Wolff-Parkinson-White (WPW) Pattern
Wolff-Parkinson-White (WPW) Pattern
Sinus rhythm with ventricular pre-excitation: a short PR, a slurred delta wave and a wide QRS, all produced by one accessory pathway.
On the trace
Read the strip in this order.
- Check the rate first, and notice it is ordinary.
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75 bpm, regular, sinus. Nothing here is fast. The finding is in the shape of each beat, not in the rhythm. - Find the P wave and measure the PR.
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The P is upright and normal, and the PR comes out at 68 ms. Under 120 ms is short, and there is no normal reason for it. - Look at how the QRS begins.
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It does not start sharply. The upstroke takes 74 ms to climb, against 24 ms on a normally conducted beat: a slow ramp that hands over to a fast one partway up. That ramp is the delta wave. - Measure the whole QRS.
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172 ms, well over 120. Wide, but not wide the way a bundle branch block is wide: the extra time is all at the front. - Join those last three up.
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The short PR and the wide QRS are not two findings. The delta pulls the start of the QRS backwards, which shortens the PR and lengthens the QRS by the same amount. One event, measured twice.
How to recognise it
| Feature | Value | Notes |
|---|---|---|
| PR interval | Under 120 ms | 68 ms here. Measured to the start of the delta, not to the R. |
| Delta wave | Slurred QRS upstroke | Its direction varies with where the pathway inserts, and it can be negative. |
| QRS | Over 120 ms | 172 ms here. Widened at its onset, not its end. |
| ST and T | Opposite to the delta | Secondary change, not ischaemia. |
| Rate and rhythm | Normal sinus | The pattern is a resting finding. |
| Prevalence | 1 to 3 per 1000 | The pattern is far commoner than the syndrome. |
The strip
Mechanism
An accessory pathway is working muscle bridging the insulating ring between atrium and ventricle. The normal route delays every impulse at the AV node; the pathway does not, so the impulse arrives at the ventricle early. But it arrives into ordinary myocardium rather than the His-Purkinje system, and muscle conducts slowly, cell to cell. So ventricular activation begins early and crawls, which draws the delta. Meanwhile the impulse that went the normal way clears the node, reaches the His-Purkinje system and overtakes, finishing the QRS at normal speed. Every pre-excited beat is a fusion of those two wavefronts, and how much of the QRS the delta occupies depends on how far ahead the pathway got.
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Pattern, or syndrome
The pattern is the ECG appearance alone. The syndrome is the pattern plus arrhythmias caused by the same pathway. Orthodromic AVRT is the commonest of those, and it often produces a normal-looking narrow tachycardia, because during the tachycardia the pathway is being used backwards and pre-excites nothing.
The dangerous one is atrial fibrillation
Up to half of patients with WPW develop atrial fibrillation, and this is what kills. The pathway conducts without decrement: unlike the AV node, it does not slow down as it is asked to go faster, so it passes fibrillatory impulses to the ventricle at rates the node would have filtered out. The result is a very fast, irregular, wide-complex rhythm that can degenerate into ventricular fibrillation. A pathway with an effective refractory period under 240 ms, or a shortest pre-excited R-R of 250 ms or less, marks the higher-risk patient.
What not to give
In pre-excited atrial fibrillation, AV nodal blocking drugs are the wrong answer and adenosine especially so. Blocking the node removes the only competing route and pushes everything down the pathway. Intravenous ibutilide or procainamide are the preferred agents, with flecainide or propafenone as alternatives. Amiodarone is no longer recommended in this setting: it can enhance pathway conduction, and ventricular fibrillation has been reported after it. If the patient is unstable, cardiovert.
The mistake it invites
Pre-excited atrial fibrillation is fast, wide and irregular, and it is most often called ventricular tachycardia. The irregularity is the clue that it is not, and the changing QRS width from beat to beat is the clue that it is pre-excited.
When there is no pattern at all
Many accessory pathways conduct only backwards. They are concealed, the resting ECG is entirely normal, and they still support AVRT. A normal ECG does not exclude a pathway.
Clinical impact
The resting pattern is mostly benign in itself. Its value is as a warning label: it tells you a pathway exists and can conduct forwards, before the day that matters.
Management
Pattern alone: assess, do not treat reflexively
An asymptomatic pattern found incidentally needs risk assessment rather than immediate therapy, weighted towards those in high-risk occupations or competitive sport.
Pre-excited AF: avoid the AV node entirely
No adenosine, no verapamil or diltiazem, no digoxin, and no amiodarone. IV ibutilide or procainamide first, with flecainide or propafenone as alternatives.
Unstable: synchronised cardioversion
A class I recommendation, and the safest option whenever the rhythm is fast, wide and poorly tolerated or the diagnosis is uncertain.
Definitive: pathway ablation
Ablation removes the pathway and with it both the AVRT circuit and the pre-excited AF risk. It is the treatment of choice for symptomatic patients and for high-risk pathways.
Differential
The tachycardia this pattern predicts. During orthodromic AVRT the pathway is used backwards, so the delta disappears and the QRS is narrow.
Ordinary atrial fibrillation is irregular and narrow. Conducted down an accessory pathway it is irregular and wide, much faster, and the QRS width varies beat to beat.
What pre-excited AF is usually mistaken for. VT is regular with a fixed QRS shape; pre-excited AF is irregular and its complexes change width.
References
- 2019 ESC Guidelines for the management of patients with supraventricular tachycardia — European Heart Journal, 2020
- Pre-Excited Atrial Fibrillation in Wolff-Parkinson-White (WPW) Syndrome: A Case Report and a Review of the Literature — Reviews in Cardiovascular Medicine, 2024
- 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia — Circulation, 2016