FRCA Notes

Wolff-Parkinson-White syndrome

WPW syndrome isn't explicitly mentioned in the curriculum but falls under the item 'abnormal electrocardiogram and arrhythmias'.

Resources

  • WPW is a specific form of AV re-entrant tachycardia
  • It is characterised by the presence of the Bundle of Kent, a fast accessory pathway between the atrium and ventricle, which conducts impulses faster than the AV node
  • Action potentials travelling down this abnormal pathway may stimulate the ventricles to contract prematurely, leading to (supra-)ventricular tachycardia
  • The incidence is 0.1 – 3.0 per 1,000
  • Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway (bypass tracts)
  • These abnormal conduction pathways are formed during cardiac development, can exist in a variety of anatomical locations and in some patients there may be multiple pathways
  • In WPW, the pathway is sometimes referred to as the Bundle of Kent

  • An action potential can be conducted in three ways
    • In both directions (majority)
    • Retrograde only, away from the ventricle (15%)
    • Anterograde only, towards the ventricle (rare)
  • The direction of conduction affects the appearance of the ECG in sinus rhythm and during tachyarrhythmias

  • Action potentials can also be left-sided or right-sided, and ECG features will vary depending on this:
    • Left-sided: produces a positive delta wave in all precordial leads, with R/S >1 in V1 - sometimes referred to as a type A WPW pattern
    • Right-sided: produces a negative delta wave in leads V1 and V2 - sometimes referred to as a type B WPW pattern

  • The features of pre-excitation may be intermittent or subtle
  • They may be more pronounced with increased vagal tone e.g. during Valsalva manoeuvres, or with AV blocking drug therapy


  • Typically a sinus rhythm
  • Short PR interval <120ms due to rapid conduction through the accessory pathway
  • Presence of a delta wave, a slurred slow-rise of the initial portion of the QRS
    • Arises due to fusion between the early depolarization via the accessory pathway and later depolarization via the AV node
  • Up to 70% of patients have a 'pseudo-infarction' pattern with a negative delta wave in aVL, which mimics the Q-wave of a lateral infarction

Tachyarrhythmias

  • <25% of those with WPW suffer episodes of sustained tachycardia
  • Circus re-entrant tachycardia, leading to SVT or even VT
  • Atrial fibrillation, leading to VF

  • Procainamide and amiodarone are the drugs of choice
  • If ventricular arrhythmias do arise they are difficult to treat

Perioperative management of the patient with Wolff-Parkinson-White syndrome


  • Standard pre-operative assessment and investigations
  • Ascertain:
    • Presence of symptoms such as syncope, which increase the risk of sudden death
    • Previous interventions e.g. radiofrequency catheter ablation of the accessory pathway, need for cardioversion
  • Cardiology input may be necessary
  • Appropriate planning e.g. plan in case of dysrhythmia

  • Patients have a tendency to SVT in the perioperative period, although AF can also occur
  • The use of anaesthesia (GA or RA) may unmask previously undiagnosed WPW syndrome

Anaesthetic technique

  • Consider pre-medication to reduce anxiety-induced tachyarrhythmia
  • Consider need for the close presence of the cardiac arrest trolley, attached defibrillator pads or pre-drawn up anti-arrhythmic (procainamide, amiodarone)
  • RA may be preferable to avoid factors that may precipitate dysrhythmia e.g. laryngoscopy, cardiovascular instability, light plane of anaesthesia

  • If GA is chosen, propofol may cause disappearance of the delta wave so is a suitable induction agent
  • Avoid light planes of anaesthesia
  • Sevoflurane and isoflurane have no impact on AV node conduction so are suitable
  • Short-acting, non-depolarising NMBA without histamine release are preferable
  • Opioids and benzodiazepines have no effect on the accessory pathway

Avoid factors which may precipitate tachyarrhythmia

  • Physiological
    • Pain
    • Hypoxia
    • Hypercarbia
    • Hypothermia
    • Electrolyte imbalances

  • Drugs
    • Anti-arrhythmics which may force conduction via the accessory pathway: adenosine, calcium-channel blockers, β-blockers, digoxin
    • Ketamine
    • Glycopyrrolate inc. in combination with neostigmine
    • Atropine

  • Multimodal analgesia to reduce risk of pain-induced tachyarrhythmia
  • Multimodal anti-emesis
  • Ongoing avoidance of factors which can precipitate dysrhythmia