- 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.
- 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.)
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 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.
- 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)
- 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).
- 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.
- 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.
- 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’.
- 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.
- 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.
- 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.
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