Atrial Flutter 

Updated: Nov 18, 2019
Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD 

Overview

Practice Essentials

Atrial flutter is a cardiac arrhythmia characterized by atrial rates of 240-400 beats/min, usually with some degree of atrioventricular (AV) node conduction block. For the most part, morbidity and mortality are due to complications of rate (eg, syncope and congestive heart failure [CHF]). See the image below.

Anatomy of classic counterclockwise atrial flutter Anatomy of classic counterclockwise atrial flutter. This image demonstrates an oblique view of the right atrium and shows some crucial structures. The isthmus of tissue responsible for atrial flutter is seen anterior to the coronary sinus (CS) orifice. The eustachian ridge is part of the crista terminalis that separates the roughened part of the right atrium from the smooth septal part of the right atrium. IVC = inferior vena cava; SVC = superior vena cava.

Signs and symptoms

Signs and symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. Typical symptoms include the following:

  • Palpitations

  • Fatigue or poor exercise tolerance

  • Mild dyspnea

  • Presyncope

Less common symptoms include angina, profound dyspnea, or syncope. Tachycardia may or may not be present, depending on the degree of AV block associated with the atrial flutter activity.

Physical findings include the following:

  • The heart rate is often approximately 150 beats/min because of a 2:1 AV block

  • The pulse may be regular or slightly irregular

  • Hypotension is possible, but normal blood pressure is more commonly observed

Other points in the physical examination are as follows:

  • Palpate the neck and thyroid gland for goiter

  • Evaluate the neck for jugular venous distention

  • Auscultate the lungs for rales or crackles

  • Auscultate the heart for extra heart sounds and murmurs

  • Palpate the point of maximum impulse on the chest wall

  • Assess the lower extremities for edema or impaired perfusion

If embolization has occurred from intermittent atrial flutter, findings are related to brain or peripheral vascular involvement. Other complications of atrial flutter may include the following:

  • Embolization (arterial)

  • CHF

  • Severe bradycardia

  • Myocardial rate–related ischemia

See Presentation for more detail.

Diagnosis

The following techniques aid in the diagnosis of atrial flutter:

  • Electrocardiography (ECG): This is an essential diagnostic modality for atrial flutter

  • Vagal maneuvers: These can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well

  • Adenosine: This drug can be helpful in making the diagnosis of atrial flutter by transiently blocking the AV node

  • Exercise testing: This can be utilized to identify exercise-induced atrial fibrillation and to evaluate the response of the ventricular rate to activity, as well as its interaction with symptoms including those of ischemic heart disease

  • Holter monitor: This can be used to help identify arrhythmias in patients with nonspecific symptoms, to identify triggers, and to detect associated atrial arrhythmias

Transthoracic echocardiography (TTE) is the preferred initial imaging modality for evaluating atrial flutter. It can evaluate right and left atrial size, as well as the size and function of the right and left ventricles, and this information facilitates diagnosis of valvular heart disease, left ventricular hypertrophy (LVH), and pericardial disease.

See Workup for more detail.

Management

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

  • Control of ventricular rate: This can be achieved with drugs that block the AV node; intravenous (IV) calcium channel blockers (eg, verapamil and diltiazem) or beta blockers can be used, followed by initiation of oral agents. Concurrent control of resting and activity-associated rates is generally required, and may be difficult to achieve.

  • Restoration of sinus rhythm: This can be achieved by means of electrical or pharmacologic cardioversion or radiofrequency ablation (RFA); successful ablation reduces or eliminates the need for long-term anticoagulation and antiarrhythmic medications

  • Prevention of recurrent episodes or reduction in their frequency or duration: In general, the use of antiarrhythmic drugs in atrial flutter is similar to that in atrial fibrillation

  • Prevention of thromboembolic complications: 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

  • Minimization of adverse effects from therapy: Because atrial flutter is a nonfatal arrhythmia, carefully assess the risks and benefits of drug therapy, especially with antiarrhythmic agents

See Treatment and Medication for more detail.

Background

Atrial flutter is a cardiac arrhythmia characterized by atrial rates of 240-400 beats/min, usually with some degree of atrioventricular (AV) node conduction block. In the most common form of atrial flutter (typical atrial flutter), electrocardiography (ECG) demonstrates a negative sawtooth pattern in leads II, III, and aVF.

Typical (or classic) atrial flutter involves a single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus. The electrical wavefront most often propagates in a counterclockwise direction. Atypical atrial flutter follows a different circuit; it may involve the right or the left atrium. (See Pathophysiology.)

Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately 60% of patients with atrial flutter have coronary artery disease (CAD) or hypertensive heart disease; 30% have no underlying cardiac disease. Uncommon forms of atrial flutter have been noted during long-term follow-up in as many as 26% of patients with surgical correction of congenital cardiac anomalies. (See Etiology.)

Symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. The most common symptom is palpitations. Other symptoms include fatigue, dyspnea, and chest pain. (See Presentation.) ECG is essential in making the diagnosis. Transthoracic echocardiography (TTE) is the preferred initial imaging modality for evaluating atrial flutter. (See Workup.)

Intervening to control the ventricular response rate or to return the patient to sinus rhythm is important. Consider immediate electrical cardioversion for patients who are hemodynamically unstable. Consider catheter-based ablation as first-line therapy in patients with typical atrial flutter if they are reasonable candidates. Ablation is usually performed as an elective procedure; however, it can also be performed when the patient is in atrial flutter. (See Treatment.)

Atrial flutter is similar to atrial fibrillation in many respects (eg, underlying disease, predisposing factors, complications, and medical management), and some patients have both atrial flutter and atrial fibrillation. However, the underlying mechanism of atrial flutter makes this arrhythmia amenable to cure with percutaneous catheter-based techniques.

Pathophysiology

In humans, the most common form of atrial flutter (typical) involves a single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus (most often in a counterclockwise direction), with an area of slow conduction located between the tricuspid valve annulus and the coronary sinus ostium (subeustachian isthmus). A 3-dimensional electroanatomic map of typical atrial flutter is shown in the video below.

3-Dimensional electroanatomic map of typical atrial flutter. Colors progress from blue to red to white and represent the relative conduction time in the right atrium (early to late). An ablation line (red dots) has been created on the tricuspid ridge extending to the inferior vena cava. This ablation line interrupts the flutter circuit. CSO = coronary sinus os; IVC = inferior vena cava; RAA = right atrial appendage; TV = tricuspid valve annulus.

Animal models have been used to demonstrate that an anatomic block (surgically created) or a functional block of conduction between the superior vena cava and the inferior vena cava, similar to the crista terminalis in the human right atrium, is key to initiating and maintaining the arrhythmia.

The crista terminalis acts as another anatomic conduction barrier, similar to the line of conduction block between the two venae cavae required in the animal model. The orifices of both venae cavae, the eustachian ridge, the coronary sinus orifice, and the tricuspid annulus complete the barrier for the reentry circuit (see the image below). Typical atrial flutter is often referred to as isthmus-dependent flutter. The rhythm is due to macroreentry, there is an excitable gap, and the rhythm can be entrained.

Anatomy of classic counterclockwise atrial flutter Anatomy of classic counterclockwise atrial flutter. This image demonstrates an oblique view of the right atrium and shows some crucial structures. The isthmus of tissue responsible for atrial flutter is seen anterior to the coronary sinus (CS) orifice. The eustachian ridge is part of the crista terminalis that separates the roughened part of the right atrium from the smooth septal part of the right atrium. IVC = inferior vena cava; SVC = superior vena cava.

Typical counterclockwise atrial flutter has caudocranial activation (ie, activation counterclockwise around the tricuspid valve annulus when viewed in the left antero-oblique fluoroscopic view) of the atrial septum (see the image below).

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.

Typical atrial flutter can also have the opposite activation sequence (ie, clockwise activation around the tricuspid valve annulus). Clockwise atrial flutter is much less common. When the electric activity moves in a clockwise direction, the electrocardiogram (ECG) will show positive flutter waves in leads II, III, and aVF, and they may appear somewhat sinusoidal. This arrhythmia is still considered typical, isthmus-dependent flutter; it is usually called reverse typical atrial flutter.

Atypical atrial flutters are less extensively studied and electroanatomically characterized. Atypical atrial flutters may originate from the right atrium, as a result of surgical scars (ie, incisional reentry), or from the left atrium, specifically the pulmonary veins (ie, focal reentry) or mitral annulus (see the image below). Left atrial flutter is common and often problematic after left atrial linear ablation procedures (for atrial fibrillation). Thus, tricuspid isthmus dependency is not a prerequisite for atypical atrial flutter.

Electrocardiogram of atypical left atrial flutter. Electrocardiogram of atypical left atrial flutter.

 

Etiology

Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately 30% of patients with atrial flutter have coronary artery disease, 30% have hypertensive heart disease, and 30% have no underlying cardiac disease. Rheumatic heart disease, congenital heart disease, pericarditis, and cardiomyopathy may also lead to atrial flutter. Rarely, mitral valve prolapse or acute myocardial infarction has been associated with atrial flutter.

In addition, the following conditions are also associated with atrial flutter:

  • Hypoxia
  • Chronic obstructive pulmonary disease
  • Pulmonary embolism
  • Hyperthyroidism
  • Pheochromocytoma
  • Diabetes
  • Electrolyte imbalance
  • Alcohol consumption
  • Obesity
  • Myotonic dystrophy in childhood (rare) [1]

Atrial flutter may be a sequela of open heart surgery. After cardiac surgery, atrial flutter may be reentrant as a result of natural barriers, atrial incisions, and other cardiac scars. Some patients develop atypical left atrial flutter after pulmonary vein isolation procedures for atrial fibrillation.

Although there are no clearly defined genetic conditions that cause atrial flutter, in many cases there is likely an underlying genetic susceptibility to acquiring it. Genome-wide association studies have identified genes associated with atrial flutter.[2]

The PITX2 (paired-like homeodomain 2) gene on chromosome locus 4q25 is known to play a major role in left-right asymmetry of the heart and has been found to have a strong association with atrial fibrillation[3] and an even stronger association with typical atrial flutter.[4] There are not yet any clinically available genetic tests that can identify persons at increased risk for atrial flutter.

Epidemiology

United States statistics

Atrial flutter is much less common than atrial fibrillation. Of the patients admitted to US hospitals with a diagnosis of supraventricular tachycardia between 1985 and 1990, 77% had atrial fibrillation and 10% had atrial flutter. On the basis of a study of patients referred to tertiary care centers, the incidence of atrial flutter in the United States is estimated to be approximately 200,000 new cases per year.[5]

Sex- and age-related demographics

In a study of 100 patients with atrial flutter, 75% were men. In another study performed at a tertiary care study, atrial flutter was 2.5 times more common in men.

Patients with atrial flutter, as with atrial fibrillation, tend to be older adults. In one study, the average age was 64 years. The prevalence of atrial fibrillation increases with age, as follows:

  • 25-35 years: 2-3 cases per 1000 population
  • 55-64 years: 30-90 cases per 1000 population
  • 65-90 years: 50-90 cases per 1000 population

Prognosis

The prognosis for atrial flutter depends on the patient’s underlying medical condition. Any prolonged atrial arrhythmia can cause a tachycardia-induced cardiomyopathy. Intervening to control the ventricular response rate or to return the patient to sinus rhythm is important. Thrombus formation in the left atrium has been described in patients with atrial flutter (0-21%). Thromboembolic complications have also been described.[6]

Because of the conduction properties of the atrioventricular (AV) node, many people with atrial flutter will have a faster ventricular response than those with atrial fibrillation. The heart rate is often more difficult to control with atrial flutter than with atrial fibrillation, because of increased concealed conduction in those with atrial fibrillation.

For the most part, morbidity and mortality result from complications of rate (eg, syncope and congestive heart failure [CHF]). In patients with atrial flutter, the risk of embolic occurrences approaches that seen in atrial fibrillation. Patients with Wolff-Parkinson-White syndrome who develop atrial flutter can develop life-threatening ventricular responses and therefore should be considered for catheter ablation of their accessory bypass tract.

Data from the Framingham study suggest that patients with atrial fibrillation do not live as long as patients without atrial fibrillation (ie, control subjects). No data are available on atrial flutter.

The prognosis for patients with typical atrial flutter who undergo catheter ablation is excellent, with a very low recurrence rate. The picture is not as clear for patients with both atrial flutter and atrial fibrillation. Some reports have documented fewer episodes of atrial fibrillation after successful flutter ablation; others have not. It is possible that atrial fibrillation may be more responsive to antiarrhythmic agents after atrial flutter has been eliminated.

Bohnen et al performed a prospective study to assess the incidence and predictors of major complications from contemporary catheter ablation procedures.[7] Major complication rates ranged from 0.8% (supraventricular tachycardia, applicable to ablation of typical atrial flutter) to 6% (ventricular tachycardia associated with structural heart disease), depending on the ablation procedure performed. Renal insufficiency was the only independent predictor of a major complication.

Numerous reports indicate that patients with atrial fibrillation who are given class IC antiarrhythmic agents may convert to atrial flutter with faster ventricular rates, even if the flutter rate is "relatively slow." Thus, patients receiving type IC agents (eg, flecainide) should also receive an AV node−blocking drug such as a beta blocker or calcium channel blocker. In patients with atrial flutter in one study, the relative risk for development of stroke was 1.4 in comparison to control subjects.[8]

A multicenter report by Stiell et al that prospectively evaluated management and 30-day outcomes in 1091 emergency department (ED) patients with recent-onset atrial fibrillation (84.7%) or atrial flutter (15.3%) found that oral anticoagulants were underprescribed and that patients discharged from the ED in sinus rhythm had a smaller likelihood of experiencing an adverse event.[9]  More than 10% of all patients had adverse events within 30 days, including one case of stroke, but no deaths were reported. Potential risk factors for adverse events included longer duration from arrhythmia onset, radiographic evidence of pulmonary congestion, previous history of stroke/transient ischemic attack, and ED discharge without being in sinus rhythm.[9]

Patients with concurrently diagnosed new rapid atrial fibrillation or atrial flutter and new reduced left ventricular ejection fraction (LVEF) appear to have  a high rate prevalence of left atrial appendage thrombi (LAAT).[10]  However, the presence of LAAT does not appear to be prognostic for eventual improvement.

Patient Education

Educating patients regarding medications and diet is important. Patients taking warfarin should avoid making major changes in their diet until they have consulted with their healthcare providers. Specifically, a sudden change in the consumption of green leafy vegetables, which are sources of vitamin K, can affect coagulation in patients taking warfarin, which inhibits vitamin K synthesis. This education is not needed with newer drugs that avoid these drug-drug or drug-food interactions, but these drugs lack the monitoring that warfarin can provide.

For patient education information, see the Heart Health Center, as well as Atrial Flutter, Arrhythmias (Heart Rhythm Disorders), Stroke, Supraventricular Tachycardia (SVT, PSVT), and Palpitations.

 

Presentation

History

Symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. Typical symptoms include the following:

  • Palpitations
  • Fatigue or poor exercise tolerance
  • Mild dyspnea
  • Presyncope

Less common symptoms include angina, profound dyspnea, or syncope resulting from compromised left ventricular function. Thromboembolic events are possible with this arrhythmia. In addition, patients may have symptoms of the conditions that are causing the atrial flutter. These may be noncardiac (eg, hyperthyroidism or pulmonary disease) or cardiac.

The clinician should attempt to elicit information about factors that may have precipitated the episode of atrial flutter, including alcohol, as well as medical conditions (eg, pneumonia or acute myocardial infarction) and surgical procedures. An effort should also be made to elicit any history of using stimulant drugs (eg, ginseng, cocaine, ephedra, or methamphetamine).

Determining when the onset of symptoms occurred is critical, in that the duration of the episode affects management. For atrial flutter lasting longer than 48 hours, anticoagulation with warfarin or transesophageal echocardiography is required to rule out thrombus in the left atrium before cardioversion to sinus rhythm. In patients with a history of atrial flutter, the history should include precipitating causes and modes of termination of the arrhythmia.

Atrial flutter rhythm itself is unstable and usually reverts either to atrial fibrillation or to sinus rhythm. It would be unusual but certainly not impossible for a patient to remain in stable chronic atrial flutter. A history of preexcitation syndrome (Wolff-Parkinson-White) indicates a need for caution; these patients are at risk for 1:1 conduction of the flutter waves, which can cause ventricular fibrillation.

Patients with concurrently diagnosed new rapid atrial fibrillation or atrial flutter and new reduced left ventricular ejection fraction typically have heavy alcohol intake and a high rate prevalence of left atrial appendage thrombi.[10]

Physical Examination

The patient’s general appearance and vital signs are important for determining the urgency of restoring sinus rhythm. Thus, the initial cardiopulmonary evaluation and monitoring for signs of cardiac or pulmonary failure help guide initial management.

Pay careful attention to the heart rate, blood pressure, and oxygen saturation. Tachycardia may or may not be present, depending on the degree of atrioventricular (AV) block associated with the atrial flutter activity.

The heart rate is often approximately 150 beats/min because of a 2:1 AV block. (This depends on the atrial firing rate, which may be influenced by medications as well as by intrinsic cardiac factors.) The venous pulsations may be more rapid at the rate of the flutter. Because the AV block may be variable, the pulse may be regular or slightly irregular. Hypotension is possible, but normal blood pressure is more commonly observed.

Other elements of the physical examination are as follows:

  • Palpate the neck and thyroid gland for goiter
  • Evaluate the neck for jugular venous distention
  • Auscultate the lungs for rales or crackles
  • Auscultate the heart for extra heart sounds and murmurs
  • Palpate the point of maximum impulse on the chest wall
  • Assess the lower extremities for edema or impaired perfusion

If embolization has occurred from intermittent atrial flutter, findings are related to brain or peripheral vascular involvement. In addition to neurologic insult, other complications of atrial flutter may include the following:

  • Embolization (arterial)
  • Congestive heart failure
  • Severe bradycardia
  • Myocardial rate–related ischemia
 

DDx

Diagnostic Considerations

Coarse atrial fibrillation may mimic atrial flutter over limited electrocardiogram (ECG) strips. Prolonged recordings will uncover an irregular rate and variation in P wave morphology (as compared to a regular rate and P wave morphology with atrial flutter). The distinction between atrial flutter and atrial tachycardia is generally arbitrarily based on the atrial rate, and does not mechanistically distinguish these rhythms.

The ECG should be reviewed for the following:

  • Artifact from tremor
  • Atrial tachycardia with atrioventricular block
  • Atrial tachycardia, multifocal
  • Narrow-complex tachyarrhythmias
  • Wide-complex tachyarrhythmias

Differential Diagnoses

 

Workup

Approach Considerations

Electrocardiography (ECG) is essential in making the diagnosis, and can provide essential information in distinguishing "typical" from "atypical" atrial flutter. Transthoracic echocardiography (TTE) is the preferred initial imaging modality for evaluating atrial flutter.

The history and physical examination findings guide laboratory studies. Although hyperthyroidism is a rare cause of atrial flutter, asymptomatic hyperthyroidism, especially in elderly patients, can manifest as atrial fibrillation or flutter and should be excluded with thyroid function studies.

Obtain a complete blood cell count if anemia is suspected or the patient has a history of recent or current blood loss associated with the presenting symptoms. Serum electrolyte levels and pulmonary function tests may be indicated based on the history. Obtain serum electrolyte and digoxin levels if appropriate. Consider obtaining blood gas measurements in patients with hypoxia or carbon monoxide intoxication.

Chest radiography may be useful in the evaluation of lung disease and the pulmonary vasculature. Chest radiographic findings are usually normal in patients with atrial flutter, but radiographic evidence of pulmonary edema may be present in subacute cases.

Electrocardiography

In the common form of typical atrial flutter, the electrocardiogram (ECG) shows sawtooth flutter (F) waves. Flutter waves are often visualized best in leads II, III, aVF, or V1 (see the image below). The flutter waves for typical atrial flutter are inverted (negative) in leads II, III, and aVF, negative in V6, and generally positive in V1 because of a counterclockwise reentrant pathway.[11] Sometimes, they are upright (positive) when the reentrant loop is clockwise. Flutter waves (particularly 2:1) can deform the ST complex in such a manner as to mimic an ischemic injury pattern on the 12-lead ECG, and often results in erroneous interpretations on computer-based ECG diagnosis.

A 12-Lead electrocardiogram of typical atrial flut A 12-Lead electrocardiogram of typical atrial flutter. Note the negative sawtooth pattern of the flutter waves in leads II, III, and aVF.

In typical atrial flutter, the atrial rate is usually 250-350 beats/min. The ventricular response may be regular or irregular. In patients with typical atrial flutter, class IA and IC antiarrhythmic drugs and amiodarone can reduce the rate to approximately 200 beats/min. If this occurs, the ventricles can respond in a 1:1 fashion to the slower atrial rate. The rate in atypical flutter is usually 350-450 beats/min.

The ventricular rate reflects a fixed mathematical relation between the flutter waves and the resulting QRS complexes. Variable atrioventricular (AV) conduction can also be seen; patients commonly present with 2:1 AV conduction. With 1:1 AV conduction, hemodynamic collapse may occur. Deterioration to 1:1 conduction can occur in patients with healthy hearts, but it is a particular risk in patients with a preexcitation syndrome (Wolff-Parkinson-White). An ECG clue to a preexcitation syndrome is a very short PR interval (< 0.115 s) and delta wave.

The morphology of the flutter wave can predict findings in the electrophysiology laboratory. A negative flutter wave in the inferior limb leads and a positive flutter wave in V1 are highly predictive of a counterclockwise circuit; however, with positive flutter waves in the inferior limb leads and negative flutter waves in V1, differentiating between clockwise typical atrial flutter and atypical forms of non–isthmus-dependent intra-atrial reentry is difficult.

Diagnostic Aids

Vagal maneuvers can be helpful in determining the underlying atrial rhythm if flutter waves are not seen well. Adenosine, administered in an intravenous (IV) push followed with an IV bolus with flush, can also be helpful in making the diagnosis of atrial flutter by transiently blocking the atrioventricular node (see the image below). Approximately 15% of atrial tachycardias will also terminate with adenosine.

Rhythm strips demonstrating typical atrial flutter Rhythm strips demonstrating typical atrial flutter unmasked by adenosine (Adenocard).

Exercise testing can be utilized to identify exercise-induced atrial fibrillation and to evaluate ischemic heart disease. A Holter monitor can be used to help identify arrhythmias in patients with nonspecific symptoms, to identify triggers, and to detect associated atrial arrhythmias.

Echocardiography

Transthoracic echocardiography (TTE) is the preferred initial imaging modality for evaluating atrial flutter. It can evaluate right and left atrial size, as well as the size and function of the right and left ventricles, thereby facilitating diagnosis of valvular heart disease, left ventricular hypertrophy, and pericardial disease.

TTE has low sensitivity for intra-atrial thrombi. Transesophageal echocardiography (TEE) is the preferred technique for detecting thrombus in the left atrium.

 

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 recommended because appendage blood flow velocity is lowest immediately after conversion and recovers slowly.

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.

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.

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]

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.

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.

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.

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]

 

Guidelines

Guidelines Summary

In August 2019, the European Society of Cardiology (ESC) in collaboration with the Association for European Paediatric and Congenital Cardiology (AEPC) released recommendations on the management of supraventricular tachycardia.[32, 33] Previous related guidelines include, but are not limited to, the 2015 American College of Cardiology, American Heart Association, and Heart Rhythm Society (ACC/AHA/HRS) guidelines for the management of supraventricular tachycardia which includes algorithms for both acute and ongoing treatment of atrial flutter.[14] These guidelines are summarized in the following sections.

2019 ESC/AEPC Guidelines for the Management of Supraventricular Tachycardia

Supraventricular Tachycardia Clinical Practice Guidelines (2019)

Several changes from the previous guidelines (2003) include revised drug grades as well as medications that are no longer considered, and changes to ablation techniques and indications.[32, 33]

Table. Medications, Strategies, and Techniques Specified or Not Mentioned in the 2019 Guidelines (Open Table in a new window)

Type of Tachycardia

Treatment (Grade)

Not Mentioned in 2019 Guidelines

Narrow QRS tachycardias

Verapamil and diltiazem; beta-blockers (now all are grade IIa)

Amiodarone, digoxin

Wide QRS tachycardias

Procainamide, adenosine (both grade IIa); amiodarone (IIb)

Sotalol, lidocaine

Inappropriate sinus tachycardia

Beta-blockers (IIa)

Verapamil/diltiazem, catheter ablation

Postural orthostatic tachycardia syndrome

Salt and fluid intake (IIb)

Head-up tilt sleep, compression stockings, selective beta-blockers, fludrocortisone, clonidine, methylphenidate, fluoxetine, erythropoietin, ergotaminel octreotide, phenobarbitone

Focal atrial tachycardia

Acute: beta-blockers (IIa); flecainide/propafenone, amiodarone (IIb)

Acute: procainamide, sotalol, digoxin

Chronic: beta-blockers; verapamil and diltiazem (all IIa)

Chronic: amiodarone, sotalol, disopyramide

Atrial flutter

Acute: ibutilide (I); verapamil and diltiazem, beta-blockers (all IIa); atrial or transesophageal pacing (IIb); flecainide/propafenone (III)

Acute: digitalis

Chronic: —

Chronic: dofetilide, sotalol, flecainide, propafenone, procainamide, quinidine, disopyramide

Atrioventricular nodal re-entrant tachycardia (AVNRT)

Acute: —

Acute: amiodarone, sotalol, flecainide, propafenone

Chronic: verapamil and diltiazem; beta-blockers (all IIa)

Chronic: amiodarone, sotalol, flecainide, propafenone, “pill-in-the-pocket” approach

Atrioventricular re-entrant tachycardia (AVRT)

Beta-blockers (IIa); flecainide/propafenone (IIb)

Amiodarone, sotalol, “pill-in-the-pocket” approach

SVT in pregnancy

Verapamil (IIa); catheter ablation (IIa when fluoroless ablation is available)

Sotalol, propafenone, quinidine, procainamide

Adapted from Brugada J, Katritsis DG, Arbelo E, et al, for the ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2019 Aug 31;ehz467. https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz467/5556821

2019 New Recommendations

For detailed recommendations on specific types of SVTs, please consult the original guidelines as listed under the references.

Class I (recommended or indicated)

For conversion of atrial flutter: Intravenous (IV) ibutilide, or IV or oral (PO) (in-hospital) dofetilide

For termination of atrial flutter (when an implanted pacemaker or defibrillator is present): High-rate atrial pacing

For asymptomatic patients with high-risk features (eg, shortest pre-excited RR interval during atrial fibrillation [SPERRI] ≤250 ms, accessory pathway [AP] effective refractory period [ERP] ≤250 ms, multiple APs, and an inducible AP-mediated tachycardia) as identified on electrophysiology testing (EPS) using isoprenaline: Catheter ablation

For tachycardia responsible for tachycardiomyopathy that cannot be ablated or controlled by drugs: Atrioventricular nodal ablation followed by pacing (“ablate and pace”) (biventricular or His-bundle pacing)

First trimester of pregnancy: Avoid all antiarrhythmic drugs, if possible

Class IIa (should be considered)

Symptomatic patients with inappropriate sinus tachycardia: Consider ivabradine alone or with a beta-blocker

Atrial flutter without atrial fibrillation: Consider anticoagulation (initiation threshold not yet established)

Asymptomatic preexcitation: Consider EPS for risk stratification

Asymptomatic preexcitation with left ventricular dysfunction due to electrical dyssynchrony: Consider catheter ablation

Class IIb (may be considered)

Acute focal atrial tachycardia: Consider IV ibutilide

Chronic focal atrial tachycardia: Consider ivabradine with a beta-blocker

Postural orthostatic tachycardia syndrome: Consider ivabradine

Asymptomatic preexcitation: Consider noninvasive assessment of the AP conducting properties

Asymptomatic preexcitation with low-risk AP at invasive/noninvasive risk stratification: Consider catheter ablation

Prevention of SVT in pregnant women without Wolff-Parkinson-White syndrome: Consider beta-1 selective blockers (except atenolol) (preferred) or verapamil

Prevention of SVT in pregnant women without Wolff-Parkinson-White syndrome and without ischemic or structural heart disease: Consider flecainide or propafenone

Class III (not recommended)

IV amiodarone is not recommended for preexcited atrial fibrillation.

2015 ACC/AHA/HRS Guideline for the Management of Supraventricular Tachycardia

Management of Acute Atrial Flutter

Hemodynamically unstable patients[14]

For rhythm control, synchronized cardioversion is recommended. (Class I recommendation)

For rate control, intravenous (IV) amiodarone is recommended. (Class IIa recommendation)

Hemodynamically stable patients[14]

For rhythm control, the following are recommended (all class I recommendations):

  • Synchronized cardioversion, oral dofetilide, IV ibutilide, and/or rapid atrial pacing
  • Rapid atrial pacing in patients who have pacing wires in place as part of a permanent pacemaker or implantable cardioverter-defibrillator or for temporary atrial pacing after cardiac surgery
  • Elective synchronized cardioversion

Note that synchronized cardioversion or rapid atrial pacing is not appropriate for rhythms that break or spontaneously recur.

For rate control, beta blockers, diltiazem, or verapamil is recommended. (Class I recommendation)[14] IV amiodarone is recommended when beta blockers are contraindicated. (Class IIa recommendation)

Management of Ongoing Atrial Flutter

Rate control[14]

Administer beta blockers, diltiazem, or verapamil. (Class I recommendation)

  • Beta blockers are generally preferred in patients with heart failure.
  • Given the potential for accelerated ventricular rates degenerating to ventricular fibrillation, beta blockers, diltiazem, and verapamil should be avoided in patients with pre-excited atrial flutter.

Rhythm control[14]

After assuring adequate anticoagulation or excluding left atrial thrombus by transesophageal echocardiography (TEE) before conversion, catheter ablation is preferred to long-term pharmacologic therapy for cavotricuspid isthmus (CTI)-dependent atrial flutter.(Class I recommendation) Other indications for catheter ablation include the following:

  • For non–CTI-dependent flutter after failure of at least one antiarrhythmic agent (class I)
  • For CTI-dependent atrial flutter that occurs as the result of flecainide, propafenone, or amiodarone used to treat atrial fibrillation (AF) (class IIa) or as primary therapy, before antiarrhythmic drugs, after carefully weighing the potential risks and benefits of treatment options (class IIa)
  • For patients undergoing catheter ablation of AF who also have a history of CTI-dependent atrial flutter (class IIa)
  • For asymptomatic patients with recurrent atrial flutter (class IIb)

Antiarrhythmic agents can be considered in patients with symptomatic, recurrent atrial flutter, with the drug choice depending on the patient's underlying heart disease and comorbidities. (Class IIa recommendation) Drug choices include the following:

  • Amiodarone
  • Dofetilide
  • Sotalol

​Flecainide or propafenone may be considered in patients without structural heart disease or ischemic heart disease who have symptomatic recurrent atrial flutter. (Class IIb recommendation)

Prevention of Thromboembolic Complications

The 2015 ACC/AHA/HRS guidelines[14] concur with the 2012 American College of Chest Physicians (ACCP) thrombosis prevention recommendation[22] that the anticoagulation strategy used for AF be followed for patients with atrial flutter. Select, specific ACCP recommendation are summarized below.[22]

No therapy for patients at low risk of stroke (eg, CHADS2 score = 0). For patients who choose therapy, use aspirin (75 mg to 325 mg daily) rather than oral anticoagulation or combination therapy with aspirin and clopidogrel. (Grade 2B)

For patients at intermediate risk of stroke (eg, CHADS2 score = 1), oral anticoagulation is preferred to no treatment (Grade 1B), aspirin daily, or combination therapy with aspirin and clopidogrel. (Grade 2B)

For patients at high risk of stroke (eg, CHADS2 score ≥2), oral anticoagulation is preferred to no treatment (Grade 1A), aspirin daily, or combination therapy with aspirin and clopidogrel. (Grade 1B)

For oral anticoagulation, use dabigatran 150 mg twice daily rather than adjusted-dose vitamin K antagonist (VKA) therapy (target INR range, 2.0-3.0) (Grade 2B)

Patients who are unsuitable for or choose not to take an oral anticoagulant (for reasons other than concerns about major bleeding), use combination therapy with aspirin and clopidogrel. (Grade 1B)

In general, when atrial flutter persists for longer than 48 hours, 4 weeks of adequate anticoagulation must be provided or the absence of thrombus on TEE documented before attempting cardioversion to sinus rhythm. Postconversion anticoagulation is recommended for a minimum of 4 weeks, because thromboembolic complications can occur spontaneously after cardioversion or ablation. (Grade 1B)

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

 

Medication

Medication Summary

Medications are usually administered in the acute setting or to patients who are not candidates for radiofrequency ablation (RFA). Agents can be used to control the ventricular rate, terminate acute episodes, prevent or decrease the frequency or duration of recurrent episodes, and prevent complications.

Drug initiation in an outpatient setting is generally accepted in patients without underlying structural heart disease who are in sinus rhythm. In addition, many specialists initiate outpatient drug therapy in patients with therapeutically anticoagulated atrial flutter who are awaiting outpatient electrical cardioversion in the near future.

Certain medications, such as sotalol and dofetilide, should be initiated in an inpatient setting because they can prolong the QT interval and be proarrhythmic. Regardless, close patient follow-up is mandated, with frequent electrocardiographic (ECG) or transtelephonic monitoring for potential signs of proarrhythmia.

Antidysrhythmics, Class IC

Class Summary

Class IC antidysrhythmics are indicated for use in patients with atrial flutter and supraventricular tachycardia (SVT) without structural heart disease. Because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) may occur with these agents, they are used in conjunction with atrioventricular (AV) nodal blocking agents in these cases.

Propafenone (Rythmol)

Propafenone treats life-threatening arrhythmias. It possibly works by reducing spontaneous automaticity and prolonging the effective refractory period. It is indicated for patients with atrial flutter and SVT without structural heart disease. Propafenone is used in conjunction with AV nodal blocking agents when administered to patients in atrial fibrillation because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) is noted.

Flecainide (Tambocor)

Flecainide treats life-threatening ventricular arrhythmias. It causes prolongation of refractory periods and decreases action potential without affecting duration. This agent blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart, with greatest effect on the His-Purkinje system.

Effects on AV nodal conduction time and intra-atrial conduction times, though present, are less pronounced than those on ventricular conduction velocity. Flecainide is used in conjunction with AV nodal blocking agents when administered to patients in atrial fibrillation because conversion to atrial flutter with 1:1 conduction (producing fast ventricular rates) is noted.

Antidysrhythmics, Class III

Class Summary

Class III antidysrhythmics are used to slow ventricular response by inhibiting AV nodal conduction during atrial fibrillation or flutter. They are also indicated for use in conjunction with class IA and IC antiarrhythmics, which slow atrial fibrillation or flutter rate and may cause more rapid ventricular response.

Beta blockers currently play more of a secondary role in rate control in atrial flutter or fibrillation. Patients receiving these agents require careful monitoring of blood pressure.

Amiodarone (Cordarone, Parcerone, Nexterone)

Amiodarone may inhibit AV conduction and sinus node function. It prolongs the action potential and refractory period in myocardium and inhibits adrenergic stimulation. It blocks sodium channels with high affinity for inactive channels, blocks potassium channels, and weakly blocks calcium channels. In addition, amiodarone noncompetitively blocks alpha- and beta-adrenergic receptors. Before administration, control ventricular rate and heart failure (if present) with digoxin or calcium channel blockers.

Dronedarone (Multaq)

Dronedarone blocks sodium channels, blocks beta1-adrenergic receptors, and alters adenyl cyclase generation (ie, it has negative inotropic effects). It blocks potassium channels (eg, hERG) and therefore prolongs cardiac repolarization.

Dronedarone is indicated for reducing the risk of cardiovascular hospitalization in patients with paroxysmal atrial fibrillation or atrial flutter who have had a recent episode of either arrhythmia, are in sinus rhythm or will be cardioverted, and have associated cardiovascular risk factors.

Sotalol (Betapace, Betapace AF, Sorine)

This class III antiarrhythmic agent blocks potassium channels, prolongs action potential duration, and lengthens the QT interval. It is a non–cardiac-selective beta-adrenergic blocker. Sotalol is be effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease. Class III effects are seen only at oral dosages of 160 mg/day or higher.

Ibutilide (Corvert)

Ibutilide is a newer class III antiarrhythmic agent that may work by increasing action potential duration and thereby changing atrial cycle length variability. It is indicated for acute termination of atrial fibrillation or flutter of recent onset. Potentially fatal arrhythmias can occur with ibutilide, usually in association with QT prolongation, during or within a number of hours after its administration.

Dofetilide (Tikosyn)

Dofetilide is the prototype of a "pure" class III agent. It has been approved by the US Food and Drug Administration (FDA) for maintenance of sinus rhythm after conversion from atrial fibrillation or atrial flutter lasting longer than 1 week. It is also indicated for conversion of atrial fibrillation and atrial flutter to normal sinus rhythm. If patients do not convert within 24 hours of initiation of therapy, electrical cardioversion should be considered.

Torsades de pointes is the only complicating arrhythmia showing a dose-response relation. The prevalence with supraventricular arrhythmia is 0.8%. The majority of torsades de pointes episodes occur within the first 3 days of therapy.

Dofetilide has no effect on cardiac output, cardiac index, stroke volume index, or systemic vascular resistance in patients with ventricular tachycardia, mild to moderate heart failure, angina, and either normal or reduced left ventricular ejection fraction (LVEF). It does not affect blood pressure.

Dofetilide blocks delayed rectifier current (IKr) and prolongs action potential duration; indeed, even at higher dosages, it has no effect on other depolarizing potassium currents (IKs and Ik1). It terminates induced reentrant tachyarrhythmias (atrial fibrillation or flutter and ventricular tachycardia) and prevents their reinduction. At clinically prescribed concentrations, it has no effect on sodium channels, which are associated with class I effects. Furthermore, no effect is noted on alpha- or beta-adrenergic receptors.

Dofetilide must be initiated with continuous ECG monitoring, and monitoring must be continued for at least 12 hours after conversion. The dosage must be individualized according to creatinine clearance (CrCl) and QTc (use the QT interval if the heart rate is below 60 beats/min). There is no information on use of this drug for heart rates lower than 50 beats/min.

Antidysrhythmics, Class IV

Class Summary

Class IV antiarrhythmic drugs are used as rate control agents. They affect calcium channels by inhibiting calcium ions from entering areas of the vascular smooth muscle and myocardium during depolarization. These agents also slow automaticity and conduction of the AV node.

Diltiazem (Cardizem, Cardizem CD, Cardizem LA, Cartia XT)

Diltiazem is a nondihydropyridine calcium channel blocker that produces relaxation of coronary vascular smooth muscle and coronary vasodilation by inhibiting calcium ions from entering the "slow channels" and myocardium during depolarization. Intravenous (IV) diltiazem is indicated for control of rapid ventricular rate in patients with atrial fibrillation or atrial flutter.

Verapamil (Calan, Isoptin, Verelan)

During depolarization, verapamil inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It can diminish premature ventricular contractions (PVCs) associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at the AV node, it can restore normal sinus rhythm in patients with paroxysmal SVT.

Antidysrhythmics, Class V

Class Summary

Cardiac glycosides decrease AV nodal conduction primarily by increasing vagal tone. They are used mainly in the context of atrial fibrillation and atrial flutter with congestive heart failure.

Digoxin (Lanoxin)

Digitalis slows sinus node and AV node conduction via a vagomimetic effect and is not very effective if sympathetic tone is increased. It has direct inotropic effects in addition to indirect effects on the cardiovascular system.

The effects on myocardium involve both direct action on cardiac muscle that increases myocardial systolic contractions and indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. This agent is generally not recommended unless depressed left ventricular function is present.

Anticoagulants, Cardiovascular

Class Summary

Anticoagulants are used to prevent thromboembolic complications.

Heparin

Heparin augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse clots but can inhibit further thrombogenesis and prevent reaccumulation of clot after spontaneous fibrinolysis. Most data are related to use of unfractionated heparin (UFH). Low-molecular-weight heparin (LMWH) is probably as effective, but results from clinical studies are not yet available.

Warfarin (Coumadin, Jantoven)

Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an international normalized ratio (INR) of 2-3.

Dabigatran (Pradaxa)

Dabigatran is a direct thrombin inhibitor that has been approved by the FDA for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The oral adult dose is 150 mg twice daily.

The American Heart Association (AHA) recommends dabigatran as a reasonable alternative to warfarin in patients who have 1 or more additional risk factors for stroke and a creatinine clearance greater than 30 mL/min. The American College of Chest Physicians (ACCP) recommends dabigatran over warfarin for primary and secondary prevention of cardioembolic stroke or transient ischemic attack.

Dabigatran is a prodrug that is converted to the active drug in vivo. It inhibits both free and fibrin-bound thrombin; it also inhibits coagulation by preventing thrombin-mediated effects. Dabigatran is not recommended for patients with a prosthetic heart valve or hemodynamically significant valve disease, severe renal failure (CrCl < 15 mL/min), or advanced liver disease.

Rivaroxaban (Xarelto)

Rivaroxaban is a direct factor Xa inhibitor approved by the FDA for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Multiple strengths are available: 10 mg, 15 mg, and 20 mg. Dosing and administration depend on the indication and the presence and degree of renal impairment. The 15-mg and 20-mg tablets can be crushed and administered via a nasogastric or gastrostomy tube (the 10-mg tablet cannot be crushed).

Rivaroxaban should be discontinued 24 hours before a scheduled surgical procedure, to reduce the risk of bleeding. Contraindications include active bleeding and hypersensitivity to rivaroxaban. It is a pregnancy category C drug.

Apixaban (Eliquis)

Apixaban is a direct factor Xa inhibitor approved by the FDA in 2012 for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The standard dose is 5 mg twice daily. Use 2.5 mg twice daily if any 2 of the following conditions are met:

* Age >80 years

* Serum creatinine level >1.5 mg/dL

* Weight < 60 kg

Apixaban is not recommended for use in patients with any of the following:

* CrCl < 15 mL/min or dialysis

* Prosthetic heart valve

* Severe hepatic impairment

Apixaban is contraindicated in patients with active bleeding or hypersensitivity to apixaban. It should be discontinued at least 48 hours before elective surgical procedures or invasive procedures with a moderate or high risk of unacceptable or clinically significant bleeding and at least 24 hours before elective surgical procedures or invasive procedures with a low risk of bleeding or in which the bleeding would be noncritical in location and easily controlled.

Edoxaban (Savaysa)

Edoxaban is a direct factor Xa inhibitor approved by the FDA in 2015 for the prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The standard dose is 60 mg once daily.

Renal function must be checked prior to starting the drug, and edoxaban should not be used in patients if the CrCl is >95 mL/minute. Dosage reduction is necessary in patients with CrCl of 15 to 50 mL/minute.

Edoxaban is not recommended for use in patients with any of the following:

* CrCl * Prosthetic heart valve or valvular heart disease* Severe hepatic impairment

Beta-Blockers, Beta-1 Selective

Class Summary

These agents are used to slow ventricular response by slowing AV nodal conduction during atrial fibrillation or flutter. They are also indicated for use in conjunction with class IA and IC antiarrhythmics, which slow atrial fibrillation or flutter rate and may cause more rapid ventricular response.

Beta blockers currently play more of a secondary role in rate control in atrial flutter and fibrillation. Patients receiving these agents require careful monitoring of blood pressure.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG.

Atenolol (Tenormin)

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 receptors.

Esmolol (Brevibloc)

Esmolol (Brevibloc)

Esmolol is excellent for use in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Its short half-life of 8 min allows titration to desired effect and quick discontinuation if necessary.

 

Questions & Answers

Overview

What is atrial flutter (AFL)?

What signs and symptoms of atrial flutter (AFL)?

What are less common symptoms of atrial flutter (AFL)?

Which physical findings are characteristic of atrial flutter (AFL)?

What is included in the physical exam for suspected atrial flutter (AFL)?

What are possible complications of atrial flutter (AFL)?

Which tests are performed in the workup of atrial flutter (AFL)?

What is the role of transthoracic echocardiography (TTE) in the diagnosis of atrial flutter (AFL)?

What are the treatment options for symptomatic atrial flutter (AFL)?

What is atrial flutter (AFL) and how is it characterized?

How do typical (or classic) and atypical atrial flutter (AFL) differ?

Which cardiac disorders are most frequently associated with atrial flutter (AFL)?

What are the symptoms of atrial flutter (AFL)?

What is the role of ventricular response rate control in the management of atrial flutter (AFL)?

How is atrial flutter (AFL) similar to atrial fibrillation (AF)?

What is the pathogenesis of typical atrial flutter (AFL)?

What is the role of an anatomic or functional block in the pathogenesis of atrial flutter (AFL) in animal models?

What is the role of crista terminalis in the pathogenesis of atrial flutter (AFL)?

What is the pathophysiology of typical counterclockwise atrial flutter (AFL)?

What is the pathophysiology of typical clockwise atrial flutter (AFL)?

What is the pathophysiology of atypical atrial flutter (AFL)?

Which cardiac disorders are associated with atrial flutter (AFL)?

Which medical conditions are associated with atrial flutter (AFL)?

What causes atrial flutter (AFL) following open heart surgery?

What are the genetic causes of atrial flutter (AFL)?

What is the prevalence of atrial flutter (AFL) in the US?

How does the prevalence of atrial flutter (AFL) vary by sex?

How does the incidence of atrial flutter (AFL) vary by age?

What is the prognosis of atrial flutter (AFL)?

What causes morbidity and mortality in atrial flutter (AFL)?

What is the life expectancy for patients with atrial flutter (AFL)?

What is the prognosis of typical atrial flutter (AFL)?

What are the major complications rates for catheter ablation procedures to treat atrial flutter (AFL)?

What causes conversion of atrial fibrillation (AF) to atrial flutter (AFL)?

What is the prognosis of atrial flutter (AFL) following emergency department (ED) treatment?

What causes left atrial appendage thrombus (LAAT) in atrial flutter (AFL)?

What is the included in the patient education Information for atrial flutter (AFL)?

Presentation

What are common symptoms of atrial flutter (AFL)?

What are less common symptoms of atrial flutter (AFL)?

What should be the focus of history in the evaluation of atrial flutter (AFL)?

What is the importance of the onset of symptoms in the evaluation of atrial flutter (AFL)?

What does preexcitation syndrome in the history of a patient with atrial flutter (AFL) suggest?

What is commonly present in the history of a patient with concurrent atrial flutter (AFL) and atrial fibrillation (AF)?

What is the role of general appearance and vital signs in the evaluation of atrial flutter (AFL)?

What should be included in the initial physical exam for suspected atrial flutter (AFL)?

Which cardiac findings are characteristic of atrial flutter (AFL)?

What elements should be included in the physical exam for atrial flutter (AFL)?

What are complications of atrial flutter (AFL)?

DDX

How is atrial fibrillation (AF) differentiated from atrial flutter (AFL)?

How should electrocardiogram (ECG) findings be reviewed in the evaluation of atrial flutter (AFL)?

What are the differential diagnoses for Atrial Flutter?

Workup

How is atrial flutter (AFL) diagnosed?

What is the role of the history and physical exam in the workup of atrial flutter (AFL)?

What is the role of a CBC count in the diagnosis of atrial flutter (AFL)?

What is the role of chest radiography in the diagnosis of atrial flutter (AFL)?

Which electrocardiogram (ECG) results are characteristic of atrial flutter (AFL)?

What is the role of atrial rate in the diagnosis of atrial flutter (AFL)?

What is the role of ventricular rate in the diagnosis of atrial flutter (AFL)?

What is the role of wave morphology in the diagnosis of atrial flutter (AFL)?

What is the role of vagal maneuvers in the diagnosis of atrial flutter (AFL)?

What is the role of exercise testing in the diagnosis of atrial flutter (AFL)?

What is the role of transthoracic echocardiography (TTE) in the diagnosis of atrial flutter (AFL)?

Treatment

What are the treatment goals for symptomatic atrial flutter (AFL)?

What is the main difference between atrial fibrillation (AF) and atrial flutter (AFL)?

What is the first-line therapy in the treatment of atrial flutter (AFL)?

What is the role of radiofrequency ablation (RFA) in the treatment of atrial flutter (AFL)?

When is cardioversion indicated in the treatment of atrial flutter (AFL)?

When should anticoagulation therapy be administered in the treatment of atrial flutter (AFL)?

When are rate- and rhythm-control strategies indicated in the treatment of atrial flutter (AFL)?

Which medications slow atrioventricular (AV) node conduction in atrial flutter (AFL)?

What is the role of anticoagulation therapy in the treatment of atrial flutter (AFL)?

What is the role of therapeutic international normalized ratio (INR) in the treatment of atrial flutter (AFL)?

What are the treatment options for atrial flutter (AFL) in patients needing cardiac surgery?

What is the role of ventricular rate control in the treatment of atrial flutter (AFL)?

What is the success rate of electrical conversion for the treatment of atrial flutter (AFL)?

What are the treatments options for atrial flutter (AFL) when cardioversion is unsuccessful?

What technique is used to perform cardioversion for the treatment of atrial flutter (AFL)?

How should electrodes be positioned in cardioversion for the treatment of atrial flutter (AFL)?

How does the efficacy of anterior-posterior electrode positioning compare to anterior-lateral positioning for cardioversion of atrial flutter (AFL)?

What is the role of dofetilide in the treatment of atrial flutter (AFL)?

What is the role of ibutilide in the treatment of atrial flutter (AFL)?

What is the role of IC antiarrhythmic agents in the treatment of atrial flutter (AFL)?

How is the risk for thromboembolic complications of atrial flutter reduced?

What is the similarities and differences between atrial fibrillation and atrial flutter (AFL) on TEE?

What is the prevalence of thrombotic events in atrial flutter (AFL)?

What is the risk of stroke in atrial flutter (AFL)?

What is the CHA2DS2-VASc score and how is it used in atrial flutter (AFL)?

How frequently do postcardioversion thromboembolic events complicate atrial flutter (AFL)?

How is postcardioversion stunning managed in atrial flutter (AFL)?

When is anticoagulation therapy indicated in patients receiving catheter ablation for atrial flutter (AFL)?

How is catheter ablation used to treat atypical atrial flutter (AFL)?

What is the role of radiofrequency ablation (RFA) in the treatment of atrial flutter (AFL)?

What are the benefits of catheter ablation for the treatment of atrial flutter (AFL)?

What are the limitations of radiofrequency ablation (RFA) for the treatment of atrial flutter (AFL)?

How is catheter ablation performed in patients with typical atrial flutter (AFL)?

What is the role of a line of conduction block during radiofrequency ablation (RFA) for atrial flutter radiofrequency ablation (RFA)?

What is the recurrence rate for atrial flutter (AFL) following radiofrequency ablation (RFA)?

What is the efficacy of radiofrequency ablation (RFA) for the treatment of atypical atrial flutter (AFL)?

What is the role of ultra-high density-activation sequence mapping (UHD-ASM) in the ablation of atypical atrial flutter (AFL)?

How is atrial flutter (AFL) managed after the initial episode is terminated?

Which treatments should be considered prior to antiarrhythmic drug therapy for atrial flutter (AFL)?

What is the efficacy of antiarrhythmic agents in the treatment of atrial flutter (AFL)?

How should antiarrhythmic agents be selected for the treatment of atrial flutter (AFL)?

What is the role of amiodarone in the treatment of atrial flutter (AFL)?

Guidelines

Which organizations have released treatment guidelines for atrial flutter (AFL)?

What are the newest guidelines for the management of supraventricular tachycardia?

What are the ESC/AEPC guidelines for the management of supraventricular tachycardia?

What are the ACC/AHA/HRS recommendations for rate control in acute atrial flutter (AFL)?

What are the ACC/AHA/HRS recommendations for rhythm control in acute atrial flutter (AFL)?

What are the ACC/AHA/HRS recommendations for rate control in ongoing atrial flutter (AFL)?

What are the ACC/AHA/HRS recommendations for rhythm control in ongoing atrial flutter (AFL)?

What are the ACC/AHA/HRS recommendations for use of antiarrhythmic agents in the treatment of ongoing atrial flutter (AFL)?

What are the thrombosis prevention guidelines for atrial flutter (AFL)?

What is the ACCP recommended anticoagulation therapy for patients with atrial flutter (AFL) at risk of stroke?

What are the ACCP recommended oral anticoagulants for atrial flutter (AFL)?

What are the ACCP anticoagulation recommendations for persistent atrial flutter (AFL)?

What are the ACCP recommendations for use of long-term anticoagulation therapy in atrial flutter (AFL)?

What is the ACCP recommended anticoagulation therapy for patients with atrial flutter (AFL) at intermediate risk of stroke?

Medications

When are medications administered for the treatment of atrial flutter (AFL)?

When are mediations indicated for the outpatient treatment of atrial flutter (AFL)?

Which medications are indicated for inpatient care of atrial flutter (AFL)?

Which medications in the drug class Antidysrhythmics, Class IC are used in the treatment of Atrial Flutter?

Which medications in the drug class Antidysrhythmics, Class III are used in the treatment of Atrial Flutter?

Which medications in the drug class Antidysrhythmics, Class IV are used in the treatment of Atrial Flutter?

Which medications in the drug class Antidysrhythmics, Class V are used in the treatment of Atrial Flutter?

Which medications in the drug class Anticoagulants, Cardiovascular are used in the treatment of Atrial Flutter?

Which medications in the drug class Beta-Blockers, Beta-1 Selective are used in the treatment of Atrial Flutter?