Atrial fibrillation (main)

(Redirected from Afib)


Non-modifiable risk factors (top left box) and modifiable risk factors (bottom left box) for atrial fibrillation. The main sequelae of atrial fibrillation are in the right box.
  • Chronic and paroxysmal a-fib are associated with thrombus formation

Atrial fibrillation categories[1]

Atrial Fibrillation Category Definition
  • Terminates spontaneously or with intervention within 7 days of onset.
  • Episodes may recur with variable frequency.
  • Continuous sustained >7 days
Long-standing persistent
  • Continuous >12 mo in duration.
  • Used when the patient and clinician make a joint decision to stop further attempts to restore and/or maintain sinus rhythm.
  • Acceptance represents a therapeutic attitude on the part of the patient and clinician rather than an inherent pathophysiological attribute.
  • May change as symptoms, efficacy of therapeutic interventions, and patient and clinician preferences evolve.
  • In the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair.
With Rapid Ventricular Response (RVR)
  • With persistent ventricular heart rate >100 beats per minute

Causes of atrial fibrillation

Clinical Features



  • Irregularly irregular heart rate

Differential Diagnosis

Narrow-complex tachycardia

Wide-complex tachycardia

Assume any wide-complex tachycardia is ventricular tachycardia until proven otherwise (it is safer to incorrectly assume a ventricular dysrhythmia than supraventricular tachycardia with abberancy)

^Fixed or rate-related



Atrial fibrillation at approximately 150 beats per minute
A 12-lead ECG showing atrial fibrillation at approximately 132 beats per minute.

ED Work-Up

  • ECG[2]
  • Eval for ACS only in:
    • Patient with ECG changes suggestive of ischemia, hypotension, angina
    • A fib is rarely only manifestation of ACS, although RVR and hypotension can provoke demand ischemia
  • Acute lab studies for all patients:
    • CBC
    • Chem-10
    • Coagulation studies (for patients requiring anticoagulation)
  • Additional labs (consider based on clinical scenario):
    • TSH & free T4 (Afib increased in sublinical hyperthyroidism)
    • BNP
    • D-dimer
    • Troponin
    • Magnesium level
    • Digoxin level (if appropriate)
  • Imaging
    • CXR (if concern for heart failure or infection)
    • Chest/Abdominal CT (if concern for sepsis)


ECG of atrial fibrillation (top) and normal sinus rhythm (bottom). The purple arrow indicates a P wave, which is lost in atrial fibrillation.

Based on one of three ECG patterns:

  1. Typical
    • Irregularly, irregular R waves
    • QRS rate 140-160/min
  2. Large fibrillatory waves
    • May look like flutter waves
      • Unlike a-flutter, the fibrillatory waves are irregular
  3. Slow, regular A-fib
    • Due to complete AV block with escape rhythm
  • Ischemic changes?
  • Rate > 250? (think preexcitation)


See atrial fibrillation with RVR for emergent treatment

Rate vs. Rhythm Control

  • Rhythm control (i.e. synchronized cardioversion)
    • Consider in the emergency department for:[3]
      • Unstable (due to rhythm)
      • Younger patients (<65 years old) with new or paroxysmal episode (<48 hours)[4]
    • Procedural anticoagulation status
      • If <48 hours of symptoms, do not need to anticoagulate prior to rhythm control (may perform in ED)[5]
      • If >48 hours of symptoms, need have rhythm control as out patient referral (if stable)
    • Method: Procedural sedation and analgesia (e.g. fentanyl and propofol). Apply pads in anterior to posterior position. Synchronized electrical cardioversion starting at 150 to 200 J.
  • Rate control for all others or cardioversion failure
    • General principal - IV medications for immediate rate control followed by PO medications for sustained rate control
    • Beta-blocker
      • Metoprolol 5 mg IV q 5 min (max 3 doses) followed by 25-100 mg PO
    • Calcium channel blocker
      • Diltiazem 0.25 mg/kg to 0.35 mg/kg IV (20 mg typical starting dose), can follow with 25 mg IV as second dose if needed
      • Followed by PO dose 60-120 mg
      • If unable to get sustained response with IV push, consider diltiazem gtt
    • Digoxin
      • Indicated if patient hypotensive and cannot get AV nodal blockade or if patient has advanced heart failure
      • Typical digitizing dose 500 mcg then 250 mcg q4hx 2 for total dose of 1000 mcg
      • Requires renal dosing if patient has impaired renal function
    • Amiodarone
      • Indicated if patient has hypotension or advanced heart failure, usually second line after digoxin
      • Typical dosing 150 mg IV x 10 min then 1 mg/min x 6 hours then 0.5 mg/minx 18 hours
      • Amiodarone can convert patient to sinus rhythm. Consider simultaneously starting empiric anticoagulation if high thromboembolism risk, see below
    • Procainamide
      • Indicated: Hemodynamically stable with systolic Blood Pressure >100 mmHg, less than 48 hrs onset, Normal Serum Potassium and Serum Magnesium
      • Ottawa protocol Method: Procainamide 1 g IV over 60 minutes. Monitor with frequent Blood Pressures, and hold Procainamide if systolic Blood Pressure <100 mmHg. Monitor telemetry for Arrhythmia, QTc Prolongation, QRS Widening and for successful cardioversion.

Anticoagulation Therapy

  • ACCP Recommendations
    • In patients with AF, including those with paroxysmal AF, with only one of the risk factors listed immediately above, we recommend long-term antithrombotic therapy (Grade 1A), either as anticoagulation with an oral VKA, such as warfarin (Grade 1A), or as aspirin, at a dose of 75-325 mg/d (Grade 1B)[6]
    • In patients with AF, including those with paroxysmal AF, who have two or more of the risk factors we recommend long-term anticoagulation with an oral VKA (Grade 1A).[6]
  • CCS Recommendations
    • Oral anticoagulants are recommended for all AF patients aged 65 or older or who have any one of the traditional CHADS2 risk factors of stroke, hypertension, heart failure, or diabetes (remember as CHADS-65). Otherwise, patients with a history of coronary artery disease or arterial vascular disease should be prescribed ASA. CCS recommends that the first choice for oral anticoagulation should be the novel direct-acting oral anticoagulants (i.e. NOACs, for non-valvular AF). The big paradigm change is that ED physicians should prescribe OACs to at-risk AF patients before they leave the ED.[7]

CHADS2-VAsc Score

Risk Factor Points
hypertension 1
DM 1
Previous stroke/TIA 2
Vascular disease (e.g. IHD, PVD) 1
Female sex 1
≥ 75 years old 2
65 to 74 years old 1
  • Score 0: consider no treatment or ASA
  • Score 1: consider warfarin or ASA
  • Score 2-6: consider warfarin (INR goal = 2-3)
  • All patients with significant valvular disease should be on anticoagulation


Used to assess 1 yr risk of bleeding on OAC medications

Risk Factor Point
Hypertension 1
Abnormal renal and/or hepatic function 1 point each
Stroke 1
Bleeding tendency/predisposition 1
Labile INR on warfarin 1
Elderly (age >65 years) 1
Drugs (aspirin or NSAIDs) and/or alcohol 1 point each
  • Score 1: 1.0 bleeds per 100 patient-years
  • Score 2: 1.9 bleeds per 100 patient-years
  • Score 3: 3.7 bleeds per 100 patient-years
  • Score 4: 8.7 bleeds per 100 patient-years
  • Score 5-9: Insufficient Data


Similar outcomes for Canadian vs. American strategies, despite lower admission rates in Canada[9]


  • "Limit hospital admission to highly symptomatic patients in whom adequate rate control cannot be achieved"[10]


Indications for hospitalization:

  • Patient with acute heart failure or hypotension after rhythm or rate control
  • AF secondary to hypertension, infection, COPD exacerbation, PE, ACS/MI
  • Age > 60 (high risk of thromboembolism, more likely to have comorbidities)
  • Initiation of heparin or other anticoagulant
  • If considering ablation of accessory pathway in patient with AF
  • Symptomatic recurrence in the ED
  • Hemodynamic instability

Indications for discharge (low-risk patients): Discharge with urgent cardiology follow up

  • <60 years old
  • No significant comorbid disease
  • No clinical suspicion for PE or MI
  • Conversion in ED or rate control


  • Hemodynamic compromise
    • A-fib lowers CO by 20-30%
    • Impaired coronary blood flow
  • Arrhythmogenesis
  • Arterial thromboembolism

See Also


  1. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary. J Am Coll Cardiol. 2014;64(21):2246-2280. doi:10.1016/j.jacc.2014.03.021
  2. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary. J Am Coll Cardiol. 2014;64(21):2246-2280. doi:10.1016/j.jacc.2014.03.021
  3. EBQ:Ottawa Aggressive ED Cardioversion Protocol
  4. Atrial Fibrillation: Would You Prefer a Pill or 150 Joules? Ann Emerg Med. 2015;66:655-657.
  5. EBQ:48hr Cardioversion for Afib]]
  6. 6.0 6.1 Singer DE et al. Antithrombotic therapy in atrial fibrillation: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).Chest. 2008 Jun;133(6 Suppl):546S-592S
  7. Verma A, et al. 2014 Focused Update of the Canadian Cardiovascular Society Guidelines for the Management of Atrial Fibrillation Canadian Journal of Cardiology 30 (2014) 1114e1130
  8. Pisters R, Lane DA, Nieuwlaat R, et al. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest 2010; 138:1093.
  9. Rising KL. Home is Where the Heart Is. Annals of Emergency Medicine. 2013;62(6):578-579
  10. Stiell, et al. Atrial Fibrilation Guidelines. Canadian Cardiovascular Society Atrial Fibrillation Guidelines 2010: management of recent-onset atrial fibrilation and flutter in the emergency department. Can J Cardiolol. 2011;27:38-46