Pediatric Atrial Flutter Treatment & Management

In children with atrial flutter, medical care should be broadly directed at the following:

• Ensuring hemodynamic stability before, during, and after conversion to sinus rhythm
• Minimizing influences favoring initiation or maintenance of atrial arrhythmias (eg, electrolyte disturbances, pericardial effusion, indwelling atrial lines or catheters)
• Excluding or managing complications (eg, ventricular dysfunction, thromboembolic phenomena)
• Restoring

Drug therapy may be indicated in some children with atrial flutter. Drug therapy in these cases can be classified under the 3 broad headings of ventricular rate control, acute conversion, and chronic suppression.

Thrombosis and thromboembolic events are recognized complications in patients with atrial flutter, particularly in the setting of repaired congenital heart disease. Patients who have thrombi identified on transesophageal echocardiography or have a history of chronic atrial flutter (>2 wk duration) should be treated with a period of anticoagulation (2-4 wk), if hemodynamically and symptomatically tolerated, before undergoing direct current (DC) cardioversion or other conversion of their rhythm.

According to a legal precedent, patients with Mustard repair of transposition of the great vessels and sick sinus syndrome should not receive quinidine without a previously implanted pacemaker. However, quinidine is now recognized to have a detrimental adverse effect profile in general, and it is essentially no longer used in the treatment of rhythm disorders following congenital heart disease. Disagreement surrounds whether this recommendation should be extrapolated to other antiarrhythmics and other forms of repaired congenital heart disease.

Go to Atrial Flutter and Emergent Management of Atrial Flutter for complete information on these topics.

Transfer considerations

As with most symptomatic arrhythmias, conversion should ideally be achieved before transfer, except in the case of a hemodynamically stable patient referred to an institution with clearly superior expertise and facilities for management of pediatric atrial flutter.

Pace-termination of atrial flutter is best performed with a programmable stimulator that is capable of sensing atrial electrograms and delivering single, double, or multiple extrastimuli at adequate output and individually programmable cycle lengths down to 100 milliseconds.

Short discrete ramps or bursts of atrial stimuli are the most likely to produce a type I conversion of atrial flutter (immediate conversion to sinus rhythm), particularly if they can be delivered in or near the flutter circuit. If such a device is unavailable, a pacemaker capable of burst pacing at a specified rate may be used.

If pacing is performed via an esophageal electrode, the device should be capable of delivering stimuli at pulse widths of 9.9-20 milliseconds and outputs of 10-26 mA.

Patients who are treated with atrial antitachycardia pacing should undergo testing to confirm that their device is effective and not proarrhythmic.

R-wave synchronized cardioversion is the mainstay of therapy in patients who are unstable or if other therapies have failed. In patients who are stable and have chronic atrial flutter, perform cardioversion only after documentation of freedom from intracardiac thrombi or following a 2-week course of anticoagulation.

Cardioversion may be performed at increasing doses of 0.5, 1, 2, and 4 J/kg. Newer biphasic waveform defibrillators may allow for lower energy applications.^[13]

Ideally, place defibrillator paddles or pads in an anteroposterior configuration, with the apex paddle located over the mid sternum and the base paddle between the scapulae. An anesthesiologist usually administers a brief general anesthetic, except in truly emergent circumstances that mandate immediate cardioversion.

Hemodynamic instability requires immediate cardioversion as described above. However, patients who are relatively stable may be allowed to remain in flutter while careful consideration of possible interventions is undertaken. The patient should rest in a supine position without undue excitement or agitation. Consider digoxin if not already in use because it frequently increases the conduction ratio and decreases the ventricular rate. However, this effect usually takes many hours.

Medications with the potential to slow the atrial rate without affecting the atrioventricular (AV) node should be used with caution because the conduction ratio often decreases to 1:1 AV association. This may result in a rapid ventricular rate and hemodynamic compromise.

Avoid adrenergic and atropinic agents during sedation or anesthesia for cardioversion. Ketamine is relatively contraindicated. Such agents may result in rapid 1:1 AV conduction, with resultant hemodynamic compromise. On the other hand, insufficient sedation during attempted esophageal overdrive pacing or a failed cardioversion may result in patient distress and 1:1 AV conduction ratio.

Currently, radiofrequency catheter ablation appears to be somewhat effective in treating postoperative intra-atrial reentrant tachycardia in children.

Because the flutter circuits and critical isthmuses are quite variable in these patients, mapping of flutter circuits may be enhanced by 3-dimensional electroanatomical display systems, identification of split potentials, and demonstration of concealed entrainment during pacing.

In patients with atrial flutter, surgical care may include one of the following procedures:

• Correction of hemodynamic lesions that could be causing atrial volume loading
• Specifically placed atrial incisions or cryoablation prophylactically to prevent atrial flutter
• Empiric or map-directed lesions to eliminate documented atrial flutter and its circuits

These surgeries include various modifications and updates to maze procedures and modifications of the Mustard and Fontan procedures. One study reported that a right-sided maze procedure in patients with atrial flutter or fibrillation undergoing congenital heart disease repair significantly reduced arrhythmia recurrence at a mean of 2.7 y after surgery.^[14] )

Aggressive strategies to convert atrial flutter and maintain sinus rhythm should be pursued in children. In rare cases of resistant chronic atrial flutter when only rate control can be accomplished, patients should avoid competitive sports. Also restrict the activities of patients likely to develop rapid conduction of intermittent acute episodes of flutter.

Atrial stretch, surgical scarring, and sinus node dysfunction all appear to play important roles in the development of atrial flutter in patients with congenital heart disease. The development of new surgical techniques to avoid atrial suture lines or dilatation and to prophylactically interrupt potential conduction isthmuses within the atria may reduce the frequency of this disorder in future surgical cohorts of patients with congenital heart disease.

Efforts directed at sparing the sinus node during surgery, coupled with more aggressive pacing strategies in patients with sinus node dysfunction, could also play an important role in prevention of atrial flutter.