Normal sinus rhythm depends on organized activation of the atria originating from the sinoatrial node and conduction to the ventricles through the AV node. This synchronized pattern is disrupted in AF. Rapid, disorganized electrical activity overwhelms the sinoatrial node and spreads continuously through the atrial myocardium in a chaotic manner. The irregular fibrillatory waves of AF prevent coordinated atrial contraction, reducing atrial emptying. Variable AV nodal conduction results in an irregular ventricular response, compromising cardiac output. Loss of atrial kick and irregular R-R intervals both contribute to hemodynamic impairment. Heart rate also becomes less responsive to autonomic modulation. Over time, persistent AF leads to electrical and structural remodeling of the atria, perpetuating the arrhythmia.
AF results from a complex interplay of triggers, substrate, and modulating factors. Ectopic foci near the pulmonary veins and superior vena cava provide triggers. Atrial stretch, fibrosis, conduction slowing, and tissue inflammation create an arrhythmogenic substrate. Autonomic tone, ischemia, valvular disease, endocrine factors, genetics, and lifestyle issues modulate AF risk.
The pathogenesis of AVNRT involves the presence of dual atrioventricular (AV) nodal pathways with different electrophysiological properties. The AV node has an unusual structure, with parallel tracks of conducting tissue that allow various routes for impulses to travel from the atria to the ventricles. One pathway has a longer refractory period but faster antegrade conduction velocity (fast pathway). The other has a shorter refractory period but slower antegrade conduction (slow pathway).
During normal sinus rhythm, impulses are conducted antegrade (from atria to ventricles) primarily through the fast pathway due to its faster conduction velocity. Retrograde conduction (from ventricles back to atria) occurs through the slow pathway. AVNRT occurs when a premature impulse traveling down the slow pathway finds the fast pathway still refractory. Instead of colliding with refractory tissue, the impulse conducts retrograde up the fast pathway, setting up a reentrant circuit. This allows repetitive activation circulating within the AV node itself.
The reentrant circuit utilizes the slow pathway for antegrade conduction towards the ventricles, and the fast pathway for retrograde conduction back to the atria. This is known as “slow-fast” AVNRT, which accounts for 95% of cases. The opposite pattern, “fast-slow” AVNRT, is less common. In either case, the end result is ineffective pumping due to the ventricles being bombarded by impulses coming down from the AV node, leading to the symptoms of rapid heart rate, palpitations, and hemodynamic instability in some patients.
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.