i. Atrial fibrillation is the most common arrhythmia, occurring in nearly 1% of the general population.
ii. Its incidence increases with age: 2% prevalence in patients younger than 65 years and 9% in those older than 65 years.
b. Pathophysiology. Requires (1) an initial atrial ectopic event (typically from a focus of the left atrial sleeve extending into the pulmonary veins) and (2) a multiple wavelet reentrant circuit that is often sustained by structural disease in the left atrium (e.g., enlargement, scar).
c. Classification. There are a number of terms used in association with atrial fibrillation.
i. Valvular generally refers to atrial fibrillation that is associated with rheumatic mitral stenosis, mechanical or bioprosthetic valve replacement, or mitral valve repair. Although rheumatic heart disease used to be responsible for most cases of atrial fibrillation, it currently accounts for less than one-third of cases. Atrial fibrillation associated with rheumatic heart disease carries a fivefold greater risk for stroke compared with “nonvalvular” atrial fibrillation.
ii. Paroxysmal refers to intermittent, brief episodes of atrial fibrillation that terminate spontaneously or with intervention within 7 days of onset.
iii. Persistent indicates atrial fibrillation that lasts 7 or more days.
iv. Long-standing persistent refers to continuous episodes of atrial fibrillation of at least 12 months’ duration.
v. Permanent atrial fibrillation is used when the patient and the treating physician jointly decide to stop further attempts to restore/maintain sinus rhythm.
vi. Lone atrial fibrillation is a historical description of atrial fibrillation occurring in young patients (<60 years) in the absence of structural heart disease (e.g., left ventricular hypertrophy, congestive heart failure [CHF], valve disease, cardiomyopathy) or hypertension. This description should not be used as the sole guide for therapeutic decisions.
vii. Isolated refers to atrial fibrillation that is secondary to another illness (e.g., hyperthyroidism, pneumonia, pulmonary embolism) and resolves when the illness is treated.
B. Clinical Manifestations of Atrial Fibrillation
a. Symptoms are due to loss of the atrial kick and an increased heart rate, which results in decreased ventricular filling, decreased cardiac output, and an increase in cardiac demand. The most common symptoms reflect these processes.
i. Fatigue (most common symptom)
iii. Chest pain
v. Dizziness or syncope
vi. Thromboembolic events
Up to 30% of patients with atrial fibrillation may not have symptoms.
b. Physical examination findings
i. Irregularly irregular pulse. An irregularly irregular pulse is the hallmark of atrial fibrillation.
ii. Pulse of varying intensity and pulse deficit. Because diastolic filling varies in length and is often reduced, pulses are of varying intensity, and not all audible ventricular beats are palpable peripherally.
iii. Absent a waves in the jugular venous pulse
iv. Variation in the intensity of the first heart sound (S1)
Patients in atrial fibrillation never have an S4.
i. The electrocardiogram (EKG) may show irregular atrial activity in the form of f waves (fine fibrillation of the atria at a rate of 350–600 beats/min) that are best visualized in lead V1. These f waves should be differentiated from more organized atrial activity (i.e., “sawtooth”) in leads II, III, and aVF that might represent atrial flutter.
ii. P waves are absent.
iii. The ventricular response will be irregularly irregular, although this may be difficult to appreciate at faster heart rates.
C. Causes of Atrial Fibrillation. Because many of the causes of atrial fibrillation are correctable, an effort should be made to pinpoint the cause of the arrhythmia.
a. Idiopathic. In approximately 10% of patients, no etiology can be found; in the absence of structural heart disease or hypertension, such patients are said to have “lone” atrial fibrillation.
b. Cardiovascular disorders, including sick sinus syndrome, Wolff-Parkinson-White syndrome, coronary artery disease, congestive heart failure, cardiomyopathy, myocarditis, hypertension, and congenital heart disease
c. Pulmonary disorders, including pulmonary embolism
d. Pericardial disease (e.g., pericarditis)
e. Metabolic disturbances, including hyperthyroidism
f. Infiltrative diseases, including amyloidosis, sarcoidosis, and hemochromatosis
g. Intoxication (e.g., alcohol, theophylline, β-adrenergic agonists)
h. Infection (e.g., endocarditis, sepsis)
i. Stress induced (e.g., postsurgery due to catecholamine surge)
Extracardiac conditions that are associated with increasing atrial fibrillation burden and therefore are important to address include obstructive sleep apnea, obesity, hypertension, and use of alcohol/drugs.
MNEMONIC: Causes of Atrial Fibrillation (“SWAMP CHILD”)
Sick sinus syndrome, Stress
Alcohol (intoxication, withdrawal, “holiday heart”)
Myocarditis, Metabolic abnormality
Pericardial disease, Pulmonary disease
CHF, Coronary artery disease, Congenital heart disease
Hypertension, Hyperthyroidism, Hypertrophic cardiomyopathy
Infiltrative disease, Infection
Dilated cardiomyopathy, Drugs
D. Approach to the Patient. Knowledge of the differential diagnosis will help direct diagnostic tests. All patients should undergo an EKG, a chest radiograph (to rule out pneumonia and other intrathoracic processes), a complete blood count (CBC), electrolyte studies, and thyroid function testing. An echocardiogram is usually obtained to examine cardiac function and atrial size as well as to rule out valve disease. Atrial fibrillation is rarely due to ischemia; stress testing is not usually necessary and should be considered on an individual basis.
E. Complications. The risk for stroke in all patients with “nonvalvular” atrial fibrillation is generally between 2% and 15% per year. It is important to assess for important factors that can allow for further estimation of the patient’s risk for stroke as calculated by the CHA2DS2-VASc score (as detailed below in Table 8.1).
a. Acute treatment. In hemodynamically unstable patients (hypotension, ongoing ischemia, cardiogenic shock), emergent electrical cardioversion should be considered. In hemodynamically stable patients, the goal of acute treatment of a patient with atrial fibrillation is rate control.
i. Pharmacologic therapy in patients without preexcitation
Table 8.1 Components of CHA2DS2-VASc and HAS-BLED Risk Calculators
Congestive heart failure
Abnormal renal or liver function
1 point each
Age greater than or equal to 75 years
Bleeding (history of major bleeding)
Stroke/transient ischemic attack/thromboembolic event
Vascular disease (prior myocardial infarction, peripheral artery disease, aortic plaque)
Age 65–74 years
Sex category (female)
a. Nondihydropyridine calcium channel blockers are first-line treatment but should be avoided in patients with decompensated heart failure.
i. Diltiazem, 5–20 mg (0.25 mg/kg) intravenously over 2 minutes with a maintenance infusion rate of 5–15 mg/hr intravenously
ii. Verapamil, 2.5–5.0 mg administered as an intravenous bolus over 2 minutes
i. Esmolol, 250–500 mcg/kg intravenously over 1 minute, followed by an intravenous maintenance infusion of 50–300 mcg/kg/min. The half-life of esmolol is only 9 minutes; thus, if during drug administration a patient becomes hypotensive, discontinuation will result in a rapid return to baseline.
ii. Metoprolol, 2.5–5 mg intravenous bolus over 2 minutes that can repeated for up to three doses
c. Digoxin, 0.5 mg intravenously followed by 0.25 mg intravenously every 6 hours to a total dose of 1 mg. Digoxin has weak AV nodal blocking properties but may be the only alternative in patients with borderline low blood pressures. Digoxin is not first-line therapy.
d. Amiodarone, 150 mg intravenously over 10 minutes, then 0.5–1 mg/min over 24 hours. Intravenous amiodarone can be useful for rate control in critically ill patients.
2. AV nodal blocking agents are contraindicated in patients with irregular, wide complex tachycardia or extremely rapid ventricular rates (>220 beats/min) until atrial fibrillation with conduction down an accessory pathway (e.g., Wolff-Parkinson-White syndrome) has been excluded. If Wolff-Parkinson-White syndrome is present, these agents can precipitate fatal ventricular fibrillation.
ii. Electrical cardioversion
1. Indications. Electrical cardioversion is indicated for any patient with rapid atrial fibrillation and life-threatening problems (e.g., ischemia, severe hypotension, or severe pulmonary edema). Begin with 200 J in the synchronized mode, but 360 J may be necessary.
2. Contraindications. Unless there is an emergent indication, no patient with atrial fibrillation should be cardioverted until anticoagulation therapy has been initiated and atrial thrombus has been excluded. This includes patients who have “new-onset” atrial fibrillation because it is often impossible to estimate the length of time the patient has been in atrial fibrillation from history alone. Patients who are cardioverted without undergoing anticoagulation therapy carry a 3%–5% risk for stroke within 30 days, even if they have returned to normal sinus rhythm on EKG.
b. Chronic treatment. The goals of chronic treatment of atrial fibrillation are minimization of symptoms and reduction of stroke risk. Data from recent trials reveal that a strategy of rate control with anticoagulation has similar mortality benefit compared with antiarrhythmic therapy. Therefore, a rhythm control strategy is reserved for individuals who are symptomatic from their atrial fibrillation despite adequate rate control.
i. Rate control. The goal is a resting heart rate lower than 80 beats/min. However, lenient rate control (less than 110 beats/min) could be considered in some symptom-free patients with normal left ventricular systolic function. Treatment should be selected after considering the patient’s other medical problems. For example:
1. In patients with hypertension or coronary artery disease, a β-blocker is a good choice because it addresses these conditions as well as the atrial fibrillation. Although often thought of as being relatively contraindicated in patients with chronic obstructive pulmonary disease (COPD) or asthma, β-blockers are often well tolerated in such patients and may be trialed in the absence of bronchoconstriction
2. In patients with CHF, β-blockers and digoxin can control the heart rate as well as improve symptoms of CHF. However, β-blockers must be uptitrated slowly, and in patients with chronic renal insufficiency, digoxin levels should be monitored very closely.
3. AV node ablation with pacemaker implantation is reserved for circumstances when rate control with drug therapy fails and rhythm control is not achievable.
ii. Rhythm control. Theoretically, conversion to normal sinus rhythm relieves all rate-related symptoms and returns the risk for stroke to baseline. However, because many patients in atrial fibrillation do not have symptoms, anticoagulation must be continued in all patients until cessation of arrhythmia is confirmed.
1. Electrical cardioversion. Unless there is an emergent indication, electrical cardioversion should be undertaken only after atrial thrombus has been excluded or at least a 3- to 4-week course of anticoagulation has been completed. After cardioversion, patients must remain on anticoagulation for at least 4 weeks because of the persistent high risk for stroke related to atrial stunning. Rarely, for patients with an episode of atrial fibrillation less than 48 hours in duration and low thromboembolic risk, intravenous heparin, low-molecular-weight heparin, novel anticoagulants, or no antithrombotic therapy can be considered with early cardioversion.
2. Antiarrhythmic therapy to prevent recurrence. Rate must be controlled before the initiation of any antiarrhythmic medication. Typically, patients who experience a change in lifestyle due to atrial fibrillation are considered for antiarrhythmic therapy.
a. Patients without structural or ischemic heart disease. The class Ic agents, propafenone and flecainide, are first-line agents for maintenance of sinus rhythm if patients do not have structural or ischemic heart disease. These medications are well tolerated from a side-effect profile but must be used with caution in patients with renal or hepatic disease. These agents should always be used in combination with AV nodal blocking agents.
b. Patients with coronary artery disease. Sotalol and dofetilide are the recommended therapy but should be used under the guidance of a cardiologist.
c. Patients with decreased left ventricular function. Amiodarone is the most efficacious antiarrhythmic overall but has significant long-term side effects that include pulmonary, neurologic, endocrine, and hepatic adverse events. Thus, amiodarone should be used with caution in younger patients, and all patients should be routinely monitored with liver function, pulmonary, and thyroid testing. Dofetilide can also be used in this patient population.
d. Dronedarone has a better safety profile than amiodarone and may be useful in some patients. However, it is less efficacious than amiodarone and is contraindicated in patients with recent decompensated heart failure, depressed left ventricular systolic function, or permanent atrial fibrillation.
3. Radiofrequency or cryoablation ablation of pulmonary vein sources is an option in select candidates with symptomatic atrial fibrillation despite antiarrhythmic therapy. The success rate for ablation can be as high as 75% from a single ablation and is highest in patients with paroxysmal atrial fibrillation as opposed to persistent atrial fibrillation.
iii. Stroke prophylaxis. Stroke is a major cause of morbidity and mortality in patients with atrial fibrillation. Anticoagulation therapy should be individualized, taking into consideration the risks for stroke and bleeding as well as patient preference.
1. Assessment of thromboembolic risk. Patients with valvular atrial fibrillation are at high risk for thromboembolic events. For patients with nonvalvular atrial fibrillation, CHA2DS2-VASc score is recommended to assess the risk for stroke, whereas the HAS-BLED score can help estimate risk for major bleeding. The decision regarding anticoagulation should be made independent of the type of atrial fibrillation (paroxysmal vs. permanent). The components of the risk calculators are summarized in Table 8.1. A general guide regarding appropriateness of anticoagulation in nonvalvular atrial fibrillation using the CHA2DS2-VASc score is as follows:
a. CHA2DS2-VASc score = 0: reasonable to omit anticoagulation.
b. CHA2DS2-VASc score = 1: In patients with one risk factor (excluding female patients with no other risk factors, i.e., only risk factor is gender), treatment with anticoagulation or aspirin may be appropriate. Observational data favor anticoagulation in this group.
c. CHA2DS2-VASc score greater than or equal to 2: oral anticoagulants are recommended unless contraindicated.
G. Therapy for Thromboembolic Risk Reduction
a. Aspirin is reserved for low-risk patients or those in whom oral anticoagulation is contraindicated.
b. Warfarin can reduce the relative risk for stroke by 40%–90%. The target international normalized ratio should be 2–3 for most patients.
c. Non–vitamin K antagonist anticoagulants, also referred to as target-specific anticoagulants, include dabigatran, rivaroxaban, apixaban, and edoxaban. These agents are limited to patients with nonvalvular atrial fibrillation. The advantages of treatment with these agents compared with warfarin are summarized in Table 8.2.
d. Nonpharmacologic stroke prevention includes procedures such as left atrial appendage occlusion (percutaneously via the WATCHMAN device or surgically via ligation) or left atrial appendage excision in patients undergoing cardiac surgery.
Table 8.2 Advantages and Disadvantages of Non–Vitamin K Antagonist Anticoagulants Compared with Warfarin
Advantage of Non–Vitamin K Antagonist Anticoagulants
Disadvantage of Non–Vitamin K Antagonist Anticoagulants
Wider therapeutic window compared with warfarin
Rapid onset of action (reduced need for bridging)
Cannot be used for valvular atrial fibrillation
Less drug-drug interactions
Limited data and use in severe renal disease
Less drug-food interactions (no dietary modifications)
Cannot be readily monitored
No need for frequent monitoring
Less readily available reversal agents
Lower risk for intracranial bleeding compared with warfarin
Short half-life (rapid decline in anticoagulation effect if doses are missed)
Suggested Further Readings
Calkins H, Willems S, Gerstenfeld EP, et al. Uninterrupted dabigatran versus warfarin for ablation in atrial fibrillation. N Engl J Med 2017;376:1627–36.Find this resource:
Heidbuchel H, Verhamme P, Alings M, et al. Updated European Heart Rhythm Association practical guide on the use of non-vitamin-K antagonist anticoagulants in patients with non-valvular atrial fibrillation: executive summary. Eur Heart J 2017;38:2137–49.Find this resource:
January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation 2014;130:2071–104.Find this resource: