Medical Care: General goals for the treatment of symptomatic atrial flutter are similar to those for atrial fibrillation and include (1) control of the ventricular rate, (2) termination of sustained episodes, (3) prevention and decreased frequency or duration of recurrent episodes, (4) prevention of thromboembolic complications, and (5) minimization of adverse effects from therapy. However, these goals can be modified for each patient. In an acute setting with pending hemodynamic collapse, follow the adult advanced cardiac life support algorithms for managing atrial fibrillation and flutter. Consider immediate electrical cardioversion for patients who are hemodynamically unstable.
" Ventricular rate control: Ventricular rate control is a priority because it may alleviate symptoms. Rate control is typically more difficult for atrial flutter than for atrial fibrillation.
o Calcium channel blockers and beta-blockers
" Ventricular rate control can be achieved with drugs that block the AV node. Intravenous calcium channel blockers (eg, verapamil, diltiazem) or beta-blockers can be used, followed by initiation of oral agents.
" Hypotension and negative inotropic effects are concerns with the use of these medications.
" A history of Wolff-Parkinson-White syndrome or evidence of ventricular preexcitation should be determined because agents that act exclusively at the level of the AV node may enhance accessory pathway conduction.
o Vagal maneuvers: These can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well.
o Intravenous adenosine: This drug, administered as an intravenous push followed with an intravenous bolus with flush, can also be helpful in making the diagnosis of atrial flutter by transiently blocking the AV node.
" Termination of sustained episodes: After determining the patient's needs for anticoagulation and ventricular rate control, the issue of restoration of the sinus rhythm can be safely addressed.
o Electrical cardioversion
" The success rate of electrical cardioversion is higher than 95%.
" Factors to consider include synchronization of shocks to R waves, adequate sedation, and electrode position (apex anterior, apex posterior, anteroposterior).
" Atrial flutter generally requires less energy for conversion than atrial fibrillation, and as few as 50 joules may be necessary. Recent data show that an initial energy of 100 joules is more effective and is less likely to induce atrial fibrillation than 50 joules.
" If cardioversion is not successful with one electrode configuration, switching may improve success. A second set of electrodes can be used with tandem or simultaneous shocks.
" Newer devices with different outputs and biphasic external waveform may be more effective in restoring sinus rhythm.
" A few points to remember about the cardioversion technique include a wide electrode separation in the anteroapex position, the application of pressure on paddles or electrodes to reduce thoracic impedance, and the placement of electrode patches under or lateral to the breasts in women.
o Pharmacological cardioversion
" Procainamide is effective for converting atrial flutter to sinus rhythm in 0-13% of patients.
" Flecainide is effective in approximately 10% of patients.
" Dofetilide is effective in 70-80% of patients.
" Ibutilide is effective, converting recent-onset atrial flutter to sinus rhythm in 63% of patients with a single infusion.
" Large single oral doses of type IC antiarrhythmic agents, such as propafenone (450-600 mg) or flecainide (200-300 mg), have also been shown to be effective in converting recent-onset atrial fibrillation to sinus rhythm. Their use in atrial flutter can be assumed to have at least equal success.
" Oral amiodarone during the loading period (>1 mo) converted 18% of atrial fibrillations or flutters to normal sinus rhythms. Intravenous amiodarone is also effective in converting atrial flutter to sinus rhythm and in slowing the ventricular rate in patients with a rapid ventricular response.
o Atrial overdrive pacing: This procedure can be performed invasively or through the use of a transesophageal electrode to pace the left atrium, with a success rate of approximately 50%.
o Combination of the above treatments: Antiarrhythmic medication prior to electrical cardioversion or rapid atrial pacing has been shown to improve the rate of conversion to sinus rhythm.
o Radiofrequency ablation: This treatment modality is not usually used in the acute setting.
" Prevention (decrease frequency or duration of recurrence episodes): After the initial episode is terminated and the underlying disease is treated, the patient may not need any further intervention except avoidance of the precipitating factor (eg, alcohol, caffeine). For atrial fibrillation, approximately 30% of patients remain in sinus rhythm at 1 year without antiarrhythmic therapy.
o Antiarrhythmic agents
" For more information on the use of antiarrhythmic agents, see Atrial Fibrillation. Data on the use of antiarrhythmic agents specifically for atrial flutter are limited. Most studies of antiarrhythmics agents and atrial fibrillation include some patients with atrial flutter (10-20%).
" In general, the use of antiarrhythmic drugs in atrial flutter is similar to that of atrial fibrillation; however, with a high success rate and low complication rate, the use of radiofrequency ablation in atrial flutter makes this procedure a favorable option compared with lifelong antiarrhythmic drug therapy because fatal proarrhythmic events (even in healthy hearts) and organ toxicity may occur.
" In general, antiarrhythmics used to treat atrial fibrillation have been shown effective in fibrillation or flutter during a 6- to 12-month follow-up. Considering the characteristic adverse effects of each antiarrhythmic agent, some guidelines are available regarding the choice of medication when taking into account the underlying cardiac pathology.
" For patients with healthy hearts, class IC or class III agents can be used safely.
" For patients with LV hypertrophy without ischemia or conduction delay, class III agents, specifically sotalol, can be used.
" For patients with an ischemic heart, sotalol or amiodarone can be used. Avoid class IC agents.
" For patients with significant systolic dysfunction, amiodarone can be used, dofetilide may be used, and class IC agents should be avoided.
o Radiofrequency ablation
" Ablation or modification of the AV node with radiofrequency ablation and pacemaker implantation is a rarely used option and is only used when the arrhythmia is not suitable for curative ablation and other options have been exhausted.
" For patients with recurrent symptomatic atrial flutter that is proven to be isthmus-dependent in the electrophysiologic laboratory, expect a success rate of higher than 90% with current technology.
o Pacemaker: In patients with paroxysmal atrial fibrillation and/or flutter in whom medical therapy has failed and who subsequently need a pacemaker, atrial or multisite atrial pacing has been shown to decrease recurrent episodes of atrial fibrillation and atrial flutter. However, this is currently under active investigation.
o Surgery: In patients who have atrial flutter and need cardiac surgery, modification of the atrial incision and creation of a cryothermal lesion, similar to the lesion created during radiofrequency catheter ablation, can be curative for atrial flutter and may prevent an incisional reentrant arrhythmia.
" Prevention of complications
o Thromboembolic
" Patients with atrial flutter are at increased risk of thromboembolic complications compared with the general population. Most clinicians anticoagulate patients with atrial flutter as they would patients with atrial fibrillation. Thus, use the same anticoagulation strategy used in patients with atrial fibrillation.
" Unlike atrial fibrillation, atrial flutter has a regular pattern of atrial contraction. TEE data have demonstrated an organized sawtooth pattern of the left atrial appendage flow with alternating filling and emptying wavelets. No difference in the left atrial appendage function is observed compared with patients in sinus rhythm. Patients with both atrial flutter and atrial fibrillation have significantly decreased left atrial appendage function, more spontaneous echo contrast, and larger left atria and accompanying appendages.
" Patients with atrial flutter and episodes of atrial fibrillation are at higher risk of thromboembolic events; however, determining whether episodes of atrial fibrillation are associated with episodes of atrial flutter is difficult.
" A large retrospective review of patients in chronic atrial flutter revealed a 14% occurrence rate of thromboembolic events over 4.5 years, with half of these events being ischemic stroke. In another large cohort of patients with atrial flutter, the occurrence rate of embolic complications in patients with chronic or recurrent atrial flutter was 12%. For stroke, this risk is estimated at approximately one third of patients with nonrheumatic atrial fibrillation. Males with hypertension, structural heart disease, LV dysfunction, and diabetes may be at higher risk of thromboembolic complications. Interestingly, associated atrial fibrillation did not significantly increase the risk of the embolic complications.
" Other reports have demonstrated thrombus in the left atrium appendage of patients with atrial flutter (as many as 43%). Most studies of non-anticoagulated patients with atrial flutter report a rate of 10-15% for patients with thrombus in the left atrium or left atrial appendage. Spontaneous echo contrast associated with increased risk of thromboembolism was found in 6-43% of patients with atrial flutter.
" Postcardioversion thromboembolic events can complicate as many as 7.3% of procedures in patients who are not anticoagulated. These events occur within 3 days after the cardioversion; almost all occur within 10 days after the cardioversion.
" In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity. This phenomenon may last as long as 4 weeks in patients with atrial fibrillation and may be related to how long patients have been in arrhythmia.
" Stunning of the left atrial appendage also occurs following conversion from atrial flutter to sinus rhythm (electrical or spontaneous), although to a lesser degree. Left atrial and left atrial appendage function decrease immediately after conversion, and, in one study, spontaneous echo contrast was noted to develop within 5 minutes after conversion in 43% of patients. This is thought to be the source of emboli in patients whose TEE findings revealed no evidence of thrombus but who had a thromboembolic event after cardioversion.
" In a recent study comparing left atrial appendage function before and after catheter ablation (immediate, 1 d, 1 wk, and 6 wk) of persistent atrial flutter, a significant increase in atrial standstill, decrease in left atrial appendage function, and new spontaneous echo contrast occurred after ablation. One patient formed a new left atrial appendage thrombus after ablation. Evidence of atrial stunning significantly improved after 1 week. Anticoagulation for at least 1 week is advocated after ablation of an atrial flutter that persists for more than 2 days.
" Adequate anticoagulation, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.
o Cardiomyopathy: Termination of long-standing atrial flutter with a rapid ventricular response has been reported to improve LV systolic function in patients without other known causes of dilated cardiomyopathy.
" Minimizing adverse effects of antiarrhythmic therapy: Because atrial flutter is a nonfatal arrhythmia, carefully assess the risks and benefits of drug therapy, especially with antiarrhythmic agents. A few points to remember that will help minimize the adverse effects include the following:
o Avoidance of precipitating factor(s) or therapy of the underlying problem may be all that is needed to prevent recurrent episodes.
o For patients with rare recurrence, cardioversion or medical, electrical, or rapid atrial pacing may be adequate.
o Of antiarrhythmic agents, amiodarone is effective and is associated with a low proarrhythmic risk but may adversely affect multiple organs, including the skin, liver, lungs, and thyroid. Quinidine may cause a lupuslike syndrome (ie, thrombocytopenia). Procainamide may cause a lupuslike syndrome (ie, agranulocytosis).
o Radiofrequency ablation may be a preferred therapeutic choice. Although many patients who were treated with radiofrequency ablation subsequently developed atrial fibrillation after long-term follow-up (56% in one study), this procedure still represents a safe alternative to antiarrhythmic agents.
" Structural heart disease prior to atrial fibrillation and inducible atrial fibrillation after ablation predict a high risk of developing atrial fibrillation after successful atrial flutter ablation; however, successful atrial flutter ablation has been shown to eliminate or reduce the frequency of atrial fibrillation episodes.
o Catheter ablation has been shown to significantly improve the quality of life in patients with atrial flutter.
o The frequency of hospital admissions and emergency department visits and the number of antiarrhythmic drugs administered are decreased significantly after ablation.
o Activity capacity significantly improves in patients with preexisting LV dysfunction.
o In general, when atrial flutter persists for more than 48 hours, 4 weeks of adequate anticoagulation or TEE is needed before attempting cardioversion to sinus rhythm.
o Thromboembolic complications occur spontaneously after cardioversion or ablation, and postconversion anticoagulation is recommended for a minimum of 4 weeks.
o Use long-term anticoagulation for patients with persistent or paroxysmal atrial flutter. As with atrial fibrillation, keep the international normalized ratio (INR) at 2-3 to optimize the therapeutic effect and minimize the risk of bleeding.
Diet: Any dietary recommendations should be appropriate for the underlying heart disease and other comorbidities (eg, diabetes).
MEDICATION :
1. BETA BLOCKERS OR ATRIOVENTRICULAR NODAL CONDUCTION BLOCKERS :
- PROPRANOLOL
- ATENOLOL
- METOPROLOL
- ESMOLOL
2. CALCIUM CHANNEL BLOCKERS ( NONDIHYDROPYRIDINE ) :
- VERAPAMIL
- DILTIAZEM
3. CARDIAC GLYCOSIDES :
- DIGOXIN
4. ANTIARRHYTHMICS :
- QUINIDINE SULPHATE
- PROCAINAMIDE
- DISOPYRAMIDE
- PROPAFENONE
- FLECAINIDE
- AMIODARONE
5. ANTICOAGULANTS TO PREVENT THROMBOEMBOLIC PHENOMENON :
- HEPARIN
- WARFARIN