Wolff-Parkinson-White Syndrome – Part 1

Wolff-Parkinson-White (WPW) Syndrome

  • Described in 1930 by Wolff, Parkinson, and White as an ECG pattern found in young, otherwise healthy adults who experienced bouts of atrial fibrillation and atrial tachycardia
  • In 1932 Holzmann and Scherf proposed that the syndrome was due to an accessory pathway between the atria and ventricles
  • In 1967 Ferrar described the syndrome as consisting of variants of pre-excitation depending on the anatomical anomaly (bundle of Kent, Mahaim’s fibers, anomalous pathway of Lown-Ganong-Levine syndrome)
  • Estimated to effect 0.15-0.2% of the general population
  • Paroxysmal tachycardias are the most important clinical manifestation and have been recorded in 13-80% of patients with the WPW pattern (depending on the population tested)
  • Radiofrequency catheter ablation is the treatment of choice for symptomatic patients

Normal conduction versus ventricular pre-excitation (WPW pattern)

Figure 1. Normal conduction (Example 1) and conduction with an accessory pathway (Example 2)

Figure 1. Normal conduction (Example 1) and conduction with an accessory pathway (Example 2)

These amazing images were created by Christopher Watford (@ecgwatford) who is a Sr. Editor at ems12lead.com. He also has his own blog over at My Variables Only Have 6 Letters.

Take a look at Figure 1. On the left (Example 1) we see normal conduction and on the right (Example 2) we see the “WPW pattern” or ventricular pre-excitation of the ventricles across an accessory pathway. This “WPW pattern” or delta wave is visible on the resting ECG in the absence of a pre-excitation-dependent tachycardia.

Let’s start with a review of normal cardiac conduction (Example 1).

The normal cardiac impulse (or depolarization wavefront) starts in the sinus node and is conducted over to the left atrium across preferred pathways known as the interatrial tract or “Bachmann’s bundle” which depolarizes the atria and corresponds to the P-wave on the surface ECG.

The impulse then passes through the AV node where it is slowed down and is conducted through the fibrous skeleton of the heart to the AV bundle (bundle of His) which corresponds to the PR interval on the surface ECG.

It should be noted that the fibrous skeleton of the heart is made of collagen (the most common structural animal protein in nature) and for the purposes of cardiac conduction it is electrically inert and insulates the ventricles from the atria. The only legitimate electrical connection between the atria and ventricles is through the AV node.

It’s worth taking a moment to think about why this should be so.

Why does the heart have a fibrous skeleton? In the first place it gives the heart structure and provides form, shape, and stability to the AV valves. We wouldn’t want them to collapse during systole!

But why should the impulse slow down? Why do we have a PR interval? It’s to allow time for ventricular filling! Atrial systole is a end-diastolic event (the “atrial kick”) and without the delay we would not have the normal “lub dub” associated with normal cardiac function.

In addition, the human animal can survive atrial fibrillation because the AV node acts as a gate keeper for the ventricles. With new onset AF the atrial rate is between 300-600/min but the ventricular rate is usually around 130/min. Why? Because the AV node does not allow 1:1 conduction across to the ventricles. If it did, atrial fibrillation (one of the most common arrhythmias in the world) might result in ventricular fibrillation (death).

Let’s get back to normal conduction.

Once the impulse travels through the AV node to the AV bundle it bifurcates (or splits) into the left and right bundle branches and Purkinje system which causes rapid and simultaneous depolarization of the ventricles which corresponds to the QRS complex on the surface ECG.

When conduction is normal we expect a narrow QRS complex with fairly tight and sharp Q, R, and S-waves.

Now let’s look at the “WPW pattern” or pre-excitation of the ventricles (Example 2).

You will note that in addition to the red arrow which passes through the AV node (the “squiggle” in the arrow notes where the impulse slows down) there is an additional arrow representing conduction across an “accessory pathway” allowing the impulse to bypass the AV node, causing early activation of the ventricles.

This arrow does not have a “squiggle” because it does not have the same properties as the specialized cardiac tissue of the AV node. In other words, it may not slow the impulse down as compared to the AV node.

This early activation of the ventricles causes some abnormalities on the surface ECG.

  • It shortens the PR interval to < 120 ms (earlier activation of the ventricles brings the QRS complex closer to the P-wave)
  • It causes a slurred upstroke (or downstroke) of the QRS complex (the “WPW pattern” or “delta wave”) where the impulse bypasses the AV node
  • This has the effect of widening the QRS complex to varying degrees (mimicking bundle branch block or left ventricular hypertrophy)
  • There is often a secondary ST/T-wave abnormality (abnormal depolarization causes abnormal repolarization)
  • Delta waves can be mistaken for Q-waves and secondary ST/T-wave abnormalities can cause ST-segment elevation (which is why WPW can be a STEMI mimic or cause a so-called “pseudo-infarct” pattern)

This illegitimate pathway also lends itself to the possibility of cardiac arrhythmias including very rapid atrial fibrillation and reciprocating tachycardias (which will be covered in Part 2).

Localization of the accessory pathway using the 12-lead ECG

With the advent of radiofrequency ablation for the treatment of tachyarrhythmias associated with WPW, it became important to precisely localize the site of the accessory pathway. Various algorithms are used to identify the site of the accessory pathway using the frontal plane QRS axis and delta wave axis.

There are those who may look upon describing the WPW pattern as Type A, B, or C as being a bit old fashioned. Some will prefer to describe a particular ECG as “suggestive of a right posterior paraseptal bypass tract” for example.

While I am impressed by their ability (especially when they don’t use a cheat sheet), it’s probably not a practical skill for the average clinician working outside of the EP lab. Most of us can’t “know it all” when it comes to electrocardiography.

Type A


In WPW pattern Type A the delta waves are predominantly upright in all of the precordial leads. If you use your imagination the QRS complex in lead V2 looks like the letter A.

Type B


In WPW pattern Type B the delta waves are predominantly negative in leads V1-V3 and predominantly positive in leads V4-V6. It can be mistaken for left bundle branch block or left ventricular hypertrophy with strain.

As a side note, you will occasionally see the computerized interpretive algorithm confuse a ventricular paced rhythm for WPW pattern Type B as pictured below. It’s just something to be aware of.


Type C

In WPW pattern Type C (which is rare) the delta waves are upright in leads V1-V4 but negative in leads V5-V6.

In Part 2 we’ll look at the tachyarrhythmias associated with Wolff-Parkinson-White syndrome and discuss appropriate treatment.


Acierno, Louis J. The History Of Cardiology. London: Parthenon Pub. Group, 1994. Print.

Ferrer, M. I. ‘New Concepts Relating To The Preexcitation Syndrome’. JAMA: The Journal of the American Medical Association 201.13 (1967): 1038-1039. Web.

Garcia, Tomas B, and Neil E Holtz. 12 Lead ECG. Boston, Ma: Jones and Bartlett, 2001. Print.

Surawicz, Borys, Timothy K Knilans, and Te-Chuan Chou. Chou’s Electrocardiography In Clinical Practice. Philadelphia: Saunders, 2001. Print.

Wolff, Louis, John Parkinson, and Paul D. White. ‘Bundle-Branch Block With Short P-R Interval In Healthy Young People Prone To Paroxysmal Tachycardia’. American Heart Journal 5.6 (1930): 685-704. Web.


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