atrial flutter

Atrial flutter results from a reentrant electrical circuit, most commonly a large loop in the right atrium that rotates around the tricuspid valve annulus using the cavotricuspid isthmus as a critical conduction pathway (typical atrial flutter). It is associated with structural heart disease, COPD, hyperthyroidism, prior cardiac surgery, and often coexists with or precedes atrial fibrillation. On ECG, the hallmark finding is regular sawtooth-shaped flutter waves (best seen in leads II, III, aVF), with atrial rates typically 250-350 bpm. Due to AV node refractoriness, conduction is often fixed (e.g., 2:1, 3:1, or 4:1), producing a regular ventricular rate; irregular conduction ratios can also occur. Clinically patients may present with palpitations, fatigue, dyspnea, or be asymptomatic; hemodynamic instability can occur with rapid ventricular rates. Like atrial fibrillation, atrial flutter carries thromboembolic risk (stroke) due to stasis in the atria, so anticoagulation decisions follow similar CHA2DS2-VASc scoring. Management includes rate control (beta-blockers, calcium channel blockers), rhythm control (antiarrhythmics, cardioversion), and definitive treatment via catheter ablation of the cavotricuspid isthmus, which has a high success rate for typical flutter. Unstable patients require immediate synchronized cardioversion. Anticoagulation should be considered before cardioversion if duration >48 hours or unknown, similar to atrial fibrillation protocols.