Mechanisms of Arrhythmogenesis in Wide Complex Tachycardia

1. Ventricular Tachycardia (VT):

   • VT originates from abnormal electrical activity within the ventricles, typically due to reentrant circuits or enhanced automaticity.
   • Reentrant VT occurs when there is a loop of electrical activity circulating within the ventricles, often secondary to scar tissue from myocardial infarction, cardiomyopathy, or other structural heart diseases.
   • Enhanced automaticity refers to an abnormal focus of cells within the ventricles that spontaneously generate rapid electrical impulses, leading to tachycardia.
   • VT may also occur in the setting of electrolyte disturbances, drug toxicity, or genetic channelopathies.

2. Supraventricular Tachycardia with Aberrancy:

   • In some cases, rapid supraventricular rhythms, such as atrial fibrillation or atrial flutter, can conduct aberrantly through the ventricular conduction system, leading to a wide complex appearance on the ECG.
   • This aberrant conduction occurs when the supraventricular impulse encounters a block or delay within the His-Purkinje system, resulting in aberrantly widened QRS complexes.

3. Preexcited Tachycardia (Wolff-Parkinson-White Syndrome):

   • Wolff-Parkinson-White (WPW) syndrome is characterized by the presence of an accessory pathway (Bundle of Kent) that connects the atria and ventricles, bypassing the normal atrioventricular conduction system.
   • During preexcited tachycardia, impulses travel simultaneously down both the normal conduction pathway and the accessory pathway, resulting in rapid depolarization of the ventricles and a wide QRS complex on the ECG.
   • This can predispose individuals to reentrant tachycardias, such as atrioventricular reentrant tachycardia (AVRT) or atrial fibrillation with rapid ventricular response.

4. Other Rare Mechanisms:

   • Other rare mechanisms of wide complex tachycardia include bundle branch reentrant tachycardia (BBRT), which involves reentrant circuits within the His-Purkinje system, and fascicular tachycardia, originating from the left or right bundle branches.

Overall, the mechanisms of arrhythmogenesis in wide complex tachycardia are diverse and often multifactorial. Differentiating between these mechanisms is essential for guiding appropriate treatment strategies, which may include antiarrhythmic medications, catheter ablation, or implantable devices such as pacemakers or defibrillators. Additionally, addressing underlying causes such as structural heart disease, electrolyte imbalances, or drug toxicity is crucial for long-term management and prevention of recurrence.

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