A comparison of the cardiovascular effects of haloperidol, thioridazine and chlorpromazine HCl.

Transient hypotension, electrocardiographic conduction changes and cardiac arrhythmias have been reported with the use of certain anti-psychotic agents. To assess these observations, we compared the effects of haloperidol, thioridazine and chlorpromazine HCl on alpha-adrenergic receptors, mean aortic pressure, myocardial contractile force and myocardial electrophysiology in anesthetized dogs. The results from these studies indicated that, on a milligram basis, chlorpromazine HCl was equipotent to haloperidol, and thioridazine was 0.5 times as potent as haloperidol as an alpha-adrenergic receptor blocker and as a myocardial depressant. Each compound induced conduction nonhomogeneity in myocardial conducting tissue. However, as a neuroleptic, when tested in dogs, haloperidol was 50 times more potent than chlorpromazine HCl and 180 times more potent than thioridazine. The therapeutic safety indices (cardiovascular effect dose/neuroleptic dose) for haloperidol regarding alpha-adrenergic blockade, hypotension, myocardial depression and ventricular conduction delay were 4, 145, 235 and 125, respectively, whereas these indices for chlorpromazine and for thioridazine were 0.06, 2, 4, 6 and 0.05, 1, 3 and 1, respectively. Therefore, because of differences in neuroleptic potency, therapeutic doses of haloperidol are less likely to cause adverse cardiovascular effects than are those of either chlorpromazine HCl or thioridazine.