- 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.)
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.
- 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).
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.
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.
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’.
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.
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.
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- 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.