• Ventricular tachycardia (VT) arises when irritable impulses are sent from ventricular automaticity foci in quick succession at a fast rate (> 100 bpm). Because the impulses don’t go through the His-Purkinje pathway, conduction to the ventricles is inefficient resulting in widened QRS complexes, which could be difficult to differentiate from SVT with aberrancy that also has widened QRS's running at a fast rate.
• There are two main types of VT: monomorphic (with identical QRS's) and polymorphic (with varying QRS's).
Monomorphic VT is further classified into scar-related VT (caused by abnormal myocardial tissue as a result of certain structural heart diseases, e.g. ischemic heart disease, hypertrophic or infiltrative cardiomyopathy) and idiopathic VT (not associated with structural heart disease)
Polymorphic VT is caused by acute myocardial ischemia (most common) that can quickly degenerate to ventricular fibrillation causing cardiac arrest, and is also seen in various inherited arrhythmias or channelopathies.
• There are 3 main mechanisms causing VT including:
Ectopy: arises from damaged or infarcted tissue in acute myocardial ischemia
Reentry: commonly arises from scarred tissue in structural heart diseases
Afterdepolarization: early or delayed afterdepolarizations in Torsades or CPVT, respectively
• VT is "sustained" if lasted ≥ 30s or related with syncope or hemodynamic instability.
