Atrial fibrillation

Last updated: July 10, 2023

Summarytoggle arrow icon

Atrial fibrillation (Afib) is a common type of supraventricular tachyarrhythmia characterized by uncoordinated atrial activation that results in an irregular ventricular response. While the exact mechanisms of Afib are poorly understood, associations with a number of cardiac (e.g., valvular heart disease, coronary artery disease) and noncardiac (e.g., hyperthyroidism, electrolyte imbalances) risk factors have been established. Individuals with Afib are typically asymptomatic. When symptoms do occur, they usually include palpitations, lightheadedness, and shortness of breath. Physical examination typically reveals an irregularly irregular pulse. Ineffective atrial emptying as a result of Afib can lead to stagnation of blood and clot formation in the atria, which in turn increases the risk of stroke and other thromboembolic complications. Diagnosis is confirmed with ECG showing absent P waves with irregular QRS intervals. Echocardiography is used to rule out structural heart disease and to evaluate for any atrial thrombi. Immediate synchronized cardioversion is required in hemodynamically unstable patients. In stable patients, treatment involves the correction of modifiable risk factors, rate or rhythm control strategies, and anticoagulation. Rate-control therapy typically involves the use of beta blockers or nondihydropyridine calcium channel blockers. Rhythm control strategies include synchronized electrical cardioversion, the use of pharmacological antiarrhythmics (e.g., flecainide, propafenone, or amiodarone), and ablation of the arrhythmogenic tissue. Patients are typically started on anticoagulation depending on their thrombotic and bleeding risk.

Atrial flutter is another common type of supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria. The risk factors for atrial flutter are similar to those of Afib. In atrial flutter, the ventricular rhythm is usually regular. Treatment is also similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter is typically more responsive to ablation therapy than Afib. Atrial flutter frequently progresses to Afib.

For the management of atrial fibrillation with a ventricular rate > 100–110/minute, see “Afib with RVR.”

Epidemiologytoggle arrow icon

  • Most common sustained arrhythmia [1]
  • Incidence: increases with age [1]
    • The lifetime risk of Afib among individuals > 40 years is 1 in 4.
    • > 95% of individuals with Afib are ≥ 60 years
  • Prevalence: approx. 1–2% of US population [2]

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

The exact causes of atrial fibrillation are unknown, but several risk factors have been identified (see table below).

Risk factors [3][4][5]

Risk factors for atrial fibrillation
Cardiovascular risk factors
Intrinsic cardiac disorders
Noncardiac disorders

Reversible causes of atrial fibrillation [7]

Approx. 15% of individuals who develop Afib have none of the above mentioned risk factors (idiopathic/lone Afib).

Remember PARASITE to memorize the major risk factors for acute Afib: PPulmonary disease; AAnemia; RRheumatic heart disease; AAtrial myxoma; SSepsis; IIschemia; TThyroid disease; EEthanol.

Classificationtoggle arrow icon

Hemodynamic stability [3][8][9]

Ventricular rate [3][8][9]

Onset and duration [3][8][9]

  • Paroxysmal Afib: Afib that resolves within 7 days of onset either following treatment or spontaneously; the frequency of recurring episodes may vary.
  • Persistent Afib: continuous Afib for > 7 days
  • Long-standing persistent Afib: continuous Afib for > 1 year
  • Permanent Afib: persistent Afib in which therapeutic attempts are no longer made to convert to or maintain sinus rhythm unless the patient and the treating physician agree to do so [3]

Method of detection [3][8][9]

  • Clinical Afib: an episode of Afib lasting ≥ 30 seconds that is documented on a surface ECG; may be symptomatic or asymptomatic
  • Subclinical Afib: asymptomatic Afib not previously detected on a surface ECG that is discovered on implanted cardiac devices and confirmed on intracardiac electrograms [8][9]

Valvular heart conditions [8]

Valvular heart conditions can affect the risk of thromboembolism. The terms valvular Afib and nonvalvular Afib have previously been used to classify patients accordingly. [8][13][14]

Patients with Afib should always be evaluated for mitral valve involvement!

Pathophysiologytoggle arrow icon

  • Atrial fibrillation is a supraventricular arrhythmia.
  • The exact mechanisms of Afib are not well understood. Suggested mechanisms include:
  • The new onset of Afib triggers a vicious circle that can ultimately lead to long-standing Afib with atrial remodeling:
    1. Afib is triggered by one or both of the following
    2. Afib is sustained by re-entry rhythms and/or rapid focal ectopic firing
      • Re-entry rhythms are more likely to occur with enlarged atria, diseased heart tissue, and/or aberrant pathways (e.g., WPW syndrome).
    3. Atrial remodeling
      • Electrophysiological changes in the atria occur within a few hours of Afib onset (electrical modeling).
      • If Afib persists, atrial fibrosis and dilatation (structural remodeling) occur within a few months.
      • Electrical and structural remodeling increase susceptibility to Afib, resulting in a vicious circle.
  • Effects of Afib


Clinical featurestoggle arrow icon

For rapid Afib, see “Clinical features of Afib with RVR.”

Individuals with Afib may be asymptomatic for a long time before a diagnosis is made.

The brain, kidney, and spleen are the three organs most likely to be damaged by emboli!

Diagnosticstoggle arrow icon

Approach [3][19]

This diagnostic approach applies to stable patients with new Afib; for approaches to patients with unstable Afib, see “Afib with RVR,” “Afib with WPW,” and “Management of unstable tachycardia.”

Assess for reversible causes of Afib, such as hyperthyroidism and electrolyte imbalances.

Consider ambulatory ECG monitoring to confirm paroxysmal Afib if the initial ECG is nondiagnostic and clinical suspicion is high.

ECG [20]

Characteristic ECG findings in atrial fibrillation [20]
  • Variable; tachycardia is common.
  • Atrial rate > ventricular rate
P waves
  • P waves are indiscernible.
  • Fibrillatory waves (f waves) are seen instead at a frequency of 300–600/minute
    • Recent-onset Afib: prominent, coarse f waves with higher amplitude in leads V1, II, III, and aVF
    • Long-standing Afib: f waves have low amplitudes and may appear as an undulating baseline.
  • PR intervals: not distinguishable
QRS complex

Wide QRS complex may indicate preexcited Afib or aberrant conduction.

Laboratory studies [3][19][21]

Routine studies

Cardiac evaluation

Additional cardiac evaluation is guided by clinical suspicion.

Afib etiologies

Obtain additional laboratory studies based on suspected underlying etiology, e.g.:

Afib can independently cause elevated D-dimer, troponin, and BNP levels. Interpret these findings along with the overall clinical suspicion for underlying PE, CHF, and/or ACS. [3][25][26][27]


TTE [3][28]

TEE for Afib [3][9][32]

TEE is performed prior to cardioversion to determine the safety of rhythm control in patients at risk of thromboemboli (e.g., Afib onset ≥ 48 hours) who cannot wait for ≥ 3 weeks of therapeutic anticoagulation.

TEE is usually not required for patients undergoing rate control and those undergoing rhythm control who have Afib onset < 48 hours or have received ≥ 3 weeks of therapeutic anticoagulation. [3][32]

Chest imaging [3]

Cardiac rhythm monitoring [3]

Specialized studies

Differential diagnosestoggle arrow icon

Differentiate Afib from other narrow complex tachycardias, e.g., SVT, multifocal AT, focal AT with variable conduction, and atrial flutter with variable conduction.

Irregularly irregular wide complex tachycardia may represent Afib with aberrant conduction, preexcited Afib, or ventricular tachycardia. If in doubt, treat it as ventricular tachycardia.

The differential diagnoses listed here are not exhaustive.

Managementtoggle arrow icon


Tachycardic or unstable patients

Patients with unstable Afib should be treated with immediate electrical cardioversion!

New diagnosis in stable patients [3][13][35]

Patients with known Afib

Patients with known Afib may seek care for acutely decompensated or recurrent Afib and/or comorbid conditions complicated by Afib (e.g., heart failure, ACS, sepsis).

Supportive care for Afib

The following measures can be applied in inpatient or outpatient settings.


See “Afib with RVR” for the disposition of patients with rapid Afib.

  • The workup and management of new stable Afib are typically started in emergency care settings and can continue in inpatient or outpatient settings depending on multiple factors, e.g.:
  • For emergency department patients, follow local protocols for hospital admission vs. discharge with rapid follow-up in consultation with a cardiologist.
  • For inpatients who develop new Afib or experience recurrence or decompensation, consult cardiology.

Treatmenttoggle arrow icon

There are two strategies for arrhythmia treatment in patients with Afib: rate control, which aims to reduce the heart rate, and rhythm control, which aims to restore normal sinus rhythm. For the management of patients with unstable Afib, see “Afib with RVR,” “Afib with WPW,” and “Management of unstable tachycardia.”

Rate control vs. rhythm control [3][8][36]

There are no strict indications for either strategy. The choice should involve shared decision-making with a specialist and varies based on disease characteristics and comorbidities, prior treatment responses, and individual patient risk factors and preferences. [37]

Rate control is typically favored [19]

Rhythm control is typically favored [39][40]

AV nodal blocking agents used for rate control are contraindicated in preexcited Afib (e.g., due to WPW), as they can precipitate ventricular tachycardia or Vfib. [3]

Rate control [3]

For goals, indications, and agents used in acute settings, see “Rate control” in “Afib with RVR.”

  • Goal: reduction of the ventricular response rate to relieve symptoms, improved quality of life, and decreased risk of developing tachycardia-induced cardiomyopathy
  • Target resting heart rate [3]
    • < 110/minute: in patients with normal LV systolic function whose symptoms are well controlled at this rate [44]
    • < 80/minute: in patients with LV systolic dysfunction or who remain symptomatic at higher rates

Pharmacological options

Surgical options

  • AV nodal ablation and implantation of a permanent ventricular pacemaker
    • Irreversible procedure
    • Eliminates the need for rate-controlling medications but leads to lifelong dependence on a pacemaker.
    • Indications
      • Recurrent Afib
      • Afib refractory to medical rate control
      • Patients who do not tolerate the pharmacological options for Afib management

Rhythm control [3]

For goals and indications in acute settings, see “Rhythm control” in “Afib with RVR.” Agents and dosages for pharmacological cardioversion are the same regardless of the setting. Consultation with cardiology is advised.

All types of cardioversion (electrical, pharmacological, and interventional) can precipitate arterial thromboembolism and stroke in at-risk patients with Afib.

Evaluate the need for pericardioversion anticoagulation for Afib in all candidates for rhythm control and consider delaying cardioversion until TEE for Afib has ruled out thrombi in high-risk patients.

Planned electrical cardioversion [3][9]

Planned cardioversion for rhythm control differs from emergency cardioversion for unstable tachycardia in terms of risk-benefit profile, preparation, setting, and aftercare.

Pharmacological cardioversion [3]

Pharmacological cardioversion agents for Afib [3][8][45][46]

The following are inpatient regimens of IV or oral antiarrhythmics:

Several antiarrhythmic agents can precipitate other arrhythmias (e.g., in patients with QTc prolongation) and clinical deterioration in patients with structural heart disease. Only start these medications in controlled settings and in consultation with a specialist.

Pill-in-pocket approach [3][9]

  • A single, self-administered dose of an anti-arrhythmic (e.g., flecainide , propafenone ) used outside of the hospital to terminate atrial fibrillation
  • Typically given in conjunction with a beta blocker or ndHP CCB
  • May be used in patients with recent onset of Afib with infrequent episodes and no history of structural or ischemic heart disease
  • Patients should be monitored on the regimen in the hospital environment before they can self-administer.

Interventional cardioversion [3]

  • Description: Creation of scar tissue that prevents the spread of ectopic impulses.
  • Indications: patients undergoing cardiac surgery for other reasons, symptomatic refractory Afib, patient preference, concurrent CHF with reduced LVEF [8][9][47]
  • Options

Pericardioversion anticoagulation for Afib [8][9]

Determine the need for pericardioversion anticoagulation based on the duration since Afib onset and the risk of arterial thromboembolism (e.g., CHA2DS2-VASc score).

In patients with unstable Afib, anticoagulate as soon as possible if indicated, but do not delay emergency electrical cardioversion for preprocedural anticoagulation.

Patients with moderate to severe mitral stenosis, mechanical heart valves, or hypertrophic cardiomyopathy are at high risk of thromboembolism regardless of duration since Afib onset or CHA2DS2-VASc score. If not already anticoagulated, consult cardiology for optimal pericardioversion management.

Pericardioversion anticoagulation for Afib [8][9]

Before cardioversion

After cardioversion
Onset < 48 hours

Low risk

(CHA2DS2-VASc score 0 in men and 1 in women)

  • Consider either:
    • No anticoagulation
    • OR anticoagulation (with heparin or a DOAC) begun as soon as possible prior to the procedure.
  • Long-term anticoagulation is not routinely required.

Moderate risk

(CHA2DS2-VASc score 1 in men and 2 in women)

  • Consider on an individual basis in consultation with cardiology. [8]

High risk

CHA2DS2-VASc score ≥ 2 in men and ≥ 3 in women)

  • Consider anticoagulation with heparin or a DOAC begun as soon as possible prior to the procedure.
Onset ≥ 48 hours or unknown Stable patients
  • At least 4 weeks of oral anticoagulation is preferred.
Unstable patients

Base decisions about postcardioversion long-term anticoagulation for Afib on individual thrombotic and bleeding risk profiles. [8]

Long-term anticoagulationtoggle arrow icon

For patients with new-onset Afib being considered for rhythm control, see “Pericardioversion anticoagulation in Afib.”


Use the same risk-benefit profile assessment for all types of Afib and atrial flutter (e.g., paroxysmal Afib, persistent Afib, or permanent Afib) and regardless of treatment strategy (i.e., rate control and/or rhythm control) or apparent maintenance of sinus rhythm. [8][9]

Prevention of thromboembolism with long-term anticoagulation is typically indicated in patients with moderate to severe mitral stenosis, mechanical heart valves, HCM, and/or a CHA2DS2-VASc score ≥ 2 in men and ≥ 3 in women.

Always consider the bleeding risk when initiating anticoagulation.

Risk assessment [8]

Evaluate thrombotic risk and bleeding risk for all patients with Afib and atrial flutter regardless of classification and treatment strategy.

Thrombotic risk in Afib and atrial flutter
Conditions Recommendation
High risk
  • Anticoagulation is recommended.
Moderate risk
Low risk
  • Anticoagulation is not routinely recommended.

Do not use CHA2DS2-VASc scores to risk stratify patients who have moderate to severe mitral stenosis, mechanical heart valves, or HCM. [8]

CHA2DS2-VASc score

CHA2DS2-VASc score [8][13][50]
Risk factor Points
Congestive heart failure or LV dysfunction 1
Hypertension 1
Age ≥ 75 years 2
Diabetes mellitus 1
Prior stroke, transient ischemic attack, or thromboembolism 2
Vascular disease 1
Age 65–74 years 1
Sex: female [51] 1

Risk of stroke [8][13]

  • 0 points (male) or 0–1 point (female): low risk
  • 1 point (male) or 2 points (female): intermediate risk
  • ≥ 2 points (male) or ≥ 3 points (female): high risk

HAS-BLED score [52]

  • Most often used to assess the risk of bleeding in patients starting anticoagulation. [8][53]
  • Consider addressing modifiable risk factors, e.g., uncontrolled hypertension, alcohol use, NSAID, or aspirin use, and reevaluating risk.
  • A high-risk HAS-BLED score is not necessarily a reason to withhold anticoagulation; these patients require more frequent monitoring. [13]
HAS-BLED score [52][53]
Characteristics Points
Uncontrolled hypertension 1
Abnormal renal or liver function 1 point each (max. 2)
Stroke 1
Bleeding history or predisposition 1
Labile INR 1
Elderly individuals (age > 65) 1
Drugs that predispose to bleeding or alcohol use 1 point each (max. 2)

Interpretation [54]

  • 0 points: low risk
  • 1–2 points: moderate risk
  • ≥ 3: high risk

Anticoagulation regimens in atrial fibrillation and atrial flutter [3][8]

Long-term anticoagulation options in atrial fibrillation and flutter [3][8][21]
Clinical applications Options Special considerations
  • Avoid in pregnancy.
  • May not be suitable in severe renal impairment
  • Preferred for patients who cannot adhere to regular INR monitoring
Vitamin K antagonists (VKAs)
  • Patients with moderate to severe mitral stenosis or mechanical heart valves
  • Patients with contraindications to DOACs
  • Patients with severe hepatic dysfunction
  • Patients with advanced CKD
  • Use LMWH with caution in renal impairment.

Avoid dabigatran in patients with Afib and mechanical heart valves as it can be harmful. [8]

Interventional alternatives to anticoagulation [8]

Atrial fluttertoggle arrow icon


Epidemiology [60]

  • Incidence: 88 per 100,000 person-years (increases with age)
  • Sex: > (incidence in men is 2.5 times greater than in women)


  • Similar to atrial fibrillation (see “Etiology” section above)
  • May additionally result from the treatment of Afib [10]


  • Type I (common; ; typical or isthmus-dependent flutter): caused by a counterclockwise (more common) or clockwise (less common) macroreentrant activation of cardiac muscle fibers in the right atrium that travels along the tricuspid annulus and passes through the cavotricuspid isthmus
  • Type II (rare; atypical atrial flutter): various reentrant rhythms that do not involve the cavotricuspid isthmus, are not well-defined, and/or occur in the left atrium

Clinical features

Diagnostics [3][21][61]

  • Similar to atrial fibrillation except for ECG findings (see “Diagnosis of atrial fibrillation”)
  • Characteristic ECG findings of atrial flutter
    • Rate: typically 75–150/minute (depending on conduction) [61]
    • Atrial rate ≥ ventricular rate
    • Regular, narrow QRS complexes
    • The rhythm may be:
      • Regularly irregular if atrial flutter occurs with a variable AV block occurring in a fixed pattern (2:1 or 4:1)
      • Irregularly irregular with a variable block occurring in a nonfixed pattern
    • Sawtooth appearance of P waves: identical flutter waves (F waves) that occur in sequence at a rate of ∼ 300/minute
    • Predominantly negative deflections in leads II, III, aVF
    • Flat deflections in I and aVL


Consult cardiology for all patients.


  • Frequently degenerates into atrial fibrillation
  • 1:1 conduction can lead to life-threatening ventricular tachycardia

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Referencestoggle arrow icon

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