eMedicine Specialties > Emergency Medicine > Cardiovascular

Wolff-Parkinson-White Syndrome: Treatment & Medication

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

Treatment

Prehospital Care

Therapy for Wolff-Parkinson-White syndrome in the prehospital setting depends upon the patient's degree of stability and the specific dysrhythmia.

Emergency Department Care

Upon presentation, immediately place an IV line in the patient and connect him or her to cardiac, blood pressure, and pulse oximetry monitors. Administer oxygen if the patient is hypoxic. Immediately perform cardioversion on a patient who is grossly unstable. Otherwise, a defibrillator should be readily available. If a patient is in cardiac arrest, treat according to advanced cardiac life support (ACLS) guidelines. Treat dysrhythmias associated with Wolff-Parkinson-White (WPW) syndrome with caution. Although a therapeutic trial of adenosine had previously been advocated by some for both irregular and regular tachycardias and in some cases to distinguish SVT with aberrancy from ventricular tachycardia, this has fallen out of favor recently because of the possibility of degradation of the rhythm to ventricular fibrillation when used indiscriminately.

• Treatment of AFib associated with WPW is necessarily different than for a patient with a normal heart. AFib is an irregular rhythm as opposed to the regular rhythm seen in CMTs.
  • The basic treatment principle in WPW AFib is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. This is in direct contradistinction to the goal of treatment of non-WPW AFib, which is to slow the refractory period of the AVN.
  • If AFib were treated in the conventional manner by drugs that prolong the refractory period of the AV node (eg, calcium channel blockers, beta-blockers, digoxin), the rate of transmission through the accessory pathway likely would increase, with a corresponding increase in ventricular rate. This could have disastrous consequences in a person with AFib in the setting of WPW, possibly causing the arrhythmia to deteriorate into V fib.
  • Thus, standard treatments for non-WPW AFib must be avoided and replaced by cardioversion with the possibility of procainamide as a potential medical therapeutic alternative. Patients presenting with AFib in WPW syndrome are typically very tachycardic and often hypotensive with evidence of hypoperfusion, thus given this unstable state, primary synchronized cardioversion should be the first-line treatment.
  • If the patient is stable, medical therapy with procainamide may be tried. Procainamide (17 mg/kg IV infusion, not to exceed 50 mg/min; hold for hypotension or 50% QRS widening) blocks the accessory pathway, but it has the added effect of increasing transmission through the AV node. Because of the potential for severe hypotension with rapid IV administration, procainamide requires a somewhat slow rate of infusion and also has a relatively slow onset of action, not reaching therapeutic blood levels for 40-60 minutes. Thus, although procainamide may control the AFib rate through the accessory pathway, it may create a potentially dangerous conventional AFib that may require treatment with other medications and/or cardioversion. Prompt cardioversion of patients with WPW syndrome and AFib may be required for any patient who is deteriorating or failing to improve.
  • Medical management may be a viable option in some patients, but it may have unpredictable results. Note that cardioversion is always the treatment of choice in unstable patients. If medical management is recommended it should be under the direction of a cardiologist.
• Treatment of CMTs (regular and generally narrow complex tachycardias) associated with WPW syndrome yields several treatment approaches. Unfortunately, there is a paucity of literature and controlled studies, which makes the chosen treatment less definitively advocated. The two common approaches include cardioversion and the use of adenosine. If adenosine is chosen, all preparations for immediate cardioversion and appropriate resuscitation should be in order in the event of degeneration of the rhythm after adenosine-induced AV nodal blockade.
  • In a stable patient with a regular narrow complex tachycardia (not known to be a result of WPW syndrome), adenosine (6 mg rapid IV push; if unsuccessful, 12 mg rapid IV push) should be the first-line treatment. (Adenosine is contraindicated in heart transplant patients and should be used with caution in patients with severe obstructive pulmonary disease and in patients with a wide QRS complex, unless the diagnosis of PSVT with aberrancy is certain.) When WPW syndrome is known or highly likely, adenosine may only be used with extreme caution and preparation for cardioversion/defibrillation should be immediately available.
  • Once the circus movement is broken, the patient usually converts to sinus rhythm. Note that whether the QRS complex is regular or irregular distinguishes CMTs from AFib on ECG.
    • If the QRS complex is regular and narrow, the arrhythmia may be treated with adenosine as if it were CMT or PSVT, as long as preparations for cardioversion/defibrillation are immediately available.
    • If the QRS complex is irregular, the arrhythmia is likely AFib. In this case, adenosine theoretically could increase the rate and cause clinical deterioration and should not be used.
    • Cardioversion, or in some cases, procainamide, are the treatment choices in these situations (ie, irregular QRS complex), providing the necessary rate control.
    • If in doubt about the regularity of the rhythm, it is safer to err on the side of treating for AFib in the context of WPW syndrome with direct cardioversion.

Consultations

Consult a cardiologist for patients presenting with WPW dysrhythmias.

Medication

The goal of pharmacologic therapy is to break the cyclical transmission of impulses using antiarrhythmics. Drugs such as adenosine and procainamide have proven useful to achieve this goal.

Antiarrhythmic agents

Alter the electrophysiologic mechanisms responsible for arrhythmia.

Adenosine (Adenocard)

Slows conduction time through the AV node, can interrupt reentry pathways through the AV node, and can restore normal sinus rhythm in PSVT, including PSVT associated with WPW syndrome.

Procainamide (Procanbid, Pronestyl)

Increases refractory period of the atria and ventricles (effectively the bypass tract). Myocardiac excitability is reduced by an increase in the threshold for excitation and inhibition of ectopic pacemaker activity.

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