Tachycardia: Difference between revisions

The pathophysiology of AF is complex and incompletely understood.<cite>Schotten</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>hais</cite> 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).<cite>Patterson</cite> These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change an move through the atria. The ability of the atria to sustain AF is dependable on atrial structural changes (fibrosis/inflammation). AF induces electromechanical changes in the atrium. These changes make it easier for AF to perpetuate; AF begets AF.<cite>Wijfels</cite> 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 AF, 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 AF are often more severe than other causes of stroke. Another complication of AF is a tachycardiomyopathy. Due to the constant chaotic activity in the atria, the AV-node can conduct these signals at high rate. The result is a irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>Packer</cite>