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  • Clinician

Atrial fibrillation


Atrial fibrillation (Afib) is a commonly seen type of supraventricular tachyarrhythmia that is characterized by uncoordinated atrial activation resulting in an irregular ventricular response. While the exact mechanisms are still 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. However, when symptoms do occur, these 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. The diagnosis is confirmed by an ECG showing indiscernible P waves and a narrow QRS complex with irregular QRS intervals. Echocardiography is used in patients with Afib to rule out structural heart disease and detect the presence of 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 involve elective synchronized cardioversion and/or the use of antiarrhythmics (e.g., flecainide, propafenone, or amiodarone). The need for anticoagulation therapy is determined based on the CHA2DS2-VASc score. Catheter-directed or surgical ablation of the arrhythmogenic tissue is used in refractory or severe Afib.

Atrial flutter is another type of commonly seen 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 atrial rate is slower than in Afib and the ventricular rhythm is usually regular. Treatment is similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter frequently degenerates into atrial fibrillation.


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

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 criteria Definition
Hemodynamic stability Unstable Afib Afib presenting 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
Heart rate Afib with rapid ventricular response Afib with a ventricular rate > 100 bpm (tachycardic Afib)
Slow Afib Afib with a ventricular rate < 60 bpm (bradycardic Afib)
Onset and duration of Afib New-onset Afib Afib less than 48 hours in duration
Paroxysmal Afib Afib that resolves within 7 days of onset either following treatment or spontaneously
Persistent Afib Continuous Afib for > 7 days
Long-standing persistent Afib Continuous Afib for > 1 year
Permanent Afib Long-standing persistent Afib that is not treated unless the patient and the treating physician agree to do so
Mitral valve involvement Valvular Afib Afib in patients with mitral valve stenosis, artificial heart valves, and/or repaired mitral valves
Nonvalvular Afib Afib in patients without mitral valve involvement

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


Clinical features

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!


ECG (initial investigation)

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


  • Transthoracic echocardiogram (TTE)
  • Transesophageal echocardiogram (TEE)
    • Indicated in patients who meet all of the following criteria:
    • Visualizes the atria and the left atrial appendage (hotspots for thrombogenesis) to identify thrombi before attempting cardioversion
    • Further assesses heart function and rules out underlying structural disease

Laboratory studies


Differential diagnoses

AFib should be differentiated from other supraventricular tachyarrhythmias with a narrow QRS complex. See supraventricular arrhythmias in the overview section of cardiac arrhythmias.

The differential diagnoses listed here are not exhaustive.


The general principles of treating atrial fibrillation include:

  1. Correcting reversible causes and/or treatable conditions (e.g., hyperthyroidism, electrolyte imbalances)
  2. Controlling heart rate and/or rhythm
  3. Providing anticoagulation

Controlling heart rate and/or rhythm

Treatment strategy Rate control Rhythm control
Goal and rationale
  • Terminating atrial fibrillation and restoring it to sinus rhythm in order to prevent atrial remodeling
  • Elderly patients
  • Failure of rate-control strategy to control symptoms
  • Younger patients
  • AF due to pre-excitation syndromes
Therapeutic measures 1st line
2nd line (ablative procedures)
  • AV nodal ablation and implantation of a permanent ventricular pacemaker

Patients with unstable AF should be treated with immediate cardioversion!


Prerequisites for cardioversion of AF

Anticoagulation therapy should be considered in all patients who are about to undergo cardioversion.

Long-term anticoagulation

CHA2DS2-VASc score Indications for long-term anticoagulation
Acronym Risk factor Points
C CHF or left-sided heart failure 1
H Hypertension 1
A2 Age ≥ 75 2
D Diabetes Mellitus 1
S2 Stroke or TIA or thromboembolism 2
V Vascular disease (prior MI, peripheral artery disease, or aortic plaque) 1
A Age 65–74 1
Sc Sex category (female sex) 1
CHA2DS2-VASc scores of 1, 2, 3, 5, and ≥6 carry an annual stroke risk of approx. 1%, 2%, 3%, 7%, and >9% respectively.

Long term anticoagulation for patients with AF in order to prevent thromboembolic complications is indicated if the patient has an underlying valvular disease and/or a CHA2DS2-VASc score ≥ 2

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


Atrial flutter

  • Atrial flutter is a supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria.
  • Epidemiology
    • Incidence: 88 per 100,000 person-years (increases with age)
    • Sex: > (5:2)
  • Etiology: similar to atrial fibrillation (see “Etiology” above)
  • Pathophysiology
    • 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 cardio-tricuspid isthmus, are not well defined, and/or occur in the left atrium
  • Clinical features
  • Diagnostics: similar to atrial fibrillation; see “Diagnostics” above
    • Sawtooth appearance of P waves: identical flutter waves (F waves) that occur in sequence at a rate of ∼ 300 bpm
    • 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
  • Treatment: similar to atrial fibrillation (see “Therapy” below)
  • Complications
    • Frequently degenerates into atrial fibrillation (see “Clinical features” above)
    • 1:1 conduction leading to life-threatening ventricular tachycardia


Acute management checklist

Hemodynamically unstable

  • Immediate synchronized cardioversion (see DC cardioversion)
  • Urgent cardiology consultation
  • ICU/CCU transfer
  • Identify and treat the underlying cause.
  • Continuous cardiac telemetry.

Hemodynamically stable

All patients

  • Identify and treat the underlying cause.
  • TTE to evaluate for valvular/structural heart disease
  • Assess the risk of stroke and consider indications for anticoagulation.

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

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last updated 09/21/2020
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