The objectives of this paper are to: 1) discuss practical aspects of antipsychotic induced QT prolongation, torsades de pointes (TdP) and sudden cardiac death, 2) discuss its possible mechanisms, 3) review data for each antipsychotic medication or class of medications and, 4) present recommendations from the literature. We performed computerized searches of the biomedical literature utilizing MEDLINE and PsycINFO computer databases (1966-2001), and by reviewing bibliographies to identify all pertinent case reports, case series, and formal studies using the following search terms: antipsychotics, sudden cardiac death, and QT prolongation. QT prolongation is a dynamic phenomena affected by various factors (mood, disease states, gender, medication, etc.). Sudden cardiac death attributable to antipsychotic medications seems to occurs in a step-wise fashion beginning with QT prolongation, leading to TdP, which can progress to cardiac arrest. Blocking the rapidly-acting potassium rectifier current appears be the primary mechanism of QT prolongation in drugs known to cause TdP and sudden cardiac death. All antipsychotic medications have been shown to cause QT prolongation, however, the degree to which this occurs and the risk of TdP varies. The risk of sudden cardiac death increases with higher doses of medications, use of phenothiazines or intravenous butyrophenones, and in patients with certain medical illnesses, especially cardiac disease. In order to prevent sudden death from antipsychotic medications, we recommend obtaining screening electrocardiograms in all at-risk patients, follow-up electrocardiograms after the initiation of medication, and using the lowest effective dose of medication. If QT prolongation occurs, the risks and benefits of therapy should be considered and medication adjustments made if warranted.