Monomorphic VT
Monomorphic VT
A rapid, regular wide-complex tachycardia with uniform beat-to-beat morphology, arising from a sustained ventricular focus.
On the trace
Read the strip in this order.
- Look at the complexes.
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Every one is wide (over 120 ms) and identical: one focus, one pathway, one shape. - Check the rhythm.
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Fast and regular, here 150 bpm. Sustained means it keeps going: past 30 seconds, or until it has to be stopped. - Hunt for P waves.
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The sinus node keeps firing at its own slower rate, so its P waves march through the VT complexes, showing up as notches and bumps that bear no relation to the QRS. That is AV dissociation. - Find the odd beats out (the arrows).
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A narrow, early beat is a capture: a sinus impulse that got through. A beat halfway between narrow and wide is a fusion: sinus and VT activating the ventricles together. Either one all but proves VT.
How to recognise it
| Feature | Value | Notes |
|---|---|---|
| Rate | 100–250 bpm | Most often 140–200. A regular wide rhythm under 100 bpm is AIVR. |
| Rhythm | Regular | Sustained irregularity in a wide tachycardia suggests AF with aberrancy or pre-excitation. |
| QRS | Wide (> 120 ms), identical | Changing shape makes it polymorphic VT. |
| Duration | Sustained | Over 30 seconds, or needing termination sooner. Shorter runs are NSVT. |
| P waves | Dissociated | Marching through at the sinus rate. Often hidden; some VT conducts back to the atria instead. |
| Capture and fusion beats | Occasional | Narrow (capture) or intermediate (fusion) beats. Their presence all but proves VT. |
The strip
Mechanism
In adults with heart disease, monomorphic VT is usually scar re-entry: the impulse circulates through surviving muscle at the edge of an old infarct, with a slow-conducting isthmus that lets the circuit keep recovering just in time. The fixed circuit gives the fixed shape and the steady rate.
In a structurally normal heart, it is more often an automatic or triggered focus, typically in the right or left ventricular outflow tract.
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Background
Monomorphic VT runs at 100–250 bpm and bypasses the His-Purkinje system entirely: the impulse spreads through the ventricular muscle cell to cell, which is why every complex is wide.
What the morphology reveals
Monomorphic VT is a PVC that will not stop, so its shape localises the origin the same way:
- Left ventricular origin: right bundle branch block pattern (dominant R in V1).
- Right ventricular origin: left bundle branch block pattern (dominant S in V1).
- Inferior axis (positive in II, III, aVF): an origin high in the heart, such as the outflow tracts. Superior axis: the inferior wall or apex.
- QR complexes: the Q is electrically silent scar, a signature of infarct substrate.
- Septal VT: relatively narrow (120–140 ms), because both ventricles are reached almost together.
Why capture and fusion beats prove VT
A capture beat is narrow because it used the normal conduction system; a supraventricular rhythm with aberrancy could not suddenly produce one narrow beat in a wide run. A fusion beat needs two separate wavefronts, one from above and one from the ventricle. Both depend on AV dissociation, which is why they are rare when the VT conducts back to the atria, and why their absence proves nothing.
Substrate and the ICD decision
Sustained VT with structural heart disease is an indication for an ICD, because the scar circuit will recur. Catheter ablation of the isthmus reduces VT and shocks but does not replace the ICD when LV function is poor. Outflow tract VT in a normal heart has an excellent prognosis and is often cured by ablation alone.
Clinical impact
Tolerance depends on the ventricle more than the rate: a preserved ejection fraction can stay alert at 200 bpm, while an ejection fraction of 25% can be peri-arrest at the same rate. Treat the patient, not the number.
Management
Unstable: synchronised cardioversion now
Hypotension, reduced consciousness, ischaemic chest pain or pulmonary oedema mean immediate synchronised cardioversion. Do not wait for drugs or a firm rhythm diagnosis. Pulseless VT is treated as VF.
Stable: terminate it anyway
Even well-tolerated VT should be stopped promptly, because it can deteriorate without warning. Cardioversion under sedation is effective. If drugs are used, the 2022 ESC guideline prefers IV procainamide over amiodarone; amiodarone is used in severe heart failure, acute infarction or end-stage renal disease. Never give verapamil or diltiazem to a wide-complex tachycardia of uncertain origin.
Find the substrate
Echocardiography for LV function and structural disease; troponin and coronary imaging to exclude ischaemia; cardiac MRI if the echo is normal, for scar from myocarditis or a cardiomyopathy.
Prevent recurrence: ICD and ablation
An ICD with structural heart disease; ablation for recurrent VT or repeated shocks; ablation alone for outflow tract VT in a normal heart.
Differential
SVT with aberrancy is 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, capture beats and fusion beats prove VT; their absence does not exclude it.
Pre-excited AF is wide and fast, but irregular, often over 250 bpm, with changing QRS width. Monomorphic VT is regular.
The same arrhythmia stopping on its own within 30 seconds, between runs of sinus rhythm.
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
- Comments on the 2022 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — Revista Española de Cardiología, 2022