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(AF; A Fib)
Atrial fibrillation (AF) is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi often form, causing a significant risk of embolic stroke. Diagnosis is by ECG. Treatment involves rate control with drugs, prevention of thromboembolism with anticoagulation, and sometimes conversion to sinus rhythm by drugs or cardioversion.
Atrial fibrillation has been attributed to multiple wavelets with chaotic reentry within the atria. However, in many cases, firing of an ectopic focus within venous structures adjacent to the atria (usually the pulmonary veins) is responsible for initiation and perhaps maintenance of AF. In AF, the atria do not contract, and the atrioventricular (AV) conduction system is bombarded with many electrical stimuli, causing inconsistent impulse transmission and an irregularly irregular ventricular rate, which is usually in the tachycardia rate range.
AF is one of the most common arrhythmias, affecting about 2.3 million adults in the US. Men and whites are more likely to have AF than women and blacks. Prevalence increases with age; almost 10% of people > 80 yr are affected. AF tends to occur in patients with a heart disorder.
The absent atrial contractions predispose to thrombus formation; annual risk of cerebrovascular embolic events is about 7%. Risk of stroke is higher in patients with a rheumatic valvular disorder, hyperthyroidism, hypertension, diabetes, left ventricular systolic dysfunction, or previous thromboembolic events. Systemic emboli can also cause malfunction or necrosis of other organs (eg, heart, kidneys, GI tract, eyes) or a limb.
AF also may impair cardiac output; loss of atrial contraction can lower cardiac output at normal heart rate by about 10%. Such a decrease is usually well tolerated except when the ventricular rate becomes too fast (eg, > 140 beats/min), or when patients have borderline or low cardiac output to begin with. In such cases, heart failure may develop.
The most common causes of atrial fibrillation are hypertension, ischemic or nonischemic cardiomyopathy, mitral or tricuspid valvular disorders, hyperthyroidism, and binge alcohol drinking (holiday heart).
Less common causes include pulmonary embolism, atrial septal and other congenital heart defects, COPD, myocarditis, and pericarditis. AF without an identifiable cause in patients < 60 yr is called lone AF.
Acute atrial fibrillation is new-onset AF lasting < 48 h.
Paroxysmal atrial fibrillation is recurrent AF that typically lasts < 48 h and that converts spontaneously to normal sinus rhythm.
Persistent atrial fibrillation lasts > 1 wk or requires treatment to convert to normal sinus rhythm.
Long-standing persistent atrial fibrillation lasts > 1 yr, but there is still the possibility of restoring sinus rhythm.
Permanent atrial fibrillation cannot be converted to sinus rhythm. The longer AF is present, the less likely is spontaneous conversion and the more difficult is cardioversion because of atrial remodeling (rapid atrial rate-induced changes in atrial electrophysiology that are dominated by a decrease in atrial refractoriness and may also include increase in spatial dispersion of atrial refractoriness slowed atrial conduction velocity, or both).
Atrial fibrillation is often asymptomatic, but many patients have palpitations, vague chest discomfort, or symptoms of heart failure (eg, weakness, light-headedness, dyspnea), particularly when the ventricular rate is very rapid (often 140 to 160 beats/min). Patients may also present with symptoms and signs of acute stroke or of other organ damage due to systemic emboli.
The pulse is irregularly irregular with loss of a waves in the jugular venous pulse. A pulse deficit (the apical ventricular rate is faster than the rate palpated at the wrist) may be present because left ventricular stroke volume is not always sufficient to produce a peripheral pressure wave at fast ventricular rates.
Diagnosis of atrial fibrillation is by ECG. Findings include absence of P waves, f (fibrillatory) waves between QRS complexes (irregular in timing, irregular in morphology; baseline undulations at rates >300/min not always apparent in all leads), and irregularly irregular R-R intervals (see Figure: Atrial fibrillation.).
Other irregular rhythms may resemble AF on ECG but can be distinguished by the presence of discrete P or flutter waves, which can sometimes be made more visible with vagal maneuvers. Muscle tremor or electrical interference may resemble f waves, but the underlying rhythm is regular. AF may also cause a phenomenon that mimics ventricular extrasystoles or ventricular tachycardia (Ashman phenomenon). This phenomenon typically occurs when a short R-R interval follows a long R-R interval; the longer interval lengthens the refractory period of the infra-Hisian conduction system, and subsequent QRS complexes are conducted aberrantly, typically with right bundle branch morphology.
Echocardiography and thyroid function tests are important in the initial evaluation. Echocardiography is done to assess structural heart defects (eg, left atrial enlargement, left ventricular wall motion abnormalities suggesting past or present ischemia, valvular disorders, cardiomyopathy) and to identify additional risk factors for stroke (eg, atrial blood stasis or thrombus, complex aortic plaque). Atrial thrombi are more likely in the atrial appendages, where they are best detected by transesophageal rather than transthoracic echocardiography.
If a significant underlying disorder is suspected, patients with new-onset AF may benefit from hospitalization, but those with recurrent episodes do not require hospitalization unless other symptoms suggest the need for it. Once causes have been managed, treatment of AF focuses on ventricular rate control, rhythm control, and prevention of thromboembolism.
Patients with AF of any duration require rate control (typically to < 100 beats/min at rest) to control symptoms and prevent tachycardia-induced cardiomyopathy.
For acute paroxysms of rapid rate (eg, 140 to 160 beats/min), IV AV node blockers are used (for doses, see Table: Antiarrhythmic Drugs (Vaughan Williams Classification)). Caution: AV node blockers should not be used in patients with Wolff-Parkinson-White syndrome when an accessory AV pathway is involved (indicated by wide QRS duration); these drugs increase frequency of conduction via the bypass tract, possibly causing ventricular fibrillation. Beta-blockers (eg, metoprolol, esmolol) are preferred if excess catecholamines are suspected (eg, in thyroid disorders, exercise-triggered cases). Nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) are also effective. Digoxin is the least effective but may be preferred if heart failure is present. These drugs may be used orally for long-term rate control. When beta-blockers, nondihydropyridine calcium channel blockers, and digoxin—separately or in combination—are ineffective, amiodarone may be required.
In patients with heart failure or other hemodynamic compromise directly attributable to new-onset AF, restoration of normal sinus rhythm is indicated to improve cardiac output. In other cases, conversion of AF to normal sinus rhythm is optimal, but the antiarrhythmic drugs that are capable of doing so (class Ia, Ic, III) have a risk of adverse effects and may increase mortality. Conversion to sinus rhythm does not eliminate the need for chronic anticoagulation.
For acute conversion, synchronized cardioversion or drugs can be used. Before conversion is attempted, the ventricular rate should be controlled to < 120 beats/min, and, many patients should be anticoagulated (see Prevention of thromboembolism during rhythm control for criteria and methods). if AF has been present > 48 h, patients should typically be given an oral anticoagulant (conversion, regardless of method used, increases risk of thromboembolism). Anticoagulation should be maintained for > 3 wk before conversion when possible and for at least 4 wk after cardioversion. Many patients need chronic anticoagulation, although the specific criteria are still being debated (see Long-term measures to prevent thromboembolism).
Synchronized cardioversion (100 joules, followed by 200 and 360 joules as needed) converts AF to normal sinus rhythm in 75 to 90% of patients, although recurrence rate is high. Efficacy and maintenance of sinus rhythm after the procedure is improved with use of class Ia, Ic, or III drugs 24 to 48 h before the procedure. Cardioversion is more effective in patients with shorter duration of AF, lone AF, or AF with a reversible cause; it is less effective when the left atrium is enlarged (> 5 cm), atrial appendage flow is low, or a significant underlying structural heart disorder is present.
Drugs for conversion of atrial fibrillation to sinus rhythm include class Ia (procainamide, quinidine, disopyramide), Ic (flecainide, propafenone), and III (amiodarone, dofetilide, dronedarone, ibutilide, sotalol) antiarrhythmics (see Table: Antiarrhythmic Drugs (Vaughan Williams Classification)). All are effective in about 50 to 60% of patients, but adverse effects differ. These drugs should not be used until rate has been controlled by a beta-blocker or nondihydropyridine calcium channel blocker. These converting drugs are also used for long-term maintenance of sinus rhythm (with or without previous cardioversion). Choice depends on patient tolerance. However, for paroxysmal AF that occurs only or almost only at rest or during sleep when vagal tone is high, drugs with vagolytic effects (eg, disopyramide) may be particularly effective. Exercise-induced AF may be better prevented with a beta-blocker.
For certain patients with recurrent paroxysmal AF who also can identify its onset by symptoms, some clinicians provide a single oral loading dose of flecainide (300 mg for patients ≥ 70 kg, otherwise 200 mg) or propafenone (600 mg for patients ≥ 70 kg, otherwise 450 mg) that patients carry and self-administer when palpitations develop (“pill-in-the-pocket” approach). This approach must be limited to patients who have no sinoatrial or AV node dysfunction, bundle branch block, QT prolongation, Brugada syndrome, or structural heart disease. Its hazard (estimated at 1%) is the possibility of converting AF to a slowish atrial flutter that conducts 1:1 in the 200 to 240 beat/min range. This potential complication can be reduced in frequency by coadministration of an AV nodal suppressing medication (eg, a beta-blocker or a nondihydropyradine calcium antagonist).
ACE inhibitors, angiotensin II receptor blockers, and aldosterone blockers may attenuate the myocardial fibrosis that provides a substrate for AF in patients with heart failure, but the role of these drugs in routine AF treatment has yet to be defined.
Patients, particularly those in whom the current episode of AF has been present > 48 h, have a high risk of thromboembolism for several weeks after pharmacologic or direct current cardioversion. If the onset of the current episode of AF is not clearly within 48 h, the patient should be anticoagulated for 3 wk before and at least 4 wk after cardioversion regardless of the patient's predicted risk of a thromboembolic event (class I recommendation).
Alternatively, therapeutic anticoagulation is started, transesophageal echocardiography (TEE) is done, and, if no left atrial or left atrial appendage clot is seen, cardioversion may be done, followed by at least 4 wk of anticoagulation therapy (class IIa recommendation).
If urgent cardioversion is required because of hemodynamic compromise, cardioversion is done and anticoagulation is started as soon as is practical and continued for at least 4 wk.
If the onset of the current episode of AF is clearly within 48 h, cardioversion may be done without prior anticoagulation if the patient has nonvalvular AF and is not at high risk of a thromboembolic event. After cardioversion, therapeutic anticoagulation is given for 4 wk (class I recommendation); although this may not be necessary in patients at low risk of a thromboembolic event (class IIb recommendation).
After 4 wk of postconversion anticoagulation therapy, some patients require long-term anticoagulation (see below) .
For patients who do not respond to or cannot take rate-controlling drugs, radiofrequency ablation of the AV node may be done to cause complete heart block; insertion of a permanent pacemaker is then necessary. Ablation of only one AV nodal pathway (AV node modification) reduces the number of atrial impulses reaching the ventricles and eliminates the need for a pacemaker, but this approach is considered less effective than complete ablation and is rarely used.
Ablation procedures that isolate the pulmonary veins from the left atrium can prevent AF without causing AV block. In comparison to other ablation procedures, pulmonary vein isolation has a lower success rate (60 to 80%) and a higher complication rate (1 to 5%). Accordingly, this procedure is often reserved for the best candidates—younger patients with drug-resistant AF who have no significant structural heart disease.
Long-term measures to prevent thromboembolism are taken for certain patients with AF during long-term treatment depending on their estimated risk of stroke vs risk of bleeding.
Patients with rheumatic mitral stenosis and patients with mechanical artificial heart valves are considered to be at high risk of a thromboembolic event as are patients with nonvalvular atrial fibrillation who have additional risk factors. The additional risk factors are identified by the CHADS2 score (see Table: CHADS2 Score) or the CHA2DS2-VASc score (see Table: CHA2DS2-VASc Score).
The guidelines for antithrombotic therapy are in a state of flux and differ in different regions. The current guidelines in the United States are as follows:.
Long-term oral anticoagulant therapy is recommended for patients with rheumatic mitral stenosis, artificial heart valve, and for nonvalvular atrial fibrillation patients with a CHA2DS2-VASc score of ≥2 (level I recommendation)
No antithrombotic therapy is recommended for patients with nonvalvular atrial fibrillation and a CHA2DS2-VASc score of 0 (level IIa recommendation)
No antithrombotic therapy, aspirin therapy, or oral anticoagulant therapy is recommended for patients with nonvalvular atrial fibrillation and a CHA2DS2-VASc score of 1 (level IIb recommendation).
Patients with AF and a mechanical heart valve(s) are treated with warfarin.
Patients with AF and significant mitral stenosis are treated with warfarin.
For patients with nonvalvular AF who are to be treated with an oral anticoagulant, a class I indication is given for warfarin with a target INR of 2.0-3.0 (level of evidence A), apixaban (level of evidence B), dabigatran (level of evidence B), and rivaroxaban (level of evidence B).
These general guidelines are altered in patients with more than moderate renal impairment.
The left atrial appendage may be surgically ligated or closed with a transcatheter device when appropriate antithrombotic therapy is absolutely contraindicated.
An individual patient's risk of bleeding may be estimated with any of a number of prognostic tools of which the most commonly used is HAS-BLED (see Table: HAS-BLED Tool for Predicting Risk of Bleeding in Patients With Atrial Fibrillation). The HAS-BLED score serves best in identifying conditions that, if modified, reduce bleeding risk rather than in identifying patients with a higher risk of bleeding who should not receive anticoagulation
HAS-BLED Tool for Predicting Risk of Bleeding in Patients With Atrial Fibrillation
Atrial fibrillation is an irregularly irregular atrial rhythm that may be episodic or continuous; paroxysms of tachycardia may occur.
QRS complexes should be narrow; a wide complex occurs with intraventricular conduction defects or Wolff-Parkinson-White syndrome.
Patients should have echocardiography and thyroid function testing.
Heart rate is controlled (typically to < 100 beats/min at rest); first-line drugs include beta-blockers and nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem).
Restoration of sinus rhythm is not as important as rate control and does not eliminate the need for anticoagulation but may help patients with continuing symptoms or hemodynamic compromise (eg, heart failure); synchronized cardioversion or drugs can be used.
Anticoagulation is usually necessary before cardioversion.
Long-term oral anticoagulation to prevent stroke is required for patients with risk factors for thromboembolism; aspirin is used for those with no risk factors.
January CT, Wann S, Alpert JS, et al: 2014 ACC/AHA/HRS Guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force of Practice Guidelines and the Heart Rhythm Society. Circulation130:2071-2104, 2014.
Drug NameSelect Trade
procainamideNo US brand name
diltiazemCARDIZEM, CARTIA XT, DILACOR XR
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