• Polymorphic ventricular tachycardia (VT) arises when irritable impulses are sent from multiple ventricular automaticity foci in quick succession at a fast rate (> 100 bpm).
• When a polymorphic VT rhythm is preceded by a prolonged QT interval, it's called torsades de pointes, which often has a twisted ribbon shape. Congenital and acquired long QT syndromes increase the risk of torsades.
• Polymorphic VT rhythm preceded by a normal QT interval is often caused by acute myocardial ischemia, and less often, is seen in various inherited arrhythmias or channelopathies.
• Another special form of polymorphic VT is bidirectional VT, often seen in CPVT and digoxin toxicity.
• If sustained, polymorphic VT can quickly degenerate to ventricular fibrillation and cardiac arrest.
• Torsades de pointes is a form of polymorphic ventricular tachycardia arising from early afterdepolarization (EAD), often triggered by prolonged QT interval.
• ECG shows irregular rhythm with varying QRS complexes and an overall shape of a twisted ribbon.
• This is seen in hypokalemia, hypomagnesemia, hereditary, and acquired long QT syndromes.
• Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a inherited disorder in which there are:
Leaky ryanodine receptor (RyR) in the sarcoplasmic reticulum (SR), which releases Ca++ ions into the cytosol
Dysfunctional calsequestrin (CASQ), a Ca-buffering protein in the SR
• As a result, there is Ca++ overload and increased risk of delayed afterderpolarizations (DAD) and ventricular arrhythmias.
• CPVT is often triggered by catecholamine (adrenergic stimulation).
• The resulting ECG rhythm is bidirectional ventricular tachycardia, which is also seen in digoxin toxicity.
