eMedicine Specialties > Emergency Medicine > Cardiovascular

Wolff-Parkinson-White Syndrome: Differential Diagnoses & Workup

Author: Thomas J Hemingway, MD, BS, Attending Physician, Department of Emergency Medicine, Wilcox Memorial Hospital
Coauthor(s): Eric Alexander Savitsky, MD, Associate Clinical Professor of Medicine, Department of Medicine, Division of Emergency Medicine, University of California at Los Angeles Medical Center; Mel Herbert, MD, MBBS, Assistant Professor of Medicine and Nursing, Department of Emergency Medicine, Olive View-University of California at Los Angeles Medical Center
Contributor Information and Disclosures

Updated: Aug 19, 2008

Differential Diagnoses

Atrial Fibrillation
Atrial Flutter
Paroxysmal Supraventricular Tachycardia
Ventricular Tachycardia

Other Problems to Be Considered

Supraventricular tachycardia

Workup

Laboratory Studies

• No specific diagnostic laboratory studies exist for Wolff-Parkinson-White syndrome. The diagnosis is typically made with formal electrocardiographic monitoring in conjunction with clues from the history and physical examination. If laboratory values are obtained, it is reasonable to check electrolytes, including potassium, magnesium, and calcium, which may all potentially contribute to dysrhythmias.

Other Tests

• Electrocardiogram
  • The classic ECG morphology of Wolff-Parkinson-White (WPW) syndrome is described as a shortened PR interval and a slurring and slow rise of the initial upstroke of the QRS complex (delta wave), a widened QRS complex with a total duration greater than 0.12 seconds, and secondary repolarization changes reflected as ST segment–T wave changes that are generally directed opposite the major delta wave and QRS complex. In reality, the ECG morphology varies greatly.
  • Depending upon the location of the accessory pathway in relation to the sinus node and the relative transmission characteristics of the accessory pathway and the AV node, the morphology of the ECG may vary from a classic presentation to near normal.
  • In some cases, the electrical impulse's arrival at the ventricles occurs slightly earlier through the accessory pathway (by not undergoing the typical slowing through the AVN), creating preexcitation.
  • The QRS interval is widened because the ventricles are initially activated via the accessory pathway, which lies outside the normal conducting system, producing an early, albeit relatively slow initial propagation of depolarization forces through the ventricular tissue. This produces the delta wave. The delta wave makes the QRS appear wider than expected and the PR interval somewhat shortened. This is known as a revealed accessory pathway because it is easily identifiable on ECG.
  • WPW syndrome has been described by some as either type A or type B, depending on the appearance of the delta wave/QRS complex in the precordial leads. Type A WPW syndrome is described as having an upright positive delta wave in all precordial leads with a resultant R greater than S amplitude in lead V1. Type B has a predominantly negative delta wave and QRS complex in leads V1 and V2 and becomes positive in transition to the lateral leads resembling that of a left bundle-branch block (LBBB).
  • LGL has a shortened PR interval due to the presence of the accessory pathway bypassing the AVN, but a normal QRS because the accessory pathway (James fibers) connects directly with the His bundle and do not depolarize the ventricles directly but do so through the typical conduction pathway through the His-Purkinje system.
  • In other WPW syndrome cases, arrival of the electrical impulse to the ventricle occurs nearly simultaneously through both the accessory pathway and the AV node.
    • When this occurs, preexcitation is absent and ECG appears normal.
    • Thus, the morphology of the ECG depends directly upon the degree of preexcitation (ie, relative conduction speeds).
  • An accessory pathway that does not manifest on ECG is revealed when the rate exceeds the refractory period of the AV node. This has been described as latent accessory pathway.
    • A latent accessory pathway can conduct both anterograde and retrograde transmissions.
    • An accessory pathway in which only retrograde transmission of impulses can occur is called concealed and is used only during circus movement tachycardias (CMT).
• Although many types of dysrhythmias can occur in a patient with WPW syndrome, the two most common are CMT and atrial fibrillation (AFib). CMT is the more common dysrhythmia of the two.
  • A critically timed premature atrial beat that occurs during the refractory period of the accessory pathway typically initiates CMT. The impulse, therefore, travels solely down the AV node but returns retrograde through the accessory pathway, resulting in CMT (orthodromic conduction).
  • This circus movement tachycardia pattern is termed orthodromic conduction. It results in a narrow complex heart rhythm limited by the refractory period of the AV node. The QRS interval is narrow because the impulses travel antegrade (orthodromically) through the AV node and regular because circus movement occurs at a regular rate.
  • Differential diagnosis of this type of WPW dysrhythmia (orthodromic conduction) includes paroxysmal supraventricular tachycardia (PSVT). Differentiating between the two in an acutely symptomatic patient with a regular rhythm, narrow complex tachycardia is difficult. Cardiac dysrhythmias with rates greater than 220 bpm in adults suggest the dysrhythmia is bypassing the AV node and is suggestive of an accessory pathway or ventricular tachycardia.
  • Orthodromic CMTs are 10-15 times more likely than antidromic CMTs.
  • Antidromic CMTs are wide and potentially faster because of the relatively short refractory period of most accessory pathways. They are termed antidromic because anterograde transmission occurs down the accessory pathway, creating preexcitation of the ventricle adjacent to it. These dysrhythmias are regular due to the nature of the circus movement.
  • The accessory pathways in antidromic CMTs conduct anterograde from the atria to the ventricles and are likely to have the classic delta wave appearance of the QRS on the resting ECG.
  • Differential diagnoses include ventricular tachycardia (V tach), which also is regular (unless it is torsade de pointes) or PSVT with aberrancy. One should initially consider any regular wide-complex tachycardia to be V tach until proven otherwise.
  • Most cases of regular wide-complex CMT associated with WPW syndrome that are treated with adenosine consequently are converted to sinus rhythm.
• AFib in patients with WPW is very common and has an incidence of 11-38%. It also is the deadliest arrhythmia for these patients because of the possibility of deterioration into ventricular fibrillation (V fib).
  • In normal hearts, an individual is protected from exceptionally high ventricular rates by the relatively long refractory period of the AV node. In patients with WPW, however, the accessory pathway often has a much shorter anterograde refractory period, allowing for much faster transmission of impulses and correspondingly higher rates.
  • In addition, sympathetic discharge secondary to hypotension may lead to further shortening of the refractory period and subsequent increases in the ventricular rate. If the rate becomes too high, V fib may result.
  • Note that AFib through an accessory pathway appears as a bizarre, wide-complex, irregular tachycardia on ECG, with rates often in the 250 bpm range or higher. Combining the variables of a rapid rate, widened QRS complex, and unusual/changing QRS complex morphologies in a young patient strongly suggest the diagnosis.²

• Search for CME/CE on This Topic »

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• Supraventricular Tachycardia, Wolff-Parkinson-White Syndrome (Pediatrics: Cardiac Disease and Critical Care Medicine)
• Programmed Electrical Stimulation (Cardiology)
• Ventricular Fibrillation (Pediatrics: Cardiac Disease and Critical Care Medicine)

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