Atrial Flutter Treatment & Management

Updated: Nov 20, 2017
  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Treatment

Approach Considerations

General treatment goals for symptomatic atrial flutter are similar to those for atrial fibrillation and include the following:

  • Control of the ventricular rate
  • Restoration of sinus rhythm
  • Prevention of recurrent episodes or reduction of their frequency or duration
  • Prevention of thromboembolic complications
  • 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 (ACLS) algorithms for managing atrial fibrillation and flutter. [12, 13] Consider immediate electrical cardioversion for patients who are hemodynamically unstable.

The main difference between atrial fibrillation and atrial flutter is that most cases of atrial flutter can be cured with radiofrequency ablation (RFA). In all available studies, catheter ablation is superior to rate-control and rhythm-control strategies with antiarrhythmic drugs.

Consider catheter-based ablation as first-line therapy in patients with typical atrial flutter if they are reasonable candidates. [14] Ablation is usually performed as an elective procedure; however, it can be done when the patient is in atrial flutter as well.

Given its high success rate and low complication rate, RFA is superior to medical therapy. Successful ablation reduces or eliminates the need for long-term antiarrhythmic medications and anticoagulation (unless the patient also has atrial fibrillation).

For atrial flutter duration shorter than 48 hours, attempt cardioversion as soon as possible. Similar to patients with atrial fibrillation, a decision on the need for postconversion anticoagulation is made after considering the individual patient’s risks of thromboembolism and bleeding. Data from transesophageal echocardiography (TEE) studies indicate that postconversion anticoagulation is a reasonable option because appendage blood flow velocity is lowest immediately after conversion.

For episodes of atrial flutter of uncertain duration or longer than 48 hours, begin anticoagulation therapy. Rate control and therapeutic anticoagulation are required for a minimum of 4 weeks prior to cardioversion. If cardioversion is needed sooner, anticoagulate patients with intravenous (IV) heparin and perform TEE as close to the time of cardioversion as possible. Patients continue to require anticoagulation for at least 4 weeks after cardioversion. If thrombus is observed or suspected on the basis of TEE findings, delay cardioversion.

In patients who are not candidates for catheter-based ablation, rate- and rhythm-control strategies should be considered. Because of the arrhythmia risk, drugs such as ibutilide, sotalol, and dofetilide should be initiated in an inpatient setting. Pause-dependent torsade de pointes can occur after conversion to sinus rhythm. The risk of proarrhythmia is probably greatest during the first 24-48 hours after the initiation of antiarrhythmics.

Preferred medications that slow atrioventricular (AV) node conduction include beta blockers (eg, atenolol, metoprolol, propranolol) and calcium channel blockers (eg, verapamil, diltiazem). These medications are used to control ventricular rates. They are also used in patients who are taking class IA or IC antiarrhythmic drugs (to prevent rapid ventricular response, which can occur when the atrial rate is slowed).

Considering anticoagulation in this patient population (at least until sinus rhythm is maintained) is a wise decision. Anticoagulant therapy (ie, warfarin) is indicated, especially when the atrial flutter is longer than 48 hours’ duration or its onset is uncertain.

Patients need to maintain a therapeutic international normalized ratio (INR) for 3 weeks before conversion and for at least 4 weeks after conversion to sinus rhythm. Long-term anticoagulation is recommended for patients with chronic atrial flutter. Closely monitor the patient’s anticoagulation therapy, with a target INR of 2-3. Take special care when additional medications (including antibiotics) are added because they may dramatically alter the INR in patients treated with warfarin.

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.

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Ventricular Rate Control

Ventricular rate control is a priority in atrial flutter because it may alleviate symptoms. Rate control is typically more difficult for atrial flutter than for atrial fibrillation.

Ventricular rate control can be achieved with drugs that block the atrioventricular (AV) node. Intravenous calcium channel blockers (eg, verapamil, diltiazem) or beta blockers can be used, followed by the 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.

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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, or anteroposterior). Atrial flutter generally requires less energy for conversion than atrial fibrillation does; as little as 50 J may be necessary.

If cardioversion is not successful with one electrode configuration, switching to another configuration may improve success. A second set of electrodes can be used with tandem or simultaneous shocks. Biphasic external waveform may be more effective in restoring sinus rhythm.

Points to remember about the cardioversion technique include the following:

  • Use a wide electrode separation in the right anterior and left posterior positions (sandwiching the atria), although the more traditional pad location (anterior and apical) will also work
  • Apply pressure on the paddles or electrodes to reduce thoracic impedance
  • In women, place the electrode patches under or lateral to the breasts

Risius et al found that in external electrical cardioversion of atrial flutter, anterior-lateral electrode positioning yields results superior to those achieved with anterior-posterior positioning. [15] In this randomized trial, 96 patients (72 of them men) received sequential biphasic waveform shocks consisting of 50, 75, 100, 150, or 200 J according to a step-up protocol.

Compared with anterior-posterior positioning, anterior-lateral positioning resulted in successful cardioversion with less mean energy (65 ± 13 vs 77 ± 13 J) and fewer mean shocks (1.48 ± 1.01 vs 1.96 ± 1.00 J). In addition, cardioversion occurred with the first 50-J shock in 73% of patients when anterior-lateral positioning was used, versus 36% with the anterior-posterior electrode position. [15]

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Pharmacologic Cardioversion

Dofetilide [16] is effective in 70-80% of patients with atrial flutter. This drug should be initiated in an inpatient setting.

Ibutilide [17, 18, 19, 20] is also effective, converting recent-onset atrial flutter to sinus rhythm in 63% of patients with a single infusion. It is the only agent available in the United States that can be used intravenously for cardioversion. Because of the risk of QT prolongation and torsade de pointes, it must be given in a monitored setting. Continuous electrocardiographic (ECG) monitoring is indicated for at least 4 hours after infusion. Ibutilide should not be used in patients with severe chronic heart failure, hypokalemia, or baseline prolonged QT.

Large single oral doses of type IC antiarrhythmic agents (eg, propafenone 450-600 mg, flecainide 200-300 mg) have also been shown to be effective in converting recent-onset atrial fibrillation to sinus rhythm. [21] Their use in atrial flutter can be assumed to have at least equal success. Giving antiarrhythmic medications before electrical cardioversion has been shown to improve the rate of conversion to sinus rhythm. Concurrent treatment with beta blockers or calcium channel blockers is suggested when oral type IC agents are used.

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Prevention of Thromboembolic Complications

Compared with the general population, patients with atrial flutter are at an increased risk for thromboembolic complications. Adequate anticoagulation has been shown to decrease these complications in patients with chronic atrial flutter and in patients undergoing cardioversion. [22]  The anticoagulation strategy used for atrial fibrillation is also recommended for atrial flutter. 

Unlike atrial fibrillation, atrial flutter has a regular pattern of atrial contraction. Transesophageal echocardiography (TEE) data demonstrate an organized sawtooth pattern of left atrial appendage flow with alternating filling and emptying wavelets. No difference in left atrial appendage function is observed in comparison to 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.

Other reports have demonstrated thrombus in the left atrial appendage of patients with atrial flutter (as many as 43%). Most studies of nonanticoagulated 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 that was associated with an increased risk of thromboembolism was found in 6-43% of patients with atrial flutter.

Patients with atrial flutter and episodes of atrial fibrillation are at higher risk for 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, left ventricular dysfunction, and diabetes may be at higher risk for thromboembolic complications. It is noteworthy that associated atrial fibrillation appears not to increase the risk of embolic complications significantly.

The CHA2DS2-VASc score has been shown to perform well at predicting whether a patient is at high or low risk for thromboembolism. [20] This score includes the following risk factors:

  • Congestive heart failure
  • Hypertension
  • Age 65-74 years
  • Diabetes
  • Previous stroke
  • Vascular disease
  • Female sex

Postcardioversion thromboembolic events can complicate as many as 7.3% of procedures in patients who are not anticoagulated. These events typically occur within 3 days after cardioversion; almost all occur within 10 days after cardioversion. [23]

In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity. [24] 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 the arrhythmia.

Stunning of the left atrial appendage also occurs after conversion from atrial flutter to sinus rhythm (whether 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 in whom TEE revealed no evidence of thrombus but who had a thromboembolic event after cardioversion.

In a study comparing left atrial appendage function before and at varying intervals (immediate, 1 day, 1 week, and 6 week) after catheter ablation of persistent atrial flutter, a significant increase in atrial standstill, decrease in left atrial appendage function, and new spontaneous echo contrast occurred after ablation. [25] One patient formed a new left atrial appendage thrombus. Evidence of atrial stunning significantly improved after 1 week. Anticoagulation for at least 30 days is advocated after ablation of an atrial flutter persisting for more than 2 days.

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Radiofrequency Ablation

Radiofrequency ablation (RFA) is often used as first-line therapy to achieve permanent restoration of sinus rhythm. This procedure is often performed electively, but it can also be performed in acute setting at centers with the capability to do this. For patients with recurrent symptomatic atrial flutter that is proved to be isthmus-dependent in the electrophysiologic laboratory, a success rate higher than 95% can be expected with current technology.

Catheter ablation has been shown to significantly improve quality of life in patients with atrial flutter. The frequency of hospital admissions and emergency department visits and the number of antiarrhythmic drugs administered decrease substantially after ablation. Activity capacity improves significantly in patients with preexisting left ventricular dysfunction.

Although many patients treated with RFA have subsequently developed atrial fibrillation on long-term follow-up (with rates increasing over time to 63% at 4 years in one study [26] ), this procedure still represents a safe alternative to antiarrhythmic agents. In patients with obstructive sleep apnea, treatment with continuous positive airway pressure (CPAP) has been shown to reduce the incidence of newly diagnosed atrial fibrillation after RFA for atrial flutter. [27]

A study by Saygi et al involving 153 randomized patients indicated that in cases of cavotricuspid isthmus (CTI)-dependent atrial flutter, RFA and cryoablation each cause a similar degree of procedural myocardial injury, as measured by increased troponin I levels after the procedure. [28]  The same investigators found similar procedural success rates between RFA and cryoablation for CTI-dependent atrial flutter, regardless of the CTI morphology (straight, concave, and pouchlike). [29]  However, patients with a longer CTI experienced a lower procedure success rate whether the energy source was RFA or cryoablation.

Typical atrial flutter

In patients with typical atrial flutter (tricuspid valve isthmus−dependent), catheter ablation is usually an outpatient procedure. The procedure involves moderate sedation and accessing the femoral veins for catheter insertion. The diagnosis of atrial flutter is confirmed by means of pacing maneuvers, and ablation is performed typically at the 6 o’clock position on the tricuspid valve isthmus.

A line of conduction block is required to interrupt the circuit (see the image below). Postablation pacing maneuvers can confirm that the substrate required for the circuit has been modified.

Typical counterclockwise atrial flutter. This 3-di Typical counterclockwise atrial flutter. This 3-dimensional electroanatomic map of a tricuspid valve and right atrium shows the activation pattern displayed in color format. Red is early and blue is late, relative to a fixed point in time. Activation travels in counterclockwise direction.

The recurrence rate is lower than 5%. Postprocedure anticoagulation with warfarin is usually continued for 4-6 weeks.

Atypical atrial flutter

Atypical atrial flutter (non−isthmus dependent) circuits are amenable to catheter ablation, especially in centers with advanced mapping systems. The ablation procedure is similar to that for typical flutter but may involve additional mapping of the left atrium (via a transseptal puncture).

Success depends on localizing the circuit and creating a line of block that includes an electrically inert anatomic structure (ie, the mitral valve annulus). Although the success rate should approach 95%, recurrence is more common than with typical atrial flutter and may also necessitate the use of antiarrhythmic agents for suppression. Patients undergoing catheter-based ablation for atrial fibrillation can develop atypical left atrial flutter or macroreentrant left atrial tachycardias, which can be challenging to map and ablate.

In a study that assessed the use of ultra-high density-activation sequence mapping (UHD-ASM) for ablating 31 atypical atrial flutters (97% in the left atrium) in 23 patients, Winkle et al was able to identify the entire circuit and the target area of slow conduction, as well as directly terminate or eliminate the atypical atrial flutter in 90.3% with ablation of the area of slow conduction or microreentry focuses without the need for entrainment mapping. [30]  At 1-year follow-up, 77% of patients did not have atrial tachycardia or atrial flutter, and 61% did not have any atrial arrhythmias.

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Antiarrhythmic Therapy

After the initial episode of atrial flutter is terminated and the underlying disease is treated, the patient may not need any further intervention except avoidance of the precipitating factor (eg, alcohol [31] ). For atrial fibrillation, approximately 30% of patients remain in sinus rhythm at 1 year without antiarrhythmic therapy, and the situation may be similar with atrial flutter.

If intervention is required, always consider catheter-based ablation before starting an antiarrhythmic agent. Radiofrequency ablation is currently the preferred therapeutic choice. With lifelong antiarrhythmic drug therapy, fatal proarrhythmic events (even in healthy hearts) and organ toxicity may occur.

Data on the use of antiarrhythmic agents specifically to treat atrial flutter are limited. Most studies of antiarrhythmics agents and atrial fibrillation include some patients with atrial flutter (10-20%). (For more information on the use of antiarrhythmic agents, see Atrial Fibrillation.) In general, antiarrhythmics used to treat atrial fibrillation have been shown to be effective in fibrillation or flutter during a 6- to 12-month follow-up.

Besides considering the characteristic adverse effects of each antiarrhythmic agent, the choice of medication should take into account the underlying cardiac pathology, as follows:

  • No structural heart disease: Class IC agents can be used safely, but in general, class III agents are more effective for patients with flutter
  • Left ventricular hypertrophy without ischemia or conduction delay: Class III agents, specifically amiodarone, can be used
  • Ischemic heart disease: Sotalol or amiodarone can be used; class IC agents should be avoided
  • Significant systolic dysfunction: Amiodarone or dofetilide may be used; class IC agents should be avoided

Amiodarone is effective and is associated with a low proarrhythmic risk, but it may adversely affect multiple organs, including the skin, liver, lungs, and thyroid. Sotalol and dofetilide can prolong the QT interval and be proarrhythmic and thus should be initiated in the inpatient setting. [14]

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