Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise ventricular pre-excitation, manage AV re-entry and pre-excited atrial fibrillation safely, and identify who needs electrophysiology risk assessment or ablation.
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.
Incomplete electrical insulation at the atrioventricular junction leaves a myocardial connection that bypasses the AV node and links atrial tissue directly with ventricular myocardium.
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.
Multiple pathways or a connection capable of very rapid antegrade conduction increases the danger during atrial fibrillation. Syncope or documented rapid episodes strengthen concern.
An antegradely conducting accessory pathway activates part of the ventricle before impulses have traversed the normal rate-limiting AV node and His–Purkinje system.
Early pathway activation merges with normal conduction, producing a short PR interval, slurred initial QRS upstroke and broadened fusion complex during sinus rhythm.
A premature beat encounters different refractory properties in the pathway and AV node, allowing conduction down one limb and return through the other.
Orthodromic AVRT travels down the AV node and returns through the pathway, usually producing a narrow rhythm; the reverse antidromic circuit produces broad complexes.
During atrial fibrillation, a rapidly conducting pathway bypasses AV nodal filtering and delivers irregular impulses to the ventricles, potentially deteriorating into ventricular fibrillation.
Short PR, delta wave and widened QRS in sinus rhythm reflect fusion between accessory-pathway and normal His-Purkinje activation.
Usually a sudden-onset regular narrow tachycardia; retrograde P waves may follow the QRS.
A regular broad tachycardia using the pathway antegradely can mimic ventricular tachycardia and warrants expert assessment.
An irregular broad tachycardia with changing QRS morphology and very short RR intervals is the critical pattern.
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.
Syncope during tachycardia, documented AF, very rapid episodes, resuscitated arrest, multiple pathways or a high-risk occupation/sport accelerate specialist assessment.
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 broadens the QRS through delayed intraventricular conduction but lacks the characteristic short PR and slurred initial upstroke of resting pre-excitation.
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.
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.
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.
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.
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.
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.
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.
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.
An incidental delta wave is ventricular pre-excitation; WPW syndrome requires a clinical tachyarrhythmia attributable to the pathway.
In pre-excited AF, blocking only the AV node can divert more atrial impulses through the accessory pathway and dangerously accelerate the ventricles.
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.
A shortest pre-excited RR interval during AF of 250 ms or less indicates a pathway capable of rapid antegrade conduction.
Abrupt loss of pre-excitation is reassuring, but syncope, documented arrhythmia, multiple pathways or high-risk occupation can still justify invasive assessment.
Giving an AV nodal blocker to an irregular broad-complex tachycardia before excluding pre-excited AF.
Using amiodarone for pre-excited AF despite current ESC/RCUK safety advice.
Calling every broad tachycardia in a person with a delta wave antidromic AVRT instead of treating uncertain cases as VT.
Equating an incidental delta wave with symptomatic WPW syndrome.
Reassuring a person with syncope and pre-excitation without electrophysiology risk assessment.
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A 25-year-old with known pre-excitation develops an irregular broad-complex tachycardia at 230/min but remains conscious with a blood pressure of 112/70 mmHg. Which is the safest immediate drug option while expert cardioversion capability is present?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
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.
Stop or slow for hypotension or marked QRS/QT prolongation; avoid combining with another QT-prolonging antiarrhythmic and seek expert help.