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 stability of atrial flutter, 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. However, a common denominator atrial interval is often present.

Table 1 summarizes the different types of atrial flutter and distinguishing features on scalar electrocardiography.

• Atrial flutter is the second most common sustained atrial tachyarrhythmia after atrial fibrillation, with an estimated 200,000 new cases annually in the U.S.
• Atrial flutter is common in patients with congestive heart failure, chronic obstructive pulmonary disease (COPD), pulmonary vascular disorders such as pulmonary embolism, or during the first week after open heart surgery.
• Atrial flutter occurs more frequently with advancing age (5/100,000 age <50 vs. 587/100,000 age >80 yr) and 2.5 times more frequently in men than in women.
• Patients taking antiarrhythmics for chronic suppression of atrial fibrillation may present with atrial flutter.
• Atrial flutter is typically seen in patients with underlying structural heart disease and is uncommon in children or young adults without congenital heart disease.
• More than 50% of patients with atrial flutter will develop atrial fibrillation in 3 yr, and more than 80% will develop atrial fibrillation within 5 yr. This is important when considering treatment options for atrial flutter, especially anticoagulation.

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 options (i.e., ablation). Type I CTI-dependent atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 250 to 350 beats/min. The reentrant loop circles the tricuspid valve in 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.

• 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. E1).
• 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. E2).
• 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 after left atrial ablation for atrial fibrillation) or may be idiopathic. One ECG feature is the lack of discordance of the flutter wave polarity between the inferior leads (leads II, III, and aVF) and V1. Flutter circuits in the left atrium (such as mitral annular flutter) often have upright flutter waves in all precordial leads.

• Palpitations
• Dizziness, light-headedness, syncope, or near syncope
• Angina
• Congestive heart failure
• Embolic phenomena from intracardiac thrombus

• Age-related degenerative changes
• Rheumatic heart disease
• Congenital heart disease
• Left ventricular dysfunction or congestive heart failure
• Acute myocardial infarction (rarely)
• Thyrotoxicosis
• Pulmonary embolism
• Mitral valve disease
• Cardiac surgery
• Chronic obstructive pulmonary disease
• Obesity
• Pericarditis
• Pulmonary hypertension
• Antiarrhythmic therapy use in patients with atrial fibrillation
• Other causes of right atrial enlargement
• Systemic infections (such as COVID-19)¹

• Atrial fibrillation
• Atrial tachycardia
• Supraventricular tachycardia:
  1. Atrioventricular node reentry
  2. Orthodromic reciprocating tachycardia (using a concealed bypass tract)
  3. Junctional ectopic tachycardia
  4. Wolff-Parkinson-White syndrome
• Sinus tachycardia

• ECG (Fig. 3)
• Laboratory evaluation
• Assessment of CHA₂DS₂-VaSc score (Table 2)

• Thyroid function studies
• Serum electrolytes, including renal and hepatic tests (anticipating antiarrhythmic therapy use)
• CBC and PT/INR values (anticipating anticoagulation therapy)

• ECG:
  1. Absence of P waves
  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). The discordance of the polarity of the flutter waves between the inferior leads and V1 is a constant finding
  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 (see Fig. E1), 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
• 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
• Echocardiography (for new diagnoses) to evaluate for structural heart disease (atrial enlargement, left and right ventricular size, thickness, and function; atrial size, and valve function)
• Transesophageal echocardiography: Consider in the setting of cardioversion in the absence of an appropriate duration of anticoagulation to ascertain the absence of intracardiac (e.g., left atrial appendage) thrombi
• Electrophysiologic studies: Required for a precise diagnosis and for ablation
• Pulmonary vascular imaging (e.g., a CT scan with contrast) if a pulmonary embolism is suspected

• Treatment choices are based on clinical circumstances. Fig. 4 describes an acute treatment of atrial flutter algorithm.² Table 3 summarizes atrial flutter therapy.
• In cases of electrocardiographic uncertainty, atrial flutter may be differentiated from SVT through vagal maneuvers that slow AV conduction (e.g., the Valsalva maneuver, carotid sinus massage, or the use of adenosine). Vagal maneuvers may reveal flutter waves but will not terminate atrial flutter.
• Direct current cardioversion is the treatment of choice for unstable patients or those with debilitating symptoms. This 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. After cardioversion, patients will need anticoagulation for at least one month due to resultant atrial stunning from the presence of atrial flutter. Subsequent anticoagulation will depend on their stroke risk (CHA₂DS₂-VASc score; Table 2).
• 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.

Figure 4 Acute Treatment of Atrial Flutter

Anticoagulation as Per Guideline is Mandatory. †for Rhythms that Break or Recur Spontaneously, Synchronized Cardioversion, or Rapid Atrial Pacing is Not Appropriate. IV, Intravenous.

Reproduced with permission from Page RL et al: 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia, JACC 67[13]:e27-e115, 2016. In Olshansky B et al: Arrhythmia essentials, ed 2, Philadelphia, 2017, Elsevier.

• Proceed with either rate control or rhythm control strategy. Data is inconclusive on which strategy is more effective, but in general, atrial flutter is more difficult to rate-control than atrial fibrillation. Atrial flutter may spontaneously convert to normal sinus rhythm with rate control strategy.
• For a rate control strategy: First-line agents are calcium channel blockers and beta-blockers. Digoxin and amiodarone may be used in those with borderline hypotension, decompensated congestive heart failure, and those unable to tolerate first-line agents.
• Avoid calcium channel blockers if known EF <40%.
• Digoxin has a narrow therapeutic window, and thus caution is recommended in patients with kidney impairment.
• Amiodarone use is typically a rhythm control agent but also has utility in rate control. It carries the risk of cardioverting a patient not on anticoagulation.
• A rhythm control strategy can be employed using either electrical or pharmacologic cardioversion.
• While electrical cardioversion is often successful, its effects are not durable. 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.
• For pharmacologic cardioversion, intravenous ibutilide is a first-line medication 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. Oral flecainide (300 mg once) or oral propafenone (600 mg) may be used as well. Cardiac telemetry monitoring is required for 4 to 6 hours after giving antiarrhythmic medications at these doses in patients receiving this therapy for the first time.

• Chronic treatment of atrial flutter is indicated to prevent symptoms and adverse remodeling of the heart (arrhythmia induced cardiomyopathy, AIC). This may either be in the form of rate control or rhythm control strategy although the latter is preferred because successful rhythm control can be achieved in >90% of cases through catheter ablation.
• Radiofrequency ablation is often offered as a first-line treatment of typical atrial flutter but is also highly effective for those with recurrent episodes. It has been shown to improve health-related quality of life.
• In those patients who fail, opt not to, or not candidates for catheter ablation, electrical cardioversion followed by pharmacologic therapy to maintain sinus rhythm may be considered.
• Elective outpatient cardioversion or ablation can be performed either immediately preceded by transesophageal echocardiography (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.
• Pharmacologic options to maintain sinus rhythm include 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. It is important to keep in mind that antiarrhythmic drugs carry the risk of toxicity and can also be proarrhythmic.
• In addition to atrial flutter control, stroke risk mitigation is also a part of atrial flutter management and prophylactic anticoagulation should also be addressed depending on stroke risk, guided by the CHA₂DS₂-VASc score. Antithrombotic therapy is recommended as in atrial fibrillation.³ Anticoagulation should be considered for patients whose CHA₂DS₂-VaSc score is ≥2 in men or ≥3 in women. Options for oral anticoagulants include warfarin (target INR 2-3) or direct oral anticoagulants (DOACs, e.g., dabigatran, rivaroxaban, apixaban, or edoxaban), although the latter is now recommended over the former (except for cases of moderate to severe mitral stenosis or mechanical heart valves). For patients with a CHA₂DS₂-VaSc score of 1 (men) or 2 (women), prescribing an oral anticoagulant to reduce stroke risk may be considered (previous recommendation for aspirin was removed).⁴ Left atrial appendage closure may also be an option in patients at high risk for bleeding with anticoagulation.

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

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

• The surface ECG is the best tool for recognizing atrial flutter and distinguishing atrial flutter from atrial fibrillation. The inferior leads (II, III, aVF) are the best for seeing the characteristic sawtooth pattern.
• 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.
• Patients with atrial flutter carry a significant risk for subsequent development of atrial fibrillation.
• Anticoagulation should be considered for all patients whose CHA₂DS₂-VaSc score is ≥2 (men) or ≥3 (women). For patients with a CHA₂DS₂-VaSc score of 1 (men) or 2 (women), risks and benefits should be considered on an individual basis.
• Although anticoagulation recommendations for atrial flutter are identical to those for atrial fibrillation, studies suggest that the absolute risk of stroke is lower from atrial flutter than from fibrillation.

Atrial Flutter (Patient Information)

Atrial Fibrillation (Related Key Topic)