Cardiac monitoring and intravenous (IV) access should be obtained in all patients who present with symptomatic atrial fibrillation. Unstable patients with atrial fibrillation with rapid ventricular response should undergo synchronized electrical cardioversion. Consideration can be made to utilize chemical cardioversion if the patient is stable. Concurrent anticoagulation should be considered with cardioversion if the time of onset is unknown.
Atrial fibrillation is the result of disordered electrical activity within the atria, resulting in a lack of coordinated atrial contraction. In normal sinus rhythm, the electrical impulse responsible for each heartbeat starts at the sinoatrial (SA) node, which allows for controlled conduction through the atria, atrioventricular (AV) node, and ventricles. In atrial fibrillation, an ectopic focus creates reentrant circuits within the atria. This also causes the AV node, which acts as an electrical filter and prevents conduction of all these electrical stimuli, to be bombarded with electrical activity. The ventricles are then activated with an irregularly irregular rhythm with an overall rate that is dependent on the electrical conductivity of the AV node.
Patients without significant AV node disease who are not on AV nodal-blocking medications will generally have significant tachycardia (known as rapid ventricular response or RVR) with the onset of atrial fibrillation, as these reentry circuits can create hundreds of atrial impulses a minute. This may lead to inadequate time for ventricular filling with subsequently poor stroke volume.
The initiation of the electrical impulses that cause atrial fibrillation is often due to an underlying mechanical irritation of the atria through increased atrial filling pressures (ie, stretching), infiltration (fibrosis), ischemia, hypertrophy, or inflammation. There are numerous causes of atrial fibrillation, including pathologies such as valvular heart disease, hypertension, cardiomyopathy, ischemia, congestive heart failure (CHF), congenital heart disease, pulmonary embolism, hyperthyroidism, and infection, and other stressors such as surgery. Other reported contributing factors include obesity, diabetes, metabolic syndrome, chronic kidney disease, family history, electrolyte abnormalities (ie, low serum magnesium), alcohol use, caffeine use, and the use of certain medications (eg, theophylline, adenosine, digitalis, and bisphosphonates). It is also sometimes associated with a somatic mutation in the GJA5 gene. In some cases, no underlying cause is apparent.
Episodes of atrial fibrillation may be paroxysmal, with restoration of normal sinus rhythm within seconds to days. In other cases, it may be persistent if medical intervention is not performed.
Atrial fibrillation carries a lifetime risk of approximately 25%. It may occur at any age but is increasingly prevalent with advancing age. The prevalence also increases with underlying heart disease. Additional risk factors include physical inactivity, obstructive sleep apnea, and smoking. There is a slightly higher prevalence in males in all age groups.
In many patients, the ventricular rate is rapid, producing sudden onset of symptoms that may include palpitations, dizziness, lightheadedness, dyspnea, and syncope or near syncope. The rapid ventricular response and sometimes extreme tachycardia can also result in hypotension, subendocardial ischemia, or CHF, particularly in those with coexistent cardiac or systemic illness. In patients with slower AV node conduction, the ventricular rate can be relatively normal and the patient may be completely asymptomatic. In such patients, atrial fibrillation is often an incidental finding on physical examination or ECG.
Patients with ventricular preexcitation (such as Wolff-Parkinson-White syndrome) require special attention. These patients possess an accessory pathway allowing conduction of fibrillation potentials from the atrium to the ventricle, which bypasses the regulatory AV node. Because of this, the ventricular rate may become extremely fast, destabilizing the ventricle and resulting in ventricular fibrillation. AV nodal-blocking medications should not be used in these patients, as this can enhance conduction down a bypass tract, increasing the ventricular rate and further destabilizing the ventricle, leading to ventricular dysrhythmias.
Patients with atrial fibrillation are at increased risk of thromboembolism and thromboembolic events such as stroke due to the lack of coordinated contractility and subsequent increased hemostasis. The risk of such events complicating atrial fibrillation increases with age, coexistent CHF, hypertension, diabetes, and prior history of a stroke. All patients with atrial fibrillation should be risk stratified for the possibility of thromboembolism, and treatment with antiplatelet and/or anticoagulant medications should be considered. In some cases, a stroke or other thromboembolic event may be the initial presentation of atrial fibrillation.
Pediatric patient considerations: Although rare among children, atrial fibrillation is nearly always an indicator of underlying structural heart disease in young patients and further cardiac workup is indicated.
I48.91 – Unspecified atrial fibrillation
49436004 – Atrial fibrillation
Differential Diagnosis & Pitfalls
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