Pathophysiolgy

Atrial fibrillation is a supraventricular arrhythmia.

The exact mechanisms of Afib are not well understood. Suggested mechanisms include:

• Volume overload, hemodynamic stress → atrial hypertrophy and/or dilatation

• Atrial ischemia

• Inflammation of the atrial myocardium

• Altered ion conduction by the atrial myocardium

The new onset of Afib triggers a vicious circle that can ultimately lead to long-standing Afib with atrial remodeling:

1. Afib is triggered by one or both of the following

   • Bursts of electrical activity from automatic foci near the pulmonary veins or in diseased, fibrotic atrial tissue

   • Pre-excitation of the atria as a result of aberrant pathways (e.g., WPW syndrome)

2. Afib is sustained by re-entry rhythms and/or rapid focal ectopic firing

   • Re-entry rhythms are more likely to occur with enlarged atria, diseased heart tissue, and/or aberrant pathways (e.g., WPW syndrome).

3. Atrial remodeling

   • Electrophysiological changes in the atria occur within a few hours of Afib onset (electrical modeling).

   • If Afib persists, atrial fibrosis and dilatation (structural remodeling) occur within a few months.

   • Electrical and structural remodeling increase susceptibility to Afib, resulting in a vicious circle.

   
   

Effects of Afib

• The atria contract rapidly but ineffectively and in an uncoordinated fashion → stasis of blood within the atria → risk of thromboembolism and stroke

• Irregular activation of the ventricles by conduction through the AV node → tachycardia