HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zemrak, W. R. Articles by Kenna, G. A. Search for Related Content PubMed PubMed Citation Articles by Zemrak, W. R. Articles by Kenna, G. A.

WESLEY R. ZEMRAK, PHARMD., is Pharmacy Practice Resident, Maine. Medical Center, Portland. GEORGE A. KENNA, PH.D., B.S.PHARM., is Assistant Professor of Psychiatry and Human Behavior (Research), Brown Medical School, Brown University, Providence, RI, and Clinical Pharmacist, The Westerly Hospital, Westerly, RI.

Address correspondence to Dr. Kenna at the Center for Alcohol and Addiction Studies, Box G-S121-5, Providence, RI 02903 (george_kenna{at}brown.edu).

Purpose. The association of antipsychotic and antidepressant drugs with Q-T interval prolongation is reviewed. Summary. Prolongation of the Q-T interval can be of particular concern to practitioners when prescribing antidepressants and antipsychotics. Patients may be at a greater risk for developing fatal arrhythmias when taking many of these drugs. In general, antipsychotics cause Q-T interval prolongation at a higher rate than do antidepressants. The typical antipsychotics thioridazine, pimozide, and intravenous haloperidol all have the highest potential for Q-T interval prolongation. The tricyclic antidepressants have a higher rate of Q-T interval prolongation than do selective serotonin-reuptake inhibitors (SSRIs), particularly at higher concentrations and in cases of overdose. In addition, nonpharmacologic risk factors such as existing heart disease, female sex, electrolyte abnormalities, hepatic insufficiency, and stimulant drug abuse contribute to the risk for developing these arrhythmias, as do pharmacologic factors such as multidrug therapy and high dosages of drugs known to prolong the Q-T interval. Risk factors may be identified in the patient’s history and demographic information. However, all pharmacists may not have this information readily available to them. Conclusion. Antipsychotics cause Q-Tc interval prolongation at a higher rate than do antidepressants, and the typical anti-psychotics thioridazine, pimozide, and i.v. haloperidol all have the highest potential for Q-Tc interval prolongation. Tricyclic antidepressants have a higher rate of Q-Tc interval prolongation than do the SSRIs, particularly at higher concentrations and in overdose situations. The frequency of adverse events associated with drug-induced Q-T interval prolongation is unknown. Index terms: Antidepressants; Antipsychotic agents; Dosage; Haloperidol; Long QT syndrome; Pimozide; Thioridazine; Toxicity

 

This article has been cited by other articles:

				E. L. Breden, M. T. Liu, and S. R. Dean Metabolic and Cardiac Side Effects of Second-generation Antipsychotics: What Every Clinician Should Know Journal of Pharmacy Practice, October 1, 2009; 22(5): 478 - 488. [Abstract] [PDF]