Wolff–Parkinson–White syndrome: Difference between revisions

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==Diagnosis==
==Diagnosis==
''Although the ECG and an electrophysiology study are diagnostic, the characteristic features are not always seen on ECG''
''Although the ECG and an electrophysiology study are diagnostic, the characteristic features are not always seen on ECG''
#Short PR interval - <0.12sec
*Short PR interval - <0.12sec
##Due to loss of normal AV node conduction delay
**Due to loss of normal AV node conduction delay
##Differentiate from [[premature junctional complex]]
**Differentiate from [[premature junctional complex]]
#Delta wave / slurred upstroke
*Delta wave / slurred upstroke
##Due to early activation of ventricular myocardium
**Due to early activation of ventricular myocardium
#QRS duration > 0.10 sec
*QRS duration > 0.10 sec
##Represents a fusion beat
**Represents a fusion beat
#Dominant R wave in V1, Type A WPW
*Dominant R wave in V1, Type A WPW
##Left sided accessory pathway
**Left sided accessory pathway
#Dominant S wave in V1, Type B WPW
*Dominant S wave in V1, Type B WPW
##Right sided accessory pathway
**Right sided accessory pathway
#Tall R waves in V1-V3 with [[T wave]] inversion
*Tall R waves in V1-V3 with [[T wave]] inversion
##Mimic RVH
**Mimic RVH
#"Negative" delta waves in III and aVF
*"Negative" delta waves in III and aVF
##Appear as pseudo-infarct Q waves
**Appear as pseudo-infarct Q waves
##Mimics prior inferior infarct
**Mimics prior inferior infarct


==Treatment==
==Treatment==

Revision as of 20:43, 2 May 2016

Background

  • Abbreviation: WPW

Orthodromic Type

  • More common type occuring ~95% of the time
  • Accessory pathway (Kent bundles) is used for retrograde reentry conduction
  • QRS narrow (delta wave absent)
  • May see ST depression, TWI
  • Rate 150-250 bpm

Antidromic Type

  • Least common type occuring ~5% of the time
  • Accessory pathway used for anterograde conduction
  • QRS wide, delta wave present

Atrial Fibrillation and Flutter[1]

  • Atrial fibrillation in up to 20% of patients with WPW
    • Irregular rhythym, 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 rhythym
    • Easily mistaken for regular rate VT
  • Treatment with AV nodal blocking agents (adenosine, BBs, CCBs, 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

Differential Diagnosis

Palpitations

Diagnosis

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

Treatment

Orthodromic

Treat like paroxysmal SVT'

  • Unstable
    • Cardioversion (synchronized)
    • Adult: 50-100 J
    • Peds: 0.5-2 J/kg
  • Stable
    • CCBs, BBs, 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: 17mg/kg IV over 30min (up to 50mg/kg or 50% widening of QRS complex)
    • Amiodarone with 'ABCD' drugs ie adenosine, BBs, CCBs, digoxin
  • Wide-complex, irregular (presumed preexcited A-fib)
    • Unsynchronized cardioversion (200J)

Atrial Fibrillation and Atrial Flutter

  • Stable - synchronized cardioversion, 100 - 200 J
  • Unstble - procainamide or ibutilide
  • Avoid AV nodal blocking agents

Disposition

  • Discharge:
    • Consider if dysrhythmia was easily terminated and can arrange outpt EP study with poss RF catheter ablation
    • C/w with cardiologist regarding outpt beta-blockers vs. more potent medications (amiodarone, sotalol, flecainide, etc.)
  • Admit or transfer to center with electrophys[2]:

See Also

WPW with AFIB

References

  1. Burns E. Wolff-Parkinson-White Syndromes. Life in the Fast Lane. http://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/.
  2. Ellis CR et al. Wolff-Parkinson-White Syndrome Treatment & Management. eMedicine. Dec 4, 2015. http://emedicine.medscape.com/article/159222-treatment#showall.