Atrial fibrillation

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.”

• 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.

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

Risk factors ^[3][4][5]

Reversible causes of atrial fibrillation ^[7]

• Hyperthyroidism, thyrotoxicosis
• Electrolyte imbalances
• Cardiothoracic surgery
• Myocarditis
• Pericarditis
• Myocardial infarction
• Alcohol use
• Excess caffeine
• Fever of any cause
• Recreational or pharmacological drug use
• Pulmonary embolism
• Other triggers of tachycardia: e.g., pain, hypovolemia, anemia

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.

Hemodynamic stability ^[3][8][9]

• 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 ^[3][8][9]

• Afib with rapid ventricular response: Afib with a ventricular rate > 100–110/minute (tachycardic Afib) ^[10][11]
• Afib with slow ventricular response: Afib with a ventricular rate < 60/minute (bradycardic Afib or slow Afib) ^[12]

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]

• Moderate to severe mitral stenosis or a mechanical heart valve
  • Significantly increased risk of thromboembolic events
  • Previously classified as valvular Afib ^[8][13][14]
• Any other valvular heart disease or no valvulopathy
  • Lower risk of thromboembolic events than moderate to severe mitral stenosis or a mechanical heart valve
  • Previously classified as nonvalvular Afib ^[8][13][14]

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:
  • Volume overload, hemodynamic stress → atrial hypertrophy and/or dilatation
  • Atrial ischemia
  • Inflammation of the atrial myocardium
  • Altered ion conduction by the atrial myocardium
• 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
     • Bursts of electrical activity from automatic foci near the pulmonary veins or in diseased, fibrotic atrial tissue
     • Pre-excitation of the atria as a result of aberrant pathways (e.g., WPW syndrome)
  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
  • The atria contract rapidly but ineffectively and in an uncoordinated fashion → stasis of blood within the atria → risk of thromboembolism and stroke
  • Irregular activation of the ventricles by conduction through the AV node → tachycardia

References:^{[15][16][17][18]}

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

• All patients
  • Irregularly irregular pulse; with or without tachycardia
  • Apex-pulse deficit
• Stable Afib
  • Most affected individuals are asymptomatic.
  • Some may present with:
    • Palpitations
    • Fatigue
    • Dyspnea
    • Lightheadedness
    • Syncope
    • Signs of underlying heart disease (e.g., murmurs of mitral stenosis)
• Unstable Afib: more likely to occur in patients with Afib with RVR and/or underlying cardiopulmonary disease
  • Ischemic chest pain
  • Altered mental status
  • Clinical features of acute heart failure
  • Clinical features of cardiogenic shock
• Complications of Afib
  • Acute left heart failure → pulmonary edema
  • Thromboembolic events: stroke/TIA, renal infarct, splenic infarct , intestinal ischemia , acute limb ischemia
  • Tachycardia-induced cardiomyopathy

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!

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.”

• Diagnostic confirmation
  • Obtain 12-lead ECG to identify ECG findings of Afib.
  • If ECG is not diagnostic and clinical suspicion is high, consider:
    • Continuous cardiac rhythm monitoring
    • Ambulatory ECG monitoring
• Identification of the underlying Afib etiology (e.g., ACS diagnostics, PE diagnostics)
  • Routine studies: CBC, CMP, and TTE
  • Additional studies based on clinical suspicion: e.g., TFTs, CXR, CTPA, toxicology screen
  • Specialized testing on an individual basis: e.g., EP study, sleep study
  • See also “Reversible causes of Afib.”
• Evaluation for factors that affect treatment
  • Risk of thrombotic complications: e.g., CHA₂DS₂-VASc score, TEE for Afib
  • Risk of bleeding: e.g., coagulation studies, HAS-BLED score
• Additional evaluation
  • Comorbid conditions: e.g., diabetes screening, CAD diagnostics
  • Complications: e.g., ischemic stroke diagnostics, AHF diagnostics

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]

• Initial investigative study to confirm Afib
• Signs of comorbid conditions and/or underlying etiologies ^[3]
  • Aberrant conduction: e.g., LBBB, RBBB, ECG findings in WPW
  • CAD: e.g., rate-dependent ST depressions, ECG findings in STEMI, ECG findings of NSTE-ACS, or evidence of previous myocardial infarction
  • Others: e.g., ECG findings in pericarditis, ECG signs of LVH

Wide QRS complex may indicate preexcited Afib or aberrant conduction.

Laboratory studies ^[3][19][21]

Routine studies

• CBC: assessment for anemia and signs of infection
• Serum electrolytes (Na⁺, K⁺, Mg²⁺, and Ca²⁺): to identify electrolyte imbalances
• BUN, serum creatinine: to identify chronic kidney disease (CKD) ^[6]
• Coagulation studies: to guide anticoagulation therapy

Cardiac evaluation

Additional cardiac evaluation is guided by clinical suspicion.

• ACS diagnostics: e.g., troponin
• Diagnostics of CHF and/or diagnostics of AHF: e.g., BNP or NT-proBNP ^[22]
• Others: See “CAD diagnostics” and “Diagnosis of hypertension.”

Afib etiologies

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

• TFTs: to screen for thyrotoxicosis
• PE diagnostics: e.g., D-dimer levels in patients with low Wells score for PE ^[23]
• Others
  • Diabetes screening ^[21]
  • Liver chemistries: to assess for liver disease ^[24]
  • Serum toxicology (e.g., ethanol level, digoxin level) and/or urine toxicology (e.g., cocaine, amphetamines)
  • Sepsis workup

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]}

Echocardiography

TTE ^[3][28]

• Goal: to assess cardiac function and rule out underlying structural heart disease (e.g., mitral valve stenosis)
• Indications
  • New Afib diagnosis
  • Known Afib with clinical deterioration of unclear etiology
• Echocardiographic findings in Afib ^{[28][29][30][31]}
  • 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., ↓ LVEF (due to cardiomyopathy), valvular heart disease, pericardial effusion

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.

• Goals
  • To evaluate for thrombi and reduce the risk of thromboembolic events
  • Visualize the atria and the left atrial appendage (hotspots for thrombogenesis)
• Indications (prior to cardioversion)
  • New-onset Afib or atrial flutter of ≥ 48 hours or unknown duration
  • No previous anticoagulant use or subtherapeutic anticoagulation
  • High stroke risk (e.g., history of stroke, left atrial thrombus, HOCM, or rheumatic fever)
• Findings of concern
  • Thrombus in the left atrium, left atrial appendage, and/or left ventricle
  • Left atrial appendage “smoke” and/or “sludge”
  • Low left atrial appendage velocities
  • Aortic atheroma ^[33]
• Interpretation
  • No thrombus identified: Safe to proceed with rhythm control
  • Thrombus identified: Anticoagulate for ≥ 3 weeks and consider repeat TEE prior to attempting rhythm control.

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]

• Goal: to evaluate for underlying cardiopulmonary comorbidities or etiologies
• CXR: e.g., CXR findings of AHF, CXR findings of pneumonia, CXR findings of COPD
• CT pulmonary angiography: See “Findings” in “CTPA.”

Cardiac rhythm monitoring ^[3]

• Indications
  • Suspected paroxysmal Afib
  • Evaluation of the adequacy of rate or rhythm control measures
  • Assessment of the relationship between symptoms and Afib (patient-activated event recorders)
• Options
  • Inpatient: continuous cardiac telemetry
  • Ambulatory ECG monitoring: Holter monitor, event recorders, loop recorders
• Findings: episodes of paroxysmal Afib; may reveal additional arrhythmias, e.g., atrial flutter

Specialized studies

• Cardiac stress test: if underlying ischemic heart disease is suspected or to assess the adequacy of rate control ^[3][19]
• EP study ^[3]
  • To identify lesions amenable to ablation (e.g., for pulmonary vein isolation)
  • To identify associated conduction abnormalities: e.g., preexcitation
  • To distinguish between ventricular tachycardia and Afib with aberrant conduction
• Sleep study: if obstructive sleep apnea is suspected ^[19]

• Tachycardia
  • See “Differential diagnosis of irregular, narrow-complex tachycardia.”
  • See “Differential diagnosis of SVT.”
  • See “Differential diagnosis of wide-complex tachycardia.”
• Palpitations ^[34]
  • Cardiac arrhythmias
  • Valvular heart disease (e.g., aortic stenosis or regurgitation, mitral valve prolapse)
  • Cardiomyopathy
  • Hyperthyroidism
  • Hypoglycemia
  • Hypovolemia
  • Drugs (e.g., alcohol, cocaine, caffeine)
  • Psychiatric disorders (e.g., panic attack, anxiety)
• Other symptoms
  • See also “Syncope.”
  • See also “Chest pain.”
  • See also “Dyspnea.”

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.

Approach

Tachycardic or unstable patients

• Unstable Afib: Perform emergency electrical cardioversion (see “Management of unstable tachycardia” for details).
• Heart rate > 100–110/minute: Start management of Afib with RVR.
• Suspected preexcited Afib: See “Afib with WPW.”

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

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

• Onset ≥ 48 hours or unknown
  • Consider rate control initially.
  • Defer consideration of rhythm control until:
    • ≥ 3 weeks of therapeutic anticoagulation is complete
    • OR thrombi are ruled out via TEE for Afib
• Onset < 48 hours
  • Consider rhythm control or rate control on an individual basis.
  • See “Rate control vs. rhythm control” for details.
• All patients
  • Begin long-term anticoagulation for Afib if favored by risk assessment.
  • Identify and treat reversible causes of Afib.
  • Provide supportive care for Afib.
  • Manage complications.

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).

• For acutely decompensated rapid Afib, see “Afib with RVR.”
• For all other stable patients:
  • Assess adherence to therapy (e.g., rate control medications, anticoagulation for Afib).
  • Identify and manage reversible Afib triggers.
  • Evaluate for and address conditions that could alter treatment efficacy (e.g., new-onset AKI, medication interactions).
  • Follow any existing treatment plan for rate control or rhythm control.
  • Consult the patient's treating cardiologist as needed.
  • Manage complications and comorbid conditions on an individual basis.

Supportive care for Afib

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

• Optimize long-term therapy for chronic underlying Afib etiologies and related comorbidities.
• Manage cardiovascular risk factors and encourage lifestyle modifications, e.g., weight loss, exercise, OSA management, reduction of alcohol consumption. ^[8][9]
• Monitor kidney and liver function regularly for patients on anticoagulation. ^[8]
• Educate patients on treatment adherence, risk of thromboembolism, and risks of anticoagulation and/or antiarrhythmic drugs.

Disposition

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.:
  • Individual patient risk profile and comorbidities
  • Optimal treatment strategy, e.g., rate control, early or delayed rhythm control
  • Risk of therapy adverse effects
  • Social support and access to health care
• 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.

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]

• Longstanding persistent or recurrent Afib ^[3][38]
• Untreated reversible cause of Afib
• High risk of thromboembolism, e.g., new Afib with onset ≥ 48 hours or unknown, known atrial thrombus, suboptimal anticoagulation
• High risk of adverse reactions to pharmacological cardioversion or electrical cardioversion

Rhythm control is typically favored ^[39][40]

• Recent-onset (< 12 months) Afib with known cardiovascular disease, especially heart failure ^[39][41][42]
• Patients < 70 years of age ^[37]
• Failure of prior rate control strategy to control symptoms or achieve target heart rate
• Treated reversible cause of Afib
• Tachycardia-induced cardiomyopathy (interventional cardioversion) ^[3][43]

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

• First-line
  • Beta blockers: e.g., metoprolol , atenolol , propranolol ^[3]
    • Preferred when Afib is due to hyperthyroidism and in pregnant patients
    • Avoid in patients with COPD and acute decompensated heart failure (ADHF).
  • OR nondihydropyridine calcium channel blockers (ndHP CCBs): e.g., diltiazem , verapamil ^[3]
    • Avoid in patients with ADHF.
    • Can be safely used in heart failure with preserved normal LV systolic function.
• Second-line: digoxin ; preferred initial therapy for patients with ADHF ^[3]
• Third-line: amiodarone ; typically reserved for patients in whom all other options have failed ^[3]

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.

• Goals
  • Termination of atrial fibrillation (or flutter)
  • Restoration and maintenance of sinus rhythm
  • Symptom improvement
  • Prevention of atrial remodeling
• Cardioversion options
  • Planned electrical cardioversion
  • Pharmacological cardioversion
  • Interventional cardioversion
• Long-term antiarrhythmic drug therapy: Consider in patients with a low risk of adverse effects.
  • Goal: to maintain sinus rhythm and reduce the frequency and duration of Afib episodes in patients with recurrent Afib ^[3]
  • Options include amiodarone, dofetilide, dronedarone, flecainide, propafenone, and sotalol.

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.

• Gradually increasing strengths of direct current shock (synchronized with the R wave) are administered under procedural sedation until sinus rhythm is restored.
• The adjunctive use of antiarrhythmic drugs prior to shock delivery may increase the likelihood of success.
• See “Management of unstable tachycardia” for the approach to emergency electrical cardioversion.

Pharmacological cardioversion ^[3]

• Consider in situations in which procedural sedation may be harmful or if the patient prefers pharmacological cardioversion.
• Most likely to be effective for arrhythmias of < 7 days duration ^[3]
• Consultation with a specialist (e.g., cardiologist, electrophysiologist) is strongly recommended.
• More effective for atrial flutter than Afib, but there is a risk of conversion to 1:1 conduction with propafenone and flecainide ^[3]

Pharmacological cardioversion agents for Afib ^{[3][8][45][46]}

The following are inpatient regimens of IV or oral antiarrhythmics:

• Flecainide ^[3]
• Dofetilide ^[3]
• Propafenone ^[3]
• Ibutilide ^[3]
• Amiodarone

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
  • 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.

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.

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

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

Approach

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]

• Assess thrombotic risk.
  • Identify patients with moderate to severe mitral stenosis, mechanical heart valves, and HCM.
  • Calculate CHA₂DS₂-VASc score in all other patients.
• Assess bleeding risk.
  • Identify contraindications to anticoagulation.
  • Calculate HAS-BLED score.
• Choose the appropriate anticoagulation regimen for Afib based on the individual risk profile.
• Consider interventional alternatives for patients with contraindications to anticoagulation and a high thrombotic risk.

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.

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

• A validated scoring system for assessing the risk of stroke in Afib. ^[49]
• Avoid use in patients with moderate to severe mitral stenosis, mechanical heart valves, or HCM. ^[8]

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]

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

• The choice of anticoagulant is predominantly based on individual patient factors.
• Educate patients on treatment adherence, bleeding risk, and risk-mitigating behavior modifications. ^[55][56]
• Antiplatelets are no longer recommended as an alternative to anticoagulation for stroke prevention in Afib or atrial flutter. ^[3][9]
• See “Pericardioversion anticoagulation in Afib” for indications and agents for anticoagulation prior to cardioversion for rhythm control.

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

Interventional alternatives to anticoagulation ^[8]

• Description: occlusion of the left atrial appendage (most common location for the formation of thrombus) ^[59]
• Options include
  • Percutaneous left atrial appendage occlusion
  • Surgical occlusion of the left atrial appendage
• Consider in patients who have contraindications to anticoagulation and have an increased risk of stroke. ^[9]

Definition

• Atrial flutter is a supraventricular tachyarrhythmia that is usually caused by a macroreentrant rhythm within the atria. ^[3]

Epidemiology ^[60]

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

Etiology

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

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 cavotricuspid isthmus, are not well-defined, and/or occur in the left atrium

Clinical features

• Most patients are asymptomatic.
• Less commonly: symptoms of arrhythmias, such as palpitations, dizziness, syncope, fatigue, and or dyspnea
• Tachycardia with a regular pulse
• Symptoms of the underlying disease (e.g., murmurs of mitral stenosis) may be present.

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

Treatment

Consult cardiology for all patients.

• Acute management of rapid atrial flutter is the same as the management of Afib with RVR.
• Long-term arrhythmia management is very similar to treatment of Afib with some minor differences:
  • Rate control: more difficult to achieve in atrial flutter than in Afib ^[21]
  • Rhythm control
    • Better results and lower recurrence compared to Afib ^[3][61]
    • Catheter ablation may be the most effective rhythm control strategy.
• Anticoagulation recommendations are the same as for long-term anticoagulation in Afib.

Complications

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

• One-Minute Telegram 67-2023-1/3: Freezing the progression of atrial fibrillation
• One-Minute Telegram 65-2022-1/3: 2022 U.S. Preventive Services Task Force: summary of recommendations
• One-Minute Telegram 63-2022-1/3: Apixaban: the right pick for atrial fibrillation?
• One-Minute Telegram 63-2022-3/3: No revelations on the best anticoagulant for patients with end-stage kidney disease
• One-Minute Telegram 62-2022-1/3: K+ may be more than OK at making bad rhythms go away
• One-Minute Telegram 59-2022-3/3: The rhythm is gonna get you: early rhythm control in low-risk AF
• One-Minute Telegram 44-2022-2/4: To screen or not to screen for atrial fibrillation: 2022 updated USPSTF recommendations
• One-Minute Telegram 15-2020-3/4: Anticoagulation for patients with bioprosthetic mitral valves: is it time for a DOAC?
• One-Minute Telegram 12-2020-4/4: Levothyroxine and AFib in older patients: what’s the right dose?

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