Wolff Parkinson White Syndrome (WPW)

Wolff Parkinson White Syndrome (WPW) is characterized by an abnormal accessory pathway in the heart leading to arrhythmias.


Pathology: Born with an accessory pathway, the bundle of Kent which connects the atria and ventricle. The electrical impulses from the SA node reach the ventricles earlier via the accessory pathway as there is no AV nodal delay in this pathway. This leads to the preexcitation of the ventricle and initiation of ventricular contraction. This ventricular contraction is prolonged when the impulse via the AV nodal pathway reaches the ventricles.


Most common location of the accessory pathway- between the left atrium and free wall of the left ventricle


ECG changes: 

  • Shortened PR interval(typically <120 ms) - because of the early initiation of ventricular depolarization.
  • Prolonged QRS duration (total duration >0.12 seconds)- because of the AV nodal impulse reaching the ventricles after the aberrant impulse.
  • Delta waves- slurred upstroke of QRS complex
  • ST-segment-T wave (repolarization) changes, generally directed opposite the major delta wave and QRS complex, reflecting altered depolarization.


The given ECG shows delta waves marked with red arrows:


The given ECG is suggestive of Wolff-Parkinson-White syndrome (WPW). Its prevalence decreases with age.


Treatment:

Catheter ablation is the treatment of choice.

Anti-arrhythmic drugs like procainamide, amiodarone, quinidine, propafenone, dofetilide are used in slowing conduction in the accessory pathway (prolong refractory period).

IV procainamide is the drug of choice in a hemodynamically stable WPW presenting with atrial fibrillation. 

DC cardioversion is done in hemodynamically unstable patients.


Rate-slowing drugs such as non-dihydropyridine calcium channel blockers (eg, verapamil, diltiazem), beta-blockers, and digoxin are contraindicated in these patients. They increase the refractoriness of the AV node with minimal or no effect on the accessory pathway. This can lead to faster ventricular rates, increasing the risk of ventricular fibrillation.




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