Polymorphic VT
Polymorphic VT
Polymorphic VT in the setting of QT prolongation, with a spindle-shaped waxing-and-waning amplitude that twists around the isoelectric line.
On the trace
Read the strip in the order it happens.
- Measure the QT on the sinus beats.
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It is long, well past half the R-R. A QTc over 500 ms is the high-risk line. - Find the short-long-short start.
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A PVC, then its compensatory pause, then a second PVC landing on the T wave of the beat after the pause (the arrow marks it). - Watch the run twist.
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The complexes grow taller, then shorter, then flip polarity and grow again, as if rotating around the baseline. - See it stop.
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The run ends on its own and the long-QT sinus rhythm returns, until the next episode.
How to recognise it
| Feature | Value | Notes |
|---|---|---|
| Baseline QT | Prolonged (QTc > 500 ms is high-risk) | Measured on the sinus beats before the run. Without it, the diagnosis is not torsades. |
| Initiating sequence | Short-long-short | PVC, compensatory pause, then a PVC on the prolonged T or U wave. |
| QRS envelope | Spindle-shaped | Amplitude waxes and wanes over 5–20 beats, twisting around the isoelectric line. |
| Rate | 150–300 bpm | Irregular, and fast enough that the complexes merge into an undulating wave. |
| Course | Usually self-terminating | Recurrent short runs cause palpitations, presyncope or syncope. A run that does not stop can degenerate into VF. |
The strip
Mechanism
A prolonged QT means a prolonged action potential plateau. During it, calcium and late sodium currents can reactivate and partially depolarise the cell again before it has recovered: an early afterdepolarisation (EAD). An EAD that reaches threshold fires a triggered beat, the PVC on the T wave.
QT prolongation is rarely uniform, so that PVC meets myocardium at different stages of recovery. This dispersion of refractoriness lets a re-entrant wavefront form and wander, producing the twisting run. The pause before it matters because a long cycle lengthens the next QT even further, widening the vulnerable window just as the second PVC arrives.
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Acquired QT prolongation
Drug-induced long QT is the most common cause of torsades in practice:
- Antiarrhythmics: sotalol, quinidine, procainamide, disopyramide, ibutilide, dofetilide.
- Psychotropics: haloperidol, phenothiazines, tricyclic antidepressants, methadone.
- Antibiotics: macrolides (erythromycin, clarithromycin), fluoroquinolones (especially moxifloxacin).
- Others: ondansetron (particularly high IV doses), chloroquine, hydroxychloroquine.
Hypokalaemia and hypomagnesaemia add to any of these. Torsades clusters in hospital because that is where the combination meets: a borderline QT, a QT-prolonging drug, low electrolytes and physiological stress.
Bradycardia, especially complete heart block with a slow escape rhythm, causes severe pause-dependent QT prolongation. Torsades in that setting is an indication for urgent temporary pacing.
Congenital long QT syndromes
Inherited potassium or sodium channel defects can stay silent until stress, exercise or a drug unmasks them:
- LQT1 (KCNQ1, slow potassium current): events during exercise, classically swimming. Beta-blockers work well.
- LQT2 (hERG, rapid potassium current): events on sudden noise (an alarm clock) or emotional stress. Very sensitive to low potassium and QT-prolonging drugs.
- LQT3 (SCN5A, sodium channel): events at rest or asleep, when the rate is slow and the QT longest. Beta-blockers help less; mexiletine or flecainide is often added.
Anyone who survives torsades without an acquired cause should be referred for genetic testing and counselling.
Why amiodarone rarely causes torsades
Amiodarone prolongs the QT, yet it causes torsades far less often than sotalol or dofetilide. It also blocks calcium and late sodium currents, which suppresses EADs, and it prolongs repolarisation evenly across the ventricle rather than creating the dispersion that re-entry needs. This explains a pharmacology puzzle; it does not make amiodarone a treatment for torsades.
Clinical impact
Because most episodes stop on their own, torsades usually presents as palpitations, dizziness or recurrent syncope rather than arrest. Unexplained syncope with a long QT should be treated as self-terminating torsades until proven otherwise; the danger is the episode that does not stop.
Management
Pulseless: defibrillate immediately
Torsades without a pulse is a cardiac arrest. Give an unsynchronised shock. The constantly changing QRS gives a synchronised shock nothing reliable to lock onto, which can delay or abort it.
IV magnesium, regardless of serum levels
Magnesium sulfate 2 g IV suppresses early afterdepolarisations and works even when the serum level is normal. Repeat if the arrhythmia recurs.
Remove the cause, replace potassium
Stop any QT-prolonging drug; that alone may be the definitive treatment. Keep potassium at 4.5–5.0 mmol/L and correct magnesium. Do not give amiodarone, which prolongs the QT further.
Shorten the QT: pacing or isoproterenol
A faster rate shortens repolarisation and closes the vulnerable window. Temporary overdrive pacing at 90–110 bpm is the most reliable option and first-line when bradycardia or heart block is driving it. Isoproterenol does the same by raising the sinus rate, but is contraindicated in congenital long QT and acute ischaemia.
Differential
Polymorphic VT with a normal QT, most often from acute ischaemia. During the run the two can look identical; the QT on the sinus beats before it is what separates them. Ischaemic polymorphic VT is treated with amiodarone and urgent angiography.
Alternates between two fixed QRS axes on every beat, a strict two-beat cycle rather than a gradual twist. Think digoxin toxicity or CPVT. The QT is normal.
References
- 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022
- Torsade de Pointes — StatPearls, 2023