ECG criteria
- Rhythm is irregular (irregularly irregular), RR intervals show no constant pattern
- Ventricular rate is very high, frequently 200–300 bpm, sometimes exceeding 300 bpm
- QRS width and morphology vary due to a changing degree of pre-excitation and fusion between AV nodal and accessory pathway conduction — ranging from narrow to wide
- Pre-excited complexes may have a slurred initial deflection corresponding to a delta wave, but on a high-rate tachycardiogram it is often indistinguishable
- Shortest pre-excited RR interval ≤250 ms during AF is not a mandatory diagnostic criterion, but a marker of high risk for rapid conduction via the accessory pathway
- P waves are not visible; atrial fibrillation waves (f waves) may be visible between complexes
- A delta wave and a short PQ interval on the sinus ECG (before or after the paroxysm) confirm manifest pre-excitation, but their absence after AF termination does not rule out accessory pathway conduction during the arrhythmia itself (intermittent pre-excitation)
What it looks like on ECG
The rhythm is irregular in all leads, P waves are absent, and a baseline wave of atrial fibrillation is visible. The main feature is QRS complexes of variable width and morphology from beat to beat within the same tracing. This results from the changing degree of fusion between AV nodal and accessory pathway conduction: some complexes tend to be narrow, others wide with a slurred initial deflection resembling a delta wave, though at high rates this wave is often smoothed out and poorly distinguishable. This polymorphic picture — complexes of different shapes and widths on a single tracing — is the key differentiator from monomorphic ventricular tachycardia.
A very high heart rate (200–300 bpm and higher), irregular rhythm, and variable morphology of wide QRS complexes combined should raise suspicion for pre-excited AF, although high rate alone is not a diagnostic criterion: in regular AF, especially in young patients or under sympathetic activation, the rate can also be high. The shortest pre-excited RR interval ≤250 ms is evaluated separately — it is not a sign confirming or excluding the diagnosis, but a marker of high risk for progression to ventricular fibrillation. At a paper speed of 25 mm/s, this corresponds to approximately 6.25 mm (6.25 small boxes); one must evaluate precisely the shortest RR between pre-excited complexes rather than an arbitrary pair of wide QRS complexes.
| Sign | Typical AF | AF in WPW |
|---|---|---|
| QRS | usually narrow, more stable morphology | narrow to wide, varying morphology |
| HR | usually up to 150–180 bpm, but can be higher | frequently 200–300 bpm |
| AV node limitation | yes (with caveats) | no (accessory pathway bypasses the node) |
After termination or during arrhythmia slowing, sinus complexes may show a typical delta wave and a short PQ interval, confirming manifest pre-excitation. However, pre-excitation can be intermittent: the absence of a delta wave on a sinus ECG after a paroxysm does not rule out that impulses traveled via the accessory pathway during the AF itself.
Mechanism
In WPW syndrome, there is an accessory pathway (bundle of Kent) connecting the atrium and ventricle directly, bypassing the AV node. The AV node physiologically slows and limits the conduction rate to the ventricles — acting as a protective filter with decremental conduction. The accessory pathway lacks such decremental conduction: it can conduct rapidly and without normal AV nodal limitation. Pathways with a short effective refractory period are particularly dangerous, as they can conduct a large number of atrial impulses to the ventricles with very short RR intervals, sometimes causing a dangerously high ventricular rate. Some impulses travel via the AV node (complexes closer to narrow), and some via the accessory pathway (complexes wider, with delta wave features), yielding a polymorphic picture. At a very high rate and short RR intervals, the ventricles may begin to contract chaotically, leading to ventricular fibrillation.
Causes
- Presence of an antegrade-conducting accessory pathway in WPW syndrome; such a pathway may also participate in antidromic or orthodromic AV reciprocating tachycardia
- Triggering factor: an actual paroxysm of atrial fibrillation in a patient with WPW (may be the initial presentation of the syndrome)
- Risk is higher with a short antegrade effective refractory period of the accessory pathway
- Sometimes triggered by alcohol intake, catecholamines, or physical exertion
Differential diagnosis
Polymorphic ventricular tachycardia — differentiation can be difficult: pre-excited AF is also irregular and can have very wide and changing complexes, and a known diagnosis of WPW does not rule out VT. When in doubt, wide-complex tachycardia should be managed as potentially life-threatening.
AF with aberrant conduction (Ashman phenomenon) — wide complexes with aberration usually present as physiological bundle branch block (most commonly right bundle branch block) with relatively stable morphology, but morphology alone cannot reliably distinguish aberration from pre-excitation.
Ventricular flutter/ventricular fibrillation — pre-excited AF with very short RR intervals can degenerate into ventricular fibrillation; when in doubt, manage as a life-threatening tachyarrhythmia.
Regular AF with high ventricular rate — QRS complexes are usually narrow and morphology is typically stable, but aberrant wide complexes may occur; high heart rate by itself only raises suspicion for pre-excitation and is not a reliable distinguishing feature.
Clinical significance and management
AF in WPW is an emergency condition carrying a risk of progression to ventricular fibrillation and sudden death, especially when the shortest pre-excited RR interval is ≤250 ms and the heart rate exceeds 200 bpm. The key rule: do not administer AV nodal blocking drugs — digoxin, verapamil, diltiazem, beta-blockers, and adenosine; intravenous amiodarone should also be avoided for rate control in this tachycardia due to the risk of accelerating accessory pathway conduction. Eliminating competing AV nodal conduction can increase the relative proportion of accessory pathway conduction and elevate the risk of ventricular fibrillation.
In the presence of hemodynamic instability, perform immediate synchronized cardioversion. If synchronization is unreliable or impossible due to an extremely irregular and polymorphic rhythm (including true fibrillation or polymorphic VT), or if pulses are absent, deliver an immediate unsynchronized shock (defibrillation) without wasting time on synchronization attempts. In stable patients, consider antiarrhythmic drugs that slow accessory pathway conduction (according to ESC guidelines on AF: procainamide, ibutilide). Following restoration of sinus rhythm, refer the patient for catheter ablation of the accessory pathway as a definitive solution.
Common interpretation errors
- Mistaking the polymorphic pattern of wide QRS complexes for ventricular tachycardia and failing to recognize rhythm irregularity
- Failing to notice the baseline delta wave on sinus complexes before or after the paroxysm, or incorrectly ruling out the diagnosis due to its absence after AF termination
- Prescribing verapamil or a cardiac glycoside for wide irregular QRS complexes without confirming the diagnosis — risking the induction of VF
- Confusing it with regular AF with aberrancy, failing to notice the extremely high heart rate and variability in QRS width
- Interpreting RR ≤250 ms as a mandatory diagnostic criterion rather than a high-risk marker, and ruling out pre-excited AF on that basis
FBI tachycardia: Fast, Broad (wide QRS), Irregular
1. Which ECG feature is most characteristic of AF in WPW syndrome?
A changing degree of fusion between AV nodal and accessory pathway conduction produces a polymorphic picture against the background of irregular AF rhythm.
2. Which medications are contraindicated in AF with WPW due to the risk of accelerating accessory pathway conduction?
AV nodal blockade eliminates the competing conduction pathway, which can enhance relative accessory pathway conduction and increase the risk of ventricular fibrillation.
3. How should the shortest pre-excited RR interval ≤250 ms be interpreted in AF with WPW?
This is not a mandatory diagnostic criterion, but a marker of high risk for rapid conduction over an accessory pathway and potential progression to VF.
Frequently asked questions
Why are verapamil or digoxin contraindicated in AF with WPW?
These drugs block conduction through the AV node. In pre-excited AF, eliminating this competing conduction pathway can increase the relative proportion of conduction down the accessory pathway and accelerate the ventricular response, raising the risk of ventricular fibrillation.
How to distinguish AF with WPW from ventricular tachycardia?
In AF with WPW, the rhythm is irregular, and the QRS width and morphology vary from beat to beat on the same tracing. Monomorphic VT is usually regular and has a constant QRS morphology. However, distinguishing it from polymorphic VT can be difficult, and when in doubt, management should follow the protocol for a life-threatening tachyarrhythmia.
Is AF with WPW dangerous?
Yes, this is one of the most dangerous tachyarrhythmias in pre-excitation: with a short pre-excited RR interval and a very high ventricular response rate, progression to ventricular fibrillation and sudden cardiac death is possible.
What should a physician do upon encountering such an ECG?
In unstable hemodynamics, immediate electrical cardioversion is performed (synchronized, or unsynchronized shock if synchronization is unreliable or pulseless). In a stable condition, antiarrhythmics that slow conduction through the accessory pathway are considered, while avoiding AV nodal blockers and amiodarone. Subsequently, the patient is referred for catheter ablation of the accessory pathway.
If there is no delta wave on the ECG after cardioverting AF, does this mean WPW is ruled out?
No. Pre-excitation can be intermittent: the accessory pathway may conduct impulses during AF while not manifesting as a delta wave and short PQ interval on sinus rhythm after the termination of the paroxysm. The absence of these signs does not rule out accessory pathway conduction during the arrhythmia.
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Related terms
More in the section «Ventricular pre-excitation»
Sources
- Surawicz, Knilans. Chou's Electrocardiography in Clinical Practice, 6th ed.
- Hampton. The ECG Made Easy
- ESC Guidelines for the management of patients with supraventricular tachycardia, 2019
- Orlov V.N. Guide to Electrocardiography
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.