Torsades de pointes secondary to intravenous haloperidol after coronary bypass grafting surgery

Perrault, Louis P.; Denault, André; Carrier, Michel; Cartier, Raymond; Bélisle, Sylvain

doi:10.1007/bf03018922

Cited by 59 publications

(25 citation statements)

References 13 publications

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“…5,[17][18][19][20][21][22]35,36 In reviewing all reported cases of cardiac complications associated with IV haloperidol, as well as the current literature, an association with QTP and TdP is likely. However, the case reports reveal that QTP and TdP generally occur in the setting of concomitant risk factors, and no cases have been reported utilizing a cumulative IV dose of <2 mg.…”

Section: Resultsmentioning

confidence: 99%

The FDA extended warning for intravenous haloperidol and torsades de pointes: How should institutions respond?

Meyer‐Massetti

Cheng

Sharpe

et al. 2010

Journal of Hospital Medicine

136

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Section: Resultsmentioning

confidence: 99%

The FDA extended warning for intravenous haloperidol and torsades de pointes: How should institutions respond?

Meyer‐Massetti

Cheng

Sharpe

et al. 2010

Journal of Hospital Medicine

136

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“…19,20 In a meta-analysis, 1,397 patients received different regimens of haloperidol, however, there were no reports of cardiac dysrhythmias. 5 5-HT 3 ] are also known to prolong the QTc interval at high dosages.…”

Section: Discussionmentioning

confidence: 99%

Haloperidol is as effective as ondansetron for preventing postoperative nausea and vomiting

Lee

Wang

Lai

et al. 2007

Can J Anesth/J Can Anesth

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Purpose: Recent warnings regarding the safety of droperidol have limited use of this drug as an antiemetic. Haloperidol, a butyrophenone derivative similar to droperidol, has not been rigorously evaluated as an antiemetic. The aim of this study was to compare the prophylactic antiemetic efficacy of haloperidol vs ondansetron for the prevention of postoperative nausea and vomiting (PONV) after general anesthesia.Methods: Ninety non-smoking female patients were eligible to participate in this randomized double-blinded study. Approximately 30 min before the end of surgery, patients were randomly assigned to receive either haloperidol 2 mg iv, or ondansetron 4 mg iv, respectively. The incidence of PONV, average pain and sedation scores, recovery times, and changes of the rate-corrected QT (QTc) interval were observed postoperatively. Results:The proportion of patients who experienced PONV in the first 24 hr was similar in the two groups (28% and 26% for haloperidol and ondansetron groups, respectively). The incidence of PONV was significantly less in both groups than predicted according to the patients' underlying risks (53% for the haloperidol group, P = 0.016; 51% for the ondansetron group, P = 0.015). Pain scores, sedation scores, and recovery times were similar in the two groups, and no prolongation of the QTc interval was observed in either group. Conclusions: Haloperidol 2 mg iv given 30 min before the end of surgery is effective in preventing PONV, with efficacy comparable to ondansetron 4 mg iv for the first 24 hr after general anesthesia.

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“…An infusion of magnesium sulfate abolished the ventricular arrhythmia (O'Brein et al 1999). Another episode of torsade de pointes not associated with QT prolongation was recorded in a patient anaesthetized with haloperidol for a coronary bypass introduction (Perrault et al 2000).…”

Section: Butyrophenonesmentioning

confidence: 97%

Drug-induced block of cardiac HERG potassium channels and development of torsade de pointes arrhythmias: the case of antipsychotics

Calderone

Testai

Martinotti

et al. 2005

Journal of Pharmacy and Pharmacology

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The prolongation of the cardiac repolarization process, a result of the blocking of the Human Ether-ago-go Related Gene potassium channel, is an undesired accessory property shared by many pharmacological classes of non-cardiovascular drugs. Often the delayed cardiac repolarization process can be identified by a prolongation of the QT interval of the electrocardiograph. In these conditions, premature action potentials can trigger a dangerous polymorphic ventricular tachyarrhythmia, known as torsade de pointes, which occasionally can result in lethal ventricular fibrillation. In this work, brief descriptions of the electrophysiological basis of torsade de pointes and of the several pharmacological classes of torsadogenic drugs are given. Attention is focused on antipsychotics, with a deeper overview on the experimental and clinical reports about their torsadogenic properties. The cardiac action potentialCardiac action potentials are generated by trans-membrane movements of ion species, flowing principally through specific channels. In a typical human cardiac action potential ( Figure 1A), five different phases can be recognized. Phase 0 is a rapid depolarization process resulting from a massive inward flow of Na þ (current I Na ). The following phase 1 is linked to the inactivation of the I Na current and to a weak and transient repolarization due to an outward flow of K þ (current I to ). Phase 2 reflects an almost iso-electric plateau generated by the simultaneous activation of a depolarizing inward Ca þþ current, a repolarizing outward rapidly activated K þ current (current I Kr ) and a repolarizing outward slowly activated K þ current (current I Ks ). Phase 3 reflects the complete membrane repolarization due to many K þ currents (mainly I Ks and I Kr ), which leads the cell to the recovery of resting membrane potential. Finally, phase 4 is the resting period, ensured by inward rectifier K þ currents (I K1 ), before a new following cardiac cycle. The QT intervalA typical electrocardiograph (ECG) tracing of a human cardiac cycle ( Figure 1B) starts with a P wave (80-110 ms) representing the atrial depolarization. The following iso-electric time (about 100 ms) reflects the propagation of the depolarization through the atrio-ventricular node to the ventricular conduction system. The QRS complex (<120 ms) represents the whole ventricular depolarization, followed by an isoelectric time (about 120 ms) starting from the J point. Finally, the T wave (230-300 ms) represents the final ventricular repolarization and the end of the cycle. Among the various ECG parameters that are useful in analysing the cardiac functions, the QT interval is the most usual one for estimating the ventricular repolarization process. Drug-induced torsade de pointesMany drugs belonging to different pharmacological classes (Table 1) can trigger lifethreatening polymorphic ventricular tachyarrhythmias, such as torsade de pointes. In particular, many non-cardiovascular drugs in common clinical use cause the prolongation

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Torsades de pointes secondary to intravenous haloperidol after coronary bypass grafting surgery

Cited by 59 publications

References 13 publications

The FDA extended warning for intravenous haloperidol and torsades de pointes: How should institutions respond?

The FDA extended warning for intravenous haloperidol and torsades de pointes: How should institutions respond?

Haloperidol is as effective as ondansetron for preventing postoperative nausea and vomiting

Drug-induced block of cardiac HERG potassium channels and development of torsade de pointes arrhythmias: the case of antipsychotics

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