- Clinical science
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.
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: P – Pulmonary disease; A – Anemia; R – Rheumatic heart disease; A – Atrial myxoma; S – Sepsis; I – Ischemia; T – Thyroid disease; E – Ethanol.
|Classification of atrial fibrillation |
|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) |
|Afib with slow ventricular response ||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 |
|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 |
|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 ||Asymptomatic Afib not previously detected on a surface ECG that is discovered on implanted cardiac devices and confirmed on intracardiac electrograms |
|Mitral valve involvement ||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 .
- 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:
- Afib is triggered by one or both of the following
- Afib is sustained by re-entry rhythms and/or rapid focal ectopic firing
- 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
- Most affected individuals are asymptomatic.
- Less commonly, affected individuals develop symptoms of such as palpitations, dizziness, syncope, fatigue, and or dyspnea.
- Signs of underlying disease (e.g., murmurs of mitral stenosis)
- Tachycardia with an irregularly irregular pulse
- Apex-pulse deficit: difference between the rate of apex heart beat and that of the peripheral pulse
- Complications of long-standing Afib
Individuals with Afib may be asymptomatic for a long time before diagnosis is made.
- 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 investigative study to confirm Afib
- To assess for evidence of risk factors that may affect treatment, such as: 
|Characteristic ECG findings in atrial fibrillation |
|P waves|| |
|QRS complex|| |
Laboratory studies 
- CBC: assessment for anemia and signs of infection
- TSH, fT4: to screen for hyperthyroidism
- Liver chemistries: to assess for liver disease 
- Consider also the following to evaluate for complications and underlying etiology:
- Troponin levels: to assess for myocardial injury or infarction
- Brain-natriuretic peptide (BNP) or NT-proBNP
- D-dimer levels: if patients have risk factors (e.g., DVT) or clinical features of pulmonary embolism 
- Serum toxicology (e.g., ethanol level, digoxin level) and/or urine toxicology (e.g., cocaine, amphetamines)
Transthoracic echocardiogram 
Indications: all patients with new-onset Afib to assess cardiac function and rule out underlying structural cardiac disease (e.g., mitral valve stenosis)
- For indications for TEE, see “Transesophageal echocardiogram for atrial fibrillation.”
- The heart may be structurally normal (more common in young people).
- Left atrial thrombus may be visible
- Atrial enlargement
- Chaotic atrial movements that are not coordinated with ventricles
- Decreased left atrial compliance and volume
- Evidence of underlying etiology, e.g., LV systolic dysfunction due to ischemic or dilated cardiomyopathy, pericardial effusion, valvular disease
Chest x-ray 
- Indication: to evaluate for pulmonary disease or heart failure
Rhythm monitoring 
- Inpatient: continuous cardiac telemetry
- Outpatient/ambulatory: Holter monitor, event recorders, loop recorders
- Assess whether rate or rhythm control measures are adequate
- Evaluate for suspected paroxysmal asymptomatic Afib
- Assessment of the relationship between symptoms and Afib (patient-activated event recorders)
- Findings: : episodes of paroxysmal Afib; may reveal additional arrhythmias, e.g., atrial flutter
- Cardiac stress test: if underlying ischemic heart disease is suspected or to assess the adequacy of rate control 
- Electrophysiological study: suspected preexcitation (delta wave on ECG), if there is suspicion for an underlying SVT triggering Afib, or to distinguish between ventricular tachycardia and Afib with aberrant conduction 
- Sleep study: if obstructive sleep apnea is suspected 
- Afib should be differentiated from other supraventricular tachyarrhythmias with a narrow QRS complex and tachyarrhythmias with wide QRS complexes .
- See “Differential diagnosis of irregular, narrow-complex tachycardia,” “Differential diagnosis of SVT,” and “Differential diagnosis of wide-complex tachycardia.”
The differential diagnoses listed here are not exhaustive.
- Unstable patients: emergent electrical cardioversion (see “Management of unstable tachycardia with a pulse”)
Stable patients: The goal is to control heart rate and/or rhythm.
- Acute management: See “Management of atrial fibrillation with RVR.”
- Long-term management:
- All patients
- Consider referral to cardiology.
- Correct reversible causes and/or treatable conditions, e.g., hyperthyroidism, electrolyte imbalances (see “Reversible causes of atrial fibrillation” in “Etiology”).
- Prevention of thromboembolic complications: Consider indications for anticoagulation (see “Anticoagulation in atrial fibrillation”).
- Encourage lifestyle modifications that reduce the risk of recurrence and decrease the likelihood of complications, e.g., weight loss, exercise, and reducing alcohol consumption. 
Patients with unstable Afib should be treated with immediate electrical cardioversion!
- The goal is to normalize the ventricular heart rate to reduce symptoms.
- Target resting heart rate 
- < 110/minute: for patients who remain asymptomatic or have normal LV systolic function 
- < 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
- Beta blockers (e.g., metoprolol , atenolol , propranolol ) 
- Nondihydropyridine calcium channel blockers (e.g., diltiazem , verapamil ) 
- Second line: digoxin ; preferred as first-line therapy in patients with decompensated HF when beta blockers are contraindicated. 
- Third line: amiodarone ; typically reserved for patients in whom all other options have failed 
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.
- Indicated in Afib that is refractory to medical rate control
Rhythm control for atrial fibrillation (i.e., cardioversion) 
The following information applies to stable patients. For emergency cardioversion of unstable patients, see “Management of unstable tachycardia with a pulse.”
- Goal: termination of atrial fibrillation (or flutter) and restoration of sinus rhythm in order to prevent atrial remodeling and improve symptoms
- Consider rhythm control in the following patient groups:
- Options include electrical cardioversion, pharmacological cardioversion, interventional cardioversion
- The choice of method of cardioversion should be made by a cardiologist.
- Contraindications (for any form of cardioversion): 
- Initiate anticoagulation before cardioversion to reduce the risk of stroke (see “Anticoagulation during cardioversion in atrial fibrillation”).
- Consider indications for TEE prior to cardioversion (see “Transesophageal echocardiogram for atrial fibrillation”)
- Following cardioversion, consider daily antiarrhythmic drugs to maintain sinus rhythm.
Cardioversion increases the risk of thromboembolic complications. All patients with Afib in whom cardioversion is planned should be considered for anticoagulant therapy.
Electrical cardioversion 
- Gradually increasing strengths of direct current shock (synchronized with the R wave) are administered under procedural sedation until sinus rhythm is restored.
- Can be performed in an emergency in unstable patients or electively in stable patients
- The use of antiarrhythmic drugs prior to planned cardioversion may increase the likelihood of successful electrical cardioversion.
- For more details on the procedure, see “Synchronized electrical cardioversion” in “Management of tachycardia.”
Pharmacological cardioversion 
- Consider if procedural sedation is deemed high risk or if the patient prefers pharmacological cardioversion.
- Most likely to be effective for arrhythmias of < 7 days' duration 
- Consultation with a specialist (e.g., cardiology, electrophysiologist) strongly recommended.
- More effective for atrial flutter when compared with Afib but there is a risk of conversion to 1:1 conduction with propafenone and flecainide 
- Inpatient regimens using intravenous or oral antiarrhythmics:
Pill-in-pocket approach 
- 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 
- 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 
Both techniques increase the risk of thromboembolic events; patients must be candidates for anticoagulation to be considered for these procedures.
Anticoagulation therapy should be considered in all patients undergoing cardioversion.
- Hemodynamically unstable patients: anticoagulate as soon as possible, but this should not delay electrical cardioversion.
- Valvular Afib: anticoagulation prior to the procedure and this should be continued long-term after the procedure
- Nonvalvular Afib: risk-stratify patients using the CHA2DS2-VASc score to determine the need for anticoagulation before and after cardioversion.
|Anticoagulation during cardioversion in patients with nonvalvular Afib |
|Type of Afib||Patient thromboembolic risk|| |
|Afib < 48 hours||Low risk (CHA2DS2-VASc score 0 in men and 1 in women)|| |
Moderate/high risk (CHA2DS2-VASc score ≥ 1 in men and ≥ 2 in women)
|Stable Afib of unknown duration or ≥ 48 hours||Any risk|
|Unstable Afib of unknown duration or ≥ 48 hours||Any risk|
Indications (prior to cardioversion) 
- New-onset atrial fibrillation or atrial flutter for > 48 hours or for an unknown duration
- No previous anticoagulant use or subtherapeutic anticoagulation
- CHF exacerbation or hemodynamic instability
- Symptomatic Afib (e.g., palpitations, chest pain, dyspnea, syncope, fatigue, lightheadedness)
- High stroke risk (e.g., history of stroke, left atrial thrombus, HOCM, or rheumatic fever)
- Findings of concern
- No thrombus identified: 3 weeks of preceding anticoagulation is not required.
- Thrombus identified: Patients should ideally receive ≥ 3 weeks of anticoagulation and a repeat TEE prior to any procedure.
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.
- Assess for absolute contraindications to anticoagulation and estimate bleeding risk.
- Assess thromboembolic risk.
- For patients with new-onset stable Afib who will undergo cardioversion:
- Need for anticoagulation depends on duration and individual risk factors (see “Anticoagulation during cardioversion in atrial fibrillation”)
- Consider TEE (see “Transesophageal echocardiogram for atrial fibrillation”) to rule out intracardiac thrombus.
- All patients starting anticoagulation: Calculate the HAS-BLED score to determine monitoring intervals and inform patients of risks.
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 
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|
|High risk|| |
|Medium risk|| |
|Low risk|| |
|CHA2DS2-VASc score |
|Congestive heart failure or LV dysfunction||1|
|Age ≥ 75 years||2|
|Prior stroke, transient ischemic attack, or thromboembolism||2|
|Age 65–74 years||1|
|Sex category: female ||1|
Risk of stroke 
HAS-BLED score 
- The HAS-BLED scoring system is used to assess the risk of bleeding in patients starting anticoagulation. 
- 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. 
|HAS-BLED score |
|Abnormal renal or liver function||1 point each (max. 2)|
|Bleeding history or predisposition||1|
|Elderly individuals (age > 65)||1|
|Drugs that predispose to bleeding or alcohol use||1 point each (max. 2)|
- The choice of anticoagulant is predominantly based on individual patient factors.
- Patients should be educated on enhanced risks of bleeding and how to reduce them. 
- Antiplatelets are no longer recommended as an alternative to anticoagulation for stroke prevention in Afib or atrial flutter. 
- Patients starting warfarin: Consider if bridging therapy with heparin is required.
|Anticoagulant regimen options in atrial fibrillation and flutter |
|Vitamin K antagonists|| |
|DOACs|| || |
|Heparin|| || |
Interventional alternatives to anticoagulation 
- Description: occlusion of the left atrial appendage (most common location for the formation of thrombus) 
- Options include
- Consider in patients who have contraindications to long-term anticoagulation and have an increased risk of stroke. 
- Immediate synchronized cardioversion
- Urgent cardiology consult
- ICU/CCU transfer
- Identify and treat the underlying cause.
- Continuous cardiac telemetry
- Afib with normal heart rate
- Consider indications for nonemergency cardioversion (e.g., first episode).
- Refer to cardiology for long-term management with either rhythm or rate control.
Afib with RVR
- < 48 hours duration: Consider rate or rhythm control.
- > 48 hours: rate control
- ICU/CCU consult and transfer if the patient has a refractory rapid ventricular rate
- Identify and treat the underlying cause.
- TTE to evaluate for valvular/structural heart disease
- Assess the risk of stroke and bleeding; consider anticoagulation.
Clinical features 
- Definition: atrial fibrillation with HR > 100–110/minute
- Patients may be unstable or stable with or without symptoms.
- ECG: to confirm the diagnosis and identify any ECG features of preexcitation.
- Assess for any underlying causes, e.g., sepsis, pulmonary embolism, hypovolemia (see “Etiology of atrial fibrillation”)
- Assess patients for hemodynamic compromise.
- Unstable: See “Management of unstable tachycardia with a pulse.”
- Stable: Treatment (rate or rhythm control) will depend on the duration of symptoms and any complications 
- Onset > 48 hours: Rate control is preferred. 
- Onset < 48 hours: Consider rate control or rhythm control (e.g., cardioversion). 
- All patients
- Consider indications for anticoagulation (see “Anticoagulation in atrial fibrillation”). 
- Consider cardiology consult for long-term therapy, anticoagulation therapy, and consideration of ablation therapy or surgery.
- Identify and treat the underlying cause.
- Identify and treat any complications.
Patients with unstable Afib should be treated with immediate cardioversion!
Rate control 
- IV agents are recommended in the acute setting; consider combination with oral medications. 
- Target resting heart rate: < 80/minute (HR < 110/minute may be acceptable in asymptomatic patients with no evidence of LV systolic dysfunction) 
- Choose from one of the following (first-line):
- Consider one of the following if the patient has contraindications to any of the above or refractory symptoms:
Rhythm control (e.g., cardioversion) 
- Hemodynamically unstable patients, ongoing myocardial ischemia, decompensated heart failure: Perform synchronized electrical cardioversion. 
- Stable patients: Consult cardiology to determine if rhythm control is appropriate (See “Rhythm control for atrial fibrillation”).
- Most patients should be started on anticoagulation prior to the procedure (see “Anticoagulation during cardioversion in atrial fibrillation”).
Management of special situations and complications
Management of Afib in acute coronary syndrome 
- Indications for urgent synchronized electrical cardioversion
- Ongoing ischemia
- Hemodynamic compromise
- Inadequate rate control
IV beta blockers
- Generally preferred for rate control
- Avoid in patients with decompensated heart failure, bronchospasm, and/or hemodynamic instability.
- Consider amiodarone or digoxin in patients with hemodynamic compromise or severe LV dysfunction and heart failure.
- Indications for urgent synchronized electrical cardioversion
Management of Afib in congestive heart failure 
- Chronic, nondecompensated CHF
- Decompensated CHF
- AV nodal blockade or rhythm control
- Management of Afib with preexcitation (e.g., WPW)
- 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 
- 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