Pre-excitation: Wolff–Parkinson–White

What it is

In Wolff–Parkinson–White (WPW) an accessory pathway, a strand of muscle that crosses the atrioventricular ring, conducts the impulse from atria to ventricles without the normal delay of the AV node. Part of the ventricle is activated early through the pathway, before the rest is activated through the His–Purkinje system, and the QRS becomes a fusion of the two. The resting ECG shows the WPW pattern: a short PR interval under 120 ms, a slurred, slow upstroke at the start of the QRS (the delta wave), a QRS widened to over 110 to 120 ms, and secondary ST and T changes in the direction opposite to the delta wave. The WPW syndrome is the pattern plus symptomatic tachyarrhythmias. The commonest is orthodromic atrioventricular re-entrant tachycardia (AVRT), which travels down the AV node and back up the pathway: a regular, narrow-complex tachycardia, often at 150 to 250 bpm, with no delta wave and with retrograde P waves in the ST segment. Antidromic AVRT goes the other way and gives a regular, wide-complex tachycardia that looks like ventricular tachycardia. The dangerous one is atrial fibrillation with pre-excitation: an irregularly irregular, very fast, wide-complex rhythm whose QRS shape changes from beat to beat; because the pathway has no protective delay, ventricular rates can exceed 250 bpm and degenerate into ventricular fibrillation. AV nodal blocking drugs (adenosine, calcium channel blockers, beta-blockers, digoxin, and intravenous amiodarone) can speed conduction down the pathway in this setting and are avoided. The polarity of the delta wave in V1 gives a rough guide to the side of the pathway, and catheter ablation is the definitive treatment.

How to recognise it

• Short PR interval: under 120 ms, with a normal P wave (sinus rhythm).
• Delta wave: slurred, slowly rising first part of the QRS, positive or negative depending on the pathway's site.
• QRS over 110 to 120 ms from fusion of early (pathway) and normal (His–Purkinje) activation.
• Secondary repolarisation changes: ST and T directed opposite to the delta wave and main QRS.
• Negative delta waves in the inferior leads can look like Q waves (pseudo-infarction); a tall R in V1 can mimic RBBB or posterior infarction.
• Positive delta wave and dominant R in V1 suggests a left-sided pathway; negative delta wave in V1 a right-sided one.
• Intermittent pre-excitation (delta wave present on some beats, absent on others) suggests a pathway with a long refractory period, a lower-risk sign.

Why it happens

• The AV node normally delays the impulse; the pathway bypasses it, so the ventricle starts early (short PR) and slowly through ordinary muscle (delta wave).
• The rest of the ventricle is activated through the His–Purkinje system, so the QRS is a fusion: the more the pathway contributes, the wider the QRS.
• Two connections between atria and ventricles form a circuit: re-entry down one and up the other causes AVRT.
• In atrial fibrillation the pathway, unlike the AV node, has no decremental delay and may let most atrial impulses through to the ventricles.

Step by step

1. Measure the PR interval in several leads — a PR under 120 ms with sinus P waves is the first clue.
2. Look at the start of each QRS for slurring — the delta wave is the mark of pre-excitation.
3. Measure the QRS width and check ST and T against the delta wave — a fusion QRS with opposite repolarisation completes the pattern.
4. Check the delta-wave polarity in V1 and the inferior leads — it hints at the pathway's side and explains pseudo-Q waves.
5. During tachycardia, decide narrow or wide and regular or irregular — this separates orthodromic AVRT, antidromic AVRT and pre-excited AF.
6. Irregular, wide and very fast with changing QRS shape: think pre-excited AF — AV nodal blockers can be lethal there.

Tachycardias in WPW

Differential and pitfalls

• Orthodromic AVRT versus AV nodal re-entry (AVNRT): in AVRT the retrograde P sits in the ST segment (RP over 70 ms); in AVNRT it is hidden in or just after the QRS.
• Antidromic AVRT and pre-excited AF mimic ventricular tachycardia; if in doubt, treat a wide-complex tachycardia as VT.
• Pre-excited AF versus AF with bundle branch block: in pre-excited AF the QRS shape varies beat to beat and rates are often over 200 bpm.
• Delta-wave pseudo-infarct Q waves and LVH-like voltages lead to false diagnoses; look for the short PR first.
• Associations: Ebstein anomaly and hypertrophic cardiomyopathy; check the echo.
• Pitfall: a subtle delta wave in a left lateral pathway may be seen only in a few leads; compare PR and QRS lead by lead.

Next step

• Unstable tachycardia with WPW: synchronised cardioversion; call a senior at once.
• Stable orthodromic AVRT: vagal manoeuvres, then adenosine with a defibrillator at hand as the protocol sets.
• Stable pre-excited AF: no AV nodal blockers; procainamide or synchronised cardioversion with specialist advice.
• Refer every patient with a WPW pattern and symptoms (palpitations, syncope) to cardiology or electrophysiology for risk assessment and ablation.
• Asymptomatic WPW pattern: refer for risk stratification (exercise test, electrophysiology study), especially in athletes and high-risk jobs.

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Elsewhere in DurgiPedia

• The cardiac conduction system
• How arrhythmias arise
• ECG basics: waves, intervals and leads

Connections

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Educational content; it does not replace supervised hands-on training, your institution's protocols or a prescriber's order. A procedure is learnt with a teacher and done only once you are trained to do it.

Sources: Wolff-Parkinson-White Syndrome (StatPearls (NCBI Bookshelf), 2023).

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