Pathophysiology

Pathophysiology of Atrial Fibrillation :
•Intrinsic changes in the electrical activity in the atrial myocytes
o commonly leading to a tachycardia that is irregularly irregular
•High rate electrical activation of the atria
•Difficult for the individual myocytes to remove calcium ions that entered during a previous activation – calcium overload
o activate intracellular enzymes known as “proteases” that can degrade a variety of important cellular proteins – calpain
o mitochondrial abnormalities, and increased production of free radicals (oxidative stress)
-loss of myofibrillar structure, and eventually myocyte death and replacement fibrosis
o If the high rate activity ends quickly, the atria can recover.
• Atrial Fibrosis :
o Normal atrial appendage is very compliant and collapses when not filled with blood.
o This appendage had become a rigid structure, with the fibrosis keeping the appendage open even when empty.
o Thus, while muscular tissue surrounds the fibrous layer, the contractility of the tissue was significantly impaired by the mechanical restraints imposed by the fibrosis.
o This can promote blood stasis in the appendage and thus clot formation.
- Thrombus formation
• At risk for embolization when atrial fibrillation converts to sinus rhythm as organized atrial contractions
• cause the dislodging or fragmentation of the atrial thrombus into the systemic circulation.

o Fibrosis can isolate muscle bundles
- loss of contractile element