Pathophysology: Ventricular Arrhythmias

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Monomorphic Ventricular Tachycardia

The pathophysiology underlying monomorphic ventricular tachycardia involves re-entry circuits within the ventricles, most often due to areas of scar tissue from prior myocardial infarction. Let’s break this down:

• Normal cardiac electrical activity originates in the sinus node, propagates through the atria to the AV node, down the bundle branches, and depolarizes the ventricles from endocardium to epicardium.
• In MVT, abnormal automaticity occurs in ventricular tissue, disrupting this organized flow of electricity.
• MVT origins are often near the borders of infarcted tissue and healthy myocardium. The scar forms areas of slowed conduction, allowing re-entry circuits to form.
• This re-entry circuit allows the depolarization wavefront to travel in a continuous loop, causing a rapid, regular ventricular rhythm.
• As this abnormal focus is localized to one area, the QRS complexes generally appear uniform or “monomorphic” on ECG.
• Factors that increase automaticity like electrolyte disturbances or medications can trigger MVT episodes in susceptible individuals.

Polymorphic Ventricular Tachycardia

Polymorphic ventricular tachycardia arises from abnormal electrical conduction and repolarization within the ventricles. The changing QRS complexes represent a propagating wavefront through ventricular tissue that is heterogenous in its repolarization state.

• Polymorphic VT is often triggered by early afterdepolarizations that occur before completion of repolarization. Early afterdepolarizations are triggered by intracellular calcium overload and represent a form of abnormal automaticity.

• Conditions that promote early afterdepolarizations and initiation of polymorphic VT include:

• Structural heart disease like myocardial infarction or cardiomyopathy. These cause regional differences in repolarization due to scar or fibrotic tissue interspersed with surviving myocardial fibers. The heterogeneous repolarization creates dispersion of refractoriness.

• Bradycardia or acquired long QT interval. The increased time spent in repolarization allows the heterogeneity in Action Potential durations to manifest and become arrhythmogenic.

• Electrolyte disturbances like hypokalemia or hypomagnesemia. These directly impair myocardial repolarization through effects on ion channels like IKr.

• Drugs that block potassium channels like class IA and III antiarrhythmics. Delayed repolarization from potassium channel blockade also increases heterogeneity.

• Congenital channelopathies like long QT syndrome. Defective ion channels, especially reduced IKs current, facilitate early afterdepolarizations.

Once triggered by early afterdepolarizations, polymorphic VT is perpetuated by re-entry as the wavefront propagates through recovered and refractory tissue. The changing QRS vectors represent different areas of heterogeneity being recruited. If uncontrolled, polymorphic VT can degenerate into ventricular fibrillation and cause sudden cardiac death. Prompt recognition and treatment is essential.