W. Victor, MD R. Vieweg, MD Christopher S. Nicholson
{"title":"扭转点室性心动过速,QT间期和精神药物","authors":"W. Victor, MD R. Vieweg, MD Christopher S. Nicholson","doi":"10.1016/S1082-7579(96)00010-6","DOIUrl":null,"url":null,"abstract":"<div><p><em>Torsade de pointes</em> (“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 <em>torsade de pointes</em>.</p><p>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 <em>torsade de pointes</em>. 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 <em>torsade de pointes</em>.</p><p>Clinically, subjects with <em>torsade de pointes</em> 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 <em>torsade de pointes</em> 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.</p><p>Identifying and withdrawing the offending agent or reversing and correcting predisposing conditions remain the cornerstone of treating <em>torsade de pointes</em> ventricular tachycardia. Because treatment of <em>torsade de pointes</em> 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.</p></div>","PeriodicalId":100909,"journal":{"name":"Medical Update for Psychiatrists","volume":"2 2","pages":"Pages 48-54"},"PeriodicalIF":0.0000,"publicationDate":"1997-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1082-7579(96)00010-6","citationCount":"7","resultStr":"{\"title\":\"Torsade de Pointes ventricular tachycardia, QT interval, and psychotropic drugs\",\"authors\":\"W. Victor, MD R. Vieweg, MD Christopher S. Nicholson\",\"doi\":\"10.1016/S1082-7579(96)00010-6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><em>Torsade de pointes</em> (“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 <em>torsade de pointes</em>.</p><p>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 <em>torsade de pointes</em>. 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 <em>torsade de pointes</em>.</p><p>Clinically, subjects with <em>torsade de pointes</em> 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 <em>torsade de pointes</em> 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.</p><p>Identifying and withdrawing the offending agent or reversing and correcting predisposing conditions remain the cornerstone of treating <em>torsade de pointes</em> ventricular tachycardia. Because treatment of <em>torsade de pointes</em> 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.</p></div>\",\"PeriodicalId\":100909,\"journal\":{\"name\":\"Medical Update for Psychiatrists\",\"volume\":\"2 2\",\"pages\":\"Pages 48-54\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S1082-7579(96)00010-6\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical Update for Psychiatrists\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1082757996000106\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Update for Psychiatrists","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1082757996000106","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.