Polymorphic VT caused by a long QT: started by a premature beat on the T after a pause, its complexes swell, shrink and flip as they twist about the baseline.
On the trace
The tracing above is the non-sustained form: a run of torsades that stops on its own, then sinus rhythm with the long QT. The first run starts about five seconds into the recording, and another starts at about 15 seconds, so the finished sheet shows one too. Each recording is new, so your numbers will differ a little.
- Measure the QT on the sinus beats. QT about 620 ms at 75 per minute, QTc about 670 ms: very long. Most patients with torsades have a QTc of 500 ms or more.
- Find the short-long-short start. A premature beat (short), then a pause of about 1.2 s while the next sinus impulse is blocked (long), then a second premature beat on the T of the beat after the pause (short).
- Measure the coupling interval of that second beat. About 490 ms from the sinus beat before it. A long coupling interval is typical of torsades: the premature beat fires late, at the end of a long action potential.
- Watch the run twist. The complexes grow taller, then shorter, pass through the baseline and come back the other way up. Fast: about 260 per minute.
- See it stop. After about four seconds the run ends on its own, and the long-QT sinus rhythm returns until the next one.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| QT on the sinus beats | Long: QTc usually 500 ms or more | QTc about 670 ms |
| Start | Pause-dependent (short-long-short), or during a speeding up | Short-long-short |
| The first beat | Long coupling interval: over 450 to 500 ms | About 490 ms |
| QRS | Changing, the size swelling and shrinking about the baseline | A twist every few beats |
| Rate | 160 to 260 per minute | About 260 per minute |
| Course | Usually stops in seconds; can degenerate into VF | Stops after about 4 s |
The QT and the start make the diagnosis, not the run: when recorded in several leads, any polymorphic VT may look twisted in some of them.
Mechanism
A long QT means a long action potential. During its prolonged plateau, the calcium current can reactivate and depolarise the cell again before it has finished repolarising: an early afterdepolarisation (EAD). On the ECG the EADs show as notched, bizarre T waves. An EAD that reaches threshold fires a beat: the premature beat on the T.
The QT is not long to the same degree everywhere: some regions, especially deep in the wall, repolarise later. A premature beat that meets this patchwork of recovery can start a re-entrant wave. The wave's path moves, and its direction turns slowly, which is the twist.
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Why the pause matters
A long QT does not shorten and lengthen normally with the heart rate. After a sudden pause (a sinus pause, or more often the pause after a premature beat), the next beat's action potential is even longer. Its T wave grows, often to a giant, bizarre T or U wave, and its EADs grow with it. The beat that fires from them falls late on that long T: the long coupling interval. Each pause brings a new premature beat, whose pause brings another: the short-long-short sequence that ends in torsades.
Pause-dependent and tachycardia-dependent
- Pause-dependent torsades is much the more common. It is the usual form in adults with acquired long QT and in congenital long QT types 2 and 3.
- Tachycardia-dependent torsades starts as the sinus rate speeds up, mainly in infants and in congenital long QT type 1. The QT fails to keep up with the faster rate, and T-wave alternans (a T wave that alternates in shape every beat) warns that torsades is close.
Acquired long QT
The long QT syndromes are listed by Viskin and colleagues:
- Drugs, the commonest. Antiarrhythmics (sotalol, quinidine, procainamide, dofetilide, ibutilide), antipsychotics and antidepressants (haloperidol, methadone), antibiotics (macrolides such as erythromycin and clarithromycin, fluoroquinolones), and others (ondansetron, hydroxychloroquine).
- Bradycardia, especially complete heart block with a slow escape rhythm.
- Hypokalaemia and hypomagnesaemia, which add to any of the others.
- After a tachycardia, an infarction or Takotsubo syndrome.
- Others: hypogonadism, and some foods, such as grapefruit juice.
Torsades clusters in hospital, where a borderline QT, a QT-prolonging drug, low potassium and physiological stress meet.
Congenital long QT
Inherited defects of potassium or sodium channels can stay silent until stress, exercise or a drug unmasks them:
- Type 1 (KCNQ1, the slow potassium current): events on exercise, classically swimming. Beta-blockers work well.
- Type 2 (hERG, the rapid potassium current): events on a sudden noise or emotion; very sensitive to low potassium and to QT-prolonging drugs.
- Type 3 (SCN5A, the sodium channel): events at rest or asleep. Mexiletine is often added.
Pseudo-torsades
Not every pause-dependent polymorphic VT with a long QT is torsades. Days after an infarction, or on amiodarone, a patient can have a long QT and polymorphic VT from another cause. Its first beat has a short coupling interval: 400 ms or less points away from a long QT syndrome even when the QT is long. It needs different treatment.
Why amiodarone rarely causes torsades
Amiodarone lengthens the QT, but causes torsades far less often than sotalol or dofetilide. It also blocks the calcium and late sodium currents that drive EADs, and lengthens repolarisation evenly across the wall. That explains a pharmacological puzzle; it does not make amiodarone a treatment for torsades.
Clinical impact
Because most runs stop on their own, torsades often presents as palpitations, dizziness or recurrent syncope rather than an arrest. Unexplained syncope with a long QT should be treated as torsades until proven otherwise.
Management
Pulseless: defibrillate
A run that does not stop, without a pulse, is a cardiac arrest: an unsynchronised shock.
Magnesium, whatever the serum level
Magnesium sulfate 2 g as a slow IV bolus suppresses the onset of torsades, even at a normal serum magnesium. Its effect is often brief, so it is first aid until the other measures work. It can be repeated; avoid a high magnesium in kidney failure.
Remove the cause
Stop every QT-prolonging drug; that may be the definitive treatment. Raise potassium to the high-normal range. Sedate (for example with IV midazolam): a rise in sympathetic tone can start the next run. Do not give amiodarone.
Prevent the pauses
For pause-dependent torsades, raise the heart rate with temporary pacing or isoproterenol, to the lowest rate that stops the pauses: a faster rate shortens the QT. Too fast can provoke tachycardia-dependent torsades. Once pacing prevents the pauses, beta-blockers can be given. Tachycardia-dependent torsades is treated with high doses of beta-blockers instead.
Differential
Polymorphic VT with a normal QT, most often from acute ischaemia. During the run the two can look alike: the QT before it, and the short coupling interval of its first beat, tell them apart. It is treated with revascularisation, not magnesium.
The same arrhythmia, from low potassium alone: flat T waves and large U waves first, a long QU, then torsades.
Changes shape every beat too, but by exactly two shapes in strict alternation, at a regular rate. The QT is normal.
A fast torsades run can look like VF. The long QT before it, and a spindle in the run, point to torsades. Pulseless, both are shocked.
References
- Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy — Circulation, 2021
- Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation — Circulation, 2010
- Treatment of torsade de pointes with magnesium sulfate — Circulation, 1988
- 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022