Wolff-Parkinson-White Syndrome – Part 2

This is Part 2 in our series on Wolff-Parkinson-White (WPW) Syndrome.

In Part 1 we went over the history of WPW and the pre-excitation syndromes and reviewed normal cardiac conduction as compared to conduction over an accessory bypass tract.

Now we’d like to look at the tachycarrhythmias associated with WPW. But first, I’d like to take this opportunity to say a little bit about supraventricular tachycardia in general.

Supraventricular tachycardia (SVT)

  • The term “SVT” is a generic, umbrella term that refers to any tachycardia that originates above the ventricles
  • A more precise definition is any tachycardia that “requires the AV node for its maintenance”

The 2005 AHA ECC Guidelines were explicit about this and listed the narrow complex tachycardias in order of frequency, which I think was quite useful.

  • Sinus tachycardia
  • Atrial fibrillation
  • Atrial flutter
  • AV nodal reentry (AVNRT)
  • Accessory pathway-mediated tachycardia (orthodromic AVRT)
  • Atrial tachycardia (ectopic and reentrant)
  • Multifocal atrial tachycardia (MAT)
  • Junctional tachycardia

Sinus tachycardia at a rate of 180/min.

The list was dropped in the 2010 AHA ECC Guidelines but they made this important statement about sinus tachycardia:

Sinus tachycardia is common and usually results from a physiologic stimulus, such as fever, anemia, or hypotension/shock. Sinus tachycardia is defined as a heart rate >100 beats per minute. The upper rate of sinus tachycardia is age-related (calculated as approximately 220 beats per minute, minus the patient’s age in years) and may be useful in judging whether an apparent sinus tachycardia falls within the expected range for a patient’s age. If judged to be sinus tachycardia, no specific drug treatment is required. Instead, therapy is directed toward identification and treatment of the underlying cause. When cardiac function is poor, cardiac output can be dependent on a rapid heart rate. In such compensatory tachycardias, stroke volume is limited, so “normalizing” the heart rate can be detrimental.

There are some important points here to consider:

  • The idea that a heart rate > 150 rules out sinus tachycardia is a myth (see: The Trouble with Sinus Tachycardia)
  • “220 minus age” is a good formula for estimating maximum sinus rate (but it can vary by 10-15%)
  • Sinus tachycardia is the most common narrow complex tachycardia and must be a part of your differential diagnosis!

Let’s move on to the tachyarrhythmias associated with Wolff-Parkinson-White syndrome.

Orthodromic AV reentrant tachycardia (AVRT)


Figure 2. Orthodromic AVRT

With orthodromic AVRT (also called orthodromic circus movement tachcycardia) antegrade conduction proceeds normally down the AV conducting system (2) and retrograde conduction proceeds up the bypass tract (3). This creates a “revolving door” or reentry circuit (4) that usually results in a narrow complex tachycardia.

This can happen in patients with so-called “concealed conduction“. There are patients for whom the bypass tract only works in the retrograde direction. These patients will not display a delta wave on the surface electrocardiogram!

It should be noted that there is more than one type of concealed conduction and patients can have more than one bypass tract.

Orthodromic AVRT is essentially indistinguishable from the more common AV nodal reentrant tachycardia (AVNRT) on the surface electrocardiogram (where the reentry circuit is confined to the tissue of the AV node).

Some have suggested that the RP interval (distance between the R-wave and retrograde P-wave) can help distinguish between AVRT and AVNRT.


Retrograde P-waves in lead V1

While I do “look for the P-waves” when analyzing any tachycardia (and find the presence of a retrograde P-wave to be helpful), I have not found the RP interval to be particularly useful during the emergency treatment of supraventricular tachycardia (SVT).

That’s probably because the treatment is exactly the same! Hemodynamically stable patients receive adenosine and hemodynamically unstable patients receive synchronized electrical cardioversion.


Reentrant SVT – this could be AVNRT or it could be orthodromic AVRT

Antidromic AV reentrant tachycardia (AVRT)


Figure 3. Antidromic AVRT

With antidromic AVRT (also called antidromic circus movement tachycardia) antegrade conduction proceeds down the accessory pathway (1) and retrograde conduction proceeds up the AV node (2-3). This creates a “revolving door” or reentry circuit (4) that results in a regular wide complex tachycardia.


Wide complex tachycardia in a patient with Wolff-Parkinson-White syndrome believed to be antidromic AVRT

This is quite rare in comparison to orthodromic AVRT and only happens spontaneously in 5-10% of patients. In fact, this may be an over-estimate because (according to Josephson) > 50% of wide complex tachycardias associated with WPW syndrome are due to atrial flutter!


1:1 atrial flutter

(Another common cause of 1:1 atrial flutter is the patient who is prescribed a Class Ic antiarrhythmic without AV nodal blocking agents which slows down the flutter rate enough to allow 1:1 conduction through the AV node.)

Antidromic AVRT should respond to adenosine and it’s reasonable to give a trial of adenosine in the setting of regular wide complex tachycardia. However, you should have a backup plan!

Anecdotally, I have reviewed several regular wide complex tachycardia cases since the 2010 AHA ECC Guidelines were published and in a majority of them the patient received 3 doses of adenosine in the prehospital setting and nothing else!

Keep in mind that an elderly patient, with a cardiac history, who presents with a regular wide complex tachycardia, has a > 80% probability of being in ventricular tachycardia! The most important criterion for VT is “wide and fast.”

It’s fine to use various algorithms to rule-in VT but failure to rule-in VT does not rule out VT.

Atrial fibrillation with accessory pathway (AF/WPW)


Figure 4. Atrial fibrillation with an accessory pathway

Atrial fibrillation in the setting of Wolff-Parkinson-White syndrome can be quite dangerous! This is an occasion where giving the wrong drugs (i.e., adenosine or a calcium channel blocker) can be a big mistake! For reasons that are not completely clear these drugs are believed to “facilitate conduction across the accessory pathway”.

As we mentioned in Part 1, the atrial rate in atrial fibrillation is typically between 300-600. When those impulses are allowed to be transmitted to the ventricles vary rapidly across an accessory pathway the result can be ventricular fibrillation (VF) and there a several case reports in the medical literature.

The ECG in AF/WPW is quite unique. It shows an irregular, polymorphic tachycardia without turning of the points. That’s how it can be distinguished from polymorphic VT or torsades de pointes. In particular, patients with AF/WPW whose shortest R-R interval on the ECG is < 6 small blocks (240 ms) are believed to be at higher risk of developing VF (note the second example below).

Although the 2010 AHA ECC Guidelines suggest that amiodarone is a viable option for these patients, many including Amal Mattu, M.D. (@amalmattu) and my old friend Andrew Bowman (@AndrewACNP1) have long argued that amiodarone should not be given.

They were recently vindicated when the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation was published in December.

Procainamide or ibutilide may be the only appropriate medications for these patients. Hemodynamically unstable patients should receive synchronized electrical cardioversion. There’s no shame in considering expert consultation! There are times when discretion is the better part of valor.

It’s worth remembering that the same potential thromboembolitic complications apply to these patients as for any other patient presenting with atrial fibrillation or atrial flutter.


The ECG of a patient with “possible AF/WPW” who was referred to cardiology


A confirmed case of AF/WPW with shortest R-R inverval is < 6 small blocks (240 ms)


Another case of AF/WPW with shortest R-R interval < 6 small blocks (240 ms)


Acierno L. The History Of Cardiology. London: Parthenon Pub. Group; 1994.

Ferrer M. New concepts relating to the preexcitation syndrome. JAMA: The Journal of the American Medical Association. 1967;201(13):1038-1039. doi:10.1001/jama.201.13.1038.

Garcia T, Holtz N. 12 Lead ECG: The Art of Interpretation. Boston, Ma: Jones and Bartlett; 2001.

Josephson M. Clinical Cardiac Electrophysiology. Philadelphia: Lippincott Williams & Wilkins; 2002.

Part 7.3: Management of Symptomatic Bradycardia and Tachycardia. Circulation. 2005;112(24_suppl):IV-67-IV-77. doi:10.1161/circulationaha.105.166558.

Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18_suppl_3):S729-S767. doi:10.1161/circulationaha.110.970988.

Rosenbaum F, Hecht H, Wilson F, Johnston F. The potential variations of the thorax and the esophagus in anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome). American Heart Journal. 1945;29(3):281-326. doi:10.1016/0002-8703(45)90333-4.

Surawicz B, Knilans T, Chou T. Chou’s Electrocardiography In Clinical Practice. Philadelphia: Saunders; 2001.

Wolff L, Parkinson J, White P. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. American Heart Journal. 1930;5(6):685-704. doi:10.1016/s0002-8703(30)90086-5.

Content Reviewer

Stephen Smith, M.D. (@SmithECGBlog)


About author

Tom Bouthillet
Tom Bouthillet - 25 posts

Tom Bouthillet (@tbouthillet) is Editor-in-Chief of ECGMedicalTraining.com (@ECGTraining) and Fire Captain/Paramedic in South Carolina where he is the Emergency Cardiac Care Program Manager and the STEMI and CARES Site Coordinator of his fire department.

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