Haloperidol-induced torsade de pointes.

OBJECTIVE: To report a case of torsade de pointes related to the administration of high-dose intravenous haloperidol for the treatment of severe agitation. CASE SUMMARY: Reports in the literature of intravenous haloperidol-induced torsade de pointes are rare. We describe the case of a 41-year-old white woman with no predisposing factors who developed torsade de pointes 55 minutes after a dose of intravenous haloperidol 80 mg (total dosage 915 mg over 7 d). The results of the electrocardiogram were consistent with torsade de pointes and showed a prolonged QTc interval of 610 milliseconds. Intravenous magnesium sulfate 2 g/100 mL NaCl 0.9% was administered, which controlled the arrhythmia. The patient received one additional 80-mg haloperidol dose six hours after the arrhythmia-triggering dose, without reoccurrence of torsade de pointes. Haloperidol was then discontinued, and the patient had no further arrhythmias. CONCLUSIONS: Our case report and others from the literature suggest that intravenous haloperidol administration may prolong QT intervals in some patients, precipitating the potentially life-threatening arrhythmia torsade de pointes. Clinicians should be aware of haloperidol's potential to induce torsade de pointes, since it is used regularly for agitation and delirium in the critical care arena.     

Amiodarone Therapy After Previous Sotalol-induced Torsade de Pointes: Analysis of AT Dispersion to Predict Proarrhythmia

BACKGROUND: Polymorphic ventricular tachycardia of the torsade de pointes type represents, potentially, the most dangerous side effect of antiarrhythmic drugs that prolong ventricular repolarization. Much effort has been devoted to the identification of the degree of drug-associated QT prolongation that might predict the occurrence of torsade de pointes. However, there is still no general agreement as to which level of QT prolongation might be the harbinger of torsade and which may simply represent the manifestation of the class III antiarrhythmic effect of a given compound. METHODS AND RESULTS: A 70-year-old woman who had survived an episode of cardiac arrest outside of a hospital was treated with dl-sotalol (320 mg/d). After 8 days of therapy, she developed two episodes of hemodynamically unstable torsade de pointes. Sotalol was withdrawn and after extensive diagnostic work, therapy with amiodarone therapy was comparable to that observed during sotalol exposure, the patient tolerated amiodarone and is now free of recurrent ventricular tachyarrhythmias over a follow-up period of 1 year. Analysis of QT dispersion in the surface electrocardiograph revealed a marked increase during sotalol therapy but not during amiodarone administration (77 vs 47 ms). During drug-free control, QT dispersion was 43 ms. CONCLUSIONS: These findings emphasize the potential usefulness of determination of QT dispersion from the surface ECG to assess disparity in ventricular recovery, which is known to favor the occurrence of torsade de pointes. These observations need to be corroborated in large prospective trials. Finally, this case report further emphasizes the low arrhythmogenic potential of amiodarone-an unexplained paradox, the understanding of which might provide insights for the development of newer antifibrillatory compounds.     

Azithromycin-induced torsade de pointes

Although erythromycin frequently induces long QT interval and torsade de pointes, the newer drug, azithromycin, has rarely been reported to be associated with torsade de pointes. We report here the occurrence of a significant typical QT prolongation within a few hours after taking azithromycin which lead to torsade de pointes.     

Long QTc interval and torsade de pointes caused by fluconazole

OBJECTIVE: To describe a patient who developed torsade de pointes while being treated with fluconazole. CASE SUMMARY: A 33-year-old woman with a 5 year history of systemic lupus erythematosus was admitted to the intensive care unit because of respiratory insufficiency due to Candida albicans pneumonia. Therapy with intravenous fluconazole 200 mg/day, with dose later adjusted according to her renal function, was started. Prolongation of the QTc interval and torsade de pointes occurred. Initially, domperidone, which had been initiated the day before fluconazole, was suspected as the possible cause and was discontinued; ultimately, both drugs were discontinued. However, torsade de pointes recurred several weeks later when the patient was treated with fluconazole for a second time and disappeared again on withdrawal of the drug. According to the Naranjo probability scale, this adverse reaction was highly probable. DISCUSSION: The risk of torsade de pointes does not correlate in a linear fashion with prolongation of the QTc interval, but an interval beyond 500 msec is considered a significant risk factor. Given that both fluconazole and domperidone are metabolized by the cytochrome P450 system, they may intensify each other's proarrhythmic effects, particularly in patients with concurrent renal dysfunction. These risks are of particular concern in patients whose baseline QTc interval is prolonged for any reason. CONCLUSIONS: From the case history, as well as use of the Naranjo scale, we concluded that fluconazole was the highly probable cause of the development of torsade de pointes in our patient.     

Lack of Triggered Automaticity Despite Repolarization Abnormalities due to Bepridil and Lidoflazine

Bepridil and lidoflazine are calcium channel antagonists that also prolong action potential duration, produce QT interval prolongation on the surface ECG, and have been associated with the distinctive form of ventricular tachycardia, torsade de pointes. It has been demonstrated that quinidine, which also prolongs QT interval and induces torsade de pointes, produces early afterdepolarizations and triggered activity in canine Purkinje fibers driven at slow rates. The effects of bepridil (1-10 microM) and of lidoflazine (5-15 microM) on the transmembrane action potential from canine Purkinje fibers were therefore studied. At long cycle lengths, unlike with quinidine, triggered activity arising during phase 3 was rare; phase 3 secondary plateaus (early afterdepolarizations) were, however, common. Arrest of transmembrane potential between -50 and -60 mV during stimulation at long cycle lengths was also frequently observed (7/20 of bepridil and 3/15 of lidoflazine-treated fibers). In preparations with prominent phase 3 secondary plateaus, addition of epinephrine resulted in triggered activity; similarly, epinephrine caused automaticity from a depolarized membrane potential in 8/9 fibers quiescent at -50 to -60 mV. Thus, the calcium channel blocking drugs bepridil and lidoflazine produced striking repolarization changes at slow stimulation rates, but unlike quinidine, triggered activity was rare. The effect of epinephrine on these drug-treated fibers suggests that the slow inward calcium current plays a role in the generation of triggered activity in the presence of prolonged repolarization.     

QT Prolongation and Torsade de Pointes Ventricular Tachycardia Produced by Ketanserin

A 65-year-old man with arterial hypertension received oral treatment with Ketanserin, a new drug, during a period of five months. He developed marked QT interval prolongation and have several Stokes-Adams attacks. A Holter recording obtained during one of these episodes showed torsade de pointes ventricular tachycardia. The arrhythmias occurred during maximum QT interval prolongation, The correlation between Ketanserin and QT interval prolongation was evaluated by using several Holter studies during administration and withdrawal of the drug. The effect of Ketanserin on the QTc interval was analyzed retrospectively in six patients who had been taking the drug orally. Following a period of four to eight months, the QTc interval was prolonged by the drug (5 to 31%, mean 17%) in five patients. We conclude that torsade de pointes is a potential hazard of long-term treatment with Ketanserin.     

Reflex sympathetic dystrophy in a patient with pre-existing torsade de pointes

A case is presented of a patient with pre-existing torsade de pointes who developed reflex sympathetic dystrophy. A trial of stellate ganglion blocks with ECG monitoring was instituted and the patient obtained relief. The pathophysiology of torsade de pointes is discussed with emphasis on the role of the stellate ganglion. Recommendations for management of similar patients are made.     

Ibutilide-induced long QT syndrome and torsade de pointes

Ibutilide is a class III antiarrhythmic agent used for the termination of atrial fibrillation and atrial flutter. It mainly affects membrane potassium currents and prolongs the cardiac action potential. This effect is reflected as QT interval prolongation on the surface electrocardiogram. Like other drugs that affect potassium currents, ibutilide is prone to induce a malignant ventricular tachycardia, torsade de pointes. We report four cases of torsade de pointes after administration of ibutilide for pharmacologic cardioversion of atrial fibrillation and atrial flutter; three of these cases required direct current cardioversion for termination of torsade de pointes. All four patients were female. We discuss the risk factors for development of ibutilide-induced torsade de pointes.     

Torsade de pointes ventricular tachycardia during low dose intermittent dobutamine treatment in a patient with dilated cardiomyopathy and congestive heart failure

The authors describe the case of a 56-year-old woman with chronic, severe heart failure secondary to dilated cardiomyopathy and absence of significant ventricular arrhythmias who developed QT prolongation and torsade de pointes ventricular tachycardia during one cycle of intermittent low dose (2.5 mcg/kg per min) dobutamine. This report of torsade de pointes ventricular tachycardia during intermittent dobutamine supports the hypothesis that unpredictable fatal arrhythmias may occur even with low doses and in patients with no history of significant rhythm disturbances. The mechanisms of proarrhythmic effects of Dubutamine are discussed.     

Torsade de pointes caused by polypharmacy and substance abuse in a patient with human immunodeficiency virus

Drug-induced QT prolongation is a potentially dangerous adverse effect of some medication combinations. When QT prolongation progresses to torsade de pointes, life-threatening or fatal outcomes may result. A 57-year-old man with a history of human immunodeficiency syndrome on abacavir, nevirapine, tenofovir, voriconazole, and methadone presented to the emergency department with a chief complaint of new-onset seizures. The physical exam was unremarkable. The electrocardiogram demonstrated sinus bradycardia and a prolonged QT_c interval of 690 ms. In the emergency department, he had several episodes of torsade de pointes (TdP) and ventricular tachycardia that resolved spontaneously. These episodes were accompanied by an alteration in mentation and generalized twitching. Magnesium and amiodarone were effective in terminating the dysrhythmia. The patient had multiple risk factors for prolonged QT syndrome including human immunodeficiency virus infection, methadone therapy, and polypharmacy leading to potential drug interactions. Physicians must be aware of multidrug interactions potentiating QT prolongation and leading to torsade de pointes.     

Doxepin Induced Torsade De Pointes

A case of torsade de pointes with normal QT interval secondary to the administration of small amounts of doxepin is presented. Electrophysiological studies during rechallenge with doxepin demonstrated replication of the patient's spontaneous arrhythmia. Evaluation of syncope in patients taking doxepin should include careful evaluation for torsade de pointes.     

Ciprofloxacin- and hypocalcemia-induced torsade de pointes triggered by hemodialysis

Torsade de pointes is a polymorphic form of ventricular tachycardia associated with prolongation of the QT interval, which may be either congenital or acquired. Etiologies for the acquired forms include drug effects, hypokalemia, hypomagnesemia, hypocalcemia, starvation, sick sinus syndrome, and atrioventricular block. We present a 76-year-old man with acute on chronic renal failure, hypocalcemia, on ciprofloxacin, and a prolonged QT interval with torsade de pointes triggered by hemodialysis. The QT prolongation was corrected by treating the hypocalcemia. Hypocalcemia and ciprofloxacin are known to independently cause prolonged QT interval and torsade de pointes; our case illustrates that dialysis can trigger torsade on a background of this risk factor combination.     

Torsade de pointes

A case is described of torsade de pointes in a 41 year old woman with pre-existing QTc prolongation, potentially exacerbated by treatment with sotalol. Previous cardiac investigations had been normal and after a second episode of ventricular fibrillation the patient was referred for electrophysiological studies. The authors review the physiology, causes, and treatment of QTc prolongation and torsade de pointes.     

Magnesium Therapy in Ventricular Arrhythmias

Magnesium (Mg) is the known activator of 300 enzymes which govern energy utilization, cell permeability, and ionic membrane currents in the cardiac conducting cells. This may explain the antiarrhythmic efficacy of Mg in specific clinical settings, despite its only modest electrophysiological effects. This review summarizes the effect of Mg administration in four clinical conditions: in digitalis toxicity; in drug-induced torsade de pointes; in patients with chronic diuretic therapy; and in acute myocardial infarction. Mg effectively abolished ventricular tachyarrhythmias associated with digitalis intoxication. This effect of Mg is related to the activation of sodium-potassium ATP-ase, which is inhibited by digitalis. Drug-induced torsade de pointes was promptly abolished by Mg sulfate in the clinical setting. Experimental studies showed that Mg suppresses the early afterdepolarizations and the triggered activity responsible for occurrence of the arrhythmia. In diuretic-treated hypertensives, potassium depletion has been associated with increased ventricular ectopy and sudden death. Mg has been found to be an important adjuvant for intracellular repletion of potassium in these patients. Several randomized, double-blind studies in patients with acute infarction showed that Mg administered on admission improved survival or reduced the incidence of complex ventricular arrhythmias. Thus, Mg should be employed as first-line therapy in digitalis intoxication and drug-related torsade de pointes, and should be considered an important adjuvant therapy in hypertensives treated with diuretics and patients with acute myocardial infarction.     

Torsade de Pointes and T-U Wave Alternans Associated with Arsenic Poisoning

Arsenic intoxication is a common form of heavy metal poisoning. Although arsenic-induced circulatory collapse, seizures, and syncope are well known, the potential for serious ventricular arrhythmias is less well recognized. Reported in this study are two cases of arsenic poisoning causing torsade de pointes. Furthermore, marked prolongation of the QT-U interval and the rarely observed phenomenon of T-U wave alternans are demonstrated. Thus, arsenic intoxication may be complicated by prolongation of the QT-U interval and torsade de pointes. T-U wave alternans occurs in the presence of a long QT-U interval and may be an electrocardiographic warning sign of torsade de pointes.     

A patient with LQTS in whom verapamil administration and permanent pacemaker implantation were useful for preventing torsade de pointes

A 21-year-old woman with long QT syndrome and missense mutation in HERG (T613M), suffered from repeated attacks of pause dependent torsade de pointes, even though she was given beta-blockers and underwent stellate ganglion block twice at the age of eight. After she received permanent pacemaker implantation and administration of verapamil, no premature beats or pause dependent torsade de pointes was observed.     

Torsade de pointes in a patient receiving intravenous vasopressin

A patient experienced hypertension, bradycardia, QT prolongation, and multiple episodes of torsade de pointes while receiving an iv vasopressin infusion. The dysrhythmias were attributed to vasopressin, but may have been potentiated by hypomagnesemia. Upon vasopressin discontinuation, ECG findings returned to normal before magnesium supplementation. Vasopressin may contribute to the development of torsade de pointes.     

Mexican Border Medications: Potential Toxicity

Abstract

A 26 year-old woman was admitted to the hospital two hours after astemizole overdose. Electrocardiograph showed a prolonged QT interval. Torsade de pointes occurred 13?h after ingestion. Plasma levels of astemizole plus hydroxylated metabolites showed an apparent plasma half-life of 17?h. The possible occurrence of torsade de pointes in astemizole overdose, and the long elimination time of astemizole and hydroxylated metabolites, makes it necessary to maintain ECG monitoring until QT interval has returned to normal.     

Drug-Assisted Intubation in the Prehospital Setting (Resource Document to NAEMSP Position Statement)

We report an emergency medical services (EMS) case of self-limited torsade de pointes after administration of droperidol for nausea andvomiting in a patient with potential predisposing factors for the development of prolonged QT interval. Despite the reported association with torsade de pointes, many clinicians still consider droperidol to be a safe medication. Rare cardiac side effects may be avoided by reviewing risk factors for prolonged QT interval in individual patients prior to administering droperidol     

Importance of QT interval determination and renal function assessment during antiarrhythmic drug therapy

A major concern associated with the use of antiarrhythmic drugs (AAD) is the occurrence of ventricular proarrhythmia, especially torsade de pointes (TdP). The AADs associated with TdP most commonly include quinidine, procainamide, disopyramide, sotalol, and the newer class III agents, such as ibutilide and dofetilide. It is not simply the administration and nature of an AAD but also several additional factors such as heart rate, ventricular hypertrophy, congestive heart failure, gender, age, concomitant drugs, and impaired drug clearance that influence TdP development. Dosing of these agents should be adjusted to take such factors into account to minimize the incidence of proarrhythmia.