Atrial Fibrillation

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.
    • Non-valvular AF: Atrial fibrillation in the absence of mechanical heart valves, rheumatic mitral stenosis, or moderate to severe non-rheumatic mitral stenosis.

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). 
MonitoringBaselineRepeat
TSHYESq6mo
Liver enzymesYESq6mo
Chest X-rayYESq1yr
ECGYESq1yr
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.

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
 
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

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
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