychotic agents, thioridazine and haloperidol—particularly intravenous administration of large doses of haloperidol—may induce polymorphic ventricular tachycardia in up to 1% of cases. The selective serotonin reuptake inhibitors (SSRIs) and nefazodone through drug-drug interactions may produce torsade de pointes.

Clinically, subjects with torsade de pointes are usually free of symptoms or only experience mild presyncopal symptoms. Overt syncope, however, can be part of this tachyarrhythmia. Occasionally, polymorphic ventricular tachycardia degenerates into ventricular fibrillation that may be fatal. Risk factors for torsade de pointes ventricular tachycardia include coronary artery disease, heart muscle disease, valvular heart disease, baseline QT interval prolongation, cardiac conduction disturbances, cardiac bradyarrhythmias, and electrolyte and metabolic disturbances.

Identifying and withdrawing the offending agent or reversing and correcting predisposing conditions remain the cornerstone of treating torsade de pointes ventricular tachycardia. Because treatment of torsade de pointes ventricular tachycardia differs from treatment of monomorphic ventricular tachycardia, distinguishing between mono- and polymorphic ventricular tachycardia is very important. Psychiatrists should become familiar with the risk factors, causes, and pathophysiology of polymorphic ventricular tachycardia. Such efforts will best protect psychiatrists and their patients from facing this rhythm disturbance.

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