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 (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

References:^[1][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

Reversible causes of atrial fibrillation ^[4]

• 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

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.

References:^{[1][2][5][6][7]}

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:^{[1][6][14][15]}

• Most affected individuals are asymptomatic.
• Less commonly, affected individuals develop symptoms of arrhythmias 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
  • Manifests when only some cardiac contractions are strong enough to transmit a pulse wave to the periphery
  • Number of cardiac contractions (perceived with stethoscope or palpated on the chest) is higher than the peripheral pulse rate (e.g., radial artery)
• Complications of long-standing Afib
  • Acute left heart failure → pulmonary edema
  • Thromboembolic events: stroke/TIA, renal infarct, splenic infarct , intestinal ischemia , acute limb ischemia
  • Life-threatening ventricular tachycardia

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!
References:^[16]

Approach ^[5][17]

• Confirm Afib with an ECG
• Perform TTE to assess cardiac function and rule out structural pathology
• Investigate the underlying cause (See “Etiology of atrial fibrillation”)

Initial evaluation

ECG ^[18]

• Initial investigative study to confirm Afib
• To assess for evidence of risk factors that may affect treatment, such as: ^[5]
  • Left ventricular hypertrophy
  • Bundle branch block
  • Preexcitation
  • Evidence of previous myocardial infarction

Laboratory studies ^[5][17][19]

• CBC: assessment for anemia and signs of infection
• BMP
  • Serum electrolytes (Na⁺, K⁺, Mg²⁺, and Ca²⁺): to identify electrolyte imbalances
  • Serum glucose: to assess for hyperglycemia ^[19]
  • BUN, serum creatinine: to identify chronic kidney disease (CKD) ^[3]
• TSH, free T₄: to screen for hyperthyroidism
• Liver chemistries: to assess for liver disease ^[20]
• HbA1c: to assess for diabetes ^[19]
• 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
    • To assess for underlying heart failure ^[21]
    • Can be elevated in persistent and paroxysmal Afib ^[5][22]
  • D-dimer levels: if patients have risk factors (e.g., DVT) or clinical features of pulmonary embolism ^[23]
  • Serum toxicology (e.g., ethanol level, digoxin level) and/or urine toxicology (e.g., cocaine, amphetamines)

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

Transthoracic echocardiogram ^[5][24]

• 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.”
• Findings ^{[24][25][26][27]}
  • 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

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

Chest x-ray ^[5]

• Indication: to evaluate for pulmonary disease or heart failure
• Findings
  • Signs of heart failure, e.g., cardiomegaly and signs of pulmonary edema
  • Signs of an underlying etiology, such as pulmonary embolism, pneumonia, or COPD (see “Etiology” section)

Additional evaluation

Rhythm monitoring ^[5]

• Options
  • Inpatient: continuous cardiac telemetry
  • Outpatient/ambulatory: Holter monitor, event recorders, loop recorders
• Indications
  • 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

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

Other

• Cardiac stress test: if underlying ischemic heart disease is suspected or to assess the adequacy of rate control ^[5][17]
• 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 ^[5]
• Sleep study: if obstructive sleep apnea is suspected ^[17]

• 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.

Approach

• 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:
    • The choice of rate control versus rhythm control depends on institutional preferences and individual patient risk factors. ^[28][29]
    • See “Rate control for atrial fibrillation” and “Rhythm control for atrial fibrillation.”
• 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. ^[9]

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

• First-line
  • Beta blockers (e.g., metoprolol , atenolol , propranolol ) ^[5]
    • Preferred when Afib is due to hyperthyroidism and in pregnant patients
    • Avoid in patients with COPD.
  • Nondihydropyridine calcium channel blockers (e.g., diltiazem , verapamil ) ^[5]
    • Avoid in patients with decompensated heart failure (LV systolic dysfunction/low ejection fraction).
    • Can be safely used in heart failure with preserved normal LV systolic function.
• Second line: digoxin ; preferred as first-line therapy in patients with decompensated HF when beta blockers are contraindicated. ^[5]
• Third line: amiodarone ; typically reserved for patients in whom all other options have failed ^[5]

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.”

Overview

• 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:
  • Failure of rate control strategy to control symptoms or achieve target heart rate
  • New-onset Afib
  • Acute illness that precipitated Afib
  • Other: tachycardia-induced cardiomyopathy, pregnancy, patient preference, younger patients
• 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): ^[17]
  • Long-standing persistent Afib for which cardioversion is unlikely to be successful ^[5]
  • Reversible causes, e.g., digoxin toxicity or electrolyte imbalances
  • High-risk of thromboembolic events, e.g., known atrial thrombus, suboptimal anticoagulation
• 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 ^[5][9]

• 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 ^[5]

• 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 ^[5]
• 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 ^[5]
• Inpatient regimens using intravenous or oral antiarrhythmics:
  • Dofetilide ^[5]
  • Ibutilide ^[5]
  • Flecainide ^[5]
  • Propafenone ^[5]
  • Amiodarone
  • Sotalol
• Pill-in-pocket approach ^[5][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 ^[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.

• 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.

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

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

• Overview
  • Can be used prior to cardioversion to evaluate for thrombus and reduce the risk of thromboembolic events
  • TEE visualizes the atria and the left atrial appendage (hotspots for thrombogenesis)
• Indications (prior to cardioversion) ; ^[33]
  • 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
  • Thrombus in the left atrium or left atrial appendage
  • Left atrial appendage “smoke” and/or “sludge”
  • Low left atrial appendage velocities
  • Aortic atheroma ^[34]
• Interpretation
  • 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.

Approach

• Assess for absolute contraindications to anticoagulation and estimate bleeding risk.
• Assess thromboembolic risk.
  • Valvular Afib: Initiate anticoagulation (if no contraindications present).
  • Nonvalvular Afib: Calculate the CHA₂DS₂-VASc score to assess risk for thromboembolism.
• 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 ^[8]

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

CHA₂DS₂-VASc score

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

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]

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

• 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. ^[43][44]
• Antiplatelets are no longer recommended as an alternative to anticoagulation for stroke prevention in Afib or atrial flutter. ^[5][19]
• Patients starting warfarin: Consider if bridging anticoagulation with heparin is required.

Interventional alternatives to anticoagulation ^[8]

• Description: occlusion of the left atrial appendage (most common location for the formation of thrombus) ^[48]
• Options include
  • Percutaneous left atrial appendage occlusion
  • Surgical occlusion of the left atrial appendage
• Consider in patients who have contraindications to long-term anticoagulation and have an increased risk of stroke. ^[9]

Hemodynamically unstable

• Immediate synchronized cardioversion
• Urgent cardiology consult
• ICU/CCU transfer
• Identify and treat the underlying cause.
• Continuous cardiac telemetry

Hemodynamically stable

• 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

All patients

• Identify and treat the underlying cause.
• TTE to evaluate for valvular/structural heart disease
• Assess the risk of stroke and bleeding; consider anticoagulation.
  • Valvular Afib: All patients require anticoagulation.
  • Nonvalvular Afib: Consider based on CHA₂DS₂-VASc score.

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.

Diagnostics

See “Diagnosis of atrial fibrillation.”

• 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”)

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

Approach

• 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 ^[5]
    • Onset > 48 hours: Rate control is preferred. ^[50][51]
    • Onset < 48 hours: Consider rate control or rhythm control (e.g., cardioversion). ^[50][52]
• All patients
  • Consider indications for anticoagulation (see “Anticoagulation in atrial fibrillation”). ^[5][53]
  • 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 ^[5][50]

• IV agents are recommended in the acute setting; consider combination with oral medications. ^[5][54]
• Target resting heart rate: < 80/minute (HR < 110/minute may be acceptable in asymptomatic patients with no evidence of LV systolic dysfunction) ^[5]
• Choose from one of the following (first-line):
  • Beta blockers
    • Esmolol ^[5]
    • Propranolol ^[5]
    • Metoprolol ^[5]
  • Nondihydropyridine calcium channel blockers (contraindicated in patients with decompensated heart failure or preexcitation)
    • Diltiazem ^[5]
    • Verapamil ^[5]
• Consider one of the following if the patient has contraindications to any of the above or refractory symptoms:
  • Digoxin ^[5]
  • Amiodarone ^[5]

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

• Hemodynamically unstable patients, ongoing myocardial ischemia, decompensated heart failure: Perform synchronized electrical cardioversion. ^[5][9]
• 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 ^[8]
  • 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.
• Management of Afib in congestive heart failure ^[5]
  • Chronic, nondecompensated CHF
    • Reduced ejection fraction: IV beta blockers, digoxin, amiodarone
    • Preserved ejection fraction: In addition to the above, consider IV ndHP CCBs.
  • Decompensated CHF
    • First-line: synchronized electrical cardioversion
    • Second-line: amiodarone or digoxin
  • Tachycardia-induced cardiomyopathy
    • AV nodal blockade or rhythm control

Avoid CCBs and beta blockers in decompensated heart failure.

• Management of Afib with preexcitation (e.g., WPW)
  • Avoid AV nodal blocking agents
  • See “Stable, wide-complex tachycardia” for the approach to diagnosis and management.

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

Definition

• Atrial flutter is a supraventricular tachyarrhythmia that is usually caused by a macroreentrant rhythm within the atria. ^[5]

Epidemiology ^[55]

• 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 ^[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

Treatment

• Same as Afib (see “Treatment of atrial fibrillation” for further details)
• Consult cardiology for all patients with atrial flutter.
• Rate control: more difficult to achieve in atrial flutter than in Afib ^[19]
• Rhythm control
  • Better results and lower recurrence compared to Afib ^[5][56]
  • Catheter ablation may be the most effective rhythm control strategy.
• The same parameters for anticoagulation in Afib are recommended (see “Anticoagulation in atrial fibrillation”).

Complications

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

• 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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