AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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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

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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

DIFFERENTIALS

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Other Problems to be Considered

Narrow complex tachyarrhythmias
Wide complex tachyarrhythmias

WORKUP

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Lab Studies

• CBC (looking for anemia, infection)
• Electrolytes and BUN/creatinine levels (looking for electrolyte disturbances or renal failure)
• Cardiac enzymes - CK and/or troponin level (to investigate myocardial infarction as a primary or secondary event)
• Thyroid function studies (looking for thyrotoxicosis, a rare, but not-to-be-missed, precipitant) may be sent from the ED, but results are not usually available to assist in decision-making.
• Digoxin level when appropriate (to look for subtherapeutic levels and/or toxicity). It is generally considered safe to administer digoxin to a patient with AF on digoxin for rate control without waiting for a level to return from the laboratory when the patient presents with AF with RVR.
• Toxicology testing

Imaging Studies

• Chest radiography findings are usually normal. Look for radiographic evidence of CHF as well as signs of lung or vascular pathology (PE, pneumonia).
• Echocardiography may be used to evaluate for valvular heart disease, left and right atrial size, LV size and function, LVH, and pericardial disease.
• Transthoracic echocardiography has low sensitivity in detecting LA thrombus, and transesophageal echocardiography (TEE) is the required modality in this case.

Other Tests

• ECG: Absent P waves, replaced by irregular, chaotic fibrillatory F waves, in the setting of irregular QRS complexes (see Media file 1). Look for aberrantly conducted beats after long-short R-R cycles (ie, Ashman phenomenon). Other features to be looked for on the ECG include LVH, preexcitation, bundle-branch blocks, acute or prior MI, and intervals (R-R, QRS, QT).
• Holter monitoring or event monitoring may be considered for those discharged from the ED (eg, in cases of paroxysmal AF not evident upon presentation).
• Exercise testing might also be used in the outpatient setting to determine adequacy of rate-control, to reproduce exercise-induced EF, and to exclude ischemic pathology.

Procedures

• Emergent electrocardioversion is indicated for an unstable patient with AF. This is not commonly required. Instability is generally considered to be present when any of the following are present and when no cause other than the AF is contributing:
• • Symptomatic hypotension
  • Altered mental status or loss of consciousness
  • Acute coronary syndrome with active myocardial ischemia evident either by symptoms (angina) or ECG, or acute myocardial infarction
  • Hypoxia
  • Presence or absence of CHF will contribute to the bedside assessment of stability.

TREATMENT

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Prehospital Care

• Care of hemodynamically unstable patients is guided by ACLS protocols, including direct current (DC) cardioversion.
• Symptomatic patients may benefit from intravenous (IV) rate-controlling agents, either calcium-channel blockers or beta-adrenergic blockers.

Emergency Department Care

The immediate role of the emergency medicine physician is to ascertain and ensure hemodynamic stability. Once this is done, the approach to atrial fibrillation is facilitated by generally accepted protocols.

• Urgently assess need for interventions, including the following:
  • Airway and oxygenation (pulse oximetry); O₂ supplementation as needed
  • Blood pressure support (often difficult until rate is controlled)
  • A patient with hemodynamic instability, mental status changes, preexcitation, or angina will require urgent synchronized DC cardioversion.
    • Obtain emergent laboratory and imaging studies (ECG, chest radiography).
    • Once the patient has been determined to be hemodynamically stable, often the first step to control ventricular tachycardia is the administration of a rate-controlling agent (as discussed elsewhere in this article, most typically a beta-blocker or a calcium-channel blocker). In a small percentage of cases, the patient may revert to sinus in response to a slowing down of the rate.
    • If the patient persists in AF, anticoagulation should be initiated with either intravenous or subcutaneous heparin. The treatment branch then divides patients into duration of AF. Patients with duration of less than or equal to 48 hours (and without significant LV dysfunction, mitral valve disease, or prior embolism) may undergo immediate pharmacologic or DC cardioversion. AF of duration of greater than 48 hours, or unknown duration, or high risk of embolization can either undergo TEE-guided DC cardioversion or be anticoagulated for 3 weeks, followed by DC cardioversion. Multiple studies have shown the safety/efficacy of TEE-facilitated early cardioversion versus conventional therapy. Although patients who have been on anticoagulation already for at least 3 weeks can be cardioverted without TEE, if any complicating factor (eg, valvular disease, LV dysfunction) is present, TEE should be considered.
• Methods of cardioversion: Cardioversion may be achieved by means of drugs or electrical shocks. Electrical cardioversion is more effective than pharmacologic cardioversion, though it requires sedation/anesthesia.
  • Electrical cardioversion
    • Direct-current cardioversion involves an electrical shock synchronized with the intrinsic activity of the heart to ensure that electrical stimulation does not occur during the vulnerable phase of the cardiac cycle. The success rate of DC cardioversion is 75-93%, with efficacy positively correlating to energy setting (360>200>100 J), and negatively correlating with duration of AF and left atrial size.
    • Paddle positions include anterior-lateral (ventricular apex and right infraclavicular) and anterior-posterior (sternum and left scapular), with at least one study suggesting increased efficacy with the anterior-posterior method.
    • Cardioversion of patients with implanted pacemakers and defibrillator devices is safe when appropriate precautions are taken. Risks of electrical cardioversion include embolic events and cardiac arrhythmias. Transient ST-segment elevations can be present after cardioversion, as well as a bump in cardiac enzyme levels without apparent myocardial damage.
    • The relapse rate after initial successful cardioversion is high: 25%-50% at 1 month and 70%-90% at 1 year.
    • While successful cardioversion in AF of duration greater than 48 hours will require 6-12 weeks of anticoagulation due to atrial stunning, no clear consensus exists for anticoagulation after cardioversion for AF of less than 48 hours. One approach is to divide these patients into low-risk (treat with aspirin) and higher-risk (traditional anticoagulation).
• • Pharmacologic cardioversion
    • Pharmacologic cardioversion appears to be most effective when initiated within 7 days after the onset of AF. Please see Medication for discussion of specific drugs.
    • The risk factors for pharmacologic cardioversion include bradyarrhythmia, QT prolongation, and ventricular arrhythmias.
• Disposition: A number of studies have looked at whether low-risk patients with new-onset AF can be treated and discharged from an emergency department setting.
• • A study by Michael et al looked at 289 patients seen during an 18-month period in an emergency department setting. Sixty-two percent (180) underwent attempted chemical cardioversion with a 50% success rate, and 28% (80) had attempted electrical cardioversion with a 89% success rate. Ninety-three percent of electrical cardioversions were performed by emergency physicians. They concluded that cardioversion and immediate discharge of patients who present to the ED with acute atrial fibrillation appears to be both safe and effective.
  • Reasons for hospitalization would include but not be limited to the following:
    • Presence of comorbidities
    • For workup or treatment of underlying etiology of AF, including evaluation for ACS or myocardial infarction
    • For elderly patients
    • For patients with underlying heart disease
    • Patients at risk of complications from AF therapies

Consultations

• Patients with AF who are treated in the ED generally require consultation with a cardiologist. Those with new-onset AF and those with associated symptoms related to rate are generally admitted to rule out MI and to evaluate for possible elective cardioversion.
• A patient's cardiologist plays a vital role in determining the most appropriate long-term strategy for a patient with AF and provides crucial follow-up.
• A cardiologist may become involved emergently if complicating factors are present or if the patient is experiencing ongoing cardiac ischemia or infarction not treatable with rate reduction measures and standard chest pain protocols. A patient with AMI and new-onset AF who is stable may benefit from simple rate-control measures (eg, intravenous beta-blockers, intravenous magnesium sulfate 2 g over 10 min) while being prepared for the catheterization laboratory and intravenous nitrates, heparin, and aspirin are begun.

MEDICATION

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Pharmacologic agents in AF fall into 1 of 2 classes: rate-controlling drugs and rhythm restoring/rhythm maintenance drugs (though some overlap exists with some drugs, such as amiodarone, exhibiting both qualities).

Rate-controlling drugs

In patients without ventricular preexcitation, rate is controlled most effectively with intravenous verapamil, diltiazem, or beta-adrenergic blockers. Beta-blockers are especially effective in the presence of thyrotoxicosis and increased sympathetic tone or in patients with myocardial ischemia/AMI. The non-hydropyridine calcium channel blockers may be chosen in patients lacking any history of heart failure and in patients with reactive airway disease.

Anecdotally, intravenous diltiazem has become many emergency medicine physician's first-line rate-controlling drug in patients without a history of heart failure.

Digoxin is ineffective in controlling ventricular rate during acute episodes.

In patients with acute or chronic heart failure, digoxin or amiodarone should be used. (Amiodarone does not currently have FDA approval for this intervention.)

Antiarrhythmic drugs

Antiarrhythmic drugs that can terminate AF include procainamide, disopyramide, propafenone, sotalol, flecainide, amiodarone, and ibutilide.

The efficacy of antiarrhythmic drugs has been linked to the duration of AF.

The American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) Guidelines make the following recommendations regarding pharmacologic conversion of AF:

• Conversion of AF less than or equal to 7 days
  • Agents with proven efficacy include dofetilide, flecainide, ibutilide, propafenone, and to a lesser degree, amiodarone and quinidine.
  • Less effective or incompletely studied agents in this scenario include procainamide, digoxin, and sotalol.
• Conversion of AF lasting greater than 7 days
  • Agents with proven efficacy include dofetilide, amiodarone, ibutilide, flecainide, propafenone, and quinidine.
  • Less effective or incompletely studied agents in this scenario include procainamide, sotalol, and digoxin.
• Conversion of AF lasting greater 90 days - Oral propafenone, amiodarone, and dofetilide have been shown to be effective at converting chronic AF to normal sinus rhythm (NSR).

A newer agent and recently approved class III antiarrhythmic is dofetilide. Another drug, azimilide, has been studied in the recent Azimilide Post-Infarct Survival Evaluation (ALIVE) trial, a post–heart attack survival study. Additional data from ALIVE further support the ongoing development of azimilide as a treatment for supraventricular arrhythmias. Fewer patients in sinus rhythm at baseline developed AF/atrial flutter during the trial on azimilide compared with placebo.

Another newer drug is dronedarone, a deiodinated derivative of amiodarone that has no organ toxicity. Its use extends to atrial and ventricular arrhythmias. At present, dronedarone is an experimental agent that has multiple actions (all 4 Von Williams class effects). Unlike amiodarone, it does not have the iodine moiety. The lack of iodination may offer a better adverse-effect profile. Dronedarone has been shown to (1) have antiadrenergic effects, (2) prolong atrial and ventricular refractory periods, and (3) prolong atrioventricular node conduction and the paced QRS complex.

In animal models, dronedarone has been shown to decrease ischemia-induced ventricular arrhythmias. The clinical effects of dronedarone are now being examined in patients with AF and in patients with internal cardioverter-defibrillators (ICDs). 

When considering drug therapy for AF, remember the treatment caveat: "Electrical cardioversion is the preferred modality in the patient whose condition is unstable."

Drug Category: Calcium channel blockers

These agents are more effective than digoxin when given orally for long-term rate control and should be the initial DOC. They reduce rate of AV nodal conduction and control ventricular response. Formulations administered IV are discussed as they apply to the control of severe symptoms related to a rapid ventricular rate in an emergent situation.

Drug Category: Beta-blockers

These agents slow the sinus rate and decrease AV nodal conduction. Beta-blockers now have more of a secondary role in AF rate control. Carefully monitor blood pressure.

Drug Category: Class IA antiarrhythmics

These agents are used only for chemical conversion. They alter the electrophysiologic mechanisms responsible for arrhythmia.

Drug Category: Class IC antiarrhythmics

These agents are used only in patients with structurally normal hearts (ie, absence of coronary artery disease or cardiomyopathy).

Drug Category: Class III antiarrhythmics

These drugs may effectively establish a chemical conversion to sinus rhythm.

Drug Category: Cardiac glycosides

These drugs slow AV nodal conduction primarily by increasing vagal tone. They are used primarily in the setting of AF with CHF.

FOLLOW-UP

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Further Inpatient Care

• Preventing complications of AF
• • Cardioversion (either electrical or chemical) carries a significant risk of embolization. Anticoagulants usually are administered to patients with AF lasting more than 48 hours. They are administered 3 weeks before to 4 weeks after cardioversion. Stunning of the atria may occur for several weeks following cardioversion, and the atrial chambers are at increased risk of developing thrombi. For this reason, antiarrhythmic agents that restore sinus rhythm should be withheld until anticoagulation has been achieved.
  • Stroke recurrence rate is high for patients with AF; therefore, long-term warfarin therapy is recommended. Aspirin offers only modest protection against stroke for patients with AF. The effect is less consistent than that of oral anticoagulation. However, for patients who cannot tolerate warfarin, aspirin is a suitable alternative. See In/Out Patient Meds.

Further Outpatient Care

• Long-term management of AF has most commonly centered around 1 of 2 strategies: rhythm control versus rate control. The discussion surrounding these strategies has been dominated by the following questions: Is AF best managed by rhythm control?, Is AF best managed by rate control?, How is sinus rhythm best maintained?, What is the best means of preventing thromboembolism? While these questions are arguably the purview of cardiologists, it behooves the emergency medicine physician to have a basic knowledge of recent developments in this area.
• Five significant randomized clinical trials have taken place in the past few years and include the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM), Paroxysmal Atrial Fibrillation (PAF 2), Pharmacological Intervention in Atrial Fibrillation (PIAF), Rate Control Versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE), and Strategies of Treatment of Atrial Fibrillation (STAF). A review of these studies yielded the following conclusions in regards to rate versus rhythm control:
• • AFFIRM and RACE both failed to demonstrate a clear benefit with rhythm control strategy.
  • All 5 studies failed to show any significant difference in all-cause or cardiovascular mortality between the two strategies.
  • With respect to stroke, no difference was noted between the two strategies. Warfarin lowers the risk of stroke in both strategies.
  • With respect to quality of life and functional status, all 5 trials failed to show any differences between rate control and rhythm control.
• In 2003, the American Academy of Family Physicians and the American College of Physicians issued clinical practice guidelines on the management of newly detected atrial fibrillation, with the following recommendations:
• • Recommendation 1: Rate control with chronic anticoagulation is the recommended strategy for the majority of patients with atrial fibrillation. Rhythm control is appropriate when based on other special considerations, such as patient symptoms, exercise tolerance, and patient preference. Grade: 2A.
  • Recommendation 2: Patients with atrial fibrillation should receive chronic anticoagulation with adjusted-dose warfarin, unless they are at low risk of stroke or have a specific contraindication (eg, thrombocytopenia, recent trauma or surgery, alcoholism) to the use of warfarin.
  • Recommendation 3: For patients with atrial fibrillation, the following drugs are recommended for their demonstrated efficacy in rate control during exercise and while at rest: atenolol, metoprolol, diltiazem, and verapamil (drugs listed alphabetically by class). Digoxin is only effective for rate control at rest and therefore should only be used as a second-line agent for rate control in atrial fibrillation.
  • Recommendation 4: For patients who elect to undergo acute cardioversion to achieve sinus rhythm in atrial fibrillation, both DC cardioversion and pharmacologic conversion are appropriate options.
  • Recommendation 5: Both transesophageal echocardiography with short-term prior anticoagulation followed by early acute cardioversion (in the absence of intracardiac thrombus) with postcardioversion anticoagulation versus delayed cardioversion with preanticoagulation and postanticoagulation are appropriate management strategies for patients who elect to undergo cardioversion.
  • Recommendation 6: Most patients converted to sinus rhythm from atrial fibrillation should not be placed on rhythm maintenance therapy since the risks outweigh the benefits.
• As stated previously, stratification of patients with AF into those at high and low risk for thromboembolism is a crucial determinant of optimal antithrombotic prophylaxis. Brass et al found that anticoagulation is underused in elderly patients with stroke and AF, even among ideal candidates.

In/Out Patient Meds

• Medications for rate control in inpatient and outpatient setting
• • Inpatient medication consists of a 24-hour diltiazem drip and/or digoxin loading dose and maintenance therapy; however, digoxin therapy is falling out of favor rapidly as a method of rate control.
  • Outpatient management consists of rate control with oral diltiazem, digoxin, or quinidine in addition to prevention of thromboembolic complications (see Stratification by embolic risk).
  • Farshi et al compared several standardized drug regimens for 24-hour ventricular rate control (digoxin, diltiazem-CD, atenolol, digoxin plus diltiazem-CD, digoxin plus atenolol). Digoxin plus atenolol produced the most effective rate control due to a synergistic effect on the AV node.
  • Because of its vagolytic effect and resultant rapid ventricular response, quinidine should not be given without prior administration of agents that slow AV nodal conduction.
  • Occasionally, treatment of patients with tachycardia-bradycardia syndrome worsens sinus node function, resulting in symptomatic bradyarrhythmias that require pacemaker support. For this reason, the author reduces the initial dose of intravenous diltiazem for rate control in the elderly (eg, unknown sick sinus syndrome) or for those on any other AV node-blocking drug, using half to one quarter of the loading dose of IV diltiazem (usually about 5-10 mg in the average adult) and titrating at equal increments every 15 minutes up to the standard mg/kg loading dose. This has proven a very effective method of preventing "bradycardic overshoot."
  • Using this method, the author has had no adverse bradycardic events from diltiazem.
  • A permanent pacemaker should be implanted in persons who have AF and cerebral symptoms that are not drug induced, such as dizziness or syncope associated with ventricular pauses longer than 3 seconds.
  • Many antiarrhythmic agents, especially flecainide and propafenone, can slow the atrial rate, which allows greater impulse conduction through the AV node, resulting in a faster ventricular rate. In fact, many episodes of wide QRS tachycardia in patients who have AF and are treated with flecainide or propafenone appear to be secondary to atrial flutter with 1:1 AV node conduction associated with QRS widening.
    • The resultant arrhythmia is often misdiagnosed as ventricular tachycardia. This situation can be prevented or treated by the addition of agents that slow AV node conduction (eg, digitalis, alpha-adrenergic blockers, calcium channel blockers).
    • The Atrial Fibrillation Follow-up Investigation in Rhythm Management (AFFIRM) study randomized 4060 elderly patients (mean age 68 +/- 9 y) to either rate control or rhythm control and assessed them for total mortality at a mean follow-up of 3.5 years. After this interval, the rate-control group trended toward lower mortality rates (306 vs 356, P=.058). Stroke events were nearly equal in both treatment groups; most occurred when patients ceased intake of warfarin (or levels were subtherapeutic). Therefore, in both groups, the need to continue antiplatelet therapy in patients with stroke risk factors (regardless of the rhythm therapy) was emphasized. Additionally, the AFFIRM trial found that significantly fewer hospitalizations were required in the rate-control group, even in the elderly patient population, indicating that further savings could be achieved by using a rate-control strategy.
    • In the Rate Control vs Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) trial, the investigators used the composite primary end point of rate of death or severe cardiovascular incident. This end point occurred in fewer patients randomized to rate control (n = 256; 17.2%) vs rhythm control (n = 266; 22.6%). When subsets of these end points were analyzed (eg, cardiovascular death, CHF, hemorrhage) they found no statistical difference between the 2 groups. Of importance, the study found that the rate of adverse events was greater in the rhythm-control vs the rate-control group, and this was also true for patients with hypertension (30.8% event rate with rhythm control vs 17.3% with rate-control).
• Inpatient and outpatient prevention of embolic problems is best achieved with vitamin K antagonists (eg, warfarin), which are highly effective in reducing risk of ischemic stroke in patients with AF.
• • High-risk patients who can safely receive anticoagulation should be treated with warfarin. For high-risk AF patients younger than 75 years, an INR range of 2-3 is safe and effective. For those older than 75 years, close surveillance of INR levels is recommended because of the apparently greater likelihood of bleeding complications. Feinberg noted that patients with AF have a stroke risk of 4.5% per year. Anticoagulation reduces this to around 1.5% per year, a 70% relative risk reduction.
  • The presence of additional risk factors, such as a recent stroke or TIA, hypertension (particularly systolic hypertension), CHF, or diabetes mellitus, greatly increases stroke risk. Patients with any of these risk factors have a stroke risk of 8% per year. In contrast, patients who are younger than 75 years and have none of these risk factors have a low risk for stroke (around 1% per year) when treated with aspirin.
  • The value of other antiplatelet agents has not been assessed in patients with AF.
  • Inpatients with new-onset AF frequently are placed on intravenous heparin initially before chemical or electrical conversion.
  • Stroke Prevention Using Oral Thrombin Inhibitor in Atrial Fibrillation (SPORTIF) III and V trials were trials performed in Europe (SPORTIF III) and in North America (SPORTIF V). Both were noninferiority trials. By definition, noninferiority trials intend to show that an experimental treatment (ximelagatran) does not produce worse results than those of a known active control (warfarin) by a specified margin (2% per year).
  • SPORTIF III was reported in the Lancet in November 2003. It was a phase 3, multicenter, randomized, controlled clinical trial that compared warfarin to ximelagatran in the treatment of 3410 patients with AF and one or more stroke factors. The primary endpoint was stroke or systemic embolism. The primary event rate by intention to treat was 2.3% per year for warfarin and 1.6% for ximelagatran (absolute risk reduction, 0.7%; relative risk reduction, 29%). Rates of disabling or fatal stroke, mortality, and major bleeding were similar, but the rate of combined minor and major hemorrhages was 29.8% per year for warfarin and 25.8% for ximelagatran (relative risk reduction, 14%; P = .007). Raised serum alanine transferase levels were more commonly observed in the ximelagatran group.
  • SPORTIF V was reported in the American Heart Journal in September 2003 and at the American Heart Association Scientific Sessions in November 2003. This study included a double-blind treatment allocation with 3922 patients. Again, the primary endpoints were strokes and systemic embolic events with a noninferiority treatment objective compared to warfarin. The study commenced in July 2000 and enrollment ended in December 2001. Data analysis was extensive and included safety monitoring. The primary event rate by intention to treat was 1.2% per year for warfarin and 1.6% for ximelagatran. The ximelagatran rate was identical in the two studies, whereas the rate for warfarin in SPORTIF V was half that noted in SPORTIF III. The reasons for this difference in the warfarin groups continue to be evaluated.
  • In both studies, the rates of intracranial and/or other major bleeding events were insignificant. However, when the event rates for major and minor bleeding are combined, ximelagatran was significantly better than warfarin (P <.001 and P <.007, respectively). Elevated alanine transaminase (ALT) levels were noted not only in SPORTIF III and V but also in all previously conducted long-term ximelagatran trials. These elevations are transient and return to normal whether or not the drug is discontinued. It appears that the ALT elevation is limited to the first 6 months of treatment with ximelagatran.

Transfer

• Transfer to a referral center if the patient has complications, including the following:
• • Bradycardia caused by sick sinus syndrome that requires pacemaker therapy
  • Unresponsive rate control despite adequate medical therapy. After electrical cardioversion, referral for electrophysiologic ablation may be appropriate. These patients generally are transferred from one inpatient facility to another.
  • Embolic complications requiring surgical therapy (arterial embolization) or CVA requiring neurointensive care

Complications

• Stroke (AF-associated stroke is particularly a problem for patients older than 75 years (see Image 2).
• Arterial embolization
• CHF
• Severe bradycardia
• Rate-related myocardial ischemia

Prognosis

• As discussed earlier, the rate of ischemic stroke among patients with nonrheumatic AF averages 5% year, which is somewhere between 2-7 times the rate of stroke in patients without AF.
• 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.

Patient Education

• In cases of intermittent AF, educating the patient on rapid access to 911 services is beneficial.
• Long-term education should be the responsibility of the primary care provider but certainly knowledge about stroke risk and prevention should be initially imparted by the emergency to the AF patient.
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Atrial Fibrillation.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Watch for development of severe bradycardia during treatment. This may cause severe hypotension and death if not carefully monitored.
• Rarely, AF may be due to pulmonary embolism, pericardial disease/effusion or carbon monoxide intoxication. Keep these rare events in mind when dealing with the unusual case that does not respond to standard therapy.
• Managed care has recently pushed for discharging stable patients with lone AF for follow-up within 24-48 hours. In these patients, carefully document normal ventricular function (using echocardiography, if possible) and obtain baseline thyroid studies. Be certain that a qualified internist or cardiologist will follow-up with the patient within this time frame. Once established in the ED, oral medication for rate control may be quite appropriate in these cases.
• Most patients with lone or paroxysmal AF will self-convert. Episodes of paroxysmal AF may last from a few seconds to several weeks. Spontaneous conversion of paroxysmal AF to sinus rhythm occurs in 68% of persons presenting with AF of fewer than 72 hours duration.
• Beware of AF in Wolfe-Parkinson-White syndrome. In young patients with this disorder, which appears as rapid wide-complex AF with a rate of more than 200 beats per minute, the use of calcium channel blockers may induce ventricular fibrillation.

Special Concerns

• For more information on this topic, please consult the following Internet site and resource text.
• • American Heart Association
  • Management of Patients with Atrial Fibrillation: A Statement for Healthcare Professionals from the Subcommittee on Electrocardiography an