08. Atrial Fibrillation

Definition

Atrial fibrillation (a-fib) is an irregular heart rhythm due to uncoordinated atrial activity with variable conduction down the AV node to the ventricles.

  • Paroxysmal: recurrent and terminates spontaneously within 7 days.
  • Persistent: sustained >7 days or requires cardioversion.
  • Long-standing persistent: continuous >1 year.
  • Permanent: AF cannot be converted and sinus rhythm is no longer being pursued.

Etiologies/Risk Factors

  • Cardiac: HTN, CAD/ischemia, CHF, valvular heart disease, left atrial enlargement, left ventricular wall thickness, pericarditis, myocarditis, cardiomyopathy, congenital heart disease, changes in myocardial wall stress.
  • Metabolic/endocrine: obesity, hyperthyroidism, diabetes.
  • Pulmonary: pneumonia, PE, lung CA, chronic lung disease, OSA.
  • Other: fever, pain, surgery (up to 1/3 of patients go into a-fib after cardiopulmonary bypass, post-valve replacement), alcohol, severe infection, exercise.

Evaluation

  • ECG or rhythm monitor to identify arrhythmia.
  • TTE to evaluate chamber size, function, valvular disease, pericardial disease.
  • TSH, renal panel, liver panel, CBC.
  • Consider ambulatory electrocardiogram to evaluate AF burden.

Anticoagulation

  • The decision for anticoagulation is based on thromboembolic risks, not type of AF. To evaluate thromboembolic risk in a-fib and atrial flutter, use CHA2DS2-VASc score:
    • Score ≥2 → usually benefit from anticoagulation (class I).
    • Score =1 → consider no anticoagulation or use of aspirin (class IIb).
    • Score =0 → reasonable to omit anticoagulation (class IIa).
  • Regardless of the CHA2DS2-VASc score, patients with mod-severe mitral stenosis and mechanical valve are at high risk of stroke and should be evaluated for anticoagulation. Other special populations: hypertrophic cardiomyopathy, hyperthyroidism, CKD.
  • Bridging: patients at high risk for thromboembolic events or with a mechanical valve should undergo bridging therapy with heparin gtt or LMWH as appropriate.   
  • Oral agents:
    • Non-vitamin K oral anticoagulants (NOACs) are recommended over warfarin if eligible (class I). Ineligible: mod-severe mitral stenosis or a mechanical heart valve. Check renal and hepatic function prior to NOAC initiation and at least yearly. See Hematology: Direct Oral Anticoagulants section for additional info.
    • Warfarin is recommended in patients with a mechanical heart valve. Check INR at least weekly initially then at least monthly once stable.
    • For patients who are at high thromboembolic risk by CHA2DS2-VASc and CrCl <15 ml/min or on dialysis, warfarin or apixaban is recommended (class IIb). For less severe renal impairment, consider NOAC dose reduction.
    • Reversal agents: idarucizumab for dabigatran, andexanet alfa (recombinant factor Xa) for reversal of rivaroxaban and apixaban.
  • Percutaneous Left Atrial Appendage occlusion remains an option to reduce thromboembolic risk in those unable to undergo oral anticoagulation.
  • Interruption and bridging AC: for patients with a mechanical heart valve that require interrupting warfarin, bridging with heparin or LMWH is recommended. For patients without a mechanical heart valve, decision should balance risk of stroke, bleeding, and duration of interruption.

Acute Rate Control

  • In patients with a-fib with rapid ventricular response who are symptomatic or hemodynamically unstable (chest pain, heart failure, hypotensive, ischemia), proceed directly to immediate electric cardioversion (do not neglect the need for anticoagulation).
    • Use 150-200J synchronized, biphasic for emergent cardioversion.
    • Address underlying etiology for RVR (the equivalent of sinus tachycardia in patients in persistent atrial fibrillation): volume overload, alcohol withdrawal, dehydration, infection, etc.
  • Metoprolol tartrate: (5mg IV pushes q5 min x 3) to slow rate and then start oral at 12.5-25mg PO q6h-q12h (conversion: 1mg IV to 2.5mg PO). Increase dose at each interval as indicated.
  • Esmolol: good for potentially unstable patient (e.g., ICU) because half-life only 9 min. Bolus 500mcg/kg, drip 50-200mcg/kg/min. RBC metabolism, so useful for liver or renal disease. 
  • Diltiazem: weight-based dosing (10-20 mg IV pushes over 2 min; can be rebolused in 15 min). Then start drip at 5-15mg/hr if unable to control rate but for less than 24 hours. Caution with patients with decompensated heart failure.
  • Amiodarone: good for controlling ventricular rate but may chemically cardiovert patient (so consider anticoagulation ramifications). Typically used in patients with hypotension. Load with 150mg IV over 10 minutes (can slow infusion to reduce incident of hypotension) then start drip at 1mg/min x 6 hrs, then 0.5mg/min x 18 hrs. Obtain baseline TSH and LFTs.
  • Digoxin: typically use in conjunction with other rate controlling agents (slow onset) and excellent in patients with hypotension and heart failure. Avoid in hypertrophic cardiomyopathy, renal insufficiency, electrolyte abnormalities (potassium).
    • Dosing: load with 0.5mg IV once, then in 6 hours 0.25mg IV q6h x 2. Watch for digoxin toxicity: increased PVC, paroxysmal atrial tachycardia, or conduction disease – life threatening.

Long-term Rate Control

  • Rate control is recommended except in patients with reversible a-fib, new-onset a-fib, or heart failure caused by AF.
  • Beta-blockers and nondihydropyridine calcium channel antagonists are the main agents in atrial fibrillation without pre-excitation. Amiodarone or even AV nodal ablation with a permanent pacemaker are also possibilities for difficult cases.
  • Goal resting heart rate is <110 (asymptomatic patient with preserved LV systolic function; RACE II trial).
  • Metoprolol tartrate (short acting) 12.5 to 100mg PO BID.
  • Metoprolol succinate (long acting) 25mg to 200mg PO daily (up to 400mg daily).
  • Diltiazem SA PO 120-360mg daily.
  • Digoxin 0.25mg increments up to 1.5mg (in 24 hours).
    • Initial: ~0.5mg followed by 0.25mg q6 hours x 2.
    • Maintenance: 0.125-0.25mg PO daily.
  • Amiodarone: IV load of ~1gm (see Acute Rate Control), followed by oral dosing for 10gm total load. Then maintenance: 100-200mg PO daily.

Important:

  • Do not use nondihydropyridine calcium channel antagonists (i.e. diltiazem or verapamil) in those with decompensated heart failure.
  • AV nodal blockade in those with pre-excitation may result in ventricular fibrillation (use procainamide or ibutilide).

Cardioversion

Every patient should be given a chance at restoring sinus rhythm if maintaining sinus rhythm is likely (e.g., a patient with rheumatic mitral stenosis with very large atria is unlikely to stay in sinus). Spontaneous cardioversion may occur in first few days for new onset a-fib.

See Acute Rate Control for emergent DC cardioversion.

  • Electrical: high success rate. Requires sedation. Use anteroposterior pad placement (on L parasternal region and on the L scapular region). Synchronize to QRS. Start with 100J biphasic. Predictors of success: short duration of a-fib, normal left atrial size.
  • Chemical: sinus rhythm can be achieved in 30-40% of patients with class Ia (procainamide), class Ic (propafenone, flecainide), or class III (amiodarone, sotalol, ibutilide) agents. Patients who have been in a-fib for greater than one year, or with enlarged left atria, are less likely to convert.
  • Maintenance of sinus rhythm: due to high rates of recurrent a-fib, many patients with chronic a-fib are started on anti-arrhythmic therapy after cardioversion. 
  • Anticoagulation peri-cardioversion of atrial fibrillation or flutter:
    • Duration >48 hours (or duration unknown): anticoagulate with warfarin (INR 2-3), factor Xa inhibitor, or direct thrombin inhibitor for 3 weeks before cardioversion and 4 weeks after cardioversion regardless of method (pharmacologic vs. electrical) used (class I). In those who are not anticoagulated prior to cardioversion, a TEE can be used to r/o atrial thrombus (class IIa).
    • Duration <48 hours and CHA2DS2-VASc ≥2 in men or ≥3 in women: prior anticoagulation is not necessary but should be continued for at least 4 weeks post-cardioversion regardless of method used.
    • Cardioversion of a HD unstable patient: anticoagulation should be initiated as soon as possible and maintained for at least 4 weeks.
    • Long term anticoagulation should be individualized and based on CHA2DS2-VASc as above.

Rhythm Control and Ablation

Initiation and management of rhythm control should be done in close consultation with cardiology or EP and will be deferred here. Structural heart disease plays a key role in selection of the appropriate agent.

  • Clinical trials (AFFIRM and RACE trials) have shown no clinical difference or net benefit for rate compared to rhythm control. In AFFIRM, disabling stroke, hospitalizations, and new arrhythmias were less in the rate control group and at 2 years of follow up, the survival curve was slightly better for the rate control group.
  • Consider rhythm control strategy for patients a) with difficult to control ventricular rates, b) those who are symptomatic from their atrial fibrillation even with adequate rate control and c) younger patients.
  • Ablation should be considered in patients with symptomatic AF and HFrEF (class IIb) and can be considered in those unable to tolerate antiarrhythmic medications in whom rhythm control strategy is favored. Anticoagulation post-ablation currently is based on CHA2DS2-VASc score rather post-procedure rhythm (e.g., persistent sinus rhythm).

Atrial Flutter

Anticoagulation risk assessment similar to a-fib. Rate control can be more challenging in atrial flutter. Electrical cardioversion can often be successful with less energy than for a-fib. “Typical” flutter can often be cured with EP ablation with high success rate therefore ablation should be considered for first-line therapy in some patients. 

Key Points

  • The two major management decisions in atrial fibrillation are 1) need for anticoagulation and 2) rate vs. rhythm control.
  • Urgent cardioversion is indicated in the setting of hemodynamic compromise.

 

January CT, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 Guideline for Management of Patients with Atrial Fibrillation. 10.1016/j.jacc.2019.01.011. ACC.org/GMSAF.

January CT, Wann L, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2014;64(21):e1-e76. doi:10.1016/j.jacc.2014.03.022.

January CT, Wann S, Alpert J, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation: Executive Summary. Circulation. 2014; 130: 2071-2104.

McNamara RL, Tamariz LJ, Segal JB, et al. Management of atrial fibrillation: Review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography. Ann Intern Med 2003;139:1018-1033.