Polymorphic VT and Torsades de Pointes (TdP)


Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction.

Torsades de pointes (TdP) is a specific form of PVT occurring in the context of QT prolongation — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.

ECG strip Torsades de pointes TDP
Torsades de pointes
  • For TdP to be diagnosed, the patient must have evidence of both PVT and QT prolongation
  • Bidirectional VT is another specific type of of PVT, most commonly associated with digoxin toxicity
  • First described by François Dessertenne (1917-2006) in 1966

Clinical Significance
  • TdP is often short lived and self terminating, however can be associated with haemodynamic instability and collapse. TdP may also degenerate into ventricular fibrillation (VF)
  • QT prolongation may occur secondary to multiple drug effects, electrolyte abnormalities and medical conditions; these may combine to produce TdP, e.g. hypokalaemia may precipitate TdP in a patient with congenital long QT syndrome
  • Recognition of TdP and the risk of TdP allows the instigation of specific management strategies (e.g. magnesium, isoprenaline, overdrive pacing, etc.)

Further review of the causes of QT prolongation

Pathophysiology of TdP
  • A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction
  • This prolonged repolarisation period also gives rise to early after-depolarisations (EADs)
  • EADs may manifest on the ECG as tall U waves; if these reach threshold amplitude they may manifest as premature ventricular contractions (PVCs)
  • TdP is initiated when a PVC occurs during the preceding T wave, known as ‘R on T’ phenomenon
  • The onset of TdP is often preceded by a sequence of short-long-short R-R intervals, so called “pause dependent” TDP, with longer pauses associated with faster runs of TdP

Electrocardiographic Pearls
  • During short runs of TdP or single lead recording the characteristic “twisting” morphology may not be apparent
  • Bigeminy in a patient with a known long QT syndrome may herald imminent TdP
  • TdP with heart rates > 220 beats/min are of longer duration and more likely to degenerate into VF
  • Presence of abnormal (“giant”) T-U waves may precede TdP

Drug-induced Torsades
  • In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better described by the absolute rather than corrected QT
  • More precisely, the risk of TdP is determined by considering both the absolute QT interval and the simultaneous heart rate (i.e. on the same ECG tracing)
  • These values are then plotted on the QT nomogram (below) to determine whether the patient is at risk of TdP
  • A QT interval-heart rate pair that plots above the line indicates that the patient is at significant risk of TdP
QT nomogram risk stratification for torsades de pointes

ECG Examples
Example 1
ECG strip Torsades de pointes TDP 2 2

Torsades de Pointes:

  • Frequent PVCs with ‘R on T’ phenomenon trigger a run of polymorphic VT which subsequently begins degenerates into VF
  • QT interval is difficult to see because of artefact but appears slightly prolonged (QTc ~480ms), making this likely to be TdP
  • This combination of mildly prolonged QTc and frequent PVCs / bigeminy is commonly seen in acute myocardial ischaemia — these patients are at high risk of deterioration into PVT / VF

Example 2
ECG hypokalaemia torsades 2

TdP secondary to hypokalaemia:

  • Sinus rhythm with inverted T waves, prominent U waves and a long Q-U interval due to severe hypokalaemia (K+ 1.7)
  • A premature atrial complex (beat #9 of the rhythm strip) lands on the end of the T wave, causing ‘R on T’ phenomenon and initiating a paroxysm of polymorphic VT
  • Because of the preceding long QU interval, this can be diagnosed as TdP

Example 3
ECG hypokalaemia torsades 3

TdP secondary to hypokalaemia:

  • Another ECG from the same patient (K+ still 1.7)
  • A brief, self-terminating paroxysm of TdP is again precipitated by a PAC causing ‘R on T’

Example 4
ECG Torsades des pointes tdp 2

Torsades de Pointes:

  • Sinus rhythm, or possibly ectopic atrial rhythm (biphasic / inverted P waves in lead II)
  • Prolonged QTc interval of 540 ms (greater than half the R-R interval)
  • Ventricular ectopics with ‘R-on-T’ phenomenon — the second PVC initiates a run of TdP

NB. See how the arterial line pressure waveform (lower tracing) is affected by the dysrhythmia. There is a reduced volume pulse during the first PVC as the heart has less time to fill. Subsequently the cardiac output drops away to almost nothing during the run of TdP – this is likely to result in syncope or cardiac arrest.

Example 5
ECG R on T 2

R on T phenomenon:

  • There is sinus rhythm with frequent PVCs in a pattern of ventricular bigeminy
  • The QT interval is markedly prolonged (at least 600ms), with each PVC falling on the preceding T wave (= ‘R on T’ phenomenon)
  • This ECG is extremely high risk for TdP – in fact this patient had a TdP cardiac arrest shortly after this ECG was taken

For the story behind this ECG, check out Cardiovascular Curveball 003.


Advanced Reading



LITFL Further Reading


MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner

Emergency Physician in Prehospital and Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education | ECG Library |

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