Approach

Hemodynamically unstable patients require urgent synchronized cardioversion. Hemodynamically stable patients can be treated with pharmacologic therapy; however, cardioversion (either electrical or pharmacologic) is an option in patients who do not respond to rate-control drugs. Patients with recurrent atrial flutter, or those who do not respond to elective cardioversion, may require catheter ablation of the cavotricuspid isthmus. Anticoagulation and treatment of any coexisting disease processes are important adjunctive therapies in all patients.

Hemodynamically unstable

If atrial flutter is associated with acute hemodynamic collapse involving symptomatic hypotension, congestive heart failure evidenced by pulmonary edema and/or elevated serum brain natriuretic peptide, or myocardial ischemia (acute ischemic ECG changes, angina), emergent direct current (DC)-synchronized cardioversion is indicated.[6][23]​ This rhythm is generally successfully cardioverted with monophasic shocks using <50 J of energy, although the higher-energy initial shocks are indicated for emergent therapy and may be needed for elective cardioversions.[4] ​In patients with hemodynamic instability, initiation of anticoagulation should not delay DC cardioversion.​[20]

Electrical (direct current) cardioversion animated demonstration
Electrical (direct current) cardioversion animated demonstration

How to perform electrical (direct current) cardioversion using a defibrillator.

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Hemodynamically stable: rate control

Most commonly, patients in atrial flutter present with 2:1 or higher grades of atrioventricular (AV) conduction block and are thus stable hemodynamically. In approximately 60% of patients, atrial flutter occurs as part of an acute disease process.[5] When the underlying process resolves, sinus rhythm is generally restored and chronic therapy is not needed.

AV-nodal blocking agents (e.g., beta-blockers, calcium-channel blockers, and amiodarone) are considered a first-line therapy for rate control in the immediate acute setting.[6][8]​ Beta-blockers are indicated for rate control in patients with atrial flutter complicating acute coronary syndromes to reduce myocardial oxygen demands.[6]​​ Beta-blockers should be used with caution in patients with COPD or asthma, because they might provoke bronchospasm; calcium-channel blockers are preferred if chronic lung disease is also present. Calcium-channel blockers are generally contraindicated or used with extreme caution in patients with heart failure.[8]​ Intravenous amiodarone is useful for acute control of the ventricular rate (in the absence of pre-excitation) in patients with atrial flutter and systolic heart failure when beta-blockers are contraindicated or ineffective.[8]

Adequate rate control is more difficult with atrial flutter than with atrial fibrillation. However, most randomized controlled trials of AV nodal-blocking agents generally do not report data for atrial flutter alone, but rather combined groups of patients with atrial fibrillation and/or flutter.[4] In addition, slowing of the atrial rate can cause rapid one-to-one AV conduction, particularly with class Ic antiarrhythmic drugs in the absence of AV nodal-blocking agents.[4][7][8]​​ For example, atrial flutter with a rate of 300 bpm that conducts 2:1 will result in a ventricular rate of 150 bpm. An antiarrhythmic drug that slows the flutter rate to 200 bpm might allow 1:1 AV nodal conduction in the absence of AV nodal blockers, thus resulting in a potentially clinically dangerous ventricular rate of 200 bpm.

Hemodynamically stable: cardioversion or pacing

If the rhythm persists despite pharmacologic therapy and treatment of the underlying cause (or in the absence of a reversible cause), elective synchronized cardioversion is generally preferred, both because atrial flutter is extremely responsive to electrical cardioversion and because it is relatively difficult to rate control chronically.[4]​​​​​[8][20]​​​ The success rate for external DC cardioversion, using 5 to 50 J of energy, is 95% to 100%.[34][35][36]​ Lower amounts are most successful with biphasic rather than monophasic waveforms. However, higher energies may be needed.[23][34][35][36]​ 

Rate-control agents are continued before cardioversion and discontinued when sinus rhythm is restored. However, they can be continued afterward to prevent rapid ventricular rate in case of recurrence. Dosage may need to be decreased after cardioversion if there is bradycardia or hypotension.

Rapid atrial pacing is useful for acute conversion of atrial flutter in patients who have pacing wires in place as part of a permanent pacemaker or an implantable cardioverter-defibrillator, or for temporary atrial pacing after cardiac surgery.[4]

The decision to perform a transesophageal echocardiogram prior to cardioversion (both electrical and chemical) to assess for left atrial or appendage thrombus should follow the recommendations for atrial fibrillation.​[20]

Hemodynamically stable: pharmacologic cardioversion

If atrial flutter persists despite resolution of acute provocation, and electrical cardioversion is unavailable or not acceptable to the patient, pharmacologic cardioversion may be attempted if the patient has a normal QT interval and no structural heart disease. It is also an option when sedation is not tolerated or available.

Intravenous ibutilide is the preferred agent for pharmacologic cardioversion; however, oral dofetilide may also be used.[4] Dofetilide is contraindicated in patients with long QT syndrome, QT prolongation, renal failure, and torsade de pointes. It requires specialist inpatient monitoring and should only be initiated by a physician experienced with its use.

Pharmacologic cardioversion is less effective than synchronized cardioversion, with potential for being proarrhythmic. The success rate is 38% to 76% for conversion of atrial flutter to sinus rhythm, with the mean time to conversion reported to be 30 minutes in those who respond. Ventricular proarrhythmia, specifically sustained polymorphic ventricular tachycardia, occurs at a rate of 1.2% to 1.7%.[37][38][39][40] For this reason, these drugs should not be given to those with severe structural heart disease and prolonged QT interval.

The major risk associated with pharmacologic cardioversion is torsade de pointes. Patients with reduced left ventricular ejection fraction are at the highest risk. Pretreatment with magnesium may reduce the risk of torsade de pointes. Continuous ECG monitoring is required during administration of these agents and for at least 4 hours after completion of therapy (ibutilide), or at least 3 days (or 12 hours after conversion to normal sinus rhythm, whichever is greater) after completion of therapy (dofetilide).

Intravenous class Ic agents and oral sotalol have relatively poor efficacy in acute conversion, are associated with significant adverse effects, and are not recommended.[4]

The decision to perform a transesophageal echocardiogram prior to cardioversion (both electrical and chemical) to assess for left atrial or appendage thrombus should follow the recommendations for atrial fibrillation.​[20]

Recurrent or refractory atrial flutter: catheter ablation

Catheter ablation of the cavotricuspid isthmus (CTI) is useful in patients with atrial flutter that is symptomatic or refractory to pharmacologic rate control, patients in whom at least one antiarrhythmic drug has failed, patients who develop atrial flutter as a result of antiarrhythmic therapy for atrial fibrillation, and patients with recurrent atrial flutter.

Catheter ablation has a class I indication in the following clinical scenarios:[4][6][41]

  • Symptomatic or refractory to pharmacologic rate control

  • Recurrent symptomatic CTI-dependent flutter after failure of at least one antiarrhythmic agent

  • Symptomatic recurrent episodes of non-CTI-dependent flutter at experienced catheter ablation centers

  • Persistent atrial flutter or atrial flutter associated with tachycardia-mediated cardiomyopathy with depressed left ventricular function.

Reasonable (class II) indications include:

  • CTI-dependent atrial flutter that occurs as the result of flecainide, propafenone, or amiodarone used for the treatment of atrial fibrillation

  • Patients undergoing catheter ablation of atrial fibrillation who also have a history of documented clinical or induced CTI-dependent atrial flutter

  • Primary therapy of recurrent symptomatic non-CTI-dependent flutter before therapeutic trials of antiarrhythmic drugs after carefully weighing the potential risks and benefits of treatment options

  • Asymptomatic patients with recurrent atrial flutter

  • First episode of symptomatic typical atrial flutter.

Catheter ablation is effective at maintaining sinus rhythm in typical atrial flutter in which the CTI is a necessary part of the arrhythmic circuit. This invasive technique involves a femoral venous approach. An ablation catheter is placed at the isthmus between the inferior vena cava and the tricuspid annulus using either fluoroscopic guidance or a 3-dimensional electroanatomic mapping system. Radiofrequency energy is then applied to create a line of ablation from the tricuspid annulus to the inferior vena cava.

The success rate for treatment of typical atrial flutter is high and has been reported at 92% for the first procedure and 97% for multiple procedures.[8][41][42][43] Atypical flutter is more difficult to ablate, particularly when associated with congenital heart disease. In such situations, referral to an experienced center ought to be considered.

Recurrent or refractory atrial flutter: long-term antiarrhythmic therapy

Chronic pharmacologic therapy is generally not required. In approximately 60% of cases, atrial flutter arises in the setting of a precipitating cause and, once that acute process resolves, sinus rhythm is restored.[5]

Most studies evaluating long-term antiarrhythmic therapy have grouped atrial flutter patients with atrial fibrillation patients. Therefore, exact efficacy rates are difficult to determine, but are probably around 50% for class I antiarrhythmics.[4]

Antiarrhythmic drug choice depends on the presence or absence of underlying heart disease and any comorbidities. Options include amiodarone, dofetilide, sotalol, flecainide, and propafenone.

AV nodal agents such as beta-blockers or calcium-channel blockers should be used in conjunction with class Ic drugs (e.g., flecainide, propafenone) because of the concern for slowing of the atrial flutter rate with resultant 1:1 AV conduction at high rates. However, class Ic drugs are contraindicated in patients with structural heart disease.

Class III agents such as oral dofetilide, sotalol, and amiodarone resulted in maintenance of sinus rhythm in 73% of atrial flutter patients.[4] Amiodarone is generally less effective than dofetilide; however, it is less proarrhythmic than other antiarrhythmics and is relatively safe in patients with structural heart disease.[44] Dofetilide is contraindicated in patients with long QT syndrome, QT prolongation, renal failure, and torsade de pointes. Continuous ECG monitoring is required during administration and for at least 3 days (or 12 hours after conversion to normal sinus rhythm, whichever is greater) after completion of therapy. It should only be initiated by a physician experienced in its use. Sotalol has both class II beta-blocking and class III properties, and thus provides rate control.

Anticoagulant therapy

The guidelines for thromboembolic prophylaxis in atrial flutter are the same as those for atrial fibrillation.​​​​[8]​​​​​​[20][22]​​[45]​​​​[46]

Selection of stroke risk reduction therapy should be guided by the patient’s risk of stroke, risks of bleeding with therapy, and their individual preferences.​[20] ​The ​American Heart Association (AHA) and European Society of Cardiology (ESC) guidelines emphasize a risk factor-based approach using a validated clinical risk score such as the CHA2DS2-VASc score system.[8][20]​​​ [ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ] ​ The CHA2DS2-VASc score is considered the most validated score; however, newer online calculators for risk scores, such as ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) and GARFIELD (Global Anticoagulant Registry in the Field-Atrial Fibrillation), in comparison to CHA2DS2-VASc, may modestly improve discrimination between high versus low risk and may offer potential advantages in specific populations.[20]​ The HAS-BLED score can be used to assess bleeding risk.​[20] [ HAS-BLED Bleeding Risk Score Opens in new window ] ​​​​​

Observational studies have demonstrated a 1.7% to 7% risk of embolization during cardioversion from atrial flutter.[47] Anticoagulation management prior to ablation should be handled similarly to that before cardioversion for atrial fibrillation. Anticoagulation after catheter ablation for atrial flutter should follow the same approach for that after atrial fibrillation ablation. The incidence of thrombus or echo-dense material in the atria in patients with atrial flutter who are not anticoagulated ranges from 0% to 34% and increases with atrial flutter duration more than 48 hours.[48] Atrial mechanical stunning has also been documented to persist for several weeks after cardioversion.[49]

The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran (a direct thrombin inhibitor), rivaroxaban, apixaban, or edoxaban (direct factor Xa inhibitors). Both vitamin K antagonists and DOACs are approved as efficacious agents for stroke prevention in this patient population.[20]​ In patients who are candidates for anticoagulation and do not have either moderate-severe rheumatic mitral stenosis or mechanical heart valves, DOACs are recommended over warfarin to reduce the risk of mortality, stroke, systemic embolism and intracranial hemorrhage.[20]​ While it is reasonable to use DOACs as first-line agents or as a subsequent replacement for warfarin in patients with atrial flutter, warfarin remains the first-line therapy in patients with AF and moderate-severe rheumatic mitral stenosis or mechanical heart valves.[20]

DOACs are recommended over warfarin in eligible patients (i.e., patients who do not have moderate-to-severe mitral stenosis or a mechanical heart valve).​​​​​​​​​​[20]​ Bridging with a parenteral anticoagulant is not necessary when initiating DOACs for this indication. DOACs do not require monitoring of anticoagulant activity; however, they must be used with caution in patients with renal impairment and a dose adjustment may be necessary.​ In the event of major bleeding, the effects of dabigatran can be reversed with idarucizumab, for reversal of apixaban, rivaroxaban, or edoxaban andexanet alfa can be used (recombinant coagulation factor Xa).[20]

​​​Edoxaban should not be used in patients with a creatinine clearance >95 mL/minute because of an increased risk of ischemic stroke.[20]​ ​Initial anticoagulation with subcutaneous low-molecular-weight heparin (LMWH) or intravenous unfractionated heparin may be necessary for patients presenting acutely with atrial flutter, pending full evaluation and selection of ongoing antithrombotic therapy; recommendations vary according to duration of symptoms and timing of cardioversion.​​​​​

Warfarin is an alternative to DOAC therapy indicated for selected patients (e.g., patients with mechanical heart valves, clinically significant rheumatic mitral stenosis. Intravenous unfractionated heparin or subcutaneous LMWH should be continued until an INR of 2-3 is achieved with warfarin therapy (bridging therapy).​[20]

If there are no risk factors for stroke, aspirin either alone or in combination with clopidogrel is not recommended to reduce the risk of stroke or to prevent thromboembolic events.[20]

Anticoagulation should be established before cardioversion and is continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[20]

For more detailed anticoagulation recommendations, see New-onset atrial fibrillation.

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