Everything you need to know about Wolff-Parkinson-White Syndrome.
History
In 1930, Louis Wolff, John Parkinson and Paul Dudley White published a case series consisting of 11 patients who experienced paroxysmal tachycardia associated with an underlying ECG pattern of sinus rhythm with short PR and bundle branch block/wide QRS. This phenomenon was subsequently named as Wolff-Parkinson-White (WPW) syndrome.
Wolf, Parkinson and White together. Image ecgpedia
Prior case reports
1893: Stanley Kent described lateral atrioventricular (AV) connections and thought these constituted the normal specialized AV conduction system. This work proved controversial and was, in fact, rejected by such notables as Sir Thomas Lewis and Keith Flack.
1893: The work of His clearly established the anatomy of the AV node and His–Purkinje system.
1906: The work of Tawara reinforces the study of His. Moreover, they (His and Tawara) proved that section of the His bundle resulted in complete AV block and described the His–Purkinje system.
1914: In a later study Dr. Kent described lateral connections with node-like structures which he felt constituted the normal AV conduction system.
1915: While the eponym Wolff–Parkinson–White (WPW) syndrome is attributed to the landmark article published by the trio in 1930, other isolated case reports of the same entity were previously reported in the literature by Wilson FN.
1921: While the eponym Wolff–Parkinson–White (WPW) syndrome is attributed to the landmark article published by the trio in 1930, other isolated case reports of the same entity were previously reported in the literature by Wedd AM.
1930: Wolff–Parkinson–White published a case series.
1937: Other pioneer observations include those of Mahaim and Benatt who described connections between the AV node or His bundle to fascicles on ventricular myocardium.
1943: It was clearly Wood et al. who first described the presence of a right-sided accessory pathway (AP) in a patient with an EKG pattern of pre-excitation.
1944: Öhnell described left-sided APs in patients with pre-excitation.
1955: In an important study, Lev and Lerner presented a detailed investigation of 33 fetal and neonatal hearts and found no evidence for any lateral AV communications. They interpreted Kent’s finding of nodal tissue as being really atrial tissue: in neonates there is sparse collagen in the AV groove, and, depending on the angle of the sections, these may be misinterpreted as AV connections. It is, therefore, surprising that the eponym “Kent” bundle is still used to describe abnormal AV connections.
How does differ WPW pattern from WPW syndrome?
- WPW pattern is considered when the pattern is present on the EKG in the absence of symptoms.
- WPW syndrome is considered when the pattern on the EKG and the symptoms coexist (eg, tachyarrhythmias, syncope, etc).
Overview
Wolff-Parkinson-White (WPW) pattern is characterized by abnormal accessory conduction pathway (bundle of Kent) between the atria and the ventricles. AV conduction over the accessory pathway bypasses the AV node resulting in preexcitation of the ventricles. Symptomatic patients (WPW syndrome) classically present with palpitations or syncope that results from supraventricular tachycardia. WPW is more common in males and younger patients.
Criteria
EKG criteria in the context of sinus rhythm.
- Normal P wave.
- PR interval <0.12 sec.
- Delta wave (slurring of initial portion of the QRS). Best seen in leads I, aVL, V5 and V6.
- QRS ≥ 0.12 sec.
- Secondary ST-T changes maybe seen.
In general, there are two types of WPW:
Type A (dominant R wave in V1 lead) may be confused with:
- Right bundle branch block
- Right ventricular hypertrophy
- Posterior myocardial infarction
Type B (negative QRS complex in V1 lead) may be confused with:
- Left bundle branch block
- Anterior myocardial infarction
Delta wave
Delta wave is slurring of initial portion of the QRS. It can be positive or negative depending on the lead and is often associated with short PR interval.
EKG
37-year-old male with history of WPW syndrome. Notice the delta waves (red arrows) in I, aVL, V4-V6 and the short PR interval. Negative delta waves are also present in leads III and aVF.
What Is an accessory pathway?
Accessory pathways (AP) are abnormal congenital connections between the atria and ventricles, bypassing the AV node altogether. Some people with an accessory pathway have a normal EKG at baseline because the accessory pathway is electrically active only when there is a fast. Therefore, some people with accessory pathways can have completely normal EKG. AP often have more rapid conduction, but longer refractory periods than the AV node. As the impulse travels through the ventricles it can conduct retrograde through the accessory pathway from ventricle to atrium. This lead a reentrant pathway that results in atrioventricular reentrant tachycardia (AVRT), which accounts for up to ~85% of SVT in WPW. Orthodromic AVRT (antegrade through AV node, retrograde through accessory pathway) accounts for ~90% of AVRT in WPW.
Accessory pathways location by EKG
1- Algorithm using the Delta wave.
- If Delta wave positive in V1, aVF and negative in aVL = Left lateral.
- If Delta wave positive in V1, aVL and negative in aVF = Left posterior/septal.
- If Delta wave positive in aVL and negative in V1/aVF = Right posterior/septal.
- If Delta wave positive in aVF/aVL and negative in V1 = Right lateral/anterior.
Where:
- (+) it means positive.
- (-) it means negative.
- (R) it means right.
- (L) it means left.
- (=) it means location.
2- Algorithm using the R/S ratio.
Based on in this paper, they studied 142 patients with a single anterogradely conducting AP.
- 55 patients with left free wall APs showed R/S-V1 ≥0.5.
- 47 (98%) of 48 patients with left anterior or lateral APs showed R/S-aVF ≥1.
- All seven patients with left posterolateral or posterior APs showed R/S-aVF <1.
- All nine patients with right-and-left midseptal or posteroseptal APs showed R/S-V1 <0.5 and R/S-V2 ≥0.5.
- Of 12 patients with right anterior, lateral or anteroseptal APs, 10 (83%) showed R/S-V1 <0.5, R/S-V2 <0.5 and R/S-aVF ≥1.
- Nine (75%) of 12 patients with right posterolateral or posterior APs showed R/S-V1 <0.5, R/S-V2 <0.5, and R/S-aVF <1.
Illustration
Treatment
A patient with known WPW pattern on baseline EKG or prior episode of WPW syndrome-related tachyarrhythmia who presents with an acute tachyarrhythmia will require acute medical management. The patient who presents with an acute tachyarrhythmia can be managed following the "2010 American Heart Association guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care" The first step in this algorithm is determining if the patient has a pulse. If no pulse is identified, CPR should be initiated, and the patient should be managed using the Advanced Cardiac Life Support (ACLS) Cardiac Arrest Algorithm. If a pulse is Identified, then management can proceed using the ACLS Tachycardia Algorithm.
According to the ACLS tachycardia algorithm, patients with persisting tachyarrhythmia who are deemed hemodynamically unstable as determined by identification of hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, or acute heart failure should undergo synchronized cardioversion or defibrillation. A trial of adenosine may be considered for a regular narrow complex tachycardia.
For patients who have WPW syndrome, high-risk factors, or strong preference, radiofrequency catheter ablation can be curative and has high success rates with low rates of complications.
Issues
Patients with atrial fibrillation and rapid ventricular response are often treated with amiodarone or procainamide. Procainamide and cardioversion are accepted treatments for conversion of tachycardia associated with Wolff Parkinson White syndrome (WPW). In acute AF associated with WPW syndrome, the use of IV amiodarone may potentially lead to ventricular fibrillation in some reports and thus should be avoided.
AV node blockers should be avoided in atrial fibrillation and atrial flutter with Wolff Parkinson White syndrome (WPW). In particular, avoid adenosine, diltiazem, verapamil, and other calcium channel blockers and beta-blockers. They can exacerbate the syndrome by blocking the heart's normal electrical pathway and facilitating antegrade conduction via the accessory pathway.
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Related articles
- Sinus arrhythmia
- Sinus bradycardia
- Sinus tachycardia
- Supraventricular tachycardia (SVT)
- Atrial fibrillation
- Focal atrial tachycardia
- Multifocal atrial tachycardia
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