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Polymorphic VT

critical
Lead II
25 mm/s10 mm/mV
HR72bpm
RR833ms
QT402ms
Type

A rapid ventricular tachycardia whose QRS changes from beat to beat with no repeating pattern, on a normal QT, most often from acute myocardial ischaemia.

Updated

On the trace

Read the strip in the order it happens.

Try each step, then check it.
  1. Measure the QT on the sinus beats.
    Show It is normal. That single fact rules out torsades and points to ischaemia.
  2. Find the trigger.
    Show A single early PVC fires straight off a normal beat and lands on its T wave (the arrow marks it). There is no pause before it.
  3. Compare the complexes.
    Show Every one differs in height, width or direction, and the rhythm is fast and irregular.
  4. Look for a pattern, and find none.
    Show The size changes at random. There is no smooth swell and shrink, which is what a torsades spindle would show.
  5. See it end.
    Show This run stops and sinus rhythm returns. In a patient it can just as easily degenerate into VF.

How to recognise it

FeatureValueNotes
Baseline QTNormal (QTc < 460 ms)Measured on the sinus beats before the run. A long QT makes it torsades instead.
InitiationShort-coupled PVCLands on the T of a normal beat, about 350 ms after it, with no pause first.
QRS morphologyContinuously changing, wideNo complex repeats, and no pattern emerges, over 10–20 beats.
Rate200–300 bpmFaster than most monomorphic VT.
RhythmIrregularThe R-R varies from beat to beat.
CourseUnstableSelf-terminates or degenerates into VF, often within seconds.

The strip

Thirty seconds of lead II with runs of polymorphic VT, drawn by the simulator. Work through the steps above on it: measure the QT on a sinus beat first, then find what starts each run.

Mechanism

Acute ischaemia makes neighbouring zones of myocardium recover at different rates. An impulse arriving into that patchwork meets some tissue still refractory and some already recovered, so instead of one stable circuit, the wavefront keeps breaking and re-forming along new paths.

Each new path activates the ventricles from a different direction, which is why every complex looks different. The activation is still organised enough to be called VT, but it is unstable, and the same substrate that sustains it can fragment it into VF.

Go deeper

The QT branch point

A polymorphic wide-complex tachycardia always raises one question: what was the QT before it started?

  • Normal QT: ischaemia most often, then CPVT or Brugada syndrome. Treated with revascularisation, beta-blockers and amiodarone.
  • Long QT: torsades de pointes, from a drug, low potassium or magnesium, or a congenital syndrome. Treated with magnesium and by shortening the QT. Amiodarone prolongs the QT and can make it worse.

If the QT cannot be measured, magnesium does no harm on either branch; amiodarone can harm on one.

Ischaemia is the usual cause

Polymorphic VT with a normal QT is most often a sign of acute coronary occlusion. Antiarrhythmics buy time, but restoring flow is the only treatment that removes the substrate, so the destination is the catheterisation laboratory.

Catecholaminergic polymorphic VT (CPVT)

In a structurally normal heart with a normal QT, polymorphic or bidirectional VT triggered by exercise or emotion suggests CPVT. Mutations in the ryanodine receptor (RYR2) or calsequestrin (CASQ2) make calcium handling unstable under adrenergic drive, and the resulting triggered activity starts the arrhythmia. Beta-blockers are the cornerstone, flecainide is added for breakthrough events, and an ICD follows cardiac arrest or syncope despite treatment.

Clinical impact

Ischaemia leaves neighbouring myocardium recovering at different rates
A short-coupled PVC starts a wavefront that keeps changing path
Uncoordinated contraction: cardiac output falls sharplyCollapse
Without treatment it degenerates into ventricular fibrillationVF

Unlike monomorphic VT, polymorphic VT rarely leaves time for assessment. The priority is a shock if there is no pulse, then treating the cause as fast as possible.

Management

1

Pulseless: defibrillate immediately

Treat it as VF: an unsynchronised shock without delay. The changing QRS gives a synchronised shock nothing reliable to lock onto.

2

Normal QT: treat the ischaemia

Emergency coronary angiography is the priority. A beta-blocker reduces the adrenergic trigger, and IV amiodarone is a reasonable bridge to the catheterisation laboratory.

3

Long or uncertain QT: magnesium, not amiodarone

Give IV magnesium, stop any QT-prolonging drug and correct potassium. Manage as torsades.

4

Exercise-triggered, normal heart: think CPVT

Beta-blocker first, flecainide for breakthrough, and an ICD after arrest or syncope.

Differential

Monomorphic Ventricular Tachycardia

Monomorphic VT repeats one wide complex at a regular rate. Polymorphic VT has no single repeating complex, and its R-R varies.

Torsades de Pointes

Also polymorphic, but on a long QT. The run swells and shrinks in a spindle as it twists around the baseline, and it starts after a pause (short-long-short) rather than straight off a normal beat.

References

  1. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022
  2. 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death — Circulation, 2018
  3. 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