Wolff–Parkinson–White syndrome: Difference between revisions
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**Except regular rhythym | **Except regular rhythym | ||
**Easily mistaken for regular rate VT | **Easily mistaken for regular rate VT | ||
*Treatment with AV nodal blocking agents (adenosine, | *Treatment with AV nodal blocking agents (adenosine, beta-blockers, CCBs, amiodarone, digoxin) may incite [[ventricular fibrillation]] or [[ventricular tachycardia]] | ||
*"Manifest WPW" = degeneration into VT or VF | *"Manifest WPW" = degeneration into VT or VF | ||
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**Peds: 0.5-2 J/kg | **Peds: 0.5-2 J/kg | ||
**Procainamide: 17mg/kg IV over 30min (up to 50mg/kg or 50% widening of QRS complex) | **Procainamide: 17mg/kg IV over 30min (up to 50mg/kg or 50% widening of QRS complex) | ||
**Amiodarone with 'ABCD' drugs ie adenosine, | **Amiodarone with 'ABCD' drugs ie adenosine, beta-blockers, CCBs, digoxin | ||
*Wide-complex, irregular (presumed preexcited A-fib) | *Wide-complex, irregular (presumed preexcited A-fib) | ||
**Unsynchronized cardioversion (200J) | **Unsynchronized cardioversion (200J) | ||
Revision as of 10:52, 3 August 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, beta-blockers, 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
- Arrhythmias:
- Non-arrhythmic cardiac causes:
- Psychiatric causes:
- Drugs and Medications:
- Alcohol
- Caffeine
- Drugs of abuse (e.g. cocaine)
- Medications (e.g. digoxin, theophylline)
- Tobacco
- Misc
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
- Due to loss of normal AV node conduction delay
- Differentiate from premature junctional complex
- 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: 17mg/kg IV over 30min (up to 50mg/kg or 50% widening of QRS complex)
- Amiodarone with 'ABCD' drugs ie adenosine, beta-blockers, CCBs, digoxin
- Wide-complex, irregular (presumed preexcited A-fib)
- Unsynchronized cardioversion (200J)
Atrial Fibrillation and Atrial Flutter
- Stable - synchronized cardioversion, 100 - 200 J
- Unstable - synchronized cardioversion
- Consider higher joule dosage and frequency of repeats than for stable
- Procainamide or ibutilide
- 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 or transfer to center with electrophys[2]
- Patients with chest pain, CHF, electrolyte imbalance, or required cardioversion
- Syncope
- Uncertain diagnosis (wide-complex tachycardia)
- Significant associated structural heart disease (MVP, cardiomyopathy)
- Family history of Sudden cardiac death
- Atrial flutter or atrial fibrillation
See Also
External Links
References
- ↑ Burns E. Wolff-Parkinson-White Syndromes. Life in the Fast Lane. http://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/.
- ↑ Ellis CR et al. Wolff-Parkinson-White Syndrome Treatment & Management. eMedicine. Dec 4, 2015. http://emedicine.medscape.com/article/159222-treatment#showall.