Wolff-Parkinson-White syndrome and pre-excitation

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

An accessory pathway can support a re-entry circuit or conduct rapid atrial activity directly to the ventricle. The danger is greatest when AF reaches the ventricles rapidly because the pathway lacks the protective rate-limiting behaviour of the AV node.

Acute treatment depends on rhythm regularity, QRS width and stability. Adenosine belongs only in a selected regular tachycardia when pre-excited AF is not present; it is specifically excluded from the irregular pre-excited rhythm.

Definitive management is electrophysiological. Pathway ablation is recommended for symptomatic AVRT and is considered for asymptomatic pre-excitation when invasive testing shows high-risk properties or the person's occupation or sport makes sudden incapacity especially hazardous.

Key points

Pre-excitation means an accessory atrioventricular pathway conducts to the ventricle outside the AV node; WPW syndrome is pre-excitation plus symptomatic tachyarrhythmia.
The sinus-rhythm ECG classically shows a short PR interval, slurred initial QRS upstroke (delta wave) and a widened QRS.
Orthodromic AV re-entrant tachycardia is usually regular and narrow because antegrade conduction uses the AV node; antidromic AVRT is broad.
Pre-excited AF is irregular and broad with beat-to-beat QRS variation and potentially extreme ventricular rates.
Do not give adenosine, beta-blockers, diltiazem, verapamil, digoxin or amiodarone to pre-excited AF; AV nodal block can favour conduction down the accessory pathway.
For stable pre-excited AF, current RCUK options are procainamide or cardioversion; instability requires cardioversion.
Catheter ablation is first-line definitive treatment for symptomatic recurrent AVRT and for pathways with high-risk conduction properties.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Congenital accessory pathway

Incomplete electrical insulation at the atrioventricular junction leaves a myocardial connection that bypasses the AV node and links atrial tissue directly with ventricular myocardium.

Manifest or concealed conduction

A pathway conducting antegradely produces resting pre-excitation; WPW syndrome additionally requires an attributable tachyarrhythmia. A retrograde-only concealed pathway leaves the sinus ECG normal but can still sustain AV re-entry.

Higher-risk pathway phenotype

Multiple pathways or a connection capable of very rapid antegrade conduction increases the danger during atrial fibrillation. Syncope or documented rapid episodes strengthen concern.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
AV nodal bypass
An antegradely conducting accessory pathway activates part of the ventricle before impulses have traversed the normal rate-limiting AV node and His–Purkinje system.
2
Ventricular fusion
Early pathway activation merges with normal conduction, producing a short PR interval, slurred initial QRS upstroke and broadened fusion complex during sinus rhythm.
3
Re-entry initiation
A premature beat encounters different refractory properties in the pathway and AV node, allowing conduction down one limb and return through the other.
4
AV re-entrant tachycardia
Orthodromic AVRT travels down the AV node and returns through the pathway, usually producing a narrow rhythm; the reverse antidromic circuit produces broad complexes.
5
Rapid pre-excited atrial fibrillation
During atrial fibrillation, a rapidly conducting pathway bypasses AV nodal filtering and delivers irregular impulses to the ventricles, potentially deteriorating into ventricular fibrillation.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Resting pre-excitation

Short PR, delta wave and widened QRS in sinus rhythm reflect fusion between accessory-pathway and normal His-Purkinje activation.

Orthodromic AVRT

Usually a sudden-onset regular narrow tachycardia; retrograde P waves may follow the QRS.

Antidromic AVRT

A regular broad tachycardia using the pathway antegradely can mimic ventricular tachycardia and warrants expert assessment.

Pre-excited AFRed flag

An irregular broad tachycardia with changing QRS morphology and very short RR intervals is the critical pattern.

High-risk pathway

At electrophysiology study, accessory-pathway effective refractory period 250 ms or less, or shortest pre-excited RR interval during AF 250 ms or less, indicates rapid conducting capacity.

Clinical red flagsRed flag

Syncope during tachycardia, documented AF, very rapid episodes, resuscitated arrest, multiple pathways or a high-risk occupation/sport accelerate specialist assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECG in sinus rhythmFirst step
Why
Confirm and localise pre-excitation and look for alternative conduction disease.
Interpretation and limitations
Delta-wave polarity can suggest pathway location, but absence of pre-excitation on one ECG does not exclude a concealed or intermittent pathway.
02
12-lead ECG during tachycardia
Why
Distinguish regular narrow AVRT, regular broad tachycardia and irregular pre-excited AF.
Interpretation and limitations
Irregularity and beat-to-beat QRS variation must be recognised before any AV nodal blocker is given.
03
Ambulatory ECG
Why
Document symptomatic episodes and intermittent pre-excitation.
Interpretation and limitations
Abrupt loss of pre-excitation can suggest a longer refractory pathway but does not replace specialist risk assessment when other high-risk features exist.
04
Exercise ECG
Why
Assess behaviour of pre-excitation with increasing rate in selected asymptomatic people.
Interpretation and limitations
Abrupt complete loss of the delta wave suggests lower-risk antegrade conduction; gradual fusion change is less reassuring.
05
Electrophysiology study
Why
Measure pathway conduction, induce tachycardia and permit ablation.
Interpretation and limitations
A shortest pre-excited RR interval or pathway refractory period of 250 ms or less is a high-risk property.
06
Echocardiogram
Why
Identify associated structural disease and establish ventricular function.
Interpretation and limitations
Structural abnormalities influence differential diagnosis and treatment planning but are not required for the ECG diagnosis.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Short PR without pre-excitation

Enhanced AV nodal conduction can shorten the PR interval but does not create a delta wave or widened fusion QRS, distinguishing it from manifest accessory-pathway conduction.

Bundle-branch block

Bundle-branch block broadens the QRS through delayed intraventricular conduction but lacks the characteristic short PR and slurred initial upstroke of resting pre-excitation.

AV nodal re-entry tachycardia

AVNRT also causes abrupt regular narrow tachycardia, often with hidden P waves. Baseline pre-excitation raises suspicion of AVRT, but electrophysiological demonstration that the pathway participates in the circuit distinguishes it from coincident AVNRT.

Ventricular tachycardia

Regular broad tachycardia may be antidromic AVRT, SVT with aberrancy or VT. Structural disease and AV dissociation support VT, but uncertain cases require a VT-safe approach.

Polymorphic ventricular tachycardia

Both it and pre-excited atrial fibrillation may appear broad and variable. Marked irregularity, changing degrees of pre-excitation and a known delta wave favour the latter.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01regular-narrowStable regular narrow tachycardiaFirst stepThe rhythm is regular, QRS is under 120 ms and there is no evidence of pre-excited AF.

1Record a 12-lead ECG and perform vagal manoeuvres while monitoring continuously.
2If unsuccessful and there is no pre-excitation in the tachycardia, give adenosine 6 mg as a very rapid IV bolus followed by a flush.
3If needed give 12 mg, then 18 mg as very rapid IV boluses while recording a multi-lead ECG; this is the March 2026 RCUK sequence.
4If adenosine fails or instability develops, obtain expert help and use synchronised cardioversion; never transfer this sequence to an irregular broad rhythm.

02pre-excited-afPre-excited atrial fibrillationIrregular broad tachycardia with suspected accessory-pathway conduction.

1Attach defibrillator pads, obtain expert help and assess immediately for shock, syncope with severe hypotension, ischaemia or pulmonary oedema.
2If unstable, deliver synchronised cardioversion with appropriate sedation if feasible without delay.
3If stable, use IV procainamide 10-15 mg/kg over 20 minutes (maximum 1 g) or perform cardioversion, with continuous ECG and blood-pressure monitoring.
4Avoid adenosine, beta-blockers, verapamil, diltiazem, digoxin and amiodarone because selective AV nodal block can accelerate pathway conduction.

03regular-broadRegular broad tachycardiaThe differential includes antidromic AVRT, SVT with aberrancy and VT.

1Treat as VT when the diagnosis is uncertain, particularly with structural heart disease.
2If unstable, deliver synchronised cardioversion; RCUK starts VT with a pulse at 120-150 J.
3Only when the rhythm is regular and an SVT with aberrancy is suspected may monitored IV adenosine be used diagnostically/therapeutically; if ineffective, treat as VT.
4Arrange electrophysiology review after recovery to define and ablate the pathway when appropriate.

04definitiveRisk assessment and ablationDefinitiveSymptoms, documented AVRT/AF, high-risk features or asymptomatic pre-excitation requiring risk stratification.

1Refer to an electrophysiologist and review syncope, occupation, competitive sport, family history and recorded rhythms.
2Use non-invasive testing selectively, but proceed to electrophysiology study when symptoms or risk context justify it.
3Offer catheter ablation for symptomatic recurrent AVRT or a pathway with high-risk invasive properties.
4Confirm loss of pathway conduction after ablation and provide recurrence and vascular-access safety advice.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Stable regular narrow-complex tachycardia, or selected regular broad tachycardia thought to be SVT with aberrancy, only when pre-excited AF is absent.

Adenosine

RCUK March 2026: 6 mg by very rapid IV bolus, then 12 mg if unsuccessful, then 18 mg if still unsuccessful, each followed by a rapid flush and given with continuous ECG recording. This resuscitation-algorithm sequence differs from the cited product SmPC's licensed 3 mg, 6 mg, then 12 mg sequence.

Do not use in irregular broad-complex tachycardia or pre-excited AF. The cited UK SmPC contraindicates bronchospastic chronic lung disease including asthma, long-QT syndrome, severe hypotension, decompensated heart failure, and sick-sinus or second-/third-degree AV block without a functioning pacemaker. Avoid with dipyridamole; if essential, stop dipyridamole 24 hours beforehand or use a greatly reduced adenosine dose under expert direction. Sensitivity after heart transplantation may be increased.

A current option for stable pre-excited AF and for stable broad-complex tachycardia when drug treatment is selected because cardioversion sedation/anaesthesia poses excess risk.

Procainamide

RCUK: 10-15 mg/kg IV over 20 minutes, maximum 1 g, with continuous ECG and blood-pressure monitoring.

Stop or slow for hypotension or marked QRS/QT prolongation; avoid combining with another QT-prolonging antiarrhythmic and seek expert help.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Recurrent AV re-entry

The accessory connection completes a stable macro-re-entry circuit, causing abrupt palpitations, chest discomfort or breathlessness and repeated urgent presentations despite normal rhythm between episodes.

Syncope and injury

Very rapid AVRT or pre-excited atrial fibrillation can transiently reduce cardiac output, causing sudden loss of consciousness with associated trauma, driving or occupational risk.

Pre-excited atrial fibrillation

Atrial fibrillation can conduct rapidly through the pathway because it lacks normal AV nodal rate limitation, producing an irregular broad rhythm and severe haemodynamic compromise.

Ventricular fibrillation and sudden death

Extremely rapid irregular ventricular activation can disorganise into ventricular fibrillation. This uncommon but critical pathway explains the importance of specialist risk assessment after high-risk presentations.

Tachycardia-induced ventricular dysfunction

Frequent or prolonged re-entrant episodes can impair ventricular function through persistent rate stress and, when ventricular activation is abnormal, dyssynchrony. Function may recover when the arrhythmia is durably controlled.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During acute treatment, continuously monitor ECG, blood pressure, oxygen saturation and level of consciousness.
Record a 12-lead ECG before and after conversion and retain the tachycardia tracing for electrophysiology review.
With procainamide, monitor QRS, QT and blood pressure throughout the infusion.
After ablation, check for disappearance of pre-excitation and monitor the access site and rhythm recurrence.
Advise prompt reassessment for syncope, an irregular very rapid episode or recurrence after ablation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Pattern versus syndrome

An incidental delta wave is ventricular pre-excitation; WPW syndrome requires a clinical tachyarrhythmia attributable to the pathway.

The AV node can be protective

In pre-excited AF, blocking only the AV node can divert more atrial impulses through the accessory pathway and dangerously accelerate the ventricles.

Adenosine dose has changed

The current March 2026 RCUK adult tachyarrhythmia algorithm uses 6 mg, 12 mg and 18 mg; older teaching commonly used 6 mg, 12 mg and another 12 mg.

Short RR interval signals risk

A shortest pre-excited RR interval during AF of 250 ms or less indicates a pathway capable of rapid antegrade conduction.

Intermittent does not mean harmless

Abrupt loss of pre-excitation is reassuring, but syncope, documented arrhythmia, multiple pathways or high-risk occupation can still justify invasive assessment.

11Common pitfallsFrequent interpretation and management errors.

01
Giving an AV nodal blocker to an irregular broad-complex tachycardia before excluding pre-excited AF.
02
Using amiodarone for pre-excited AF despite current ESC/RCUK safety advice.
03
Calling every broad tachycardia in a person with a delta wave antidromic AVRT instead of treating uncertain cases as VT.
04
Equating an incidental delta wave with symptomatic WPW syndrome.
05
Reassuring a person with syncope and pre-excitation without electrophysiology risk assessment.