Atrial flutter, also known as intra-atrial re-entrant tachycardia, is a regular or regularly irregular tachycardia characterized by atrial activity at a rate of 250–400 beats/min. These contractions are thought to be due to a re-entrant or circus rhythm originating in the atria and involving a micro-re-entrant loop within the atrial tissue and some form of anatomic obstacle that creates a discontinuity in conduction (fibrosis, surgical suture site, valve annulus). Because the AV node cannot transmit such rapid impulses, some degree of AV block is virtually always present, and the ventricles respond to every 2nd–4th atrial beat. Occasionally, the response is variable and the rhythm appears irregular.
In older children, atrial flutter usually occurs in the setting of congenital heart disease; neonates with atrial flutter frequently have normal hearts.
Atrial flutter may occur during acute infectious illnesses but is most often seen in patients with large stretched atria, such as those associated with long-standing mitral or tricuspid insufficiency, tricuspid atresia, Ebstein anomaly, or rheumatic mitral stenosis. Atrial flutter can also occur after palliative or corrective intra-atrial surgery. Uncontrolled atrial flutter may precipitate heart failure. Vagal maneuvers (such as carotid sinus pressure or iced saline submersion) or adenosine generally produce a temporary slowing of the heart rate.
The diagnosis is confirmed by electrocardiography, which demonstrates the rapid and regular atrial saw-toothed flutter waves.
Atrial flutter usually converts immediately to sinus rhythm by synchronized DC cardioversion, which is most often the treatment of choice. Patients with chronic atrial flutter in the setting of congenital heart disease may be at increased risk for thromboembolism and stroke and should thus undergo anticoagulation before elective cardioversion. Digitalis slows the ventricular response in atrial flutter by prolonging conduction time through the AV node. After digitalization, a type I agent such as quinidine or procainamide is usually needed to maintain adequate control. Type III agents such as amiodarone and sotalol have shown promise and may be useful in patients refractory to type I agents. Other modalities, including radiofrequency and surgical ablation, have been used in older patients with congenital heart disease with moderate success. Neonates with normal hearts who respond to digoxin may be treated for 6–12 mo, after which the medication can often be discontinued.