Atrial Fibrillation – Causes, Symptoms, Diagnosis, Treatment and Ongoing care
This topic covers both atrial fibrillation (Afib) and atrial flutter (Aflut).
- Afib: Continuous or paroxysmal arrhythmia characterized by chaotic atrial electrical activity and an irregularly irregular ventricular response
- In some patients, ventricular response is rapid (>110 bpm), because AV node is bombarded with nearly continuous atrial electrical impulses.
- Aflut: Continuous or paroxysmal arrhythmia with regular atrial electrical activity, typical atrial rate 250–350, manifested as sawtooth flutter waves on ECG. A 2:1 or 4:1 conduction through the AV node to the ventricle is common, so the ventricular response is frequently regular at a rate of 150 or 75 bpm.
- Clinical pattern:
- Persistent: Sustained >7 days, usually requiring pharmacologic or DC cardioversion to restore sinus rhythm
- Paroxysmal (PAF): Self-terminating episodes, usually <7 days
- Permanent: Sinus rhythm cannot be restored; cardioversion has failed or has not been attempted.
- Incidence/prevalence increases with age.
- Predominant gender: Male > Female
- Afib: Age <40, <0.1%/year; >80, >1.5%/year, less for atrial flutter
- Lifetime risk: 25% for those ≥40 years
- Estimated 0.4–1% of general population <60
- ∼2–5%, 7th decade; 5–10%, 8th decade
In US, hypertension/coronary disease most common. See Etiology.
Familial forms rare, but do exist. Multiple culprit genes have been identified.
Ethanol may trigger AF in some; so-called “holiday heart syndrome.” Adequate HTN control may prevent development of AF due to hypertensive heart disease.
- In patients with PAF and no/minimal structural heart disease, triggering premature atrial beats and/or bursts of tachycardia emanate from the pulmonary venous ostia or other sites.
- In patients with persistent/permanent AF and significant structural heart disease, multiple reentrant wavelets within atria may be the cause.
- Cardiac: Hypertensive heart disease, valvular/rheumatic disease, CAD, acute MI, cardiomyopathy, CHF, pericarditis, infiltrative heart disease, sick sinus syndrome
- Pulmonary: Pulmonary embolism, COPD, pneumonia
- Ingestion: (e.g., ethanol in holiday heart), digoxin toxicity (AFlut)
- Endocrine: Hyperthyroidism
- Postoperative (e.g., cardiothoracic surgery)
- Idiopathic: Including lone AF (<60 without clinical or electrocardiogram [EKG] evidence of cardiopulmonary disease, including HTN)
Commonly Associated Conditions
- Sick sinus syndrome.
- Afib and Aflut are frequently associated with each other. Aflut tends to be a more unstable rhythm and tends to not last as long.
- Symptoms vary from none–mild (palpitations, lightheadedness, fatigue, poor exercise capacity) to severe (angina, dyspnea, syncope). Symptoms frequently more serious in patients with structural heart disease.
- In patients with Wolff-Parkinson-White syndrome and other types of bypass tracts, Afib may lead to an extremely rapid ventricular rate that may swiftly degenerate into ventricular fibrillation.
- Afib: Irregularly irregular pulse, frequently tachycardic
- Aflut: Regular pulse, frequently tachycardic
Diagnostic Tests & Interpretation
- Afib: EKG is diagnostic; low-amplitude fibrillatory waves without discrete P waves; irregularly irregular pattern of QRS complexes
- Aflut: Sawtooth P-waves are the classic sign. Narrow complex QRS. Frequent tachycardia.
- Holter monitor and event monitor helpful in diagnosing PAF and monitoring for recurrence.
Initial lab tests
TSH, CMP, cardiac enzymes, PT/INR (if anticoagulation is contemplated), consider digoxin level (if appropriate) and CBC
Follow-Up & Special Considerations
Occasional Holter monitoring and/or exercise stress testing to assess for adequacy of rate control
- Chest x-ray (CXR) for cardiopulmonary disease
- EKG for structural heart disease, signs of ischemia, heart blocks, and other arrhythmias
- Spiral chest computed tomography (CT) (or other tests such as D-dimer, ventilation-perfusion scan, or pulmonary angiography) if pulmonary embolus possible etiology for new-onset disease
- Transesophageal echocardiogram to detect left atrial appendage thrombus if cardioversion planned
Electrophysiologic studies should be considered in patients with recurrent Aflut to map the source of the arrhythmia for possible ablation.
- Atrial dilatation and fibrosis
- Atrial injury (chronic or acute)
- Atrial thrombus, especially in atrial appendage
- Sclerosis/fibrosis of sinoatrial node
- Coronary artery disease, valvular/rheumatic disease, cardiomyopathy, pulmonary embolus
- Tachycardia-induced cardiomyopathy
- Multifocal atrial tachycardia
- Sinus tachycardia with frequent atrial premature beats
- Atrial flutter/atrial fibrillation
- Anticoagulation guidelines (same for Afib and Aflut):
- Unless contraindicated, patients with AF with any high-risk factors for stroke (prior transient ischemic attack (TIA)/cerebrovascular accident (CVA)/thromboembolism, mitral stenosis, prosthetic valve) should receive warfarin to maintain INR of 2.0–3.0. Patients with mechanical valves should maintain INR >2.5.
- CHADS2 score: Patients with ≥2 moderate risk factors (CHF, HTN, Age >75 and/or DM), should receive warfarin (INR 2.0–3.0) unless contraindicated.
- Patients with 1 moderate risk factor should be treated with warfarin (INR 2.0–3.0) or aspirin (81–325 mg/d). Discuss with patient risks and benefits.
- Patients at low risk of thromboembolic complications or in whom warfarin is contraindicated should receive aspirin (81–325 mg/d) or clopidogrel.
- Anticoagulation recommendations are independent of AF pattern (paroxysmal, persistent, permanent).
- So-called “rate control” and “rhythm control” strategies have approximately equivalent outcomes in terms of mortality. Rhythm control tends to have more adverse reactions.
- Control of ventricular rate:
- Nondihydropyridine calcium channel blockers:
- Diltiazem (Cardizem)
- Class contraindications: Hypotension, documented sensitivity, 2nd- or 3rd-degree AV block, severe CHF, sick sinus syndrome
- Precautions: Use caution with CHF, left ventricular (LV) dysfunction, liver or kidney disease. Adverse reactions: Hypotension, CHF, peripheral edema, AV block.
- Interactions: May increase digoxin levels; with amiodarone or beta-blockers, may severely decrease cardiac output, trigger complete heart block
- Metoprolol (Lopressor)
- Contraindications: Hypotension, documented sensitivity, 2nd- or 3rd-degree AV block, severe CHF, sick sinus syndrome
- Precautions: Use caution with CHF, LV dysfunction, kidney disease, asthma
- Interactions: Bradycardia with digoxin; with amiodarone or calcium channel blockers, may severely decrease cardiac output or trigger complete heart block
- Adverse reactions: Hypotension, CHF, peripheral edema, AV block
- Nondihydropyridine calcium channel blockers:
- Digoxin (Lanoxin):
- Indicated for CHF, hypotension
- Contraindications: Documented sensitivity, sick sinus syndrome, hypertrophic cardiomyopathy
- Precautions: Use caution with electrolyte abnormalities (especially hypokalemia, hypercalcemia), impaired renal function, thyroid disease, acute myocardial infarction (MI), AV block
- Interactions: Unpredictable effects with many antiarrhythmics; additive bradycardia with calcium channel blockers, beta-blockers
- Adverse reactions: AV block, bradycardia, mental disturbances, nausea
- Rate control usually achieved in 4 hours (1).
- Conversion to/maintenance of sinus rhythm:
- DC cardioversion
- Caution: Antiarrhythmic therapy for chemical cardioversion and maintenance of sinus rhythm following cardioversion may be proarrhythmic.
- Ibutilide, an IV type III agent, for chemical cardioversion of AF and flutter of short duration (<90 days)
- If duration of AF is >24–48 hours or unknown, treat with warfarin for ≥3 weeks before cardioversion. Or, once anticoagulation is established, perform transesophageal EKG. If no atrial thrombus, may cardiovert. Anticoagulation should be continued for ≥4 weeks following cardioversion.
- Long-term, perhaps indefinite, anticoagulation should be considered in patients with thromboembolic risk factors with chronic or recurrent AF.
- Chronic oral antiarrhythmic therapy to suppress AF recurrences:
- Type IA (procainamide, disopyramide, quinidine): Generally not used
- Type IC (flecainide, propafenone) in patients with structurally normal hearts or mild hypertensive heart disease. Concomitant use of β-blocker recommended.
- Type III (sotalol, amiodarone, dofetilide)
- Type IC drugs are contraindicated in patients with coronary artery disease, cardiomyopathy, and significant LVH.
- Type IA and III drugs should not be used in patients with torsade de pointes history or long QT. The risk of torsade de pointes increases with the extent of QT interval prolongation (the QTc), so these medications should be used with great caution, if at all, in patients on medications that prolong the QT.
- Precautions: Avoid hypokalemia and hypomagnesemia.
- With type IC drugs, stress testing to exclude exercise-induced arrhythmia or QRS widening
- With amiodarone, careful surveillance for hepatic, thyroid, pulmonary, skin, ophthalmologic adverse effects
- In many patients, adequate medical therapy of AF will cause bradycardia, necessitating a permanent pacemaker.
- According to a recent Cochrane Review, several class IA, IC, and III drugs are effective in maintaining sinus rhythm but increase adverse events, including pro-arrhythmia, and disopyramide and quinidine are associated with increased mortality. Any benefit on clinically relevant outcomes (embolisms, heart failure, mortality) remains to be established (1).
Issues for Referral
AF refractory to medical therapy (unable to achieve adequate rate control or significant bradycardia) should be considered for more definitive therapy such as pacemaker +/-AV node ablation. Antiarrhythmic therapy should be prescribed by experienced practitioners.
- Current guidelines reserve catheter ablation in Afib to highly symptomatic patients who have failed at least 1 course of antiarrhythmic drug therapy [C]. It is the treatment of choice for patients who are in chronic Aflut, with a number needed to treat (NNT) of 2.2 to prevent rehospitalization, vs antiarrhythmics.
- Catheter ablation success rates vary with the type of Afb (paroxysmal > persistent > permanent) and the presence of structural heart disease, particularly left atrial enlargement. May require ≥2 ablation procedures to achieve clinical success.
- Cardiac surgery (e.g., the maze procedure or minimally invasive epicardial procedures) may be considered in severely symptomatic, medically refractory patients.
- Permanent dual-chamber pacing may reduce incidence of new-onset AF and reduce frequency of PAF episodes in patients with sick sinus syndrome.
Acute therapy for hemodynamically compromised patients:
- Heparin for anticoagulation (not generally necessary; may just initiate warfarin without “bridge” therapy)
- IV β- or calcium channel blocker for control of ventricular rate if blood pressure (BP) adequate
- Urgent cardioversion if hemodynamically unstable:
- DC cardioversion is best treatment (2)[C].
- Begin with dose of 50 J (with biphasic defibrillator) or 200 J (with monophasic defibrillator) and increase as needed (2)[C].
- Atrial overdrive pacing also effective
- Inpatient if:
- Significant symptoms
- Extremely rapid ventricular rate
- Initiating antiarrhythmic therapy
- AF triggered by acute process (acute myocardial infarction, congestive heart failure [CHF], pulmonary embolus)
- High risk for stroke (rheumatic heart disease, prior TIA/stroke)
- Outpatient management for low-risk patients with controlled ventricular rates
Adequate rate or rhythm control without symptoms. Long-term plan for anticoagulation established.
There continues to be debate about whether rate or rhythm control is best for treating patients with chronic Afib/Aflut. Mortality is the same for both. Risk of stroke is higher for electrical cardioversion, but there are some measures of symptom control and quality of life that appear to be improved. Pharmacologic cardioversion is associated with more adverse events and hospitalization in elderly patients. Take into account the patient with their associated health conditions when deciding what path to take (3,4).
- Monitor warfarin levels.
- EKG to monitor QTc interval if on antiarrhythmic therapy
Avoid potential triggers: Ethanol, caffeine, nicotine
Warfarin anticoagulation reduces annual embolic stroke rate from ∼5% to 1–2%. Aspirin reduces risk to 3–4% annually. AF increases risk of morbidity and mortality, but prognosis is a function of underlying heart disease.
- Embolic stroke
- Peripheral arterial embolization
- Bleeding with anticoagulation
- Tachycardia-induced cardiomyopathy with prolonged periods of inadequate rate control
1. Lafuente-Lafuente C, Mouly S, Longas-Tejero MA, Bergmann JF, et al. Antiarrhythmics for maintaining sinus rhythm after cardioversion of atrial fibrillation. Cochrane Database Syst Rev. 2007;CD005049.
2. Fuster, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation. Circulation. 2006;114:e257–354.
3. Mead GE, Elder AT, Flapan AD, Kelman A, et al. Electrical cardioversion for atrial fibrillation and flutter. Cochrane Database Syst Rev. 2005;CD002903.
4. Cordina J, Mead G, et al. Pharmacological cardioversion for atrial fibrillation and flutter. Cochrane Database Syst Rev. 2005;CD003713.
- 427.31 Atrial fibrillation
- 427.32 Atrial flutter
- 49436004 Atrial fibrillation (disorder)
- 5370000 Atrial flutter (disorder)
- There continues to be debate about whether rate or rhythm control is best for treating patients with chronic Afib/Aflut. Mortality is the same for both. When in doubt and in absence of other contraindications, rate control appears to have the best outcome data.
- AF with rapid ventricular rates may be the initial presentation of tachy/brady syndrome with underlying sinus node dysfunction, particularly in the elderly. Exercise caution when initiating AV nodal-blocking agents in the elderly patient with rapid AF.