eMedicine Specialties > Emergency Medicine > Cardiovascular

Atrial Fibrillation

Author: Jeffrey Lazar, MD, MPH, Chief Resident, Section of Emergency Medicine, Yale New Haven Hospital
Coauthor(s): Alan D Clark, MD, Director, St Johns.com/Healthy People Magazine, Former Department Chairman, St. John's Emergency Trauma Center, St John's Regional Health Center, Springfield, Missouri
Contributor Information and Disclosures

Updated: Mar 5, 2007

Introduction

Background

Atrial fibrillation (AF), the most commonly encountered arrhythmia in clinical practice, is defined by the absence of coordinated atrial systole. AF results from multiple reentrant electrical wavelets that move randomly around the atria.

P waves are replaced by irregular, chaotic fibrillatory waves, often with a concomitant irregular ventricular tachycardia. The rate at which the atrial electrical impulses are transmitted to the ventricle is determined by a number of factors including relative refractory period within the atrioventricular (AV) node, hydration status, and presence or absence of pharmacologic agents used to control the rate. When ventricular rate increases to tachycardic levels, a situation of atrial fibrillation with rapid ventricular response (AF with RVR) ensues. This in turn can lead to decompensation in the form of either myocardial ischemia or creation of congestive heart failure (CHF).

AF may increase mortality up to 2-fold, primarily due to embolic stroke. This risk exists as the lack of coordinated atrial contraction leads to unusual fluid flow states through the atrium that are permissive for formation of thrombus that is then at risk to embolize. This risk is theoretically particularly present upon return to normal sinus rhythm when coordinated atrial contraction can entrain a thrombus into flow. The risk of embolism associated with cardioversion is stated to be as high as 2%. Thus, part of the challenge for emergency physicians is the question of managing rate versus rhythm in the ED and the issue of when cardioversion through any mechanism should be attempted.

The incidence of atrial fibrillation increases significantly with advancing age.

Managing AF in the ED, for the most part, involves a straightforward approach. Generally accepted guidelines and protocols for managing AF are of great value in the decision-making process (see Media files 1-6).

The cardiologist's approach to AF is well covered in Dr Rosenthal's article, Atrial Fibrillation. Emergency physicians are more concerned with the acute life threat and appropriate ED treatment of patients with AF; however, readers who are interested in topics such as catheter ablation and clinical electrophysiology of AF are referred to Dr Rosenthal's article. For additional resources, please also visit Medscape's Atrial Fibrillation Resource Center.

Pathophysiology

Multiple reentrant waveforms within the atria bombard the AV node, which becomes relatively refractive to conduction due to the frequency of upstream electrical activity.

Three mechanisms that have been shown to play a role in the initiation and maintenance of AF include the following:

• Enhanced automaticity in the left atrium extending to proximal 5-6 mc portions of the pulmonary veins
• Electrical remodeling of the atria with resultant shortening of the atrial refractory period increases the duration and stability of AF, well-described by the phrase "atrial fibrillation begets atrial fibrillation"
• In chronic AF, areas of functional conduction block further divide and maintain a persistently chaotic electrical state.

Inflammation is believed to play an as-of-yet undefined role in the pathogenesis of AF.

AF occurs in 3 distinct clinical circumstances:

• As a primary arrhythmia in the absence of identifiable structural heart disease
• As a secondary arrhythmia in the absence of structural heart disease but in the presence of a systemic abnormality that predisposes the individual to the arrhythmia
• As a secondary arrhythmia associated with cardiac disease that affects the atria

While differing classification schemes exist, AF is commonly broken down into acute versus chronic AF, with chronic AF then being subcategorized into one of the following:

• Paroxysmal - Duration less than 7 days, with spontaneous termination
• Persistent - Duration greater than 7 days and would last indefinitely unless cardioverted
• Permanent - Duration greater than 7 days, with restoration to sinus rhythm not possible
• Lone AF has been used to describe AF in individuals without structural or cardiac or pulmonary disease, with low risk for thromboembolism. It has traditionally been applied to patients younger than 60 years.

The 3 primary ways AF affects hemodynamic function include the following:

• Loss of atrial kick (synchronized atrial mechanical activity)
• Irregularity of ventricular response
• Inappropriately rapid heart rate

Frequency

United States

Approximately 2.5 million Americans, or close to 1% of the total population, currently have atrial fibrillation.

Atrial fibrillation can be considered a disease of aging, and with the projected increase in the elderly population in America, the prevalence is expected to more than double by the year 2050.

Mortality/Morbidity

• The rate of ischemic stroke among patients with nonrheumatic AF averages 5% a year, which is somewhere between 2-7 times the rate of stroke in patients without AF. The risk of stroke is not due solely to AF; it increases substantially in the presence of other cardiovascular disease.
• The attributable risk of stroke from AF is estimated to be 1.5% for those aged 50-59 years, and it approaches 30% for those aged 80-89 years.
• The total mortality rate is approximately doubled in patients with AF compared with patients in normal sinus rhythm and is linked with the severity of underlying heart disease.
• AF complicates acute myocardial infarction (AMI) in 5-10% of cases. The causes of AF in AMI are thought to be due to any number of factors, such as atrial infarction, atrial ischemic injury, atrial distension, or, perhaps, pericarditis. According to Rathore et al, patients who developed new-onset AF during the course of myocardial infarction (MI) were at higher risk than patients who presented with chronic AF. Patients with AMI and AF tend to be older, be less healthy, and have poorer outcomes during hospitalization and after discharge than individuals without AF. AF is independently associated with an increased mortality rate.

Race

• Atrial fibrillation appears to be more common in whites than in blacks.
• Blacks have less than half the age-adjusted risk of developing AF than is seen in whites.

Sex

Incidence is significantly higher in men than in women in all age groups.

Age

The prevalence of atrial fibrillation increases almost exponentially with age.

AF is uncommon in childhood except after cardiac surgery.

• The prevalence of AF among persons younger than 55 years is 0.1%.
• The prevalence of AF among persons 60 years or older is 3.8%.
• The prevalence of AF among persons 80 years or older is 10%.

Clinical

History

In addition to eliciting symptoms listed below, history taking of any patient presenting with suspected AF should include questions relevant to temporality, precipitating factors (including hydration status, recent infections, alcohol use), history of pharmacologic or electric interventions and responses, and presence of heart disease. Occasionally, a patient may have clear and strong belief about the onset of symptoms that may be helpful in determining a course of action.

• Palpitations
• Fatigue or poor exercise tolerance
• Dyspnea
• Chest pain (true angina)
• Presyncope or syncope
• Generalized weakness

Physical

• Pertinent physical findings are limited to the cardiovascular system or, if embolization has occurred, the brain and/or peripheral vasculature. These include the following:
  • Irregular pulse, with or without tachycardia, is typically described as the irregularly irregular rhythm.
  • Hypotension and poor perfusion caused by decrease in atrial filling pressures and decrease in stroke volume are common findings. This may be either rate related or because of the lack of normal atrial kick.
  • Congestive heart failure, if present, may be indicated by rales, jugular venous distension, peripheral edema, and a gallop, which may be difficult to auscultate due to rapid rate.
  • Signs of embolization, including transient ischemic attack (TIA), stroke, and peripheral arterial embolization (eg, cold, pulseless extremities), may be identified.

Causes

Risk factors for atrial fibrillation include age, male sex, long-standing hypertension, valvular heart disease, left ventricular hypertrophy, coronary artery disease (with or without depressed left ventricular function), diabetes mellitus, smoking, and any form of carditis.

Causes of atrial fibrillation can be divided into cardiovascular versus noncardiovascular causes.

• Important cardiovascular causes include the following:
  • Long-standing hypertension
  • Ischemic heart disease
  • CHF
  • Any form of carditis
  • Cardiomyopathy
  • Infiltrative heart disease of any type
  • Sick sinus syndrome
• Noncardiovascular causes of atrial fibrillation include the following:
  • Hyperthyroidism
  • Low levels of potassium, magnesium, or calcium
  • Pheochromocytoma
  • Sympathomimetic drugs, alcohol, electrocution
• Noncardiovascular respiratory causes include the following:
  • Pulmonary embolism
  • Pneumonia
  • Lung cancer
  • Idiopathic: Lone AF is idiopathic and defined as the absence of any known etiologic factors plus normal ventricular function by echocardiography. Most patients with lone AF are younger than 65 years, although age is not used to define lone AF.
  • Hypothermia

• Search for CME/CE on This Topic »

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