Etiology

Pathophysiology

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 vein ostia (left atrium) 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, especially in atrial appendage → risk of thromboembolism and stroke
- Irregular activation of the ventricles by conduction through the AV node → tachycardia

Typically narrow QRS complex (< 0.12 seconds)
Wide QRS complex may be seen in some situations:
- Aberrant conduction, e.g., bundle branch block or preexcitation (as seen in Afib with WPW)
- Complete AV block with a ventricular escape rhythm
- Ashman phenomenon: intermittent aberrant ventricular conduction results in isolated or short runs of wide QRS complexes

Warning

Wide QRS complex may indicate preexcited Afib or aberrant conduction.

First-line
- Beta blockers: e.g., metoprolol, atenolol, propranolol
  - Via blockade of sympathetic tone
  - Work well both during rest and exercise
  - Preferred when Afib is due to hyperthyroidism and in pregnant patients
  - Avoid in patients with COPD and acute decompensated heart failure (ADHF).
- OR nondihydropyridine calcium channel blockers (ndHP CCBs): e.g., diltiazem, verapamil
  - Work well both during rest and exercise
  - Avoid in patients with ADHF.
  - Can be safely used in heart failure with preserved normal LV systolic function.
Second-line: digoxin; preferred initial therapy for patients with ADHF
- Via increased parasympathetic tone
- This mechanism is effective at rest, when sympathetic tone is low, but it poorly controls ventricular rate during exercise, when high levels of sympathetic tone accelerate AV node conduction.
Third-line: amiodarone; typically reserved for patients in whom all other options have failed