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Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting over 33 million people worldwide and associated with significantly increased risk of stroke, heart failure, and mortality. Its prevalence increases sharply with age.
AF results from disorganized electrical activity in the atria, most commonly triggered by rapidly firing foci near the pulmonary vein ostia and perpetuated by atrial remodeling. Loss of coordinated atrial contraction reduces cardiac output by 10-30%, and blood stasis in the left atrial appendage promotes thrombus formation and cardioembolic stroke.
Clinical reasoning in AF centers on four decisions: (1) hemodynamic stability — unstable AF requires immediate cardioversion; (2) rate vs. rhythm control strategy; (3) anticoagulation based on CHA₂DS₂-VASc score; (4) identifying and treating reversible causes (thyrotoxicosis, infection, PE, alcohol). The HAS-BLED score estimates bleeding risk. Differentials for irregular rhythm include multifocal atrial tachycardia and frequent ectopy. New-onset AF in a young patient warrants workup for structural heart disease and accessory pathways.
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CHA₂DS₂-VASc estimates stroke risk in non-valvular atrial fibrillation. Points are assigned for CHF, Hypertension, Age ≥75 (2 points), Diabetes, prior Stroke/TIA (2 points), Vascular disease, Age 65-74, and female Sex. Anticoagulation is recommended for scores ≥2 in men, ≥3 in women.
Rate control targets heart rate <110 bpm at rest using beta-blockers, calcium channel blockers, or digoxin without restoring sinus rhythm. Rhythm control aims to restore and maintain sinus rhythm using cardioversion, antiarrhythmics, or ablation. Both strategies have similar outcomes in most patients.
Common precipitants include cardiac causes (heart failure, valvular disease, CAD), pulmonary causes (PE, pneumonia, COPD), metabolic causes (thyrotoxicosis, electrolyte abnormalities), and external triggers (alcohol, caffeine, surgery, sepsis).