Re-entry ventricular arrhythmia

Re-entry ventricular arrhythmia a type of paroxysmal tachycardia occurring in the ventricle.

It is caused by the electric signal not completing the normal circuit, but rather an alternative circuit looping back upon itself.

It develops aa a self-perpetuating rapid and abnormal activation. 

Anatomically defined, a re-entry has a fixed anatomic pathway. 

Anomalous conduction via accessory pathways creates the re-entry circuit that exists between the atria and ventricles. 

Wolff–Parkinson–White syndrome (WPW) is an example of anatomically defined re-entry. 

WPW syndrome is an atrioventricular re-entrant tachycardia (AVRT), secondary to an accessory pathway that connects the epicardial surfaces of the atrium and ventricle along the AV groove.

The majority of time symptomatic WPW syndrome fits the definition of AVRT, however AVNRT (dual AV nodal physiology) exist in ~10% of patients with WPW syndrome creating the possibility of spontaneous atrial fibrillation degenerating into ventricular fibrillation (VF). 

WPW patients are young and do not have structural heart disease, lead to using catheter ablation of the APs with the elimination of the atrial fibrillation as well as the episodes of re-entrant ventricular tachycardia. 

Re-entry does not require the alternative anatomically defined circuit accessory pathways and it may not reside in just one location.

Ventricular fibrillation (VF) that follows ventricular tachycardia (VT) may be described as a functionally defined re-entry problem caused by multiple mini re-entrant circuits spontaneously created within the ventricular myocardium. 

Re-entry due to changes in the properties of the cardiac tissue’s functional core as a result of ischemia, electrolyte, pH abnormalities, or bradycardia are potential causes of functionally defined re-entry.

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