Wolff-Parkinson-White syndrome

Question 1

What is the only electrical connection between the atria and ventricles?

Answer 1

His bundle

Question 2

What is WPWS?

Answer 2

An accessory electrical pathway between the atria and ventricles in addition to the His bundle. Usually found on the left side of the heart and has no AV node to delay conduction causing ventricular pre-excitation which manifests as a slurred upstroke ‘delta wave’ on ECG.

Question 3

What is the difference between WPW syndrome and pattern?

Answer 3

Syndrome = symptomatic patients with typical ECG abnormality

Pattern = asymptomatic patient with typical ECG abnormalities

Question 4

How common is WPWS? Who does it usually affect?

Answer 4

Prevalence of WPW in general population 0.1-0.3%

Male to female ratio is 2:1

At any age but most common in 30-40yrs

Question 5

What are the risk factors for WPW?

Answer 5

Usually congenital accessory pathway

Risk factors:

• Ebstein’s anomaly - strong
• congenital cardiac defects - ASD, VSD, TGA, CoA
• dextrocardia
• cardiac rhabdomyomas (in tuberous sclerosis)
• mitral valve prolapse
• HOCM or other cardiomyopathies
• Marfan’s

NB: Ebstein’s anomaly - malformation of tricuspid valve and RV.

Question 6

Where is the accessory pathway usually found in WPW?

Answer 6

• 40-60% left lateral
• 20% right or posteroseptal area

90% are rapidly conducting (unlike AV node which slows stimulation rates)

Question 7

What is the typical ECG finding in WPWS?

Answer 7

Delta wave - slurred upstroke at the initiation of the QRS complex

Usually there is physiological delay of conduction at AV whereas in WPW conduction from AP causes part of ventricle to be pre-excited early

Question 8

What is the typical heart rate in WPWS?

Answer 8

When it causes a tachycardia this can be between 150-240 bpm - no P waves will be seen

Question 9

What are the most common arrhythmias diagnosed in WPWS?

Answer 9

• AVRT - MOST COMMON arrhythmia in WPW affecting 70-80% -
  
  • ORT (orthordromic) - AV node → His → PFs → AP → rapid atrial activation = narrow complex tachycardia with a short RP interval
  • ART (antidromic) - AP → Purkinje fibres = wide QRS tachycardia and therefore confused with VT
• atrial fibrillation - 10-35% - can result in VF due to rapid ventricular stimulation and cause death
• atrial flutter/tachy - 5-10% - can result in VF
  *

Question 10

What are the signs and symptoms of WPWS?

Answer 10

Asymptomatic or

Symptomatic presenting with AVRT or other acute arrhythmia:

• Palpitations
• Dizziness (acute arrhythmia*)
• SOB *
• Chest pain *
• Atrial fibrillation/flutter - HR 150-240bpm in both
• Congenital cardiac abnormalities

Uncommon:

• sudden cardiac death - usually in fast HR
• syncope and presyncope

Question 11

What investigations would you do for WPWS?

Answer 11

1st line - ECG - diagnosis and localisation of the accessory pathway for ablation

Then:

Echo- up to 20% have congenital abnormalities in WPW so check ?hypertrophic cardiomyopathy, Ebstein’s anomaly and other congenital heart disease

Treadmill exercise test - increases sympathetic stimulation so may see intermittent pre-excitation or disappearance of pre-excitation in exercise

Electrophysiology study - location and physiology of AP, number of APs and properties

Question 12

How can you tell where the accessory pathway is located from an ECG?

Answer 12

Question 13

What abnormalities are shown?

What is this condition ?

1. Normal variant
2. Sick sinus syndrome
3. Wolff-Parkinson-White syndrome
4. Long QT syndrome
5. Hyperkalaemia
6. Torsade de pointes tachycardia

Answer 13

• Short PR interval (pre-excitation),
• slurred upstroke to QRS (delta wave)
• and broad QRS are present on the ECG.

This is WPW syndrome - because of preexcitation on ECG and paroxysmal narrow complex tachycardia (AVRT symptoms) is WPW. Due to prresence of an accessory pathway that links the atria and ventricles. Left sided is more common. IMPORTANT because if they develop AF in this syndrome, it will be conducted rapidly down the accessory path and can cause VF and sudden death (?FH). So must refer to cardiologist to ablate this pathway to cure them of the syndrome.

• Hyperkalaemia = tall tented T waves, wide QRS, absent P waves and “sine wave” appearance*
• Torsades de pointed = VT with a varying access due to a raised DT interval*

Question 14

Question 15

Must there be delta waves to diagnose WPWS?

Answer 15

No - they may be absent in concealed retrograde-only AP or an AP with intermittent pre-excitation.

Question 16

Is this a right or left AP?

Answer 16

Right lateral accessory pathway

In a patient with Ebstein’s anomaly

Question 17

What is shown?

Answer 17

WPW

Question 18

Answer 18

Adenosine is diagnostic not therapeutic primarily.

Question 19

Describe the conduction pathways of the heart.

Answer 19

Starts at SA node in RA then travels to AV node as below etc etc

Question 20

What are the causes of RBBB vs LBBB?

Answer 20

RBBB - atrial septal defect

LBBB - aortic stenosis and ischaemia

Question 21

What type of SVT is shown?

Answer 21

Atrial flutter with pre-excitation due to accessory pathway

Question 22

What is the management of WPW?

Answer 22

Acute management:

If haemodynamically unstable → DC cardioversion

Stable tachycardia → Valsalva/carotid sinus massage then IV adenosine → temporary pacemaker → DC cardioversion

Treat AF/flutter as normal.

Long term management:

Catheter ablation - offered to all symptomatic or high risk patients e.g. bus drivers or pilots. If asymptomatic may be monitored. Should not be done during pregnancy.

+/- anti-arrhythmics - flecainide, sotalol, amiodarone etc.

Question 23

What are the complications of WPW?

Answer 23

Sudden cardiac death

Catheter ablation complications e.g. vascular access, catheter manipulation, septal puncture, bleeding, haematoma, DVT, fistula, pseudoaneurysm. Major ones include valvular damage, dissection of coronary arteries, perforation of myocardium.

Question 24

What is the prognosis with WPW?

Answer 24

If symptomatic should have catheter ablation as this has high efficacy and low risk

Asymptomatic patients are unlikely to progress but may be monitored.