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Atrial fibrillation


Atrial fibrillation (AF, Afib) is a common supraventricular tachyarrhythmia that is caused by uncoordinated atrial activation resulting in an irregular ventricular response. The exact mechanisms that lead to AF are poorly understood, but a number of cardiac and noncardiac risk factors are associated with AF. Patients are often asymptomatic but have an irregularly irregular pulse on physical examination. When present, symptoms usually include palpitations, lightheadedness, shortness of breath or features of embolic stroke. The relative stagnation of blood in the atria due to ineffective atrial emptying promotes clot formation, which in turn increases the risk of stroke and other thromboembolic complications. The diagnosis is confirmed by an ECG that shows indiscernible P waves and a narrow but irregular QRS complex. A Holter monitor or event recorder is used to diagnose intermittent episodes. Echocardiography is useful in ruling out structural heart disease and to detect the presence of atrial thrombi. AF with symptoms of hemodynamic instability should always be treated with immediate synchronized cardioversion. Treatment of AF among hemodynamically stable patients consists of anticoagulation therapy to prevent thromboembolic complications and the use of rate or rhythm control strategies to prevent the symptoms of AF and atrial remodeling. The need for anticoagulation therapy is determined based on the CHA2DS2-VASc score. Therapy should be individualized in high-risk patients after considering the risks (particularly life-threatening bleeding) versus benefits (reduced risk of stroke) of 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 such as flecainide, propafenone, ibutilide, dofetilide, or amiodarone. Rate control therapy is usually preferred but the preferred treatment strategy may vary depending on the treatment center and the presence or absence of other comorbidities. Catheter directed or surgical ablation of the arrhythmogenic tissue is a newer modality used in refractory or severe AF.

Atrial flutter is another common 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 AF. However, the atrial rate is slower, the QRS rhythm is usually regular, and characteristic saw-toothed P waves are seen on an ECG. Treatment is similar to that of AF, consisting of anticoagulation, and rate or rhythm control strategies. Atrial flutter frequently degenerates into atrial fibrillation.



Epidemiological data refers to the US, unless otherwise specified.


While direct causes of atrial fibrillation are not known, many risk factors for AF exist .

Risk factors for atrial fibrillation
Cardiovascular risk factors Intrinsic cardiac disorders Noncardiac disorders
  • The exact mechanisms by which these risk factors lead to AF are not well understood, but some of the suggested mechanisms include:

In approx. 15% of cases, AF occurs in the absence of any of the above risk factors (idiopathic / lone AF).



Classification criteria Definition
Hemodynamic stability Unstable AF AF patients who present with chest pain, altered mental status, acute pulmonary edema, hypotension and/or other signs of shock
Stable AF AF patients who are hemodynamically stable
Heart rate AF with rapid ventricular response AF with a ventricular rate > 100 bpm (tachycardic AF)
Slow AF AF with a ventricular rate < 60 bpm (bradycardic AF)
Onset and duration of AF New-onset AF AF less than 48 hours in duration
Paroxysmal AF AF that terminates within 7 days of onset either following treatment or spontaneously
Persistent AF Continuous AF for > 7 days
Long-standing persistent AF Continuous AF for > 1 year
Permanent AF Long-standing persistent AF that is not treated following a joint decision by the patient and the physician
Mitral valve involvement Valvular atrial fibrillation AF in patients with mitral valve stenosis, artificial heart valves, and/or repaired mitral valves
Non-valvular atrial fibrillation AF in patients without mitral valve involvement → moderately elevated risk of thromboembolic events

Mitral valve involvement should always be assessed in patients with AF!



  • Atrial fibrillation is a supraventricular arrhythmia.
  • Three steps, which perpetuate a vicious cycle are responsible for the pathogenesis of AF:
    1. AF is initiated by one or both of the following mechanisms:
    2. AF is sustained by re-entry rhythms and/or rapid focal ectopic firing
    3. Atrial remodeling
  • Effects of AF
    • The atria contract rapidly but ineffectively and in an uncoordinated fashion → stasis of blood within the atria → risk of thromboembolism
    • Irregular activation of the ventricles by conduction through the AV nodetachycardia


Clinical features

Patients with atrial fibrillation may be asymptomatic for long periods of time!

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


  • ECG (initial investigation)
    • Irregularly irregular RR intervals
    • P-waves are indiscernible
    • Tachycardia
    • Narrow QRS complex (< 0.12 seconds)

In a patient, who presents with risk factors for AF and symptoms suggestive of arrhythmias, Holter ECG monitoring may be used to detect paroxysmal AF.


Differential diagnoses

The differential diagnosis of AF include other tachyarrhythmias. See specifically “supraventricular tachyarrhythmias, which typically have a narrow QRS complex.

The differential diagnoses listed here are not exhaustive.

Atrial flutter

  • Atrial flutter is a supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria.
  • Epidemiology
  • Etiology: similar to atrial fibrillation (see “Etiology” above)
  • Clinical features
  • Diagnostics (similar to atrial fibrillation; see “Diagnostics” above)
    • Sawtooth appearance of P waves (flutter waves or F waves), at a rate of ∼ 300 bpm
    • Regular, narrow QRS complexes
  • Treatment: similar to atrial fibrillation (see “Therapy” above)
  • Complications:
    • Frequently degenerates into atrial fibrillation (see “Clinical features” above)
    • 1:1 conduction leading to life-threatening ventricular tachycardia



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
  • Long-standing persistent AF
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

  • New onset AF (< 48 hours) in patients with:
  • AF ≥ 48 hours or of unknown duration in patients with:
    • Unstable AF (require urgent cardioversion): IV heparin or LMWH immediately before cardioversion followed by warfarin for up to 4 weeks after cardioversion
      • TEE to rule out atrial thrombi recommended if anticoagulation has not been administered at least 3 week prior to cardioversion
    • Stable AF (do not require urgent cardioversion): warfarin with bridging therapy for 3 weeks before and up to 4 weeks after cardioversion

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


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.
    • Patients with nonvalvular Afib: Assess stroke risk with the CHA2DS2-VASc score and weigh risks of bleeding with the HAS-BLED score.
    • Patients with a mechanical heart valve: Start warfarin.
    • Patients undergoing nonemergency cardioversion [13]
      • New-onset Afib (< 48 hours): Start anticoagulation before cardioversion.
      • Afib > 48 hours or duration unknown
        • At least 4 weeks of oral anticoagulation and then cardioversion
        • TEE to look for thrombi if cardioversion is required earlier

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 02/26/2020
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