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Atrial fibrillation
is a rapid, irregularly irregular atrial rhythm. Symptoms include
palpitations and sometimes weakness, 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 (AF) 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 it than women and blacks. Prevalence increases with age; almost 10% of people > 80 yr are affected. It tends to occur in patients with a heart disorder, sometimes precipitating heart failure because cardiac output decreases. 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, eye) or a limb.
Etiology
The most common causes 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.
Classification
Acute AF is new-onset AF lasting < 48 h.
Paroxysmal AF is recurrent AF that typically lasts < 48 h and that converts spontaneously to normal sinus rhythm.
Persistent AF lasts > 1 wk and requires treatment to convert to normal sinus rhythm.
Permanent AF 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 and/or slowed atrial conduction velocity).
Symptoms and Signs
AF 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
Diagnosis 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 Fig. 10: Arrhythmias and Conduction Disorders: 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 produce 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 most likely in the atrial appendages, where they are best detected by transesophageal rather than transthoracic echocardiography.
Treatment
If a significant underlying disorder is suspected, patients with new-onset AF may benefit from hospitalization, but those with recurrent episodes do not require it unless other symptoms suggest it. Once causes have been managed, treatment of AF focuses on ventricular rate control, rhythm control, and prevention of thromboembolism.
Ventricular
rate control:
Patients with AF of any duration require rate control (typically to < 80 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 2: Arrhythmias and Conduction Disorders: 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. β-Blockers (eg, metoprolol , esmolol ) are preferred if excess catecholamines are suspected (eg, in thyroid disorders, exercise-triggered cases).Nondihydropyridine Ca 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 β-blockers, nondihydropyridine Ca channel blockers, and digoxin —separately or in combination—are ineffective, amiodarone may be required.
Rhythm control:
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 necessarily 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, if AF has been present > 48 h, patients should be anticoagulated (conversion, regardless of method used, increases risk of thromboembolism). Anticoagulation with warfarin (see Arrhythmias and Conduction Disorders: Prevention of thromboembolism) should be maintained for > 3 wk before conversion when possible and continued indefinitely because AF may recur. Alternatively, the patient can be anticoagulated with heparin , and transesophageal echocardiography done; if there is no intra-atrial clot, cardioversion can be done immediately.
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 to sinus rhythm include class Ia ( procainamide , quinidine , disopyramide ), Ic ( flecainide , propafenone ), and III ( amiodarone , dofetilide , ibutilide , sotalol ) antiarrhythmics (see Table 2: Arrhythmias and Conduction Disorders: 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 β-blocker or nondihydropyridine Ca 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, and exercise-induced AF may be better prevented with a β-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 those who have no SA 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.
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.
Ablation procedures:
For patients who do not respond to or cannot take rate-controlling drugs, radiofrequency ablation of the AV node may be done to produce 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 producing 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.
Prevention of
thromboembolism:
Measures to prevent thromboembolism are necessary at the time of cardioversion and during long-term treatment of most patients.
Warfarin titrated to an INR of 2 to 3 should be given for ≥ 3 wk before elective cardioversion of lone AF present for > 48 h and continued for 4 wk after successful cardioversion. Anticoagulants should be continued indefinitely for patients with recurrent paroxysmal, persistent, or permanent AF in the presence of risk factors for thromboembolism. Healthy patients with a single episode of lone AF are anticoagulated for 4 wk.
Aspirin is less effective than warfarin but is used for patients with no risk factors for thromboembolism or those with contraindications to warfarin . Direct thrombin inhibitors that do not require INR monitoring, may be equivalent to warfarin for stroke prevention in high-risk patients, but they require further study before being recommended for mainstream use. The left atrial appendage may be surgically ligated or closed with a transcatheter device when warfarin and antiplatelet drugs are absolutely contraindicated.
Last full review/revision January 2008 by L. Brent Mitchell, MD
Content last modified January 2008
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