Introduction
- 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
Definitions
- 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
Cardiac
- 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
Non-Cardiac
- 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
History
- 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)
Management
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
Rate-Control:
- 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.
Rhythm-control:
- 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).
Monitoring | Baseline | Repeat |
---|---|---|
TSH | YES | q6mo |
Liver enzymes | YES | q6mo |
Chest X-ray | YES | q1yr |
ECG | YES | q1yr |
PFT (with DLCO) | YES | Only if sx |
Ophthalmic exam | If visual impairment | Only if sx |
Please refer to CCS Part 4 Rhythm Management guidelines, Table 7 for full details of “Pill-in-Pocket” Therapy.
Cardioversion:
- 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)

Anticoagulation:
- 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
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
- Hold 5 days before procedure
- 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
- Cardiology: A practical handbook by David Laflamme
- Management of Atrial Fibrillation: Complete CCS Guidelines Listing
Authors
- 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 feedback@cardioguide.ca