Polymorphic VT & Torsades de Pointes

Definitions

• Polymorphic ventricular tachycardia (PVT) is a form of  ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration.  The commonest cause of PVT is myocardial ischaemia.
• Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia occurring in the context of QT prolongation; it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.
• For TdP to be diagnosed, the patient has to have evidence of both PVT and QT prolongation.
• Bidirectional VT is another type of polymorphic VT, most commonly associated with digoxin toxicity.

Torsades de pointes

Clinical Significance

• TdP is often short lived and self terminating, however can be associated with hemodynamic 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.)

For a review of the causes of QT prolongation, click here. 

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 preceeding 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 (this concept is discussed in more detail here)

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 risk of TdP.
• From the nomogram, you can see that QTc-prolonging drugs that are associated with a relative tachycardia (e.g. quetiapine) are much less likely to cause TdP than those that are associated with a relative bradycardia (e.g. amisulpride).

ECG Examples

Example 1

Torsades de Pointes:

• Frequent PVCs with ‘R on T’ phenomenon trigger a run of polymorphic VT which subsequently begins to degenerate to VF.
• QT 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 and is high-risk for deterioration to PVT / VF.

Example 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

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

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 

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 Chris Nickson’s Cardiovascular Curveball 003.

Related Topics

• Hypokalaemia
• Hypomagnesaemia
• QT interval

Further Reading

• ECG BASICS – Waves, Intervals, Segments and Clinical Interpretation
• ECG CLINICAL CASES – Your favourite ECG’s placed in clinical context with a challenging Q&A approach
• ECG and Cardiology Eponymous Syndromes – Cheats guide to eponymous emancipation
• ECG Reference Sites on the WEB – the best of the rest

Author Credits

• Words – John Larkin
• ECG Examples (pictures + interpretations) – Ed Burns
• Web Editing – Ed Burns

References

• Chan A, Isbister GK, Kirkpatrick CM, Dufful SB. Drug-induced QT prolongation and torsades de pointes: evaluation of a QT nomogram. QJM. 2007 Oct;100(10):609-15. Epub 2007 Sep 19 [full text].
• Kirchhof P, Franz MR, Bardai A, Wilde AM. Giant T-U waves precede torsades de pointes in long QT syndrome: a systematic electrocardiographic analysis in patients with acquired and congenital QT prolongation. J Am Coll Cardiol. 2009 Jul 7;54(2):143-9 [full text].
• Viskin S. Long QT syndromes and torsades de pointes. Lancet 1999;354:1625-33 [abstract].
• S Viskin, R Fish, D Zeltser, B Belhassen, K Heller, D Brosh, S Laniado, H V Barron.  Arrhythmias in the congenital long QT syndrome: how often is torsade de pointes pause dependent? Heart 2000;83:661–666 [full text].
• Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
• Brady WJ, Truwit JD. Critical Decisions in Emergency & Acute Care Electrocardiography. Wiley Blackwell 2009.
• Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice. 6th Edition. Saunders Elsevier 2008.