A regular wide-complex tachycardia, every beat the same, from a re-entrant circuit round an old infarct's scar, with the P waves dissociated and now and then a capture or fusion beat.
On the trace
The tracing above is sustained monomorphic VT. Each recording is new, so your numbers will differ a little from the ones here. Turn on the Normal switch under the tracing to draw a normal ECG at 75 per minute in grey behind it. Its beats are narrow; every VT beat is wide.
- Measure the QRS. About 156 ms: wide. Every complex in the run has the same shape in every lead.
- Measure the R-R. 384 ms, the same beat after beat: a regular rhythm at 156 per minute.
- Find the axis. I, II and aVF are negative and aVR is positive: an extreme axis, about −155°. Neither the normal conduction system nor a bundle branch block points the heart's activation there.
- Look at V1 and the chest leads. V1 is upright, like right bundle branch block. V2 is half up, half down. V3 to V6 are deeply negative.
- Hunt for P waves. The sinus node keeps firing at 75 per minute. Its P waves land anywhere in the VT complexes, as notches and bumps that bear no relation to the QRS: AV dissociation. About twelve in ten seconds.
- Find the odd beat out. Now and then a narrow beat comes early: a capture, a sinus impulse that reached the ventricles between two VT beats. The next VT beat comes a full cycle after it. Not every recording has one.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| Rate | 100 to 250 per minute, most often 140 to 200 | 156 per minute |
| Rhythm | Regular | R-R 384 ms |
| QRS | Wide, over 120 ms, the same every beat | About 156 ms |
| Axis | Often extreme (−90° to ±180°) | About −155° |
| P waves | Dissociated: their own rate, unrelated to the QRS | Sinus at 75 marching through |
| Capture and fusion beats | Occasional | A capture in some recordings |
| Duration | Sustained: over 30 seconds, or needing termination | The whole recording |
Several findings each make VT very likely in a regular wide-complex tachycardia. This tracing has four of them:
- AV dissociation;
- a capture or fusion beat;
- an extreme axis;
- an initial R wave in aVR (the aVR criterion of Vereckei and colleagues).
Mechanism
After an infarction, bundles of surviving muscle run through the scar. Their cells rest partly depolarised and are separated by fibrosis, so a wave crosses them slowly. That bundle is the circuit's isthmus. A wave that leaves the isthmus at its exit spreads round the scar through healthy muscle and comes back to the entrance. If the trip takes longer than the isthmus takes to recover, the wave enters it again, and the circuit turns without end.
The circuit sets the rate: the length of the loop over the speed of the wave. The exit sets the shape: the ventricles are activated from there, cell to cell, not through the bundle branches. That slow spread is why every complex is wide, and the fixed exit is why every complex is the same.
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What the shape tells you
A monomorphic VT is a premature ventricular beat that will not stop, so its shape localises the exit the same way:
- Left ventricular exit: right bundle branch block-like, with a dominant R in V1, as here.
- Right ventricular exit: left bundle branch block-like, with a dominant S in V1.
- Superior axis (negative in II, III and aVF): an exit low in the heart, the inferior wall or the apex, as here.
- Inferior axis: an exit high in the heart, such as the outflow tracts.
- QR complexes: the Q is electrically silent scar, a sign of infarct substrate.
- A relatively narrow VT (120 to 140 ms): an exit in or near the septum, or the conduction system.
Why capture and fusion beats prove VT
A capture beat is narrow because it used the normal conduction system. A supraventricular rhythm with aberrant conduction could not produce one narrow beat in the middle of a wide run. A fusion beat needs two wavefronts at once, one from above and one from the ventricle. Both depend on AV dissociation.
They are rare, and their absence proves nothing. The VT wave penetrates the AV node and the bundle branches from below on every beat, which leaves them refractory: most sinus impulses are blocked before they get near the ventricles. Some VT conducts back to the atria, and then there are no dissociated P waves at all.
Polymorphic VT is a different arrhythmia
When the QRS changes from beat to beat, the arrhythmia is polymorphic VT. It has different causes (acute ischaemia, a long QT syndrome, catecholamine-sensitive VT) and a different emergency treatment, and it is far less stable (Viskin and colleagues, 2021).
The drugs on the circuit
Procainamide blocks sodium channels, and the cells of the isthmus, already partly depolarised, are the most sensitive to it. It slows the wave in the isthmus, so the VT slows, and then it stops the wave leaving the isthmus, and the VT ends. Amiodarone lengthens the refractory period and closes the gap between the wave's head and its tail. Adenosine and the calcium-channel blockers act on the AV node, not on this circuit, so they do not stop it.
Substrate and the ICD
Sustained VT with structural heart disease is an indication for an ICD, because the scar circuit will turn again. Catheter ablation of the isthmus reduces VT and shocks, but does not replace the ICD when the left ventricle is poor. Outflow-tract VT in a structurally normal heart has an excellent prognosis and is often cured by ablation alone.
Clinical impact
Tolerance depends on the ventricle more than on the rate. A patient with a preserved ejection fraction can stay alert at 200 per minute, while one with an ejection fraction of 25% can be peri-arrest at the same rate. Treat the patient, not the number.
Management
Unstable: synchronised cardioversion now
For hypotension, a decreased level of consciousness, ischaemic chest pain or pulmonary oedema. Do not wait for drugs or a firm diagnosis. Pulseless VT is treated as VF: an unsynchronised shock.
Stable: terminate it anyway
Even well-tolerated VT can deteriorate without warning. Cardioversion under sedation is effective. If a drug is used, the 2022 ESC guideline prefers IV procainamide; amiodarone in severe heart failure or acute infarction. Never give verapamil or diltiazem to a wide-complex tachycardia of uncertain origin.
Find the substrate
Echocardiography for left ventricular function and structure; troponin and coronary imaging to exclude ischaemia; cardiac MRI if the echocardiogram is normal, for scar from myocarditis or a cardiomyopathy.
Prevent recurrence
An ICD with structural heart disease; catheter ablation for recurrent VT or repeated shocks; ablation alone for outflow-tract VT in a normal heart.
Differential
Also a regular wide-complex tachycardia. Assume VT until proven otherwise: calling VT an SVT is the dangerous error, and verapamil given to VT can cause collapse. Dissociated P waves, captures and fusions prove VT; their absence does not exclude it.
A bundle branch block with a fast sinus or atrial rhythm is wide too, but each QRS has its P, at a fixed PR, and the axis and shape are those of the block.
The QRS changes from beat to beat, and the R-R varies. A different cause and a different emergency treatment.
A wide, regular, slow-to-moderate rhythm in kidney failure can be the sine wave of hyperkalaemia. Give calcium, not an antiarrhythmic.
References
- 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
- Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy — Circulation, 2021
- New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia — Heart Rhythm, 2008