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Atrial Flutter Treatment & Management

  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 30, 2015
 

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.[9, 10] 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 type I typical atrial flutter if they are reasonable candidates.[11] Ablation is usually done as an elective procedure; however, it can be done when the patient is in atrial flutter as well.

Given the high success rate and low complication rate, RFA is superior to medical therapy. Successful ablation reduces or eliminates the need for long-term anticoagulation and antiarrhythmic medications.

For atrial flutter of less than 48 hours in duration, attempt cardioversion as soon as possible. Postconversion anticoagulation is usually unnecessary, though 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 greater than 48 hours, begin anticoagulation therapy. 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. Rate control and therapeutic anticoagulation are required for a minimum of 4 weeks.

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 torsades 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, and propranolol) and calcium channel blockers (eg, verapamil and 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 of more 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 cause dramatic 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 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 AV node. IV calcium channel blockers (eg, verapamil and 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.

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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:

  • A wide electrode separation in the right anterior and left posterior positions (sandwiching the atria), though the more traditional pad location (anterior and apical) will also work
  • Application of pressure on paddles or electrodes to reduce thoracic impedance
  • In women, placement of 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. 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.[12]

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Pharmacological Cardioversion

Dofetilide[13] is effective in 70-80% of patients. This drug should be initiated in an inpatient setting.

Ibutilide[14, 15, 16, 17] is 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 IV for cardioversion. Because of the risk of QT prolongation and torsades 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 or flecainide 200-300 mg) have also been shown to be effective in converting recent-onset atrial fibrillation to sinus rhythm.[18] 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 increased risk for thromboembolic complications. The anticoagulation strategy used for atrial fibrillation is also recommended for atrial flutter. Adequate anticoagulation, as recommended by the American College of Chest Physicians, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.

In general, when atrial flutter persists for more than 48 hours, 4 weeks of adequate anticoagulation must be provided or the absence of thrombus on TEE documented before cardioversion to sinus rhythm is attempted. Postconversion anticoagulation is recommended for a minimum of 4 weeks because thromboembolic complications can occur spontaneously after cardioversion or ablation.

Use long-term anticoagulation for patients with persistent or paroxysmal atrial flutter. As with atrial fibrillation, keep the INR at 2-3 to optimize the therapeutic effect and minimize the risk of bleeding.

Unlike atrial fibrillation, atrial flutter has a regular pattern of atrial contraction. 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 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.

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 associated with 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.[19] This score includes the following risk factors:

  • Congestive heart failure (CHF)
  • 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.[20]

In atrial fibrillation, postcardioversion stunning of the left atrial appendage is thought to contribute to thrombogenicity.[21] 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), though 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. One patient formed a new left atrial appendage thrombus. Evidence of atrial stunning significantly improved after 1 week. Anticoagulation for at least 1 week is advocated after ablation of an atrial flutter persisting for more than 2 days.

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Radiofrequency Ablation

RFA is often used as first-line therapy to achieve permanent restoration of sinus rhythm. This procedure is often performed electively, rather than in the acute setting. 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 improve quality of life significantly 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[22] ), 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.[23]

(A study by Saygi et al 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. The study included 153 randomized patients.[24] )

Type I atrial flutter

In patients with type I atrial flutter (tricuspid valve isthmus−dependent), catheter ablation is typically 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.

Type I counterclockwise atrial flutter. This 3-dim Type I counterclockwise atrial flutter. This 3-dimensional electroanatomic map of tricuspid valve and right atrium shows activation pattern displayed in color format. Red is early and blue is late, relative to 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.

Type II atrial flutter

Type II 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 type I 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 type I and may also necessitate the use of antiarrhythmic agents for suppression. Patients undergoing catheter-based ablation for atrial fibrillation can develop type II left atrial flutter or macroreentrant left atrial tachycardias, which can be challenging to map and ablate.

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Antiarrhythmic Therapy

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 or caffeine). 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. RFA 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 can prolong the QT interval and be proarrhythmic and thus should be initiated in the inpatient setting.[11]

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Contributor Information and Disclosures
Author

Lawrence Rosenthal, MD, PhD, FACC, FHRS Associate Professor of Medicine, Director, Section of Cardiac Pacing and Electrophysiology, Director of EP Fellowship Program, Division of Cardiovascular Disease, University of Massachusetts Memorial Medical Center

Lawrence Rosenthal, MD, PhD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, Massachusetts Medical Society, American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia Anne Ennis, DO Assistant Professor, University of Massachusetts Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

Brian Olshansky, MD Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, and Heart Rhythm Society

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Anatomy of classic counterclockwise atrial flutter. This demonstrates oblique view of right atrium and shows some crucial structures. Isthmus of tissue responsible for atrial flutter is seen anterior to coronary sinus orifice. Eustachian ridge is part of crista terminalis that separates roughened part of right atrium from smooth septal part of right atrium.
Type I counterclockwise atrial flutter. This 3-dimensional electroanatomic map of tricuspid valve and right atrium shows activation pattern displayed in color format. Red is early and blue is late, relative to fixed point in time. Activation travels in counterclockwise direction.
12-Lead ECG of type I atrial flutter. Note negative sawtooth pattern of flutter waves in leads II, III, and aVF.
Atypical left atrial flutter.
3-Dimensional electroanatomic map of type I atrial flutter. Colors progress from blue to red to white and represent relative conduction time in right atrium (early to late). Ablation line (red dots) has been created on tricuspid ridge extending to inferior vena cava. This interrupts flutter circuit. RAA = right atrial appendage; CSO = coronary sinus os; IVC = inferior vena cava; TV = tricuspid valve annulus.
Type I atrial flutter unmasked by adenosine (Adenocard).
 
 
 
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