Answer

Torsade de pointes (a subtype of polymorphic ventricular tachycardia [PVT]): PVT is defined as a ventricular rhythm faster than 100 bpm. It is characterized by clearly defined QRS complexes with frequent and rapid changes in morphology, axis, or both (Passman, 2001). Torsade de pointes is a subtype of polymorphic ventricular tachycardia and occurs in the setting of prolonged repolarization, which appears as a prolonged QT interval (QTc) of greater than 450 ms on an ECG. Rates are typically 160-250 bpm.

Dessertenne originally described this disturbance in 1966, referring to cycles of ventricular tachycardia with alternating electric polarity and amplitude, such that the peaks of the QRS complexes appeared to be twisting around an isoelectric line. Thus, the term torsade, or twisting of the points, originated (Dessertenne, 1966). The rhythm is usually self-terminating, but it may degenerate into ventricular fibrillation or, in rare cases, sustained monomorphic ventricular tachycardia.

Torsade de pointes is almost always associated with drugs that prolong the QT interval, including various antidysrhythmic agents (eg, quinidine, procainamide), antibiotics (eg, erythromycin, azole antifungals), sedatives (eg, droperidol, haloperidol), and antipsychotics (eg, thioridazine, ziprasidone). Other etiologies include acute coronary syndrome, electrolyte abnormalities (hypokalemia, hypomagnesemia), toxins, CNS disease, and structural heart disease.

On the ECG shown in Figure 1, the QTc interval is approximately 500 ms, and the classic pause-dependent early after depolarization (EAD) is observed prior to the first beat of torsade de pointes. PVT may actually result from an R-on-T phenomenon. The twisting or undulating nature of the dysrhythmia is obvious on this ECG.

This patient was given a 2-g bolus of magnesium and a 100-mg bolus of lidocaine, which converted the ventricular tachycardia to the patient^s prior natural rhythm of sinus tachycardia (Figure 2). Had this treatment been unsuccessful, immediate overdrive pacing and defibrillation could have been performed at the bedside.

Initial management is dependent on the patient^s hemodynamic status. Electric defibrillation according to advanced cardiac life support (ACLS) guidelines for pulseless ventricular tachycardia/ventricular fibrillation is usually successful in terminating the unstable arrhythmia. However, the arrhythmia may recur, and multiple defibrillation attempts may be required. Stable patients require removal of the offending agent, IV magnesium (2-g bolus followed by a 2- to 4-mg/min infusion), or IV lidocaine (as a bolus). Overdrive ventricular pacing at a rate of 100 bpm decreases prolonged repolarization (Atkins, 2001; Kahn 2002). Isoproterenol 2-10 mg/min has also been used. IV amiodarone may be used in refractory cases, but this medication can prolong the QTc in rare cases. Interestingly, prehospital patients with both PVT and torsade de pointes have outcomes similar to those of patients with monomorphic ventricular tachycardia when given standard ACLS (Brady, 1995; Brady, 1999).

For more information about torsade de pointes, see the eMedicine articles (Medicine/Surgery) Torsade de Pointes and (Emergency Medicine) Torsade de Pointes.

References

Atkins DL, Dorian P, Gonzalez ER, et al. Treatment of tachyarrhythmias. Ann Emerg Med 2001;37(4 Suppl):S91-109.

Brady WJ, DeBehnke DJ, Laundrie D. Prevalence, therapeutic response, and outcome of ventricular tachycardia in the out-of-hospital setting: a comparison of monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and torsade de pointes. Acad Emerg Med 1999;6(6):609-17.

Brady W, Meldon S, DeBehnke D. Comparison of prehospital monomorphic and polymorphic ventricular tachycardia: prevalence, response to therapy, and outcome. Ann Emerg Med 1995;25(1):64-70.

Dessertenne F. Ventricular tachycardia with two variable opposing foci. Arch Mal Coeur Vaiss 1966;59:263-72.

Hudson KH, Brady WJ, et al. Electrocardiographic features of ventricular tachycardia. J Emerg Med 2003;25(3):303-14.

Kao LW, Kirk MA, Evers SJ, et al. Droperidol, QT prolongation and sudden death: what is the evidence? Ann Em Med 2001;37(4 Suppl):S91-109.

Khan IA. Long QT syndrome: diagnosis and treatment. Am Heart J 2002;143(1):7-14.

Passman R, Kadish A. Polymorphic ventricular tachycardia, long QT syndrome and torsades de pointes. Med Clin North Am 2001;85(2):321-41.

BACKGROUND

The patient is an 18-year-old man who had undergone a heart transplantation for complex congenital heart disease. His stay in the coronary care unit was prolonged because of presumed acute rejection with multiple complications, including respiratory failure and ventricular fibrillation induced by subclavian line placement. The patient was slowly recovering in the hospital when he complained of sudden weakness and dizziness while watching television. What is the diagnosis?

Hint

Is this a ^twisted^ case?

Author: Claire U. Plautz, MD, and William J. Brady, MD, Associate Professor, Departments of Internal Medicine and Emergency Medicine, Vice-chair, Department of Emergency Medicine, University of Virginia School of Medicine

University of Virginia Department of Emergency Medicine, Charlottesville

eMedicine Editor: John Vozenilek, MD

Division of Emergency Medicine, Evanston Northwestern Healthcare

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