Atrial Fibrillation

Atrial fibrillation (AF or Afib) is a supraventricular tachyarrhythmia and the most common kind of arrhythmia. It is caused by rapid, uncontrolled atrial contractions and uncoordinated ventricular responses. There are many conditions that can cause AF, usually damage to the heart (e.g., coronary artery disease, previous myocardial infarction). Diagnosis is confirmed by an electrocardiogram that will show an “irregularly irregular” heartbeat with no distinct P waves and narrow QRS complexes. AF increases the risk of thromboembolic events. Treatment is primarily based on ventricular rate and rhythm control, which can be achieved through drugs and/or cardioversion. Anticoagulation is administered if the patient is at significant risk for thromboembolic events.

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Epidemiology and Etiology


  • Most common form of cardiac arrhythmia
  • Incidence increases with age
  • 70% of patients with atrial fibrillation (AF) are > 65 years old
  • More common in men (but if affected, women are more likely to be symptomatic and develop complications)
  • More common in Caucasians than African Americans, Hispanics, and Asians

General risk factors for cardiovascular disease

  • Advanced age
  • Hypertension
  • Diabetes mellitus
  • Smoking
  • Obesity
  • Sleep apnea

Risk factors for AF

  • Usually associated with some underlying heart disease
  • Most common chronic disease associations are hypertensive heart disease and coronary heart disease
  • 15%–30% of cases are idiopathic or not associated with any known risk factor
Cardiac risk factors Non-cardiac risk factors
  • Myocardial infarction
  • Coronary artery disease
  • Congestive heart failure
  • Cardiomyopathy (specifically hypertrophic)
  • Other arrhythmias
  • Valvular heart disease
  • Congenital heart disease
  • Myocarditis
  • Wolff-Parkinson-White syndrome (WPW)
  • Electrolyte disturbances (e.g., hypokalemia)
  • Drugs (e.g., theophylline, adenosine, digoxin)
  • Surgery (e.g., coronary artery bypass grafting, valvular repair)
  • Hyperthyroidism
  • Hypothermia
  • Pulmonary causes: chronic obstructive pulmonary disease (COPD), pulmonary embolism
  • Chronic kidney disease
  • Excessive sympathetic stimulation:
    • Pheochromocytoma
    • Cocaine or amphetamines
    • Sepsis
  • Heavy alcohol use (e.g., holiday heart syndrome)
  • Metabolic syndrome
Mnemonic: Etiology of acute AF = PIRATES
P Pulmonary diseases:
  • Obstructive sleep apnea
  • Pulmonary embolism
  • COPD
  • Pneumonia
  • Ischemia (CAD)
  • Infarction (MI)
  • Rheumatic heart disease
  • Mitral regurgitation
  • Anemia
  • Atrial myxoma
  • Alcohol
  • Thyrotoxicosis
  • Toxins
  • Ethanol
  • Electrolytes
  • Endocarditis
  • Sepsis
  • Sick sinus syndrome

Pathophysiology and Classification


  • AF is caused by re-entrant electric conduction.
  • Re-entrant pathways can be due to:
    • Fibrosed tissue
    • Atrial dilation (e.g., congenital defect or post-MI)
    • Abnormal accessory pathways (e.g., WPW syndrome)
  • Most common site of the rapid atrial firing that triggers AF is the pulmonary veins.
Re-entrant phenomena

The pathophysiology of re-entrant pathways

  1. An ectopic focus initiates a cardiac action potential, which travels in the form of a unidirectional conduction wave. If a conduction barrier is present (e.g., cardiac tissue damaged by ischemia), the wave will travel around it.
  2. In healthy tissue, the conductive wave will meet refractory tissue upon completing the circuit.
  3. If the refractory period is shorter than the time it takes the wave to complete the circuit, re-entrant electric conduction may occur.
  4. If the conduction barrier becomes large enough, the conduction wave will meet repolarized tissue and re-entry may occur.
  5. If the conduction wave is slowed down by a damaged section of atrial tissue, re-entry may occur.
Image by Lecturio.
  • Heart rate: 
    • Atrial rate > 300/min
    • Some beats are irregularly modulated by the atrioventricular (AV) node
    • Ventricular rate = 90–170/min
  • Effects: 
    • Atrial remodeling: irregular impulses and contractions lead to progressive dilation and fibrosis of the atria → higher risk for AF → vicious cycle of pathology 
    • Asynchronous contractility → atria lose systolic function 
    • Rapid uncontrolled atrial contractions ( > 300/min) → slower pass through the AV node → uncoordinated ventricular contractions (90–170/min) → tachycardia
    • Decreased cardiac output → stasis of blood →  promotes thromboembolism 
    • Decreased cardiac output → heart failure


  • Paroxysmal: AF that starts spontaneously and terminates spontaneously or with intervention within 7 days of onset; episodes may occur with variable frequency
  • Persistent: AF that fails to self-terminate within 7 days, requires pharmacologic or electrical cardioversion to terminate
  • Long-standing persistent: AF that has lasted for more than 12 months
  • Permanent: AF that is unresponsive to treatment, patient and doctor decide to no longer pursue a rhythm control strategy
  • Lone: paroxysmal, persistent, or permanent AF with no structural heart disease, typically in persons < 60 years old, the lowest risk of complications → patients have a CHA2DS2-VASc score of “0”
  • Secondary: due to underlying condition, treatment focuses on the underlying condition to resolve AF
  • Subclinical: AF in asymptomatic individuals without a prior diagnosis of AF, often found in the context of implantable cardiac monitoring devices

Clinical Presentation

  • AF is often asymptomatic.
  • If patients experience symptoms, these are often nonspecific and variable.
    • Palpitations
    • Tachycardia
    • Chest pain
    • Fatigue
    • Dyspnea
    • Syncope
    • Confusion
    • Mild dyspnea
    • Embolic event
  • If symptoms are atypical → notice signs of the underlying disorder (e.g., exophthalmos in hyperthyroidism, murmur in the case of a valvular defect)
  • Complications of long-standing AF:
    • Signs of heart failure (pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea, dyspnea at rest, pitting edema, S3, S4)
    • Signs of embolization (stroke/transient ischemic attack [TIA] presenting with focal neurologic deficits such as paresis, vision loss, or renal, splenic, or intestinal infarct)


Electrocardiogram (ECG): confirms diagnosis

  • Irregularly irregular (pathognomonic)
  • RR intervals follow no repetitive pattern
  • No distinct P waves
  • Narrow QRS complexes (< 0.12 seconds)

Echocardiogram: used to identify etiology and complications, not for diagnosis

  • Transthoracic echocardiogram (TTE)
    • Used to assess cardiac function
    • Rules out or confirms structural cardiac disease (e.g., valve stenosis)
  • Transesophageal echocardiogram (TEE)
    • Rules out or confirms the structural cardiac disease
    • Indicated if AF lasted for > 48 hrs or if the duration is unknown
    • Indicated if planning cardioversion on patients who haven’t received anticoagulation therapy for at least 3 weeks
    • Used to detect thrombi within the left atrium or left atrial appendage

Other tests to rule out underlying conditions:

  • Cardiac enzymes → myocardial infarction
  • BNP → heart failure
  • TSH/fT4 → hyperthyroidism
  • CBC → infection/sepsis
  • BUN, creatinine → kidney function
  • CT pulmonary angiography → pulmonary embolism
  • Electrolytes (potassium, calcium, or magnesium) → electrolyte imbalances
  • Urine drug screen → cocaine, amphetamines, digoxin, or alcohol
  • Exercise testing → ischemic heart disease, also guides pharmacotherapy


Algorithm for the management of atrial fibrillation

Algorithm for the management of atrial fibrillation

Image by Lecturio.

AF management consists of the following:

  • Determination of hemodynamic status
  • Rate control OR rhythm control
  • Anticoagulation therapy
  • Treatment of the underlying cause

Special considerations:

  • Newly discovered AF < 24-48 hours → electrical cardioversion (without anticoagulation)
  • If concurrent WPW syndrome → IV procainamide or IV amiodarone (not nodal blockers)
  • Ablative therapy for tracts or pulmonary vein foci (long-term management)
  • Use heparin only if there is a current clot in the atrium.
AF Management principles
Hemodynamic status
  • Hemodynamically unstable AF → immediate cardioversion
  • Hemodynamically stable AF → rate control with beta-blockers or calcium channel blockers (CCB)
Rate control vs. rhythm control Rate control
  • Elderly patient
  • Long-standing AF without aberrant pathways
  • 1st: beta-blockers or non-dihydropyridine CCB (diltiazem, verapamil)
  • 2nd: digoxin/amiodarone (refractory to beta-blockers or CCB or with heart failure)
Rhythm control
  • Recent onset
  • Young patient
  • Symptomatic
  • Electrical cardioversion (with appropriate anticoagulation protocol)
  • Pharmacological cardioversion (e.g., flecainide, propafenone)
  • Surgical or catheter ablation
Anticoagulation Warfarin, novel oral anticoagulants (NOAC) Indication:
  • Non-valvular AF (CHA2DS2-VASc ≥ 1)
  • In all valvular causes
Aspirin Indication:
  • CHA2DS2-VASc < 1
  • With coronary artery disease
Cardioversion protocol (electrical or pharmacological) 3 weeks prior and 4 weeks post-cardioversion
Treat underlying cause Hypertension, coronary artery disease, valvular heart disease, chronic obstructive pulmonary disease, thyrotoxicosis, sick sinus syndrome, etc.
CHA2DS2-VASc Score: assesses thromboembolic risk and the risk for stroke in patients with AF
C Congestive heart failure 1
H Hypertension 1
A Age (≥ 75 years) 2
D Diabetes mellitus 1
S Stroke, TIA, or thromboembolism 2
V Vascular disease 1
A Age 65–74 years 1
Sc Sex category (female) 1
Scores of 1, 3, 5, and ≥ 6 carry an annual stroke risk of approximately 1%, 3%, 7%, and > 9%, respectively.

Differential Diagnosis

The following conditions are differential diagnoses for AF:

  • Atrial flutter: an irregular heart rhythm of the atria. It is classified as supraventricular tachycardia. Symptoms include palpitations. Complications include increased risk of stroke and congestive heart failure. 
    • Key difference: Flutter is a regular rhythm whereas fibrillation is irregular. 
  • Paroxysmal supraventricular tachycardia: a type of supraventricular tachycardia characterized by narrow QRS complexes and a fast heart rhythm, typically between 150 and 240 beats per minute
  • Multifocal atrial tachycardia: a type of atrial arrhythmia characterized by rapid heart rate with at least 3 or more P wave morphologies. It is called multifocal since the signals arise from various zones within the atria other than the sinus node. 
  • Premature atrial contractions: common ectopic beats generated from foci in atria, triggering premature heartbeats

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