Special Feature

Polymorphic VT

By William Brady, MD

Ventricular tachycardia (vt) can be classified as monomorphic or polymorphic based on the morphologic features of the QRS complex. Monomorphic ventricular tachycardia (MVT), the most commonly encountered form of VT, is a subtype of VT with a stable QRS complex configuration (a uniform beat-to-beat QRS complex morphology). Polymorphic ventricular tachycardia (PVT) is defined as VT with an unstable (continuously varying) QRS complex morphology in any single electrocardiographic lead; variation in both the R-R interval and electrical axis are also noted features of this ventricular arrhythmia. (See Figure 1 and Figure 2.) Multiple terms for PVT—including cardiac ballet, torsades de pointes, pleomorphic VT, atypical VT, and transient recurrent ventricular fibrillation (VF)—are found throughout the medical literature, causing confusion regarding rhythm etiology and therapy. PVT should be the single term used to describe this subtype of VT. The term torsades de pointes (TdP) should be employed only when delayed repolarization (prolongation of the QT interval) is noted on the ECG—TdP is therefore one subtype of PVT and not an equivalent term. Figures 1 and 2 are rhythm strips showing PVT. Without a knowledge of the QT interval, both examples can only be termed PVT.


PVT is noted in the setting of sudden cardiac death (SCD), particularly when the patient is encountered early in the process; it frequently is the initial rhythm, which then degenerates into either MVT or VF. PVT has been found in victims of prehospital cardiac arrest,1-3 in patients undergoing ambulatory monitoring,4,5 in survivors of prehospital SCD,4,6,7 and in patients admitted to the CCU.8,9 Concerning the prehospital VT SCD population, PVT was noted to occur in 26%-30% of such patients.1,2 Reports of patients experiencing SCD while undergoing ambulatory monitoring suggest that PVT is a relatively common arrhythmia among patients with pre-existing myocardial disease, occurring as either the initial or primary arrest rhythm in 30-43% of instances.4,5,10,11 PVT is also noted in approximately 20% of patients resuscitated from cardiac arrest who survive to electrophysiologic (EP) study.4,12,13 When PVT is encountered in the EP laboratory in survivors of SCD, it frequently degenerates into VF.4,12,13 PVT has been noted in patients with acute coronary syndromes; Wolfe et al and Grenadier et al reported a somewhat less frequent occurrence of PVT in patients with acute ischemia.8,9

Figure 1

Polymorphic VT in a patient with known CAD and recent chest pain

The post-arrest ECG demonstrated a normal QT interval.

Figure 2

Polymorphic VT in a patient on procainamide for atrial fibrillation

The post-arrest ECG demonstrated QT interval prolongation, confirming the clinical suspicion of TdP.

Resuscitative Therapy

A discussion of the resuscitative treatment of PVT is plagued by considerable controversy, similar to the confusion surrounding the proper terminology. Many reports are found in the literature in which standard ACLS therapy for VT in patients with PVT was partially effective, ineffective, or potentially dangerous (i.e., proarrhythmic).1-3,8,9,14,15 In the prehospital VT cardiac arrest group,1,2 standard ACLS therapy was used to a similar extent in patients with both MVT and PVT; patients with both VT subtypes had similar outcomes. White et al noted a variable response to ACLS antiarrhythmic medication in the prehospital management of four patients with PVT.3 Wolfe et al, in their series of 11 patients with PVT related to acute ischemic heart disease, reported a patient population in which traditional antiarrhythmic therapy (lidocaine, procainamide, bretylium, and magnesium) produced a variable response.8 Grenadier et al had even less success in their series of nine patients with PVT occurring in the setting of AMI; lidocaine, procainamide, and bretylium were uniformly ineffective in the treatment of PVT.9 Nguyen et al described the clinical characteristics of 45 patients with PVT; lidocaine appeared to be effective in only half of the patients in which it was administered, while bretylium was associated with an increased frequency of PVT.15 Sclarovsky et al reported 34 patients with PVT, characterizing their response to lidocaine treatment that was successful in only 20% of patients.14

Transthoracic electrical cardioversion/defibrillation (ECD) is generally believed to be less effective in the treatment of PVT. In the prehospital population, electrical cardioversion was used in a similar fashion with equivalent outcomes in patients with both MVT and PVT.1,2 Grenadier et al reported a 66% response rate to electrical cardioversion, while Sclarovsky et al described seven successful cases in which ECD terminated the PVT in a series of 34 patients.9,14 Kerber et al demonstrated that PVT behaves more like VF than MVT in its response to ECD.16 Using increasingly higher energy shocks for the three arrhythmias, they found that MVT is successfully converted to a stable rhythm at lower electrical currents when compared to both PVT and VF. They also noted that the response to electrical therapy of PVT was similar to VF and not to MVT.

Torsades de Pointes

It is important to recall that the rhythm diagnosis of TdP requires confirmation of abnormal repolarization—that is, prolongation of the QT interval. In patients initially encountered in cardiac arrest, whether in the prehospital or ED setting, such measurements are difficult, if not impossible. In fact, one prehospital study of 476 VT cardiac arrest cases reported that only 10% of patients had an EMS-witnessed cardiac arrest—the situation in which QT interval determinations could be made.1 Additional work within a similar prehospital population revealed that only 8% of patients with out-of-hospital PVT had TdP.2 White et al reported four cases of out-of-hospital SCD involving PVT with only one patient demonstrating abnormal repolarization on the ECG.3

When one specifically considers the TdP subgroup of PVT, therapeutic recommendations are equally controversial, if not outright confusing. Standard ACLS pharmacotherapy was used in similar fashion in out-of-hospital patients with TdP, MVT, and PVT with comparable rates of resuscitation and hospital discharge.2 Nguyen et al reported 45 patients with PVT (approximately 50% of this series experiencing TdP); lidocaine was effective in only half of the cases in which it was administered, while bretylium appeared to be proarrhythmic.15 Sclarov sky et al described a series of patients, the majority with TdP, and noted that lidocaine was successful in a minority of patients.14 Type I-A antiarrhythmic agents should be avoided, due to the potential for further QT interval prolongation, if the physician suspects TdP; diphenylhydantoin may be used safely due to its membrane-stabilizing effects. Magnesium has been suggested as a specific pharmacologic treatment for patients with TdP. Aimed at normalizing repolarization abnormality, magnesium may be used in a slow IV push fashion in SCD, or over 15-30 minutes after resuscitation. Patients experiencing TdP have responded to medical measures aimed at increasing the heart rate, such as isoproterenol, which was used successfully by Sclarovsky et al in 10 patients, or Nguyen et al, who effectively employed overdrive pacing in 13 cases.14,15 Electrical cardiac overdrive pacing is also successful in patients with PVT. Transthoracic electrical cardioversion is effective as noted above; unfortunately, TdP has a tendency to recur frequently, requiring numerous applications of ECD.


PVT is a relatively common arrhythmia encountered in patients experiencing SCD, particularly when these patients are encountered early in cardiac arrest. In order to make the diagnosis of TdP, the physician must have some knowledge of the QT interval, which is difficult in many cases of SCD encountered in emergency medicine. Regarding management issues, patients with both PVT and TdP appear to have varying responses to standard ACLS resuscitation measures. In the two largest studies investigating the prevalence of PVT1,2 and one investigation exploring the subtype TdP,2 patients with these two rhythm disturbances fared as well as patients with MVT. Specific adjustment in therapy for all patients with PVT does not appear warranted.

In patients with known or suspected TdP, whether based on an analysis of the ECG or a review of the medical history, additional therapies that may benefit the patient include magnesium and electrical cardiac pacing. Recognizing that certain agents (e.g., procainamide and bretylium) may be dangerous to the patient, while other antiarrhythmic treatments (lidocaine) may not be as effective, the physician may tailor resuscitative therapies in select cases of TdP to increase the possibility of good outcome. (Dr. Brady is Assistant Professor of Emergency Medicine and Internal Medicine and Medical Director of the Chest Pain Center at the University of Virginia in Charlottesville, VA.)


1. Brady W, et al. Comparison of prehospital monomorphic and polymorphic ventricular tachycardia: Prevalence, response to therapy, and outcome. Ann Emerg Med 1995;25:64-70.

2. Brady W, et al. The prolonged QT interval in patients with out-of-hospital ventricular tachycardia cardiac arrest. Prehosp Disaster Med 1996;2:113. Abstract.

3. White RD, Wood DL. Out-of-hospital pleomorphic ventricular tachycardia and resuscitation: Association with acute myocardial ischemia and infarction. Ann Emerg Med 1992;21:1282-1287.

4. DiMarco JP, Haines DE. Sudden cardiac death. Curr Probl Cardiol 1990;15:187-232.

5. Denes P, et al. Clinical, electrocardiographic and follow-up observations in patients having ventricular fibrillation during Holter monitoring. Am J Cardiol 1981;49:9-16.

6. Wellens HJJ, et al. Programmed electrical stimulation of the heart in patients with life-threatening ventricular arrhythmias: What is the significance of induced arrhythmias and what is the correct stimulation protocol? Circulation 1985;72:1-7.

7. Horowitz LN, et al. Torsades de pointes: Electrophysiologic studies in patients without transient pharmacologic or metabolic abnormalities. Circulation 1981;63:1120-1128.

8. Wolfe CL, et al. Polymorphous ventricular tachycardia associated with acute myocardial infarction. Circulation 1991;84:1543-1551.

9. Grenadier E, et al. Polymorphous ventricular tachycardia in acute myocardial infarction. Am J Cardiol 1984; 53:1280-1283.

10. Panadis JP, Morganroth J. Sudden death in hospitalized patients: Cardiac rhythm disturbances detected by ambulatory electrocardiographic monitoring. J Am Coll Cardiol 1983;2:798-805.

11. Kempf FC, Josephson ME. Cardiac arrest recorded on ambulatory electrocardiograms. Am J Cardiol 1984;53:1577-1582.

12. Roy D, et al. Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: Relation to inducibility at electrophysiologic testing. Am J Cardiol 1983;52:969-974.

13. Stevenson WG, et al. Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction. Circulation 1985;71:1146-1152.

14. Sclarovsky S, et al. Polymorphous ventricular tachycardia: Clinical features and treatment. Am J Cardiol 1979;44:339-344.

15. Nguyen PT, et al. Polymorphous ventricular tachycardia: Clinical characterization, therapy and the QT interval. Circulation 1986;74:340-349.

16. Kerber RE, et al. Ventricular tachycardia rate and morphology determine energy and current requirements for transthoracic cardioversion. Circulation 1992;85:158-163.