Atrial Flutter (AFL)

Recognize it on the monitor - a regular narrow-complex tachycardia locked near 150 is 2:1 flutter until proven otherwise. The 12-lead shows flutter waves with no isoelectric line between QRS complexes, a picket-fence or sawtooth pattern in the inferior leads, and conduction that may be 2:1, 3:1, 4:1, or variable from Wenckebach.

Rate control first - esmolol 0.5 mg/kg IV bolus followed by 50 to 300 mcg/kg/min, or a calcium channel blocker such as verapamil 5 to 10 mg IV or diltiazem. The RACE II target of under 110 bpm is adequate; strict control below 80 buys nothing but polypharmacy.

Unstable patient - synchronized cardioversion. New-onset atrial flutter often converts with only 50 J, monophasic or biphasic; escalate as needed.

Before an elective cardioversion - be certain the flutter is new-onset and exclude intracardiac thrombus. TEE is the modality of choice because it visualizes the atrial appendage, where thrombus usually sits.

Chemical conversion - ibutilide 1 mg in 10 mL saline infused over 10 minutes converts new-onset flutter about 90% of the time and may be repeated once, but it can induce torsades, so monitor for 4 to 8 hours after the dose. Amiodarone 150 mg IV over 10 minutes, then 1 mg/min for 6 hours and 0.5 mg/min for 18 hours, also converts flutter.

Postop prophylaxis - beta blockers and calcium channel blockers prevent atrial flutter after thoracic and cardiac surgery.

Hunt the trigger - send electrolytes, thyroid function, and a CBC for anemia, and look for infection and hypoxia. Correcting these lowers the threshold for controlling rate and symptoms; pulmonary function testing is worth having, since lung disease correlates strongly with atrial arrhythmias.

Stroke risk equals atrial fibrillation - CHA2DS2-VASc stratifies annual embolic stroke risk, roughly 1.3% per year at one point and 2.2% at two.

Preop echo - the value is in what underlies the flutter. Dilated atrial chambers signal chronicity and fibrosis, LV ejection fraction may be the cause or the consequence through tachycardia-induced cardiomyopathy, and atrial or ventricular thrombus changes the cardioversion plan.

EP lab cases - radiofrequency ablation of the cavotricuspid isthmus cures typical flutter about 95% of the time. Sedation with an opiate plus a benzodiazepine is one approach; general anesthesia is preferred when extensive ablation or external cardioversion is expected, and in children and young adults. Antiarrhythmics are usually stopped 3 to 5 half-lives, about 2 to 3 days, beforehand, patients fast at least 6 hours, and remote defibrillation pads go on so the sterile field is not compromised.

Atrial flutter (AFL) is a macro-reentrant atrial tachycardia and the second most common arrhythmia after atrial fibrillation. The atria depolarize around a fixed circuit at roughly 300 beats per minute; the AV node filters the impulses, most often 2:1, producing the classic ventricular rate near 150. Typical, cavotricuspid isthmus-dependent flutter circles the right atrium bounded by the tricuspid annulus, crista terminalis, inferior vena cava, and coronary sinus os, giving sawtooth flutter waves with no isoelectric line in II, III, and aVF. Atypical flutter uses non-isthmus circuits, usually around atriotomy scars or prior ablation lines.

It clusters with COPD, pulmonary hypertension, and heart failure, and isolated flutter in a structurally normal heart is rare. Sustained rapid conduction causes hypotension, syncope, tachycardia-induced cardiomyopathy, and embolic stroke.