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Acute Coronary Syndromes: A Focus on STEMI10 Topics3 Quizzes
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Acute decompensated heart failure10 Topics3 Quizzes
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Hypertensive Urgency and Emergency Management11 Topics3 Quizzes
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Acute aortic dissection8 Topics2 Quizzes
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Supraventricular Arrhythmias (Afib, AVNRT)10 Topics2 Quizzes
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Ventricular Arrhythmias10 Topics2 Quizzes
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Atrial Fibrillation
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.
Analogy for Atrial Fibrillation
Think of the heart as an orchestra, with the sinoatrial node acting as the conductor. In a healthy heart, the conductor sets a regular rhythm and all sections of the orchestra (the heart’s chambers) follow this rhythm, resulting in a harmonious performance (effective blood pumping).
In atrial fibrillation, it’s as if multiple members of the orchestra start playing their own rhythms, ignoring the conductor. This results in a chaotic, disorganized performance (irregular heartbeats). The music (blood flow) becomes erratic and less effective, which can lead to various complications.
The triggers for AF can be compared to factors that might disrupt an orchestra’s performance, such as a disruptive audience member (ectopic foci), a broken instrument (atrial stretch or fibrosis), or a tired musician (ischemia, valvular disease).
Supraventricular Tachycardia (AVNRT)
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.
Analogy for AVRNT
Think of the AV node as a two-lane highway connecting two cities (the atria and ventricles). One lane is a fast lane with a longer waiting period at the toll booth (longer refractory period but faster conduction velocity), and the other is a slow lane with a shorter waiting period at the toll booth (shorter refractory period but slower conduction).
During normal traffic flow (sinus rhythm), most cars (impulses) prefer to take the fast lane due to its faster speed. Some cars, however, choose to return to the first city (retrograde conduction) via the slow lane.
Now, imagine a situation where a car (premature impulse) traveling down the slow lane reaches the toll booth while the fast lane is still closed (refractory). Instead of crashing into the closed fast lane, the car takes a U-turn and travels back up the fast lane, creating a circular traffic pattern (reentrant circuit).
This circular traffic pattern uses the slow lane for forward travel (antegrade conduction) and the fast lane for backward travel (retrograde conduction). This is like the “slow-fast” AVNRT, which is the most common type. Occasionally, the pattern can be reversed, which is the “fast-slow” AVNRT.
In either case, the result is a traffic jam (ineffective pumping) due to the cities being bombarded by cars coming from the highway (impulses from the AV node), leading to the symptoms of rapid heart rate, palpitations, and hemodynamic instability in some patients.
Reference:
- Wijffels MC, Kirchhof P, Dorp WL, Allessie MA. Pathophysiological mechanisms of atrial fibrillation: A translational appraisal. Physiol Rev. 2009 Oct;89(4):1173-200. doi: 10.1152/physrev.00031.2009.
- Zipes DP, Libby P, Bonow RO, Mann DL, Tomaselli GF, Braunwald E. Braunwald’s heart disease: A textbook of cardiovascular medicine. 11th ed. Philadelphia, PA: Elsevier; 2022.