Atrial Flutter

• Daniel R. Frisch, M.D.

 Basic Information

Definition

Typical atrial flutter is the term commonly applied to the atrial macroreentrant circuit that circulates around the tricuspid annulus in the right atrium. The critical isthmus of the circuit is the tissue between the inferior vena cava and the tricuspid annulus, and a more precise name for this arrhythmia is cavotricuspid isthmus-dependent atrial flutter, or CTI flutter. Because of its anatomic and physiologic stability, the result is regular atrial depolarizations, typically at a rate of 250 to 350 beats/min. Regular, macroreentrant atrial arrhythmias at this rate that do not use the CTI are referred to as atypical atrial flutter. Because of the circuit’s stability, conduction through the atrioventricular node (AVN) is often predictable at a common mathematical denominator. For example, when the flutter rate is 300 beats/min, 2:1 conduction results in a ventricular rate of 150 beats/min. By extension, 3:1 conduction results in a ventricular rate of 100 beats/min, 4:1 in a rate of 75 beats/min, and 5:1 in a rate of 60 beats/min. If the regular atrial impulses conduct at a variable rate through the AVN, the result may be an irregular QRS pattern.

ICD-10CM CODES
I48.3	Typical atrial flutter
I48.4	Atypical atrial flutter
I48.92	Unspecified atrial flutter

Epidemiology & Demographics

1. •

   Atrial flutter is the second most common atrial tachyarrhythmia after atrial fibrillation, with an estimated 200,000 new cases annually in the United States.

2. •

   Atrial flutter is common in patients with congestive heart failure, COPD, or during the first week after open-heart surgery.

3. •

   Atrial flutter occurs more frequently with advancing age (5/10,0000 age <50 vs 587/100,000 age >80 yr) and 2.5 times more frequently in men than in women.

4. •

   Patients taking antiarrhythmics for chronic suppression of atrial fibrillation may convert to atrial flutter.

5. •

   Atrial flutter is typically seen in patients with underlying structural heart disease and is uncommon in children or young adults.

6. •

   More than 50% of patients with atrial flutter will develop atrial fibrillation in 3 years, and more than 80% will develop atrial fibrillation within 5 years. This is important when considering treatment options for atrial flutter.

Classification

Historically, the Wells classification designated atrial flutter as type I and type II. However, it is now recognized that tachycardias satisfying either of the definitions for type I or type II can be caused by reentrant circuits or by rapid focal atrial tachycardia, and this classification is infrequently used. Designating atrial flutter based on whether or not it is CTI dependent is more useful because of the management (i.e., ablation) options. Type I CTI-dependent atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 350 beats/min. The reentrant loop circles the right atrium, passing through the CTI, a body of fibrous tissue in the lower atrium between the inferior vena cava and the tricuspid valve. CTI flutter can revolve around the tricuspid annulus in either direction (counterclockwise or clockwise) when viewing the tricuspid annulus en face.

1. •

   Counterclockwise atrial flutter is the more common type (∼75%). The flutter waves are “sawtooth” and negative on the surface ECG leads II, III, and aVF; positive in V1; and negative in V6 (Fig. 1).

2. •

   Clockwise atrial flutter is less common (∼25%): The reentry loop cycles in the opposite direction; thus, the flutter waves are upright in leads II, III, and aVF; negative in V1; and positive in V6 (Fig. 2).

Atypical atrial flutter is defined by absence of CTI dependence and may occur in patients with prior cardiac surgery, congenital heart disease, or prior radiofrequency ablation (especially left atrial ablation for atrial fibrillation) or may be idiopathic. One ECG feature is the lack of discordance between the inferior leads (leads II, III, and aVF) and V1. Flutter circuits in the left atrium often have upright flutter waves in all precordial leads.

Physical Findings & Clinical Presentation

1. •

   Palpitations

2. •

   Dizziness, lightheadedness, syncope, or near syncope

3. •

   Angina

4. •

   Congestive heart failure

5. •

   Embolic phenomena from intracardiac thrombus

Etiology

1. •

   Age-related degenerative changes

2. •

   Rheumatic heart disease

3. •

   Congenital heart disease

4. •

   Left ventricular dysfunction or congestive heart failure

5. •

   Acute myocardial infarction (rarely)

6. •

   Thyrotoxicosis

7. •

   Pulmonary embolism

8. •

   Mitral valve disease

9. •

   Cardiac surgery

10. •

    Chronic obstructive pulmonary disease

11. •

    Obesity

12. •

    Pericarditis

13. •

    Pulmonary hypertension

14. •

    Antiarrhythmic therapy use in patients with atrial fibrillation

Diagnosis

Differential Diagnosis

1. •

   Atrial fibrillation

2. •

   Atrial tachycardia

3. •

   Supraventricular tachycardia:

   1. ○

      Atrioventricular node reentry

   2. ○

      Orthodromic reciprocating tachycardia (using a concealed bypass tract)

   3. ○

      Junctional ectopic tachycardia

   4. ○

      Wolff-Parkinson-White syndrome

4. •

   Sinus tachycardia

Workup

1. •

   ECG

2. •

   Laboratory evaluation

3. •

   Assessment of CHA₂DS₂-VaSc score

Laboratory Tests

1. •

   Thyroid function studies

2. •

   Serum electrolytes, including renal and hepatic tests (anticipating antiarrhythmic therapy use)

Imaging Studies

1. •

   ECG:

   1. 1.

      Absence of P waves

   2. 2.

      Regular, “sawtooth,” or “F” (flutter)” wave pattern without an isoelectric baseline in leads II, III, and AVF (seen most commonly with counterclockwise typical CTI-flutter)

   3. 3.

      There is rarely 1:1 atrioventricular (AV) conduction in atrial flutter (unless pre-excitation is present). Rather, AV conduction is usually in a 2:1 (Fig. 1), 3:1, or 4:1 fashion, with corresponding usual ventricular rates of 150, 100, or 75 beats/min, respectively (assuming an atrial rate of 300 beats/min). With high vagal tone or AV block, ventricular rates may be slow in atrial flutter.

      

      

2. •

   Echocardiography (for new diagnoses) to evaluate for structural heart disease (ventricular size, thickness, and function; atrial size, and valve function).

3. •

   Transesophageal echocardiography: consider in patients with associated structural or functional heart disease to ascertain the presence of intracardiac thrombi, in the absence of an appropriate duration of anticoagulation.

4. •

   Holter monitoring or event recorder to assess for paroxysmal atrial flutter or rate control or to identify the arrhythmia if symptoms are nonspecific or to identify triggering events.

5. •

   Electrophysiologic studies: required for a precise diagnosis, for mapping pathway, and for ablation.

Treatment

Nonpharmacologic Therapy

1. •

   Vagal maneuvers (e.g., the Valsalva maneuver or carotid sinus massage) may transiently slow the ventricular rate (by increasing AV block) and may make flutter waves more evident. Adenosine may be similarly helpful for diagnostic purposes, allowing the unmasking of the atrial rhythm in the absence of ventricular activity. Maneuvers that affect AV conduction would be unlikely to terminate atrial flutter.

2. •

   Direct current cardioversion is the treatment of choice for acute management of atrial flutter associated with hemodynamic instability or debilitating symptoms such as angina, congestive heart failure, or hypotension. Electrical cardioversion may be successful with energies as low as 25 joules, but because 100 joules is virtually always successful, this may be a reasonable initial shock strength. If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore normal sinus rhythm. Sedation of a conscious patient is highly recommended before cardioversion is performed. The use of external defibrillators with biphasic waveforms decreases the amount of energy required for cardioversion and improves cardioversion success rate. Patients should be therapeutically anticoagulated for at least a month or longer depending on their stroke risk (CHA₂DS₂-VASc score; Table 1).

   TABLE1 CHA₂DS₂-VASc Risk Score for Prediction of Stroke Risk in Atrial Fibrillation

   Risk Factor	Points
   CHF/LV dysfunction	1
   Hypertension	1
   Age ≥75 years	2
   Diabetes mellitus	1
   Stroke/TIA/embolism	2
   Vascular disease	1
   Age 64-74 years	1
   Sex category (female)	1
   Maximum score	9
   CHF, congestive heart failure; LV, left ventricular; TIA, transient ischemic attack.

3. •

   Overdrive pacing in the atrium may also terminate atrial flutter. This method is especially useful in patients who have recently undergone cardiac surgery and still have temporary atrial pacing wires and in patients who have an implanted pacemaker or defibrillator with an atrial lead.

4. •

   Radiofrequency ablation to interrupt the atrial flutter is highly effective for patients with chronic or recurring atrial flutter and is generally considered first-line therapy in those with recurrent episodes of atrial flutter and may be offered for a first-ever episode of atrial flutter. It has been shown to improve health-related quality of life. Despite successful ablation of atrial flutter, however, the risk of future atrial fibrillation remains.

Acute Rx

1. •

   Treatment choices are based on clinical circumstances. Fig. 3 describes an acute treatment of atrial flutter algorithm. Table 2 summarizes atrial flutter therapy.

   

   TABLE2 Atrial Flutter TherapyFrom Olshansky B, Chung MK, Pogwizd SM, et al.: Arrhythmia essentials, ed 2, Philadelphia, 2017, Elsevier.

   Acute therapy for poorly tolerated AFL or continuous rapid ventricular rate	• If prolonged (i.e., >48 to 72 h), anticoagulation with heparin followed by therapeutic warfarin or NOAC as cardioversion may be associated with thromboembolic risk. Anticoagulation guidelines for cardioversion are the same as for atrial fibrillation and may indicate need for a TEE for prolonged episodes. Adenosine and carotid massage can be used to help to diagnose AFL masquerading as sinus rhythm. • First line: DCC under anesthesia with anticoagulation as necessary. Consider the length of the episode. • Second line: Ibutilide or procainamide may be attempted for conversion prior to DCC attempts. Ibutilide may be 70% effective if AFL has been present for <48 h, although often this is not known with certainty. Procainamide may help maintain sinus rhythm. • Alternate: Rapid atrial pacing (esophageal, epicardial, or endocardial, depending on the situation). To pace terminate, pace for 10 to 15 s at a rate of 10% to 20% faster than rate of flutter. If ineffective, burst pace 10 bpm faster at a time for 10 to 15 s at a time until conversion to AF or sinus rhythm. Adding procainamide may help pace termination efficacy; however, it may speed AV conduction if the ventricular response is not adequately controlled with AV nodal blocker drugs (see Chronic prevention, below); 20% to 30% will pace to AF and 10% to 20% will have no effect from pacing, depending on patient selection for the procedure. When AF occurs, it is usually short lived and terminates spontaneously within 24 h. If persistent, DCC can be attempted with or without antiarrhythmic drugs. Rapid AFL (atrial rate >350) and atrial fib/flutter usually cannot be pace terminated. However, slower AFL (rate <350) of any flutter wave morphology can often be pace terminated. • Oral drug loading alone to terminate AFL is rarely useful. • If recurrent episodes, use class IC or III antiarrhythmic drugs until steady state is achieved, then attempt cardioversion. These drugs (particularly 1C drugs) may stabilize the flutter circuit. It may also create another form of AFL—“IC” AFL—from AF. Ablation remains first-line therapy, especially if AFL is isthmus dependent. • Consider ablation for all persistent, refractory, or symptomatic AFL. However, despite AFL ablation, AF may occur, especially in individuals with underlying structural heart disease. • AV nodal ablation, although not preferable, could be considered when ventricular rate control cannot be achieved and flutter cannot be ablated, or if symptomatic, refractory, and/or if associated with tachycardia-induced cardiomyopathy. This option may be considered in cases where individuals have multiple forms of nonablatable AFL or AF and especially for those who do have non-isthmus-dependent AFL.
   Chronic prevention	• If structural heart disease without CHF: sotalol (initiate in the hospital), dofetilide, amiodarone. • If structural heart disease with CHF: amiodarone, dofetilide. • If no structural heart disease: propafenone, flecainide, sotalol, dofetilide, or amiodarone, but propafenone or flecainide may need concomitant AV nodal blocking drugs to prevent 1:1 conduction. • If class I or III drugs are used, first control the ventricular response rate with an AV nodal blocking drug. Otherwise, the vagolytic effects of class IA drugs can enhance AV nodal conduction, and both 1A and 1C drugs can lead to AFL with 1:1 AV conduction. • Drug therapy alone for pure AFL flutter is usually not effective. • Consider radiofrequency catheter ablation early; it has become first-line therapy.
   Nonresponders with severe symptoms	• If type I AFL, radiofrequency ablation of the right atrial isthmus. • Atypical AFL is more difficult to ablate and depends on the location of reentrant circuit. Success rates are lower than that for typical AFL. It is more difficult when there is congenital heart disease, valve disease, or prior surgery in which significant areas of scar are present. • Ventricular rate control, antiarrhythmic drugs, or AV node ablation (less preferable) can be performed for atypical, nonablatable AFL. • If AV node ablation and pacing is performed and AFL is intermittent, mode-switching function should be programmed “ON.”
   MI	• If hemodynamic intolerance or ongoing refractory myocardial ischemia, emergent cardioversion. AFL may increase MVO2 due to rapid ventricular rate, causing further ischemia, diastolic dysfunction, and pulmonary congestion and edema. • If recurrent, IV amiodarone or procainamide. • Consider temporary antitachycardia pacing if recurrent and poorly tolerated.
   Preoperative	• For cardiac surgery, convert AFL to NSR if adequate anticoagulation has been achieved, or ensure that ventricular response is well controlled. • If surgery is elective and AFL is chronic, antiarrhythmic drugs or catheter ablation may be considered. However, anticoagulation should be continued at least 3 wk after conversion of longer-term (>48 h) AFL prior to elective surgery. • For more urgent surgery in which anticoagulation cannot be used, consider rate control without cardioversion. • For short-duration (<48 h) AFL, DCC can be performed (may consider heparin prior to DCC with surgical consultation as to risk).
   Postoperative	• AFL occurs in 10%-20% of all patients after cardiac surgery; it typically occurs with AF. Incidence peaks at days 2-3. It is more common in older patients. It rarely occurs after other types of surgery. The AFL may resolve spontaneously; however, the rhythm can increase the length of hospital stay, exacerbate heart failure, slow the recovery process, and cause symptoms. • Control rate with β-adrenergic blocker if no CHF or bronchospastic disease and good LVEF (> 40%). Diltiazem is often successful as a second-line drug, but use with caution in patients with poor LVEF. Digoxin for rate control is less effective but may be considered, particularly in patients with poor LV function. • IV amiodarone may be useful for persistent and poorly tolerated AFL; amiodarone or other antiarrhythmic drugs may be helpful for recurrent episodes. • DCC or atrial pace termination (if atrial pacing leads are present) is often successful, especially when employed early after the AFL onset. • Discontinue inotropic drugs, if possible.
   AF, Atrial fibrillation; AFL, atrial flutter; AV, atrioventricular; CHF, congestive heart failure; DCC, direct current cardioversion; IV, intravenous; LV, left ventricle; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MVO2, myocardial oxygen consumption; NOAC, non-vitamin K oral anticoagulants; TEE, transesophageal echocardiography.

2. •

   If the patient is unstable, proceed directly to electrical cardioversion.

3. •

   In the hemodynamically stable patient, proceed with rate control or rhythm control strategy.

4. •

   AV blocking agents such as calcium channel blockers, beta-blockers, and digitalis (second-line treatment) may all be used for rate control. Atrial flutter may spontaneously convert to normal sinus rhythm with this strategy.

5. •

   In general, atrial flutter is more difficult to rate-control than atrial fibrillation.

6. •

   The rate of recurrence of atrial flutter with cardioversion alone is difficult to determine because most published data combine atrial flutter with atrial fibrillation. However, the recurrence rate is substantial, perhaps 50% at 1 yr.

7. •

   Intravenous ibutilide is a first-line medication for pharmacologic cardioversion of atrial flutter in patients with normal systolic function and QT intervals. The success rate is approximately 60%, and it is more effective than procainamide, sotalol, or amiodarone.

Chronic Rx

1. •

   Few data exist to decide on the choice of rate control versus rhythm control in patients with atrial flutter. However, rate control may be difficult in atrial flutter, and ablation success exceeds 90%. Although ablation results in more durable freedom from atrial flutter recurrence, there are several pharmacologic options to help maintain sinus rhythm after cardioversion of atrial flutter, such as dofetilide, amiodarone, flecainide, propafenone, or sotalol. The choice of antiarrhythmic therapy is, in part, dictated by the presence or absence of underlying structural heart disease.

2. •

   Elective outpatient cardioversion or ablation can be performed either immediately preceded by TEE to evaluate the left atrium and the left atrial appendage for thrombus or after a period of at least 3 weeks of documented therapeutic anticoagulation before cardioversion. At least 4 weeks of anticoagulation should be administered after cardioversion, if not longer, depending on the overall thromboembolic risk of the patient as determined by the CHA₂DS₂-VASC score.

Disposition

More than 85% of patients convert to regular sinus rhythm after cardioversion. Ablation success rates exceed 90%.

Referral

Refer patients who are considered for rhythm control of atrial flutter to cardiologists, especially patients who are candidates for radiofrequency ablation.

Pearls & Considerations

Comments

1. •

   The surface ECG is the best tool for recognizing atrial flutter and distinguishing atrial flutter from atrial fibrillation.

2. •

   Ablation for typical atrial flutter is highly effective, straightforward, and relatively safe. It should be considered for patients with recurrent episodes and even for a first-ever episode.

3. •

   Patients with atrial flutter carry a significant risk for subsequent development of atrial fibrillation.

4. •

   Anticoagulation should be considered for all patients whose CHA₂DS₂-VaSc score is ≥2. Anticoagulation is generally not recommended in patients with a CHA₂DS₂-VaSc score of zero. For patients with a CHA₂DS₂-VaSc score of 1, low-dose aspirin or oral anticoagulants (warfarin, dabigatran, rivaroxaban, apixaban, or edoxaban) are appropriate options.

5. •

   Though anticoagulation recommendations for atrial flutter are identical to atrial fibrillation, studies suggest that the absolute risk of stroke is lower from atrial flutter than from fibrillation.

Suggested Reading

• 2014 AHA/ACC/HRS Guideline for the management of patients with atrial fibrillation, 20162014 AHA/ACC/HRS Guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 36:2242–2246 2016

Related Content

Atrial Flutter (Patient Information)

Atrial Fibrillation (Related Key Topic)