Wolff–Parkinson–White syndrome: Difference between revisions

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==Clinical Features==
==Clinical Features==
*Suspect in any patient with ventricular rate >300
*Suspect in any patient with ventricular rate >300
*Many are asymptomatic
===Infants===
===Infants===
*Irritability, feeding intolerance
*Irritability, feeding intolerance

Revision as of 20:06, 18 March 2019

Background

  • Abbreviation: WPW
  • Congenital pre-excitation syndrome
  • Presence of an accessory electrical pathway between atria and ventricles predisposing to supraventricular tachycardia
  • Associated with certain genetic predispositions, Ebstein anomaly, and hypokalemic periodic paralysis[1] [2]

Type A

  • Delta wave and QRS complex predominantly upright in precordial leads [3]
  • Dominant R wave (greater than S amplitude) in V1 may have appearance of right bundle branch block [4]

Type B

  • Delta wave and QRS complex predominantly negative in V! and V2
  • Delta wave and QRS complex predominantly positive in other precordial leads [5]
  • Appearance of left bundle branch block [6]

Orthodromic Type

  • Most common variant (~95% of cases)
  • Accessory pathway (Kent bundles) allows retrograde reentry conduction
  • QRS narrow (delta wave absent)
    • Referred to as 'concealed' accessory pathway [7]
  • May see ST depression, TWI
  • Rate 150-250 bpm

Antidromic Type

  • Least common variant (~5% of cases)
  • Accessory pathway used for anterograde conduction
  • QRS wide, delta wave present
  • Rate 160-220 bpm, regular

Atrial Fibrillation and Flutter[8]

  • Atrial fibrillation in up to 20% of patients with WPW
    • Irregular rhythm, wide QRS complexes
    • Changing QRS complexes in shape and morphology
    • Axis remains stable as opposed to polymorphic VT
  • Atrial flutter in ~7% of patients with WPW
    • Similar features to atrial fibrillation with WPW
    • Except regular rhythm
    • Easily mistaken for monomorphic ventricular tachycardia
    • Note that if unclear, always safest to assume VT and treat with shock
  • Treatment with AV nodal blocking agents (adenosine, beta-blockers, calcium-channel blockers, amiodarone, digoxin) may incite ventricular fibrillation or ventricular tachycardia
  • "Manifest WPW" = degeneration into VT or VF

Clinical Features

  • Suspect in any patient with ventricular rate >300
  • Many are asymptomatic

Infants

  • Irritability, feeding intolerance
  • CHF
  • Intercurrent febrile illness

Children

  • Chest pain, palpitations
  • Shortness of breath
  • Syncope/near-syncope

Adults

  • Sudden onset "racing heart"

Differential Diagnosis

Palpitations

Evaluation

Workup

Evaluation

Although the ECG and an electrophysiology study are diagnostic, the characteristic features are not always seen on ECG

  • Short PR interval - <0.12sec
  • Delta wave / slurred upstroke
    • Due to early activation of ventricular myocardium
  • QRS duration > 0.10 sec
    • Represents a fusion beat
  • Dominant R wave in V1, Type A WPW
    • Left sided accessory pathway
  • Dominant S wave in V1, Type B WPW
    • Right sided accessory pathway
  • Tall R waves in V1-V3 with T wave inversion
    • Mimic RVH
  • "Negative" delta waves in III and aVF
    • Appear as pseudo-infarct Q waves
    • Mimics prior inferior infarct

Management

Orthodromic

Treat like paroxysmal SVT

  • Unstable
    • Cardioversion (synchronized)
    • Adult: 50-100 J
    • Peds: 0.5-2 J/kg
  • Stable
    • Calcium channel blockers, beta-blockers, procainamide, or adenosine
    • Procainamide safe irrespective of type of pathway conduction

Antidromic

Treat like ventricular tachycardia

  • Synchronized cardioversion
    • Adult: 50-100 J
    • Peds: 0.5-2 J/kg
    • Procainamide: 20-50mg/min IV over 30min (up to 17mg/kg, hypotension, or 50% widening of QRS complex); mainenance 1-4 mg/min
      • Avoid if prolong QT or CHF
    • Amiodarone with 'ABCD' drugs ie adenosine, beta-blockers, calcium-channel blockers, digoxin
  • Wide-complex, irregular (presumed preexcited A-fib)
    • Unsynchronized cardioversion (200J)

Atrial Fibrillation and Atrial Flutter

  • Stable
    • Procainamide 20-50 mg/min until arrhythmia suppressed
    • Synchronized cardioversion, 100 - 200 J
  • Unstable - synchronized cardioversion
    • Consider higher joule dosage and frequency of repeats than for stable
  • Avoid AV nodal blocking agents

Disposition

Discharge

  • Consider if dysrhythmia was easily terminated and can arrange outpatient EP study with possible RF catheter ablation
  • Consider consulting cardiologist regarding outpatient beta-blockers vs. more potent medications (amiodarone, sotalol, flecainide, etc.)

Admit[9]

See Also

External Links

WPW with AFIB

References