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

Clinical features

Diagnostics

ECG

QRS complex

• 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

Treatment

• 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