What is Torsades de Pointes?
Torsades de pointes is a life-threatening polymorphic ventricular tachycardia that occurs in the setting of QT interval prolongation, characterized by a distinctive twisting pattern of QRS complexes around the isoelectric line. 1
Definition and Core Features
Torsades de pointes is polymorphic ventricular tachycardia that specifically occurs when the QT interval is prolonged, with a characteristic waxing and waning QRS amplitude that creates the appearance of "twisting points." 1
The arrhythmia should be distinguished from other polymorphic ventricular tachycardias—the term should be confined to those polymorphic tachycardias with marked QT-interval prolongation (>500 ms) and QT-U deformity, as they represent a distinct mechanistic and therapeutic entity. 1
Electrocardiographic Characteristics
Distinctive ECG Pattern
The QRS complexes show changing amplitude and morphology (twisting) around the isoelectric line, though this characteristic twisting may not be evident in all ECG leads. 1, 2
The heart rate ranges from 160 to 240 beats per minute, which is notably slower than ventricular fibrillation and allows individual QRS complexes to remain visible. 1, 2
Initiation Pattern
Episodes typically start with a short-long-short pattern of R-R cycles: a premature ventricular complex (PVC) followed by a compensatory pause, then another PVC that falls close to the peak of the T wave. 1
The arrhythmia often has a long coupling interval to the first ventricular tachycardia beat, distinguishing it from idiopathic ventricular fibrillation which has short coupling intervals. 1
A "warm-up phenomenon" is typical, with the first few beats showing longer cycle lengths than subsequent complexes. 1
Termination Pattern
Torsades frequently terminates spontaneously, with the last 2 to 3 beats showing slowing of the arrhythmia. 1, 2
However, it can degenerate into ventricular fibrillation and cause sudden cardiac death in some cases. 1, 2
Distinction from Ventricular Fibrillation
Torsades maintains identifiable QRS complexes with a characteristic twisting pattern, whereas ventricular fibrillation shows rapid, grossly irregular electrical activity with no discernible QRS complexes. 2
Ventricular fibrillation typically has rates >300 bpm with cycle lengths <200 ms, making individual complexes indistinguishable. 1, 2
Unlike ventricular fibrillation that requires defibrillation to terminate, torsades frequently self-terminates. 1, 2
Clinical Context and Causes
Torsades occurs in the setting of acquired or congenital long QT syndrome, most commonly precipitated by QT-prolonging drugs (particularly class IA antiarrhythmics like quinidine and disopyramide). 3, 4
Predisposing factors include electrolyte imbalances (hypokalemia, hypomagnesemia), bradycardia, and high-grade AV block that leads to the long-short sequence initiating the arrhythmia. 1, 4, 5
Risk increases exponentially as QTc exceeds 500 ms, with a 2- to 3-fold higher risk at this threshold. 1
Clinical Presentation
The arrhythmia typically presents with self-limiting bursts causing dizziness and syncope, though it may progress to ventricular fibrillation and sudden death. 3
- Episodes may present with salvos of nonsustained ventricular tachycardia before sustained runs develop. 1