Wolff-Parkinson-White syndrome EKG

Wolff-Parkinson-White syndrome Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Differentiating Wolff-Parkinson-White syndrome from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
Approach
History and Symptoms
Electrocardiogram
EKG Examples
Other Diagnostic Studies
Treatment
Risk Stratification
Cardioversion
Medical Therapy
Catheter Ablation
Prophylaxis
Consensus Statement
Case Studies
Case #1
Wolff-Parkinson-White syndrome EKG On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Wolff-Parkinson-White syndrome EKG
CDC onWolff-Parkinson-White syndrome EKG
Wolff-Parkinson-White syndrome EKG in the news
Blogs on Wolff-Parkinson-White syndrome EKG
Directions to Hospitals Treating Deep vein thrombosis
Risk calculators and risk factors for Wolff-Parkinson-White syndrome EKG

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

The Electrocardiogram in WPW

1. Two pathways between the atrium and the ventricle are present.
2. There is a shortened PR interval
   • PR less than 0.12 seconds
   • In most cases it varies between 0.08 and 0.11 seconds
3. A wide QRS with a delta wave.
   • The QRS is 0.11 second or longer
   • Is inversely proportional to the PR (i.e. the shorter the PR, the longer the QRS secondary to greater pre-excitation).
   • The combination of the shortened PR interval and widened QRS is of normal duration
4. The delta wave occurs as the ventricle is activated first via the accessory pathway (AP) and then normal activation follows down the normal pathway.
   • The duration of the delta wave is 0.03 to 0.06 seconds
5. The pattern of ventricular activation is determined by several factors:
   • The location of the accessory pathway: The closer the accessory pathway to the SA node, the quicker the impulse will reach the atrial insertion site of the AP. In contrast, in those patients in whom the AP is located in the far lateral region of the left ventricle, contribution to the AP during NSR may be minimal.
   • The intra-atrial conduction time: Left atrial pathology will prolong the time necessary to reach the left sided AP, drugs can also prolong the time to reach a left-sided pathway.
   • The conduction time over the accessory pathway: The conduction time over the AP depends on the length of the AP and velocity with which the impulse is conducted. Investigators have found that the accessory pathway may vary in length from 1 to 10 mm.
   • The AV conduction time over the normal AV nodal-His-Purkinje pathway
6. Secondary T wave changes:
   • Because of the early asynchronous activation of the ventricle, the sequence of repolarization will be different leading to T wave changes.
   • The T wave polarity is opposite in direction to the delta wave
7. Concealed bypass tracts:
   • If the accessory pathway's contribution to ventricular activation is minimal because of the coincidental arrival of the excitation wavefront over the normal pathway, then this should not be called a concealed accessory pathway.
   • Concealed accessory pathways are those that conduct in a retrograde fashion (ventriculoatrial) only.
   • Antegrade conduction in these patients is absent because the refractory period of the AP in the antegrade direction is longer than the sinus cycle length.
   • When a recurrent tachycardia occurs in association with such concealed bypass, the conduction is called concealed WPW syndrome
   • Are usually located on the left side of the cardiac chambers
   • Consider this if during the tachycardia there is a negative P wave in lead V1, if there is a P wave after the QRS complex
8. Findings are intermittent in 1/2 the cases

Determining the location of the accessory pathway

Check lead V1
Negative delta wave in V1 = right ventricle				Positive delta wave im V1= left ventricle
Negative delta wave and QRS in II, III, AVF	Left axis	Inferior axis		Negative delta wave and QRS in II, III, AVF	Isoelectric or negative delta I, AVL, V5, V6
Posteroseptal	Right free wall	Anteroseptal		Posteroseptal	Lateral

Oversimplification

Histological studies have found that the AP fibers may insert in the septum and not the free wall as above. The location of AP may be impossible to determine in NSR, as it can be complicated by the existence of more than one AP in some patients, the coexistence of congenital lesions, the occasional superimposition of the P wave on the initial portion of the delta wave, and differences in the activation depending on whether the AP is epicardially or endocardially located.

Associated Cardiovascular Abnormalities

1. Type B is found in 5% to 25% of the reported cases of Ebstein's anomaly. Suspect this if there is Type B WPW with RBBB.
2. Also been found in patients with corrected transposition of the great arteries, tricuspid atresia, endocardial fibroelastosis, MVP, cardiomyopathies (hypertrophic obstructive and congestive).

Clinical Manifestations

1. The most common form of paroxysmal tachycardia in these patients is a circus movement tachycardia (CMT) incorporating the AP.
2. The CMT utilizes the following structures: the AV node, the His-Purkinje system, the ventricular myocardium (from the terminal portion of the His system to the ventricular end of the AP), the AP itself, and the atrial myocardium itself from the atrial insertion of the AP to the AV node.
3. This circuit can conduct in both directions:
   • Type I A CMT:

     1. This is the usual form of the CMT in patients with WPW.
     2. Is antegrade through the AV node, VA conduction through the AP.
     3. The QRS complex during the tachycardia shows either normal intraventricular conduction or typical bundle branch block configuration.
     4. Symptoms: Palpitations (97%), dyspnea (57%), anginal pain (56%), perspiration (55%), fatigue (41%), anxiety (30%), dizziness (30%),polyuria (26%).
     5. This is also called orthodromic reentrant tachycardia.
     6. There is no delta wave.
     7. The rate is 140 to 250 bpm.
     8. It is faster than the rate of tachycardia due to reentry in the AV node.
     9. Often triggered by a PAC

1. • Type I B CMT:

     1. Anterograde down the accessory pathway, retrograde in the AVN-His pathway.
     2. The QRS is widened (wide QRS)
     3. This form is rare.
     4. Also called antidromic reentrant tachycardia.

1. • Type II CMT (intra-AV nodal):

     1. Anterograde pathway is an AV nodal slow pathway, the retrograde pathway is an AV nodal fast pathway.
     2. No evidence of ventricular pre-excitation during the tachycardia.

   • Type III CMT (uses two accessory pathways):

     1. Conducts anterograde down one accessory pathway and retrograde up a second accessory pathway.
     2. These patients can also experience atrial tachycardias and ventricular tachycardias.

Atrial Fibrillation in WPW

Can cause life-threatening ventricular rates due to the exclusive AV conduction over the accessory pathway.

1. • Reduces cardiac output.
   • May degenerate into VF, particularly in those with multiple bypass tracts.
2. The only marker identified for degeneration into VF in the literature was the occurrence of RR intervals equal to or less than 205 msec during the a fib
3. Seen in 78 of 256 of Wellen's patients with WPW. Reported incidence is 20 to 35% in other studies.
4. The degree of ventricular preexcitation observed in the EKG during NSR bears no relationship whatsoever to the risk of developing life-threatening ventricular rates during the a.fib.
5. The QRS complexes are wide and bizarre as a result of preexcitation.
6. The ventricular rate is 220 to 360 beats per minute due to the short effective refractory period of the accessory pathway.
7. It is often mistaken for VT.
8. If the atrial rate in atrial fibrillation is greater than 200 BPM then suspect this. The rhythm will also be grossly irregular if it is due to atrial fibrillation. Such a rapid rate would be unusual if it were due to conduction by way of the normal AV conduction system.

Examples

Shown below is an EKG of Wolff-Parkinson-White syndrome demonstrating slurred upstroke of the QRS complex (>110 milli sec), resulting in a delta-wave (arrow). The EKG also shows a short PR interval.

Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/Main_Page

---

Shown below is an EKG showing a slurred upstroke QRS complex which is best appreciated in the precordial leads and a PR interval of less than 120 ms (short PR interval) suggesting WPW syndrome.

Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/Main_Page

---

Shown below is an EKG demonstrating a delta wave in leads V₂, I, aVL, with wide QRS complexes and left axis deviation suggesting WPW syndrome.

Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/Main_Page

---

Shown below is an EKG showing a short PR interval of less than 120 ms, delta waves in leads I, aVF, aVL and chest leads with wide QRS complexes indicating WPW syndrome.

Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/Main_Page

---

For more EKG examples of Wolff-Parkinson-White syndrome click here.