Tachycardia: Difference between revisions

The pathophysiology of atrial fibrillation is complex and incompletely understood.<cite>Schotten</cite> In atrial fibrillation there is chaotic depolarization from multiple wavelets, self-perpetuating micro re-entry circuits. In most patients the trigger of atrial fibrillation results from extra beats in from the pulmonary veins. This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (e.i. the autonomic nerve system). These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. The ability of the atria to sustain atrial fibrillation is dependable on atrial structural changes (fibrosis/inflammation). Atrial fibrillation induces electromechanical changes in the atrium. These changes make it easier for AF to perpetuate; AF begets AF. Due to the fast and rapid activation of the atria, there is no functional mechanical activity left. This results in the most feared complication of atrial fibrillation, namely forming of blood clots (with for instance stroke as a result). The atrial standstill does not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage. The strokes resulting from atrial fibrillation are often more severe than other causes of stroke.