A wide-complex tachycardia whose QRS changes from beat to beat, about 220 per minute, started by a premature beat on the T in acute ischaemia, with a normal QT before it.
On the trace
The tracing above is acute ischaemia: sinus rhythm, then a premature beat on a T wave starts polymorphic VT that does not stop. The run starts about five seconds into the recording, so watch the first sweep; the finished sheet is all VT. Each recording is new, so your numbers will differ a little.
- Measure the QT on the sinus beats. QT 354 ms, QTc 381 ms: normal. That one measurement says this is not torsades de pointes.
- Find the beat that starts it. A single wide premature beat lands on the T of a sinus beat, 280 ms after it: a short coupling interval. There is no pause before it.
- Compare the complexes in the run. Every one differs in height, width and direction. No complex repeats.
- Look for a pattern in the size. There is none: no regular swelling and shrinking about the baseline, which is what a torsades run shows.
- Count the rate. About 220 per minute, and irregular.
- Look for anything organised. No P waves and no sinus beats once the run has started: it has taken the ventricles over.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| QT on the sinus beats | Normal | QTc 381 ms |
| The first beat | Short coupling interval: on the T of the beat before | 280 ms |
| QRS | Wide, changing from beat to beat, no pattern | No complex repeats |
| Rate | 200 to 300 per minute, irregular | About 220 per minute |
| Course | Stops in seconds, or degenerates into VF | Sustained |
Viskin and colleagues (2021) give a three-step approach to any polymorphic VT, after excluding look-alikes:
- Is there a long QT syndrome? If so, it is torsades de pointes.
- If not, is there heart disease? Acute ischaemia, or coronary disease without it.
- Is it related to exercise? Catecholamine-sensitive polymorphic VT (CPVT), or exercise-induced ischaemia.
The coupling interval of the first beat helps at every step. A first beat on the T (in their series 305 ± 53 ms in ischaemic VF) points away from a long QT syndrome. Torsades starts with a long coupling interval, over 450 to 500 ms. A coupling interval of 400 ms or less points away from a long QT syndrome even when the QT is long.
Mechanism
Minutes after a coronary artery closes, the cells in its territory lose potassium, and it builds up outside them. They rest partly depolarised: they conduct slowly, their action potentials shorten, and they take longer to recover after them. Their recovery now differs from the healthy muscle around them.
A premature beat that arrives while some of the ventricles have recovered and some have not can conduct into the first and block at the second. It travels round the block and comes back: re-entry. There is no scar to anchor the circuit, so the wave turns round a core of tissue it has just made refractory, and the core moves. The wave leaves the ischaemic zone somewhere new each cycle, and each QRS is different.
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The vulnerable window
After each beat there is a short span of coupling intervals, near the peak of the T, in which a premature beat finds the ventricles partly recovered. A beat earlier than that cannot conduct; a beat later finds everything recovered and conducts normally. Ischaemia widens the window. A premature beat in it starts re-entry only where the ventricles can hold one: in a normal heart, the same beat is just a premature beat.
Polymorphic VT or VF
Early, mild ischaemia gives a fast re-entry. When it turns faster than the healthy muscle around it can recover, that muscle cannot follow it beat for beat: the wave breaks up and the rhythm becomes ventricular fibrillation within a few beats. More severe ischaemia gives a slower re-entry that the muscle can follow, and the result is sustained polymorphic VT, as on this tracing. This is why VF is most common in the first minutes of an infarction.
Ischaemic VF on the ECG
In ischaemic polymorphic VT and VF, the run starts when the ST elevation is at its highest, and the first beat has a very short coupling interval: as short as in idiopathic VF. More ST elevation means a higher risk.
Polymorphic VT in coronary disease without ischaemia
Days after an infarction or bypass surgery, some patients develop storms of polymorphic VT with no new ischaemia. The triggering beats come from Purkinje fibres in the border of the scar, and have a single shape and a short coupling interval (358 ± 38 ms). About 40% of these patients have a long QT, from the healing infarct or from amiodarone, and their VT can start after a pause. That is not torsades: Viskin and colleagues call it pseudo-torsades. Its coupling interval is short (360 ± 38 ms against 600 ± 173 ms in torsades). It responds to quinidine, not to the treatment of torsades.
Other causes with a normal QT
- Brugada syndrome: ST elevation in V1 and V2, arrest at rest or asleep, often in a young man. A short-coupled trigger.
- Short QT syndrome: a QTc usually 340 ms or less. An ultra-short-coupled trigger.
- Idiopathic VF: a normal ECG and the shortest coupling interval of all, from a Purkinje trigger.
- Catecholamine-sensitive polymorphic VT: with exercise or emotion, in a normal heart.
- Polymorphic VT from the right ventricular outflow tract: in patients who also have benign monomorphic outflow-tract VT.
Once ischaemia is excluded, the storms of the first three respond to quinidine and to isoproterenol.
Look-alikes
- Pre-excited AF or atrial tachycardia: an accessory pathway can conduct rapid atrial activity to the ventricles with changing degrees of pre-excitation. It is irregular and wide, and can look like polymorphic VT.
- Movement artefact: the real QRS complexes march through the artefact at their own rate, the "rate" is often over 350 per minute, and when it ends there is no pause before the next sinus beat.
Clinical impact
Polymorphic VT rarely leaves time to assess it. The first clinical sign of coronary disease in many people is a cardiac arrest from ischaemic VF.
Management
Pulseless: defibrillate
Treat it as VF: an unsynchronised shock without delay. The changing QRS gives a synchronised shock nothing reliable to lock onto.
Normal QT, ischaemia: revascularise
Urgent coronary angiography and revascularisation is the treatment: it removes the substrate. Guidelines endorse IV beta-blockers and deep sedation for recurrent episodes, and amiodarone and lidocaine should be considered.
Long or unknown QT: magnesium
If the QT before the run is long, or cannot be measured, manage it as torsades: IV magnesium, stop QT-prolonging drugs, correct potassium. Magnesium does no harm on either branch; amiodarone can harm on one.
Storms days after an infarction or bypass
Check the stent or graft. If there is no new ischaemia, storms from Purkinje triggers often fail amiodarone and respond to quinidine. Ablation of the triggering Purkinje fibres can be lifesaving.
Differential
Also polymorphic, but the QT before it is long. It starts after a pause, with a long coupling interval, and its complexes swell and shrink as they twist about the baseline.
One wide complex, repeated, at a regular rate. The QRS of polymorphic VT changes every beat, and its R-R varies.
Polymorphic, with a normal QT, but in a structurally normal heart, set off by exercise or emotion during a sinus tachycardia.
If no QRS complexes can be picked out at all, it is VF. Pulseless, the two are treated the same.
References
- Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy — Circulation, 2021
- Polymorphic ventricular tachycardia, ischaemic ventricular fibrillation, and torsade de pointes: importance of the QT and the coupling interval in the differential diagnosis — European Heart Journal, 2021
- 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022
- 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death — Circulation, 2018