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Sustained Monomorphic Ventricular Tachycardia Pathogenesis

Sustained Monomorphic Ventricular Tachycardia: Pathogenesis Structural Heart Disease: (90% of cases) A ventricular scar forms (in the setting of coronary artery disease or cardiomyopathy) that cannot conduct electrical activity The scar is surrounded by a circular conduction pathway consisting of an ⍺- limb (slow conduction with a fast refractory period) and a β-limb (fast conduction but a slow refractory period) A correctly timed depolarization impulse arrives during the refractory period of the β-limb so it can only propagate through the ⍺-limb The β-limb’s refractory period ends just before the impulse leaves the ⍺-limb of the circular pathway Retrograde depolarization occurs into the ⍺ -limb, creating a self-sustaining closed- loop circuit within the ventricle “Re-entry” cause of tachyarrhythmia Idiopathic Causes: (10% of cases) Structurally normal heart on imaging Trigger(s) such as catecholamines ↑ cyclic adenosine monophosphate Intracellular calcium overload occurs in some ventricular myocytes ↑ Intracellular calcium activates sodium- calcium exchangers Sodium influx into the myocytes During normal myocyte repolarization, the net calcium-mediated depolarization reaches the myocyte threshold for an action potential A triggered action potential (termed a “delayed afterdepolarization”) repeatedly occurs within the ventricle “Triggered activity” cause of tachyarrhythmia Authors: Rahim Kanji Reviewers: Stephanie Happ, Raafi Ali, Derek Chew* * MD at time of publication Sustained Monomorphic Ventricular Tachycardia A wide QRS complex tachycardia originating from the ventricles lasting > 30 seconds. Common mechanisms include re-entry (e.g., scar-mediated) or a ventricular ectopic focus with increased automaticity. Refer to Sustained Monomorphic Ventricular Tachycardia: Clinical findings for details Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 22, 2023 on www.thecalgaryguide.com