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ECG Topic - Wolff Parkinson White (WPW) Pattern
ECG Topic - Wolff Parkinson White (WPW) Pattern

ECG Topic - Wolff Parkinson White (WPW) Pattern

Last updated August 17, 2025

Introduction

Wolff Parkinson White is a pre-excitation syndrome caused by an accessory atrioventricular pathway (the Bundle of Kent). Recognition of this ECG pattern is an important skill as it predisposes patients to tachyarrhythmias and potentially sudden cardiac death.

Classic Triad

Across all 12 leads, WPW is characterized by:

  • Short PR interval (<120 ms): due to atrial impulse bypassing the AV node.
  • Delta wave: slurred upstroke of the QRS as the ventricle is activated early through the accessory pathway.
  • Widened QRS: typically >120 ms, though may be narrower in subtle cases

Not every beat will manifest pre-excitation; intermittent or concealed pathways can hide the diagnosis.

Example: WPW

Source: LITFL
Source: LITFL

Electro-Pathophysiology

The Normal Pathway

  • Atrial impulse → AV node (delays conduction ~120 ms) → His-Purkinje → rapid, synchronized ventricular activation.
  • The AV node is the “gatekeeper” that both slows conduction and prevents rapid ventricular rates during atrial arrhythmias.

What Changes in WPW

  • An accessory pathway (the bundle of Kent) directly connects atrium to ventricle, bypassing the AV node.
  • This pathway is fast-conducting (like myocardium, not specialized conduction tissue) and non-decremental (doesn’t slow with faster atrial rates).
  • Result: Pre-excitation — ventricles get activated earlier than they should.
Adapted from LITFL
Adapted from LITFL

How this creates the ECG findings

Short PR
Because the impulse doesn’t pause at the AV node, the atrium quickly conducts to the ventricle, shortening the PR interval
Delta Wave
The accessory pathway activates a portion of the ventricle slowly via myocyte-to-myocyte spread (instead of the fast His-Purkinje). This creates the slurred upstroke of the QRS.
Wide Qrs
Fusion of two activation waves: Early slurred delta wave from the accessory pathway and the normal wave from AV node/His-Purkinje. Combined, this makes the QRS longer.

Types of WPW

Type A (Left-sided pathway)

  • Location of accessory pathway: left atria —> left ventricle
  • Precordial leads: Positive in V1-V6
  • QRS axis: Normal or rightward.
  • Mimic: Looks like LVH or LBBB with tall R waves across precordium.
  • Teaching Pearl: Easy to confuse with true LVH or LBBB; delta wave slurring is the giveaway.

Approximately 9–10% of patients with Wolff-Parkinson-White (WPW) pattern have a normal PR interval on surface ECG. This atypical presentation is most commonly associated with left lateral accessory pathways

Example: Type A WPW

image

Type B (Right-sided pathway)

  • Location of accessory pathway: right atria —> right ventricle
  • Precordial leads: Negative in V1 (dominant S wave).
  • QRS axis: Leftward or normal.
  • Mimic: Anterior infarct with poor R wave progression.
  • Teaching Pearl: The pseudo-infarct pattern in anterior leads (Q waves or absent R in V1–V3) can be mistaken for ischemia.

Example: Type B WPW

image

Type C (Multiple pathways)

  • Location of accessory pathway: posteroseptal or multiple pathways of origin
  • Precordial Leads: Positive in V1 and negative in V5/V6
  • Axis: Often extreme axis deviation.
  • Teaching Pearl: Rare compared to A and B, but important—can simulate bizarre intraventricular conduction delay. Often linked with multiple accessory pathways and higher arrhythmia risk.

Example: Type C WPW

image

Tachyarrhythmias

Epidemiology

  • Prevalence
    • WPW pattern is found in about 0.1–0.3% of the population.
  • Progression to SVT
    • Roughly 50–60% of patients with a WPW ECG pattern will develop paroxysmal tachyarrhythmias most often atrioventricular reentry tachycardia (AVRT)
    • Approximately 15% will develop atrial fibrillation
    • The remaining 40–50% may remain asymptomatic for life.
  • Sudden death risk (if untreated): Rare but real, estimated around 0.1x–0.6% per year in high-risk patients (younger age, multiple pathways, short anterograde accessory pathway, atrial fibrillation).

Example: Orthodromic AVRT (narrow)

image

Example: Antidromic AVRT (wide)

Source: LITFL
Source: LITFL

Dangers of Atrial Fibrillation and WPW

  • Normally, the AV node protects the ventricles during atrial fibrillation/flutter by limiting conduction.
  • In WPW, the accessory pathway has no rate-limiting function. However atrial rates of 300 bpm in atrial fibrillation can conduct 1:1, leading to ventricular rates >250 bpm and degeneration into VF and sudden death.
  • The use of AV nodal blockers including adenosine can lead to unopposed accessory conduction which can precipitate ventricular fibrillation

Example: Atrial Fibrillation with WPW

Source: ECG Wave-Maven
Source: ECG Wave-Maven

Key Points

  • WPW is a mimic: Type A can look like LVH/LBBB, Type B like anterior MI — delta wave recognition is essential.
  • Normal PR doesn’t rule it out: ~10% of patients with WPW may have a normal PR interval, especially with left lateral pathways.
  • Half become symptomatic: 50–60% of patients with WPW pattern will develop tachyarrhythmias; ~15% develop AF.
  • AF with WPW is life threatening: Avoid AV nodal blockers — unopposed accessory conduction can degenerate into VF.

Related Posts

  • The PR interval
  • Atrioventricular Re-Entry Tachycardia (AVRT)
  • VT vs. SVT with aberrancy
  • Lown Ganong Levine Syndrome

References

  1. Brady WJ, Mattu A, Tabas JA. Critical Decisions in Emergency and Acute Care Electrocardiography. Wiley-Blackwell; 2009.
  2. Burns E, Buttner R. WPW Syndrome. Life in the Fast Lane ECG Library. Published October 2024. Accessed August 2025. https://litfl.com/wolff-parkinson-white-syndrome-wpw/
  3. Cain N, Irving C, Webber S, Beerman L, Arora G. Natural history of Wolff-Parkinson-White syndrome diagnosed in childhood. Am J Cardiol. 2013;112(7):961-965. doi:10.1016/j.amjcard.2013.05.035
  4. Chou TC, Surawicz B. Chou’s Electrocardiography in Clinical Practice. 6th ed. Saunders/Elsevier; 2008.
  5. Davila E. The ECG.. Self-published; 2024.
  6. Garcia TB. 12-Lead ECG: The Art of Interpretation. 2nd ed. Jones & Bartlett Learning; 2013.
  7. Janson CM, Millenson ME, Okunowo O, et al. Incidence of life-threatening events in children with Wolff-Parkinson-White syndrome: analysis of a large claims database. Heart Rhythm. 2022;19(4):642-647. doi:10.1016/j.hrthm.2021.12.009
  8. Lampert R, Chung EH, Ackerman MJ, et al. 2024 HRS expert consensus statement on arrhythmias in the athlete: evaluation, treatment, and return to play. Heart Rhythm. 2024;21(10):e151-e252. doi:10.1016/j.hrthm.2024.05.018
  9. Mattu A, Brady WJ, Perron AD. ECGs for the Emergency Physician 1. BMJ Books; 2003.
  10. Mattu A, Brady WJ, Perron AD. ECGs for the Emergency Physician 2. BMJ Books; 2008.
  11. Obeyesekere MN, Leong-Sit P, Massel D, et al. Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis. Circulation. 2012;125(19):2308-2315. doi:10.1161/CIRCULATIONAHA.111.055350
  12. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67(13):e27-e115. doi:10.1016/j.jacc.2015.08.856
  13. Pappone C, Vicedomini G, Manguso F, et al. Risk of malignant arrhythmias in initially symptomatic patients with Wolff-Parkinson-White syndrome: results of a prospective long-term electrophysiological follow-up study. Circulation. 2012;125(5):661-668. doi:10.1161/CIRCULATIONAHA.111.065722
  14. Podrid PJ. Podrid’s Real-World ECGs: Vol 6. Paced Rhythms, Congenital Abnormalities, and Electrolyte Disturbances. Cardiotext Publishing; 2016.

This post is for education and not medical advice

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