Torsade de Pointes Associated with the Use of Intravenous Haloperidol

  1. Jeffrey L. Wilt, MD;
  2. Ann Mary Minnema, MD;
  3. Robert F. Johnson, MD; and
  4. Andrew M. Rosenblum, MD
  1. From St. Mary's Health Services and Blodgett Memorial Medical Center, Grand Rapids, Michigan. Requests for Reprints: Jeffrey L. Wilt, MD, Section of Pulmonary and Critical Care Medicine, P.O. Box 9166, West Virginia University, Morgantown, WV 26506-9166. Acknowledgments: The authors thank David Vidro for help with figure production and Dr. Angela Tiberio for help with manuscript preparation.

    Intensive-care-unit delirium requires rapid treatment to prevent morbidity [1]. Intravenous haloperidol (Haldol, McNeil Pharmaceuticals, Spring House, Pennsylvania) has been used frequently in recent years to combat intensive-care-unit delirium. Its advantages include minimal cardiac effects, even at doses greater than 100 mg/d [2]. We present four cases of haloperidol-associated torsade de pointes [3] developing in intubated patients with intensive-care-unit delirium.

    Case Reports

    Patient 1

    A 39-year-old woman with bacterial meningitis developed acute congestive heart failure on hospital day 20 and required reintubation and intravenous haloperidol (5-mg increments) and lorazepam (Ativan, Wyeth-Ayerst Laboratories, Philadelphia, Pennsylvania) administration for sedation. Progressive Q-T interval widening was noted (Figure 1). On day 23, torsade de pointes developed Figure 1, and the haloperidol was discontinued (dosage, 580 mg over a 4-day period). Atropine was administered, the QTc interval normalized Figure 1, and no further dysrhythmia was noted. Concurrent medications included furosemide, penicillin G, methylprednisolone, digoxin, terazosin, and nitroglycerin.

    Figure 1. Values are expressed in milliseconds (ms). All tracings were averaged at the time of measurement. The baseline strip (A, standard lead II) and tracings at 4 hours (B, standard lead II), 48 hours (C, standard lead II), and 72 hours (D, lead MCL ) after starting intravenous haloperidol are shown. A sample of the torsade de pointes (TdP) is shown in tracing E (lead MCL ). The QTc gradually returned to baseline after discontinuing the haloperidol; a representative strip from 6 days later (F, lead MCL ) is shown. Sequential tracings for patient 1 with corresponding QTc intervals.111

    Patient 2

    A 19-year-old woman with status asthmaticus received sedation with intravenous haloperidol (5- or 10-mg increments) and lorazepam. She experienced progressive Q-T interval widening Figure 2 and developed monomorphic ventricular tachycardia that was unresponsive to defibrillation. She responded transiently to intravenous …

    « Previous | Next Article »Table of Contents