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Torsade de Pointes Associated with the Use of Intravenous Haloperidol

Jeffrey L. Wilt, MD; Ann Mary Minnema, MD; Robert F. Johnson, MD; and Andrew M. Rosenblum, MD
[+] Article and Author Information

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.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;119(5):391-394. doi:10.7326/0003-4819-119-5-199309010-00007
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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.

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Figure 1.
Sequential tracings for patient 1 with corresponding QTc intervals.111

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.

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Figure 2.
Sequential tracings for patient 2 with corresponding QTc intervals.

Values are expressed in milliseconds (ms). Standard lead II is shown in all tracings. All tracings were averaged at the time of measurement. A baseline strip (A) and a tracing at 12 hours (B) after initiating intravenous haloperidol are shown. Note the prolonged QTc interval at baseline. A sample of the torsade de pointes (TdP) is shown in tracing C. Atrial pacing was instituted (D) and eventually discontinued. The QTc interval gradually returned to below baseline; a representative strip from 8 days later (E) is shown.

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Figure 3.
Sequential tracings for patient 3 with corresponding QTc intervals.

Values are expressed in milliseconds (ms). Standard lead II is shown in all tracings. All tracings were averaged at the time of measurement. The baseline strip (A) is shown, as are strips at 24 hours (B) and 48 hours (C) after the initiation of intravenous haloperidol. Note that T-U augmentation is seen in strip C and is important in determining Q-T intervals (see reference 3). A sample of the torsade de pointes (TdP) is shown in tracing D. The tracings gradually returned to baseline after discontinuation of haloperidol; a representative strip from 8 days later (E) is shown.

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Figure 4.
Sequential tracings for patient 4 with corresponding QTc intervals.

Values are expressed in milliseconds (ms). All tracings were averaged at the time of measurement. A baseline strip (A, standard lead II) shows the patient in atrial fibrillation. A sample of the torsade de pointes (TdP) is shown in tracing B, also standard lead II. Note the long-short initiating sequence leading to TdP (see reference 4). A tracing from 8 days later (with the patient in sinus rhythm) is shown in tracing C (standard lead II).

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