Atrial Fibrillation


  • Atrial fibrillation is a common supraventricular tachycardia 
  • Incidence in Canada is up to 4.5% per year, with lifetime risk estimated at 25% among those older than 40 years of age
  • Prevalence is 1-2% in the general population in developed countries
  • Evaluation of the patient involves:
    • Determining the underlying cause of atrial fibrillation
    • Rate- or rhythm-control strategy
    • Role of anti-coagulation


  • Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function.
  • On an electrocardiogram (ECG), AF is described as the replacement of consistent P waves with rapid oscillations or fibrillatory waves that vary in size, shape, and timing, and are associated with an irregular, frequently rapid ventricular response.
  • Different types of AF:
    • Paroxysmal AF: Recurrent atrial fibrillation that terminates spontaneously, lasting up to 7 days, but usually < 48 hours.
    • Persistent AF: Atrial fibrillation that is sustained for > 7 days or requires termination by cardioversion.
    • Long-standing persistent AF: Atrial fibrillation persists for > 1 year.
    • Permanent AF: Atrial fibrillation where the patient and physician agree to stop attempts to restore normal sinus rhythm because the atrial fibrillation can no longer be converted.
    • Lone AF: An historic term used to describe atrial fibrillation in younger patients (such as patients < 65 years old) with no clinical history or echocardiographic evidence of cardiovascular disease, hypertension, or diabetes. Lone AF lacks a standard definition and may be paroxysmal, persistent, or permanent.
    • Valvular AF: Atrial fibrillation in the presence of any mechanical heart valve, or in the presence of moderate to severe mitral stenosis (rheumatic or nonrheumatic)

Differential Diagnosis

  • The differential diagnosis for tachycardia is broad. Tachycardia is usually classified based on morphology of the QRS (wide complex or narrow complex), rhythm, and presence or absence of p-waves.
  • Please refer to the following sites for further details:

Risk Factors


  • Hypertension
  • Coronary artery disease with prior myocardial infarction
  • Heart failure
  • Left ventricular dysfunction (systolic and diastolic; Including hypertrophic, dilated and
    restrictive cardiomyopathies)
  • Valvular heart disease
  • Congenital heart disease (early repair of atrial septal defect)
  • Pericardial disease
  • Post-surgery (particularly cardiac surgery)
  • Sick sinus syndrome
  • Atrial fibrillation as a result of ventricular pacing
  • Supraventricular tachycardia (including Wolff-Parkinson-White syndrome, atrial tachycardia, atrial flutter or other)
  • Genetic/familial


  • Excessive alcohol ingestion (acute or chronic)
  • Hyperthyroidism
  • Vagally-mediated (i.e. habitual aerobic training)
  • Pulmonary disease (pneumonia, COPD, pulmonary embolism, pulmonary hypertension)
  • Obstructive sleep apnea
  • Obesity
  • Chronic kidney disease
  • Tobacco use
  • Diabetes

History and Physical


  • May have symptoms or be completely asymptomatic 
  • Symptoms may include:
    • Palpitations
    • Shortness of breath (with heart failure)
    • Chest pain
    • Lightheadedness/dizziness (presyncope/actual syncope uncommon)
    • Focal neurological deficit (with embolic stroke)
  • Heterogenous history, symptoms vary according to ventricular response and overall functional status of individual patient
  • To assess, must:
    • Establish pattern – new onset, paroxysmal, persistent, permanent
    • Establish severity, including impact on quality of life
    • Identify potentially treatable or reversible causes such as endocrine abnormalities (hyperthyroidism), obstructive sleep apnea, excessive alcohol consumption
    • Identify risk factors for recurrence or poor prognosis (as listed above)
    • Establish bleeding risk and bleeding symptoms
  • Past Medical History: Any previous cardiac problem, HTN, diabetes
  • Social history including tobacco, alcohol and drug use
  • Family History
Physical Exam:
  • Irregular jugular venous pulsations (JVP)
  • Elevated JVP with concomitant heart failure
  • Irregularly irregular rhythm detected by palpation of pulse or auscultation
  • Heart sounds heard during auscultation may include
    • Variable intensity of first heart sound (S1)
    • Absence of a fourth heart sound (S4) heard previously during sinus rhythm
  • Pedal or sacral edema
  • Bibasilar rales/crackles (with concomitant heart failure)

Diagnostic Work-up

Testing Overview

  • Baseline evaluation should include:
    • EKG to document presence of atrial fibrillation
    • Transthoracic echo to assess cardiac function
    • Blood work at least once in the evaluation of atrial fibrillation
    • Chest x-ray if clinical findings suggest pulmonary abnormality
      • Useful to detect underlying concurrent pulmonary disease and evaluate for signs of heart failure
      • As baseline testing in patients taking amiodarone
  • Other tests to consider:
    • Ambulatory electrocardiogram (Holter monitor, event monitor, loop monitor) 
    • Ambulatory blood pressure monitoring (if borderline hypertension)
    • 6-minute walk test (if adequacy of rate control uncertain)
    • Exercise treadmill testing
      • If adequacy of rate control uncertain
      • To reproduce exercise-induced atrial fibrillation
      • For suspected myocardial ischemia
    • Electro-physiological study (for consideration of curative ablation)
    • Sleep study (ambulatory oximetry or polysomnography)
    • Genetic testing in rare cases of apparent familial disease (especially if onset at young age)

Blood Tests

  • Blood tests to be considered at least once in evaluation of atrial fibrillation:
    • Electrolytes (including magnesium, phosphate and calcium)
    • Thyroid-stimulating hormone (TSH)
    • Renal function tests
    • Liver function tests
    • Complete blood count
    • Coagulation profile
    • Fasting lipid profile
    • Fasting glucose
    • Serum levels of B-type natriuretic peptide (BNP)


Mainstay of treatment for atrial fibrillation is rate-control and reduction of stroke risk.

Two strategies to manage atrial fibrillation are rhythm- and rate-control.

  • Shown to be equivalent in AFFIRM and AF-CHF trials 


  • Goal is to minimize effect on quality of life
  • Aim for a resting heart rate of < 100 beats per minute in permanent atrial fibrillation
    • RACE II: Among patients with permanent atrial fibrillation, lenient rate-control (HR < 110 bpm) is as effective as strict rate-control (HR < 80 bpm) in preventing cardiovascular events
  • Initial therapy should be beta blockers or nondihydropyridine calcium channel blockers
    • Beta blockers should be used in patients with myocardial infarction or systolic dysfunction
    • Calcium channel blockers should be avoided in patients with systolic dysfunction
    • Digoxin should NOT be used as initial therapy
      • It can be used in sedentary individuals or those with systolic dysfunction
      • It can be used in individuals who have contraindications
      • It can be used in individuals who are unable to tolerate or have inadequate response to beta blockers or calcium channel blockers
      • Dosing should be adjusted according to renal function
      • Potential drug interactions should always be considered.


  • Recommend a rhythm-control strategy for patients with atrial fibrillation who are symptomatic with adequate rate-control therapy or in whom rate-control therapy is unlikely to control symptoms
  • Classes of antiarrhythmic agents are listed below; these can be used in acute management of atrial fibrillation
  • An AV-blocking agent should be used in patients with AF or AFL being treated with a class I antiarrhythmic drug (eg, propafenone or flecainide) in the absence of advanced AV node disease
  • Intermittent antiarrhythmic drug therapy (“pill in the pocket” as shown in the figure below) in symptomatic patients with infrequent, longer-lasting episodes of atrial fibrillation is an alternative to daily antiarrhythmic therapy
  • To be avoided in patients with advanced sinus or AV nodal disease

Rhythm-control agents in patients without CHF 

(Class I agents should be used in conjunction with AV nodal blocking agents and avoided in CAD)

    • Drodenadone (use with caution with digoxin)
    • Flecainide
    • Propafenone
    • Sotalol (use with caution in individuals at risk of Torsades – e.g. female, age > 65, and renal failure)

Rhythm-control in individuals with CHF:

  •  Determine ejection fraction
    • If EF>35%: Amiodarone or Sotalol
    • If EF<35%: Amiodarone
  • If above strategies fail – can move to catheter ablation

Amiodarone is a common antiarrhythmic medication for atrial fibrillation

  • Acutely, IV amiodarone acts as a beta-blocker and can help rate control atrial fibrillation. However, stopping IV amiodarone will lead to its diffusion into tissues, and serum levels drop off rapidly.
  • Chronically, amiodarone is the most effective medications for atrial and ventricular arrhythmias, including atrial fibrillation. Patients require a total of 10 grams to saturate their tissues such that their serum levels remain high. At that point, the half-life becomes very long and it becomes an effective anti-arrhythmic medication.
  • Drug monitoring:
    • Chronic amiodarone is rarely a long-term solution for patients with atrial fibrillation due to risk of side effects.  (discussed elsewhere). 
Liver enzymesYESq6mo
Chest X-rayYESq1yr
PFT (with DLCO)YESOnly if sx
Ophthalmic examIf visual impairmentOnly if sx

Please refer to CCS Part 4 Rhythm Management guidelines, Table 7 for full details of “Pill-in-Pocket” Therapy.


  • To be discussed below in anticoagulation section

Catheter Ablation:

  • Can be used in patients who are highly symptomatic despite adequate rhythm-control trial (drug-refractory) and in whom rhythm control is desired
  • Can be utilized in select individuals are first line therapy (e.g. paroxysmal atrial fibrillation that is highly symptomatic) or individuals with pre-excitation atrial fibrillation with an accessory pathway
  • Can be utilized as first line therapy or as a reasonable alternative to pharmacologic rhythm- or rate-control therapy patients with symptomatic typical atrial flutter 
  • Since catheter ablation is an invasive procedure, risks and benefit must be balanced; the chart below will outline some risks and benefits of catheter ablation

Management of Atrial Fibrillation or Atrial Flutter in the acute setting:

  • Stable patients: proceed with rhythm- or rate-control
  • Hemodynamically stable patients with AF/AFL of known duration <48 hours in whom a control strategy has been selected:
    • Rate-slowing agents alone are acceptable while awaiting spontaneous conversion to sinus rhythm
    • Synchronized electrical cardioversion (150-200 joules biphasic) or pharmacologic cardioversion may be used. If criteria below are met (please refer to diagram below – Figure 7)
      • Hemodynamically unstable (AF/AFL is the direct cause of instability with hypotension, acute coronary syndrome, or pulmonary edema)
      • Anticoagulation for at least three weeks before cardioversion (based on described criteria in Figure 7)
        • Trans-esophageal echo may be used instead of anticoagulation for three weeks to rule out intra-cardiac thrombus
        • Anticoagulation for patients post cardioversion for 4 weeks then use CHADS-65 score to determine need for long term anticoagulation
      • NOTE: Antiarrhythmic drugs may be used to pre-treat patients before electrical cardioversion (to decrease early recurrence of AF and to enhance cardioversion efficacy)
    • Aside: Treatment of WPW/rapid response in patients with rapid ventricular preexcitation during AF (Wolff-Parkinson-White syndrome)
      • Electrical cardioversion if unstable
      • Intravenous antiarrhythmic agents (procainamide or ibutilide) in stable patients
      • AV nodal blocking agents (digoxin, calcium channel blockers, beta-blockers, adenosine) are contraindicated (can degenerate into ventricular fibrillation spontaneously or it can be facilitated by the
        administration of specific agents)



  • See the CCS algorithm below for anti-coagulation in non-valvular atrial fibrillation and atrial flutter
    • Note: For individuals < 65 years of age and no risk factors, anticoagulation is not recommended, with anti-platelet therapy based on coronary or peripheral artery disease presence
    • NOACs are preferred as first line anticoagulation in atrial fibrillation (non-valvular)
      • Greater ease of use compared with warfarin
      • RCT data shows that NOACs are either non-inferior or superior to warfarin in stroke prevention
      • NOACs have no more major bleeding or less bleeding vs warfarin and especially less intracranial hemorrhage.
      • Apixaban dose should be reduced in individuals meeting 2/3 following criteria
        • Age 80
        • Creatinine > 133 micromol/L
        • Weight < 60 kg
    • Warfarin is preferred over NOACs in individuals with valvular atrial fibrillation, mechanical valve, and CrCl <30
    • Patients whose risk of stroke warrants OAC therapy, but who refuse any OAC, should receive ASA 81 mg/day plus clopidogrel 75 mg/day
    • Renal function should be monitored on an annual basis in patients on OAC
  • Bleeding risk can be assessed with the HAS-BLED tool 

Anticoagulation is based on renal function and appropriate adjustments

Anti-thrombotic therapy in patients with Atrial Fibrillation

  • 20-30% of patient with AF have CAD
  • Risks and benefits of anti-thrombotic therapy need to be balanced carefully
  • A list of factors that may help with balancing risk and benefit of anti-platelet and anticoagulation therapy
  • Some recommendations to reduce bleeding risk:
    • Avoid using prasugrel and ticagrelor in conjunction with oral anticoagulants
    • May need to target a lower threshold for warfarin (INR 2.0-2.5)
    • Avoid NSAIDs
    • Consider use of proton pump inhibitors
  • For management of antithrombotic therapy in patients with atrial fibrillation (AF) and coronary artery disease (CAD)/peripheral artery disease (PAD): (Figure Below)
    • Note that some NOAC doses differ
    • Note that for patients with NVAF/AFL aged < 65 years with no CHADS2 risk factors, CCS suggests no antithrombotic therapy for stroke prevention unless there is any CAD/PAD
    • Ideally, this should be discussed with interventional cardiology
Anti-platelet and Anticoagulation -CCS Guidelines
Dosing of OAC+Antiplatelets

Peri-Operative Atrial Fibrillation Management:

  • The decision to continue or stop anticoagulation should be based on risk of bleeding during procedure
  • Aspirin or clopidogrel should be stopped 5-7 days before a procedure, or 7-10 days before a procedure if risk of bleeding is very high 
  • Warfarin
    • Hold 5 days before procedure
      • INR < 1.5 for low risk procedure
      • INR < 1.2 for intermediate or high risk procedure
    • Restart after discussion with surgeon
      • 24-48 hours if low risk of bleeding
      • 48-72 hours if intermediate or high risk of bleeding
  • NOACs
    • Hold 1-2 days prior to procedure if low risk procedure
    • Hold 2-3 days prior to procedure if intermediate or high risk procedure
    • No need for bridging
    • Can re-start one day after adequate hemostasis is established after discussion with surgeon
  • Heparin
    • Bridging therapy with LMWH or UFH should be instituted when the INR is below therapeutic level only in patients at high risk of thromboembolic events (CHADS2 ≥ 4, mechanical heart valve, stroke/TIA within 3 months, rheumatic heart disease)
    • To be restarted after the procedure when hemostasis is established; discuss with surgeon
      • 24 hours for a procedure with a low risk of bleeding
      • 48-72 hours for a procedure with an intermediate or high risk of bleeding 
      • Should be prophylactic dosages for the first 24 to 72 hours and then increased to therapeutic dosages. Bridging is then continued until INR is in the therapeutic range

Further Reading


  • Primary Author: Dimitar Saveski (MD, Internal Medicine Resident)
  • Author/Reviewer: pending (MD, FRCPC, Cardiology Fellow)
  • Staff Reviewer: pending (MD, FRCPC[Cardiology])
  • Copy Editor: Perri Deacon (medical student)
  • Last Updated: June 24, 2020
  • Comments or questions please email
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