Atrial fibrillation

Last updated: June 29, 2022

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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 (replaced by fibrillatory 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. Anticoagulation therapy is used in patients with high-risk comorbidities, such as valvular disease and cardiomyopathy, and may be used in patients categorized as lower-risk depending on the CHA2DS2-VASc score.

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 frequently progresses to Afib.

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


Epidemiological data refers to the US, unless otherwise specified.

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

Risk factors

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

Reversible causes of atrial fibrillation [4]

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.


Classification of atrial fibrillation [5][8][9]
Terminology Definition
Hemodynamic stability Unstable Afib Afib manifesting with signs of hemodynamic instability (e.g., chest pain, altered mental status, acute pulmonary edema, hypotension, or cardiogenic shock)
Stable Afib Afib without signs of hemodynamic instability
Ventricular rate Afib with rapid ventricular response Afib with a ventricular rate > 100–110/minute (tachycardic Afib) [10][11]
Afib with slow ventricular response [12] Afib with a ventricular rate < 60/minute (bradycardic Afib or slow Afib)
Onset and duration New-onset Afib New presentation or diagnosis of Afib, regardless of duration [13]
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 [5]
Method of detection Clinical Afib An episode of Afib lasting ≥ 30 seconds that is documented on a surface ECG; may be symptomatic or asymptomatic
Subclinical Afib [9] Asymptomatic Afib not previously detected on a surface ECG that is discovered on implanted cardiac devices and confirmed on intracardiac electrograms [8][9]
Mitral valve involvement [8] Valvular Afib Afib in patients with moderate to severe mitral valve stenosis or an artificial (mechanical) heart valve
Nonvalvular Afib Afib in patients without moderate to severe mitral valve stenosis or a mechanical heart valve

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

  • 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


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

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

Approach [5][17]

  • Suspected Afib: Obtain an ECG.
    • Confirmed Afib (new diagnosis): Perform TTE.
    • Afib is not confirmed on initial ECG but strong clinical suspicion remains: rhythm monitoring
  • All patients: Investigate the underlying cause (see “Etiology of atrial fibrillation”).
    • Obtain laboratory studies.
    • Imaging and advanced cardiac testing depends on the suspected underlying cause

Initial evaluation

ECG [18]

Characteristic ECG findings in atrial fibrillation [18]
  • 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

Laboratory studies [5][17][19]

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

Transthoracic echocardiogram [5][24]

Chest x-ray [5]

Additional evaluation

Rhythm monitoring [5]

Holter ECG monitoring should be used in ambulatory patients with risk factors and symptoms of arrhythmia to rule out paroxysmal Afib.


The differential diagnoses listed here are not exhaustive.


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

Rate control for atrial fibrillation [5]

  • The goal is to normalize the ventricular heart rate to reduce symptoms.
  • Target resting heart rate [5]
    • < 110/minute: for patients who remain asymptomatic or have normal LV systolic function [30]
    • < 80/minute: for patients who continue to be symptomatic with a lenient rate
  • Consider rate control strategy especially in elderly patients
  • Contraindications: Afib due to preexcitation syndromes

Pharmacological options for rate control

Surgical options for rate control

  • 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 for atrial fibrillation (i.e., cardioversion) [5]

The following information applies to stable patients. For emergency cardioversion of unstable patients, see “Management of unstable tachycardia with a pulse.”


Cardioversion increases the risk of thromboembolic complications. All patients with Afib in whom cardioversion is planned should be considered for anticoagulant therapy.

Electrical cardioversion [5][9]

Pharmacological cardioversion [5]

Interventional cardioversion [5]

  • Description: Creation of scar tissue that prevents the spread of ectopic impulses.
    • Catheter radiofrequency ablation of atrial tissue around pulmonary vein openings (pulmonary vein isolation) [9]
    • Maze ablation: a series of incisions are made in the atrial endocardium either via a catheter or surgically to prevent atrial macroentry.
  • Indications: patients undergoing cardiac surgery for other reasons, symptomatic refractory Afib, patient preference, concurrent CHF with reduced LVEF [8][9][31]

Both techniques increase the risk of thromboembolic events; patients must be candidates for anticoagulation to be considered for these procedures.

Anticoagulation during cardioversion in atrial fibrillation [8][9]

Anticoagulation therapy should be considered in all patients undergoing cardioversion.

Anticoagulation during cardioversion in patients with nonvalvular Afib [8]
Type of Afib Patient thromboembolic risk

Before cardioversion

After cardioversion
Afib < 48 hours Low risk (CHA2DS2-VASc score 0 in men and 1 in women)
  • Consider anticoagulation therapy.
  • If the decision is made to anticoagulate, start heparin or a DOAC as soon as possible before cardioversion.
  • Long-term anticoagulation therapy is not routinely required.

Moderate/high risk (CHA2DS2-VASc score ≥ 1 in men and ≥ 2 in women)
  • At least 4 weeks of oral anticoagulation therapy after cardioversion
Stable Afib of unknown duration or ≥ 48 hours Any risk
Unstable Afib of unknown duration or ≥ 48 hours Any risk
  • Initiate anticoagulation as soon as possible with heparin or a DOAC.

Unstable patients should receive immediate anticoagulation therapy with rapid-acting anticoagulants before synchronized electrical cardioversion.

Transesophageal echocardiogram for atrial fibrillation [5][9][32]

Atrial fibrillation is associated with an increased risk of thromboembolic complications (e.g., ischemic stroke). The decision of whether to start anticoagulation in patients with atrial fibrillation and atrial flutter requires careful consideration of the risk of bleeding and the risk of thromboembolism in each individual patient. The choice of anticoagulant depends on patient factors and the urgency of anticoagulation.


Long-term anticoagulation for patients with Afib in order to prevent thromboembolic complications is indicated if the patient has an underlying valvular disease, hypertrophic cardiomyopathy, and/or a CHA2DS2-VASc score ≥ 2 in men and ≥ 3 in women.

The risk of bleeding due to anticoagulation should always be taken into consideration when initiating anticoagulation therapy.

Risk assessment [8]

Consider in all patients with Afib and atrial flutter regardless of classification and treatment strategy.

Risk assessment for long-term anticoagulation in Afib and atrial flutter
Conditions Recommendation
High risk
  • Anticoagulation is recommended.
Medium risk
  • Consider anticoagulation (risks and benefits should be discussed with the patient).
Low risk
  • Anticoagulation is not routinely recommended.

CHA2DS2-VASc score

CHA2DS2-VASc is a validated scoring system for assessing the risk of stroke in nonvalvular Afib. [36]

CHA2DS2-VASc score [8][37][38]
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 [39] 1

Risk of stroke [8][38]

  • 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 [40]

  • The HAS-BLED scoring system is used to assess the risk of bleeding in patients starting anticoagulation. [8][41]
  • Bleeding risk assessment should focus on modifiable risk factors, e.g., uncontrolled hypertension, alcohol use, NSAID or aspirin use.
  • A high-risk HAS-BLED score is not necessarily a reason to withhold anticoagulation; these patients require more frequent monitoring. [38]
HAS-BLED score [40]
Characteristics Points
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 [42]

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

Anticoagulation regimens in atrial fibrillation (and atrial flutter) [5]

Anticoagulant regimen options in atrial fibrillation and flutter [5][19]
Indications Special considerations Options
Vitamin K antagonists
  • Avoid in pregnancy.
  • May not be suitable in severe renal impairment
  • In renal impairment, use low molecular weight heparins (LMWHs) with caution.

Interventional alternatives to anticoagulation [8]

Hemodynamically unstable

Hemodynamically stable

All patients

Due to the risk of ventricular fibrillation, avoid digoxin, nondihydropyridine calcium channel blockers, and amiodarone in patients with Afib with preexcitation.

Clinical features [49]

  • Definition: atrial fibrillation with HR > 100–110/minute
  • Patients may be unstable or stable with or without symptoms.


See “Diagnosis of atrial fibrillation.”

Management of atrial fibrillation with RVR [5][50]


Patients with unstable Afib should be treated with immediate cardioversion!

Rate control [5][50]

Rhythm control (e.g., cardioversion) [5][8][50]

Management of special situations and complications

Avoid CCBs and beta blockers in decompensated heart failure.

Avoid CCBs, digoxin, and adenosine in patients with preexcitation because of the risk of the arrhythmia converting to ventricular fibrillation


Epidemiology [55]

  • 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 [5][19][56]

  • Similar to atrial fibrillation except for ECG findings (see “Diagnosis of atrial fibrillation”)
  • Characteristic ECG findings
    • Rate: typically 75–150/minute (depending on conduction) [56]
    • 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



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

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