Atrial Fibrillation Research Paper

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Atrial fibrillation is an irregularity in the atria’s electrical impulses, causing a disorderly and rapid rhythm. Paroxysmal atrial fibrillation (also termed intermittent atrial fibrillation) is occurrences of AF that spontaneously halt within 7 days of starting. Episodes of AF can last from a few seconds up to a few days in Paroxysmal atrial fibrillation. The sinoatrial (SA) node is the dominant pacemaker of the heart. Located at the junction of the superior vena cava and the right atrium, it initiates electrical impulses that travel through the atria, causing them to contract and push blood into the ventricles. The impulses then reach the atrioventricular (AV) node, synchronizing
the atria and ventricles, and therefore forming optimal function of the heat. Ectopic foci are abnormal pacemaker sights within the heart (outside of the SA node) that firing randomly and at an abnormal rate. Ectopic atria foci are thought to occur via delayed afterdepolarizations or early afterdepolarizations. Atrial fibrillation includes multiple ectopic foci. Incoordination and chaotic firing of the electrical impulses is the cause of AF (The Pathophysiology, 2017). Triggers are a large category in the pathogenesis of atrial fibrillation.
Triggers to AF include sympathetic or parasympathetic stimulation, bradycardia, tachycardia, atrial premature beats, accessory AV pathways, and acute atrial stretch. After being initiated, atrial fibrillation may be ephemeral (Paroxysmal AF). With the persistence of the triggers and initiators that prompt AF, longer periods will ensue, however AF can persist even in their absence. Persistence in their absence may result from electrical or structural remodeling. The longer AF persists, the more difficult it is to restore sinus rhythm and prevent recurrence (Andadre,
2014). Normal atrial action potentials display voltage changes through the heart beat.
Starting at a negative intracellular membrane potential (resting potential), they become positive when fired (depolarized) during phase 0. They then go through a series of repolarization steps to get back to resting potential. This is an automatic process as an increase in time-dependent depolarization currents carried by Na+ or Ca2+ (making the cell interior more positive) or a decrease in repolarization currents carried by K+ (which keep the cell interior negative) causes progressive time-dependent cell depolarization. As a threshold potential is reached, the cells fire, producing electrical impulses that make the heart beat (Wakili 2011). Abnormalities in Ca2+, Na+, and/or K+ contribute to ion channel dysfunction and structural remodeling of AF (Andrade, 2014). Irregular rhythm of contraction of muscles in the atria usually exceed 200-400 bpm in AF (The Pathophysiology, 2017). The AV node is unable to conduct beats that fast, thus it does so spasmodically. This results in an irregular ventricular rhythm, pooling of blood in the heart chambers, and on average 20% decrease in cardiac output (Leach,
2017). Atrial fibrillation causes electrical and structural remodeling of the heart. Atrial enlargement, cellular hypertrophy, dedifferentiation, fibrosis, apoptosis, and loss of contractile apparatus can result from AF (De Jong, 2011). Over time, myocardial fibrosis develops within the atrial tissue to support the maintenance of AF by shortening affected tissue refractory periods (Cantillon,2014). Fibrosis may increase the number of fibroblasts and alter their properties, promoting AF due to alterations of the electrophysiological behavior of cardiomyocytes attached to fibroblasts (Andrade, 2014).