Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

INITIAL

hemodynamically unstable

1st line – DC cardioversion

Back
INITIAL
|
hemodynamically unstable
1st line – 

DC cardioversion

Used immediately if the patient is hemodynamically unstable with chest pain, shortness of breath, dizziness or syncope, hypotension, and rapid heart rate.

Direct current (DC) cardioversion is performed under adequate short-acting general anesthesia and involves delivery of an electrical shock synchronized with the intrinsic activity of the heart by sensing the R wave of the ECG (i.e., synchronized). The energy output for successful termination of new-onset AF varies from 200 J to a maximum of 400 J depending on the body size and the presence of other comorbid conditions. Lower energy of 100 J may be used as the starting level when biphasic energy is used.

For patients with hemodynamically unstable AF, initiation of anticoagulation should not delay DC cardioversion. It is reasonable to consider administering intravenous bolus of unfractionated heparin followed by infusion, or low molecular weight heparin or direct-acting oral anticoagulant and to continue this after cardioversion unless contraindicated.[1]

ACUTE

hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown

1st line – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown
|
without heart failure
1st line – 

rate control with beta-blocker and/or calcium-channel blocker

Rate-control therapy is required until cardioversion is successful.

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers. 

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour infusion; 180-480 mg orally (extended-release) once daily

Plus – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown
|
without heart failure
Plus – 

anticoagulation or left atrial appendage occlusion

Treatment recommended for ALL patients in selected patient group

Anticoagulation is recommended in all patients with AF due to the high risk of thromboembolic events. The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​ 

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111] Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Anticoagulation should be established before and is recommended to be continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[1][43]​​

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

-- AND --

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

Plus – electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Back
ACUTE
|
hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown
|
without heart failure
Plus – 

electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Treatment recommended for ALL patients in selected patient group

Cardioversion should only be attempted once the patient has been established on anticoagulation with a target INR of 2 to 3 for 3-4 weeks, and following a repeat transesophageal echocardiogram (TEE), if available, to confirm left atrial thrombus. If TEE cannot be performed, the patient should be treated as for presumed thrombus and recommendations for confirmed left atrial thrombus should be followed.[Figure caption and citation for the preceding image starts]: Transesophageal echocardiogram showing left atrial appendage clot. LA=left atrium; LAA=left atrial appendage; LV=left ventricleFrom the collection of Dr Bharat Kantharia [Citation ends].com.bmj.content.model.Caption@18e89b5c

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, a prolonged observation period is recommended in patients who have received ibutilide.[150]

Anticoagulation is continued for at least 4 weeks after cardioversion.[1][43]​​

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

OR

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

OR

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

1st line – rate control with beta-blocker, digoxin, or amiodarone

Back
ACUTE
|
hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown
|
with heart failure
1st line – 

rate control with beta-blocker, digoxin, or amiodarone

Beta-blockers, digoxin, or amiodarone may be used for rate control in patients with AF and heart failure.[1][15] These drugs may be used in combination or as monotherapy. 

Choice of pharmacologic agent/s in patients with heart failure is dictated by the degree of heart failure and type of heart failure (i.e., reduced or preserved ejection fraction [EF]). Drugs that potentially accentuate cardiac contractility are therefore avoided. Thus, calcium-channel blockers, which may be used in heart failure (HF) with preserved EF, are not recommended in patients with reduced EF (heart failure with reduced ejection fraction [HFrEF]). Beta-blockers such as carvedilol, metoprolol, and bisoprolol that are recommended for HF in patients with reduced and preserved EF may be used for rate control as well.

Digoxin is not considered a first-line agent for the purpose of rate control, but it can be useful in patients with heart failure. One study explored whether digoxin use was independently associated with increased mortality in patients with AF; compared with propensity score–matched control participants, the risk of death and sudden death was significantly higher in new digoxin users.[106] In patients with AF taking digoxin, the risk of death was independently related to serum digoxin concentration and was highest in patients with concentrations of ≥1.2 ng/mL (≥1.54 nmol/L).[106]

In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

Primary options

carvedilol: 3.125 to 25 mg orally twice daily

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

digoxin: 0.25 to 0.5 mg intravenously as a loading dose, followed by 0.25 mg every 6 hours (maximum 1.5 mg/24 hours), then 0.0625 to 0.25 mg orally once daily

OR

amiodarone: 150-300 mg intravenously as a loading dose, followed by 10-50 mg/hour infusion over 24 hours, then 100-200 mg orally once daily

More

Plus – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown
|
with heart failure
Plus – 

anticoagulation or left atrial appendage occlusion

Treatment recommended for ALL patients in selected patient group

Anticoagulation is recommended in all patients with AF due to the high risk of thromboembolic events. The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​​

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3- 4 weeks before cardioversion is attempted.

Anticoagulation should be established prior to and should be continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[1][43]​​

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

-- AND --

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

Plus – electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Back
ACUTE
|
hemodynamically stable with left atrial thrombus, or presence of thrombus unknown/duration of AF unknown
|
with heart failure
Plus – 

electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Treatment recommended for ALL patients in selected patient group

Cardioversion should only be attempted once the patient has been established on anticoagulation with a target INR of 2 to 3 for 3-4 weeks, and following a repeat transesophageal echocardiogram (TEE), if available, to confirm left atrial thrombus. If TEE cannot be performed, the patient should be treated as for presumed thrombus and recommendations for confirmed left atrial thrombus should be followed.[Figure caption and citation for the preceding image starts]: Transesophageal echocardiogram showing left atrial appendage clot. LA=left atrium; LAA=left atrial appendage; LV=left ventricleFrom the collection of Dr Bharat Kantharia [Citation ends].com.bmj.content.model.Caption@6becc2dd

DC cardioversion is fast, safe, and efficient.

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, a prolonged observation period is recommended in patients who have received ibutilide.[150]

Anticoagulation should be established before cardioversion and is recommended to continued for at least 4 weeks after cardioversion.[1][43]​​

Primary options

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

hemodynamically stable without left atrial thrombus: symptom onset <48 hours

1st line – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
without heart failure: CHA₂DS₂-VASc score 0-1
1st line – 

rate control with beta-blocker and/or calcium-channel blocker

Rate-control therapy is required until cardioversion is successful.

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers.

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour infusion; 180-480 mg orally (extended-release) once daily

Plus – electrical or pharmacologic cardioversion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
without heart failure: CHA₂DS₂-VASc score 0-1
Plus – 

electrical or pharmacologic cardioversion

Treatment recommended for ALL patients in selected patient group

Patients with low thromboembolic risk presenting with new-onset AF within 48 hours can undergo immediate cardioversion without the need for anticoagulation. There is no significant difference in terms of outcome between DC and pharmacologic cardioversion. Timing of cardioversion in patients who are hemodynamically stable and minimally symptomatic is a topic of research. Some studies suggest no benefit of early cardioversion over a "wait and see" approach; others suggest outcomes are improved when cardioversion is performed early.[107][108]

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, prolonged observation period is recommended in patients who have received ibutilide.[150]

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

OR

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

OR

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

1st line – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
without heart failure: CHA₂DS₂-VASc score ≥2
1st line – 

rate control with beta-blocker and/or calcium-channel blocker

Rate-control therapy is required until cardioversion is successful.

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers.

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour infusion; 180-480 mg orally (extended-release) once daily

Plus – electrical or pharmacologic cardioversion + heparin

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
without heart failure: CHA₂DS₂-VASc score ≥2
Plus – 

electrical or pharmacologic cardioversion + heparin

Treatment recommended for ALL patients in selected patient group

Intravenous heparin (activated partial thromboplastin time [aPTT] of 45-60 seconds) or subcutaneous low molecular weight heparin should be started before cardioversion. There is no significant difference in terms of outcome between DC and pharmacologic cardioversion. Timing of cardioversion in patients who are hemodynamically stable and minimally symptomatic is a topic of research. Some studies suggest no benefit of early cardioversion over a "wait and see" approach; others suggest outcomes are improved when cardioversion is performed early.[107][108]

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, prolonged observation period is recommended in patients who have received ibutilide.[150]

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

or

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

or

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

or

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

-- AND --

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

Plus – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
without heart failure: CHA₂DS₂-VASc score ≥2
Plus – 

anticoagulation or left atrial appendage occlusion

Treatment recommended for ALL patients in selected patient group

Anticoagulation is recommended in all patients with AF due to the high risk of thromboembolic events. The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​​

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Anticoagulation is continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[1][43]

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

1st line – rate control with beta-blocker, digoxin, or amiodarone

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
with heart failure
1st line – 

rate control with beta-blocker, digoxin, or amiodarone

Patients with heart failure are considered at high risk of thromboembolism. Additional risk factors may also be present, including age ≥75 years, structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and left ventricular ejection fraction is ≤35%.

Beta-blockers, digoxin, or amiodarone may be used for rate control in patients with AF and heart failure.[1][15] These drugs may be used in combination or as monotherapy.

Choice of pharmacologic agent/s in patients with heart failure is dictated by the degree of heart failure and type of heart failure (i.e., reduced or preserved ejection fraction [EF]). Drugs that potentially accentuate cardiac contractility are therefore avoided. Thus, calcium-channel blockers, which may be used in heart failure (HF) with preserved EF, are not recommended in patients with reduced EF (heart failure with reduced ejection fraction [HFrEF]). Beta-blockers such as carvedilol, metoprolol, and bisoprolol that are recommended for HF in patients with reduced and preserved EF may be used for rate control as well.

Digoxin is not considered a first-line agent for the purpose of rate control, but it can be useful in patients with heart failure. One study explored whether digoxin use was independently associated with increased mortality in patients with AF; compared with propensity score–matched control participants, the risk of death and sudden death was significantly higher in new digoxin users.[106] In patients with AF taking digoxin, the risk of death was independently related to serum digoxin concentration and was highest in patients with concentrations of ≥1.2 ng/mL (≥1.54 nmol/L).[106]

In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]​​

Primary options

carvedilol: 3.125 to 25 mg orally twice daily

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

digoxin: 0.25 to 0.5 mg intravenously as a loading dose, followed by 0.25 mg every 6 hours (maximum 1.5 mg/24 hours), then 0.0625 to 0.25 mg orally once daily

OR

amiodarone: 150-300 mg intravenously as a loading dose, followed by 10-50 mg/hour infusion over 24 hours, then 100-200 mg orally once daily

More

Plus – electrical or pharmacologic cardioversion + heparin

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
with heart failure
Plus – 

electrical or pharmacologic cardioversion + heparin

Treatment recommended for ALL patients in selected patient group

Intravenous heparin (activated partial thromboplastin time [aPTT] of 45-60 seconds) or subcutaneous low molecular weight heparin should be started before cardioversion. There is no significant difference in terms of outcome between DC and pharmacologic cardioversion. Timing of cardioversion in patients who are hemodynamically stable and minimally symptomatic is a topic of research. Some studies suggest no benefit of early cardioversion over a "wait and see" approach; others suggest outcomes are improved when cardioversion is performed early.[107][108]  

DC cardioversion is fast, safe, and efficient.

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, prolonged observation period is recommended in patients who have received ibutilide.[150]

Primary options

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

or

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

-- AND --

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

Plus – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset <48 hours
|
with heart failure
Plus – 

anticoagulation or left atrial appendage occlusion

Treatment recommended for ALL patients in selected patient group

Anticoagulation is recommended in all patients with AF due to the high risk of thromboembolic events. The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​​

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Anticoagulation is continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[1][43]

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours

1st line – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
without heart failure: CHA₂DS₂-VASc score 0-1
1st line – 

rate control with beta-blocker and/or calcium-channel blocker

Rate-control therapy is required until cardioversion is successful.

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers.

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour infusion; 180-480 mg orally (extended-release) once daily

Plus – heparin

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
without heart failure: CHA₂DS₂-VASc score 0-1
Plus – 

heparin

Treatment recommended for ALL patients in selected patient group

Heparin (unfractionated or low molecular weight) should be started, and cardioversion should be delayed until the patient is established on heparin with a target activated partial thromboplastin time of 45-60 seconds.

Primary options

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

OR

enoxaparin: 1 mg/kg subcutaneously every 12 hours

Plus – electrical or pharmacologic cardioversion once heparin anticoagulation established

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
without heart failure: CHA₂DS₂-VASc score 0-1
Plus – 

electrical or pharmacologic cardioversion once heparin anticoagulation established

Treatment recommended for ALL patients in selected patient group

Cardioversion may be carried out once heparin is established provided the transesophageal echocardiogram is negative. There is no significant difference in terms of outcome between DC and pharmacologic cardioversion. Timing of cardioversion in patients who are hemodynamically stable and minimally symptomatic is a topic of research. Some studies suggest no benefit of early cardioversion over a "wait and see" approach; others suggest outcomes are improved when cardioversion is performed early.[107][108]

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, prolonged observation period is recommended in patients who have received ibutilide.[150]

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

OR

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

OR

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

1st line – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
without heart failure: CHA₂DS₂-VASc score ≥2
1st line – 

rate control with beta-blocker and/or calcium-channel blocker

Rate-control therapy is required until cardioversion is successful.

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers.

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour; 180-480 mg orally (extended-release) once daily

Plus – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
without heart failure: CHA₂DS₂-VASc score ≥2
Plus – 

anticoagulation or left atrial appendage occlusion

Treatment recommended for ALL patients in selected patient group

Anticoagulation is recommended in all patients with AF due to the high risk of thromboembolic events. The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​​

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Anticoagulation should be established before and is recommended to be continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[1][43]​​

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

-- AND --

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

Plus – electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
without heart failure: CHA₂DS₂-VASc score ≥2
Plus – 

electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Treatment recommended for ALL patients in selected patient group

Cardioversion should only be attempted once the patient has been established on anticoagulation with a target INR of 2 to 3 for 3-4 weeks.

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, a prolonged observation period is recommended in patients who have received ibutilide.[150]

Anticoagulation is continued for at least 4 weeks after cardioversion.[1][43]​​

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

OR

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

OR

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

1st line – rate control with beta-blocker, digoxin, or amiodarone

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
with heart failure
1st line – 

rate control with beta-blocker, digoxin, or amiodarone

Patients with heart failure are considered at high risk of thromboembolism. Additional risk factors may also be present, including age ≥75 years, structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and left ventricular ejection fraction is ≤35%.

Beta-blockers, digoxin, or amiodarone may be used for rate control in patients with AF and heart failure.[1] These drugs may be used in combination or as monotherapy. 

Choice of pharmacologic agent/s in patients with heart failure is dictated by the degree of heart failure and type of heart failure (i.e., reduced or preserved ejection fraction [EF]). Drugs that potentially accentuate cardiac contractility are therefore avoided. Thus, calcium-channel blockers, which may be used in heart failure (HF) with preserved EF, are not recommended in patients with reduced EF (heart failure with reduced ejection fraction [HFrEF]). Beta-blockers such as carvedilol, metoprolol, and bisoprolol that are recommended for HF in patients with reduced and preserved EF may be used for rate control as well.

Digoxin is not considered a first-line agent for the purpose of rate control, but it can be useful in patients with heart failure. One study explored whether digoxin use was independently associated with increased mortality in patients with AF; compared with propensity score–matched control participants, the risk of death and sudden death was significantly higher in new digoxin users.[106] In patients with AF taking digoxin, the risk of death was independently related to serum digoxin concentration and was highest in patients with concentrations of ≥1.2 ng/mL (≥1.54 nmol/L).[106]

In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed if the acute precipitant persists.[43]

Primary options

carvedilol: 3.125 to 25 mg orally twice daily

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

digoxin: 0.25 to 0.5 mg intravenously as a loading dose, followed by 0.25 mg every 6 hours (maximum 1.5 mg/24 hours), then 0.0625 to 0.25 mg orally once daily

OR

amiodarone: 150-300 mg intravenously as a loading dose, followed by 10-50 mg/hour infusion over 24 hours, then 100-200 mg orally once daily

More

Plus – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
with heart failure
Plus – 

anticoagulation or left atrial appendage occlusion

Treatment recommended for ALL patients in selected patient group

Anticoagulation is recommended in all patients with AF due to the high risk of thromboembolic events. The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​​

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Anticoagulation should be established before and is recommended to be continued for at least 4 weeks after cardioversion, and may be required for longer in some patients.[1][43]​​

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

-- AND --

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

Plus – electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: symptom onset ≥48 hours
|
with heart failure
Plus – 

electrical or pharmacologic cardioversion following 3-4 weeks of anticoagulation

Treatment recommended for ALL patients in selected patient group

Cardioversion should only be attempted once the patient has been established on anticoagulation with a target INR of 2 to 3 for 3-4 weeks.

DC cardioversion is fast, safe, and efficient.

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, a prolonged observation period is recommended in patients who have received ibutilide.[150]

Anticoagulation is continued for at least 4 weeks after cardioversion.[1][43]

Primary options

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

hemodynamically stable without left atrial thrombus: asymptomatic

1st line – observation

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score 0-1
1st line – 

observation

Most cases of new-onset AF revert to sinus rhythm spontaneously. Cases that revert spontaneously usually do so in the first 24 hours.[105]

Patients should be observed to see whether AF resolves spontaneously.

In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed, and AF is less likely to resolve spontaneously, if the acute precipitant persists.[43]

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

2nd line – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score 0-1
2nd line – 

rate control with beta-blocker and/or calcium-channel blocker

If AF does not resolve spontaneously, rate-control therapy is required until cardioversion is successful. However, rate- and rhythm-control strategies have comparable clinical outcomes in many patients with AF; shared decision-making with the patient is recommended.[1]

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers.

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used.

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour infusion; 180-480 mg orally (extended-release) once daily

Plus – anticoagulation

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score 0-1
Plus – 

anticoagulation

Treatment recommended for ALL patients in selected patient group

Anticoagulation should be established before cardioversion (in patients who require cardioversion) and is continued for at least 4 weeks afterward, and may be required for longer in some patients.[1][43]

The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

-- AND --

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

Plus – electrical or pharmacologic cardioversion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score 0-1
Plus – 

electrical or pharmacologic cardioversion

Treatment recommended for ALL patients in selected patient group

If AF does not resolve spontaneously, cardioversion should only be attempted once the patient has been established on anticoagulation. If there is evidence of LA thrombus on TEE, or the presence of thrombus is unknown or the duration of AF is unknown or for 48 hours or more, all eligible patients should preferably be put on a DOAC for at least 3-6 weeks; after this, imaging such as TEE should be repeated to rule out intracardiac thrombus before elective cardioversion.

There is no significant difference in terms of outcome between DC and pharmacologic cardioversion. Timing of cardioversion in patients who are hemodynamically stable and minimally symptomatic is a topic of research. Some studies suggest no benefit of early cardioversion over a "wait and see" approach; others suggest outcomes are improved when cardioversion is performed early.[107][108]

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, prolonged observation period is recommended in patients who have received ibutilide.[150]

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

OR

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

OR

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

1st line – anticoagulation or left atrial appendage occlusion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score ≥2
1st line – 

anticoagulation or left atrial appendage occlusion

Patients with higher thromboembolic risk require immediate anticoagulation.

The key options for anticoagulation are a vitamin K antagonist such as warfarin, or a direct oral anticoagulant (DOAC) such as dabigatran, rivaroxaban, apixaban, or edoxaban. DOACs are approved for stroke prevention and have a more favorable side-effect profile than vitamin K antagonists in patients with nonvalvular AF.

In patients with AF 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.[1]​ If CHA₂DS₂-VASc score is ≥2, all eligible patients should preferably be started on a DOAC.

DOACs should be used with caution in patients with renal impairment. If a DOAC is suitable, depending on the degree of renal impairment and the indication for use, a dose adjustment may be required. Consult the prescribing information for specific guidance on use in patients with renal impairment.

DOACs should not be used in patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis, due to an increased risk of stroke, heart attack, and blood clot in these patients, nor should they be used in combination with heparin (including low molecular weight heparin), heparin derivatives, or warfarin.[111]

Patients with diabetes are at risk of complications of diabetes when treated with oral anticoagulants; this risk seems to be lower with DOACs compared with vitamin K antagonists. Dabigatran is favored for its efficacy and lower rates of adverse effects in this patient group.[132][133]

In DOAC-ineligible patients, start concomitant heparin and warfarin therapy, and continue heparin until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3-4 weeks before cardioversion is attempted.

Anticoagulation is continued for at least 4 weeks after cardioversion (in patients who require cardioversion), and may be required for longer in some patients.[1][43]​​

In the setting of AF, the left atrial appendage can play a role in blood stasis and clot formation, and consequently be a source of emboli.[11]​ Although oral anticoagulation is the standard of care to reduce the risk of ischemic stroke in patients with AF, it is contraindicated in some patients due to an excess risk of major bleeding.[1]

Left atrial appendage occlusion may be considered as an alternative for stroke prevention in patients with a moderate to high risk of stroke (CHA₂DS₂-VASc score ≥2) when there are absolute contraindications to the use of anticoagulants (due to a nonreversible cause), or the risk of bleeding outweighs the benefits.[1][2][18][136]​​​ For more information on this treatment see Established atrial fibrillation.

Primary options

dabigatran etexilate: 150 mg orally twice daily

OR

apixaban: 2.5 to 5 mg orally twice daily

OR

edoxaban: 60 mg orally once daily

OR

rivaroxaban: 20 mg orally once daily

OR

heparin: see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds

or

enoxaparin: 1 mg/kg subcutaneously every 12 hours

-- AND --

warfarin: 2-5 mg orally once daily initially, adjust dose according to target INR

More

Plus – observation

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score ≥2
Plus – 

observation

Treatment recommended for ALL patients in selected patient group

Most cases of new-onset AF revert to sinus rhythm spontaneously. Cases that revert spontaneously usually do so in the first 24 hours.[105]

Patients should be observed to see whether AF resolves spontaneously.

In addition, identification and treatment of any potential triggers of new-onset AF is very important, because rate and rhythm control measures are less likely to succeed, and AF is less likely to resolve spontaneously, if the acute precipitant persists.[43]

Consider – rate control with beta-blocker and/or calcium-channel blocker

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score ≥2
Consider – 

rate control with beta-blocker and/or calcium-channel blocker

Treatment recommended for SOME patients in selected patient group

If AF does not resolve spontaneously, rate-control therapy is required until cardioversion is successful.

Beta-blockers and nondihydropyridine calcium-channel blockers (i.e., diltiazem or verapamil) slow atrioventricular nodal conduction of cardiac impulses and subsequently reduce ventricular rate.

Intravenous administration may be necessary for rapid control of ventricular rate. Furthermore, in the event of hemodynamic adverse effects, the infusion may be discontinued promptly.

Beta-blockers are particularly useful when new-onset AF is associated with an acute myocardial infarction or angina, and when new-onset AF is precipitated after exercise.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.

Nondihydropyridine calcium-channel blockers are useful in ventricular rate control in the absence of preexcitation. They provide reasonable rate control and also improve AF-related symptoms compared with beta-blockers.[1]​ They are preferred in patients with chronic lung disease where bronchospasm may occur with beta-blockers.

Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.

If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used.

[ Atrial Fibrillation CHA(2)DS(2)-VASc Score for Stroke Risk Opens in new window ]

Primary options

esmolol: 500 micrograms/kg intravenously as a loading dose, followed by 50-300 micrograms/kg/minute infusion

OR

metoprolol tartrate: 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 25-200 mg orally (immediate-release) twice daily

OR

propranolol hydrochloride: 1 mg intravenously initially, may repeat every 2 minutes to a total of 3 doses; 10-40 mg orally (immediate-release) three to four times daily

OR

atenolol: 25-100 mg orally once daily

OR

nadolol: 10-240 mg orally once daily

OR

bisoprolol: 2.5 to 10 mg orally once daily

OR

carvedilol: 3.125 to 25 mg orally twice daily

OR

diltiazem: 0.25 mg/kg intravenous bolus initially, may give a second bolus of 0.35 mg/kg after 15 minutes if necessary, followed by 5-15 mg/hour infusion; 120-360 mg orally (extended-release) once daily

OR

verapamil: 5-10 mg intravenous bolus initially, may give a second and third bolus of 5-10 mg after 15-30 minutes, followed by 5-20 mg/hour infusion; 180-480 mg orally (extended-release) once daily

Consider – electrical or pharmacologic cardioversion

Back
ACUTE
|
hemodynamically stable without left atrial thrombus: asymptomatic
|
CHA₂DS₂-VASc score ≥2
Consider – 

electrical or pharmacologic cardioversion

Treatment recommended for SOME patients in selected patient group

If AF does not resolve spontaneously, cardioversion should only be attempted once the patient has been established on anticoagulation. If there is evidence of LA thrombus on TEE, or the presence of thrombus is unknown or the duration of AF is unknown or for 48 hours or more, all eligible patients should preferably be put on a DOAC for at least 3-6 weeks; after this, imaging such as TEE should be repeated to rule out intracardiac thrombus before elective cardioversion.

DC cardioversion is fast, safe, and efficient.

Class IC agents (flecainide, propafenone) have a higher mortality in patients with coronary artery disease (CAD) and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.

Flecainide has strong evidence of efficacy for pharmacologic conversion (odds ratio [OR] 24.7, 95% CI 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours.[150]

Propafenone also has strong evidence of efficacy for pharmacologic conversion (OR 4.6, 95% CI 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment.[150]

Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.

To improve success of restoration of sinus rhythm and its maintenance, especially in patients with persistent AF, pre-treatment with amiodarone 1-6 weeks before electrical cardioversion may be considered.[1][151]

Ibutilide prolongs repolarization of the atrial tissue by enhancing the slow inward depolarizing Na+ current in the plateau phase of repolarization. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacologic conversion (OR 29.1, 95% CI 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3-6 hours, prolonged observation period is recommended in patients who have received ibutilide.[150]

Primary options

flecainide: body weight <70 kg: 200 mg orally as a single dose; body weight ≥70 kg: 300 mg orally as a single dose

OR

propafenone: body weight <70 kg: 450 mg orally as a single dose; body weight ≥70 kg: 600 mg orally as a single dose

OR

amiodarone: 150 mg intravenously initially over 10 minutes, followed by 1 mg/minute infusion for 6 hours, and then 0.5 mg/minute infusion for 18 hours; 600-800 mg/day orally given in 2-3 divided doses up to a total loading dose of up to 10 g, followed by 200 mg orally once daily

More

OR

ibutilide: body weight <60 kg: 0.01 mg/kg intravenously as a single dose; adults body weight ≥60 kg: 1 mg intravenously as a single dose; may repeat dose after 10 minutes if no response

back arrow

Choose a patient group to see our recommendations

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

Use of this content is subject to our disclaimer