eMedicine Specialties > Cardiology > Arrhythmias

Atrial Fibrillation: Differential Diagnoses & Workup

Author: Lawrence Rosenthal, MD, PhD, Associate Professor of Medicine, Director, Section of Cardiac Electrophysiology and Pacing, Fellowship Director of Clinical Cardiac Electrophysiology, Department of Internal Medicine, Division of Cardiovascular Medicine, University of Massachusetts Memorial Medical Center
Coauthor(s): David D McManus, MD, Assistant Professor of Medicine, Cardiac Electrophysiology Section, Cardiology Division, University of Massachusetts Medical Center
Contributor Information and Disclosures

Updated: Oct 29, 2009

Differential Diagnoses

Atrial Flutter
Atrial Tachycardia
Atrioventricular Nodal Reentry Tachycardia (AVNRT)
Paroxysmal Supraventricular Tachycardia
Wolff-Parkinson-White Syndrome

Other Problems to Be Considered

Digoxin toxicity
Hyperthyroidism
Pulmonary disease
Cardiac ischemia secondary to rapid ventricular rate

Workup

Laboratory Studies

• An electrocardiogram (ECG) should be obtained to establish the diagnosis of atrial fibrillation; look for pre-excitation; determine heart rate; and evaluate for left ventricular hypertrophy, bundle-branch block, or prior MI. The ECG is also useful to follow the QT and QRS intervals of patients receiving anti-arrhythmic medications for atrial fibrillation.
• Complete blood count, thyroid, hepatic, and renal function panels are often helpful, especially when ventricular rate is difficult to control.
• A toxicology screen or ethanol level may be appropriate to rule out acute intoxication.

Imaging Studies

• Transthoracic echocardiogram (TTE)
  • Evaluate for valvular heart disease
  • Evaluate atrial and ventricular chamber and wall dimensions
  • Estimate ventricular function and evaluate for ventricular thrombi
  • Estimate pulmonary systolic pressure (pulmonary hypertension)
  • Evaluate for pericardial disease
• Transesophageal echocardiogram (TEE)
  • Evaluate for left atrial (LA) thrombus (particularly in the LA appendage)
  • To guide cardioversion (if thrombus is seen, cardioversion should be delayed)
  • When TEE is planned, the concurrent use of TTE may increase cost without providing significant additional information.
• Computed tomography (CT) or magnetic resonance imaging (MRI): If atrial fibrillation ablation is planned, then 3-dimensional imaging technologies (CT scan or MRI) are often helpful to evaluate atrial anatomy. Imaging data can be processed to create anatomic maps of the left atrium and pulmonary veins.
• Chest radiography: May help evaluate lung parenchyma and pulmonary vasculature in the appropriate clinical context.

Other Tests

• Electrocardiogram
  • ECG findings usually confirm the diagnosis of atrial fibrillation.
  • The ventricular rate is typically irregular.
  • Discrete P waves are absent; instead, undulating fibrillatory (f) waves are present (see Media file 1).
    
    

    

    Ventricular rate varies from 130-168 beats per minute. Rhythm is irregularly irregular. P waves are not discernible.

    [ CLOSE WINDOW ]

    

    Ventricular rate varies from 130-168 beats per minute. Rhythm is irregularly irregular. P waves are not discernible.

• Six-minute walk test or exercise test
  • Six-minute walk or exercise testing can help assess the adequacy of rate control.
  • Exercise testing can exclude ischemia prior to treatment of patients with Class Ic drugs and can be used to reproduce exercise-induced atrial fibrillation.
• Holter monitoring or event recording: Helpful to establish diagnosis and evaluate rate control.
• Electrophysiology study
  • May help identify the mechanism of a wide-QRS-tachycardia.
  • May help identify a predisposing arrhythmia.
  • May help identify sites for curative ablation or AV node ablation. 

Procedures

Electrical cardioversion

• Direct-current (DC) cardioversion is synchronized to the R wave to prevent a shock from being delivered during the vulnerable phase of the T wave. This reduces the likelihood of inducing ventricular fibrillation.
• Elective DC cardioversion is used to restore sinus rhythm if patients are anticoagulated adequately with a therapeutic international normalized ratio (INR) and remain in atrial fibrillation.
• In most patients, the procedure can be performed safely in an outpatient setting.
• Administration of either moderate sedation (according to sedation guidelines) or general anesthesia is necessary for patient comfort and safety during elective atrial fibrillation cardioversion.
• Defibrillating patches can be positioned in several locations, including the right anterior and left posterior positions. This position allows the defibrillation vector to include the atria. Standard placement in the anterior and lateral positions is also acceptable.
• A high initial success rate should be expected. Some patients remain in sinus rhythm only transiently and quickly revert back to atrial fibrillation. If initially unsuccessful, check patch placement and consider use of an anti-arrhythmic such as ibutilide (see Medication section) to reduce the defibrillation threshold and increase the likelihood of cardioversion. Use of defibrillators with biphasic waveforms have consistently been demonstrated to be more efficacious in converting atrial fibrillation to sinus rhythm.¹⁰
• Patients with atrial fibrillation of less than 48 hours' duration may be considered for immediate cardioversion as the risk of thromboembolic sequelae from cardioversion in these patients is small.
• If the precise duration of the atrial fibrillation cannot be determined or if duration of atrial fibrillation is longer than 48 hours, TEE should be used to guide cardioversion. Alternatively, if the patient is able to tolerate atrial fibrillation, anticoagulation for 4 weeks can circumvent the need for TEE prior to cardioversion.
• Regardless of long-term anticoagulation strategy or duration of atrial fibrillation, administration of anticoagulation with heparin or enoxaparin is recommended prior to cardioversion.
• Body habitus and urgency can be used to guide shock energy. An obese patient with a large anteroposterior diameter will probably require higher energy (ie, 360 J monophasic). A thinner person may require lower energy (200 J). Required energies are always lower with biphasic waveforms (100-200 J).
• Two sets of patches can be used to successfully cardiovert patients in whom a single maximal shock with 1 set of patches fails. Two external defibrillators and 2 sets of defibrillation patches are required. Vectors are crossed so that 1 set of patches is placed anteriorly left of the sternum and posteriorly right of the spine. The second set of patches is placed anteriorly right of the sternum and posteriorly left of the spine. The 2 defibrillators may be activated simultaneously, in synchronized fashion, or with a slight delay after the first discharge. This method may succeed when a single set of patches fails.
• Internal cardioversion is also possible but must be performed in the electrophysiologic laboratory. Intracardiac catheters can be positioned in the right atrium and in the coronary sinus. Synchronized shocks are then delivered between the 2 catheters, with energies from 1-100 J. Alternatively, a defibrillating current may be passed between a single intracardiac catheter (right atrium, coronary sinus) and a single cutaneous patch placed anteriorly or posteriorly.
• In patients with an implantable cardioverter-defibrillator, device-delivered shock, synchronized to the QRS complex, may be used to attempt cardioversion of atrial fibrillation. Rarely, external cardioversion of patients with an implanted device can result in device damage, and device function should generally be re-evaluated following external cardioversion.

Chemical cardioversion

• Hemodynamically stable patients with atrial fibrillation can be converted to sinus rhythm using oral or intravenous agents. Oral dosing of Class Ic agents [flecainide (300 mg) or propafenone (450-600 mg)] has been shown to be efficacious in patients with atrial fibrillation of shorter duration (<7 d).¹¹ These drugs require monitoring for side-effects (ie, ventricular tachycardia and heart failure). Coadministration of an AV-nodal blocking agent (ie, beta-blocker or nondihydropyridine calcium channel blocker) is generally recommended to prevent conversion to atrial flutter with rapid ventricular response.
• While inpatient loading of Class Ic agents is not required for those without structural heart disease, it is frequently practiced. Use of flecainide and propafenone is contraindicated in patients with structural heart disease (left ventricular hypertrophy or prior myocardial infarction), baseline QRS or QT prolongation (QTc longer than 460 ms) or in those receiving concomitant antiarrhythmic therapy.
• Intravenous procainamide (Class Ia, <18 mg/kg/h) or ibutilide (Class III, 1 mg over 15 m) may also be used for chemical cardioversion of atrial fibrillation or to increase likelihood of successful electrical cardioversion. Both of these agents should only be used in a highly monitored, inpatient setting. These drugs predispose to ventricular tachycardia and they should not be used in those with significant structural heart disease, QT prolongation, or electrolyte abnormalities. Some clinicians preadminister magnesium to attempt to reduce the risk of ventricular tachycardia. Frequent monitoring of blood pressure, heart rate, and telemetry are advised.
• Oral dosing of other Class III agents (dofetilide, amiodarone) may also be used for chemical cardioversion or to increase the likelihood of successful electrical cardioversion. Sotalol is not generally recommended for chemical cardioversion. Amiodarone can be initiated as outpatient therapy in the appropriate clinical context (in patients without structural heart disease or other comorbidities). Initiation of dofetilide must be performed as inpatient therapy with a specified dose adjustment nomogram, including age, renal function, and changes in QT interval. Amiodarone and dofetilide are efficacious in patients with structural heart disease, including those with prior myocardial infarction or heart failure. Monitoring for bradycardia, electrolyte disturbances, and QT prolongation is strongly recommended.

Staging

Several classification schemas have been proposed for the study of atrial fibrillation, but none fully accounts for all aspects of atrial fibrillation. A number of different labels and nomenclature have been used to describe patterns of atrial fibrillation, including acute, chronic, paroxysmal, intermittent, and permanent. The vagaries of each of these definitions make comparing the results of studies assessing the magnitude and treatment of atrial fibrillation difficult.

Published guidelines from expert committees of the American College of Cardiology/American Heart Association and European Society of Cardiology on the treatment of patients with atrial fibrillation suggest that atrial fibrillation be classified into 3 patterns (see Media file 2). These include a first detectable episode, irrespective of whether it is symptomatic or self-limited, also recognizing that there may be some uncertainty about the duration of the episode and any prior undetected episodes. Recurrent atrial fibrillation is considered to be present when a patient has 2 or more episodes of atrial fibrillation. If atrial fibrillation terminates spontaneously, then recurrent atrial fibrillation is designated as paroxysmal; if this arrhythmia becomes sustained, then atrial fibrillation is considered persistent (irrespective of whether atrial fibrillation is terminated with pharmacologic therapy or electrical cardioversion).

Persistent atrial fibrillation may be either the first presentation of atrial fibrillation or the result of recurrent episodes of paroxysmal atrial fibrillation. Patients with persistent atrial fibrillation also include patients with long-standing atrial fibrillation in whom cardioversion has not been indicated or attempted, often leading to permanent atrial fibrillation. Permanent atrial fibrillation is recognized as the accepted rhythm, and the main treatment goals are rate control and anticoagulation. While it is possible to reverse the progression from paroxysmal to persistent and to permanent, this task can be challenging.

Some patients with paroxysmal atrial fibrillation, typically younger patients, have been found to have distinct electrically active foci within their pulmonary veins. These patients generally have many atrial premature beats noted on Holter monitoring. Isolation or elimination of these foci can lead to elimination of the trigger for paroxysms of atrial fibrillation.

Patients can also have atrial fibrillation as a secondary arrhythmia associated with cardiac disease that affects the atria (eg, congestive heart failure, hypertensive heart disease, rheumatic heart disease, coronary artery disease). These patients tend to be older, and atrial fibrillation is more likely to be chronic. Paroxysmal atrial fibrillation may progress to permanent atrial fibrillation, and aggressive attempts to restore and maintain sinus rhythm may prevent comorbidities associated with atrial fibrillation.

Persistent atrial fibrillation with an uncontrolled, rapid ventricular heart rate response can cause a dilated cardiomyopathy and can lead to electrical remodeling in the atria (atrial cardiomyopathy). Therapy, such as drugs or atrioventricular nodal ablation and permanent pacemaker implantation, to control the ventricular rate can improve left ventricular function and improve quality-of-life scores.

New developments aimed at curing atrial fibrillation are being actively explored. By reducing the critical mass required to sustain atrial fibrillation with either surgical or catheter-based compartmentalization of the atria (ie, MAZE procedure), fibrillatory wavelets collide with fixed anatomic obstacles, such as suture lines or complete lines of ablation, thus eliminating or reducing the chance of chronic atrial fibrillation. Some patients with focal origins of their atrial fibrillation also may be candidates for catheter ablation. Still, much remains to be accomplished before either of these procedures is appropriate for primary treatment.

• Search for CME/CE on This Topic »

• Atrial Fibrillation (Emergency Medicine)
• Atrial Fibrillation, Diagnosis and Management (Cardiology)
• Toxicity, Clonidine (Emergency Medicine)
• Atrial Flutter (Cardiology)

• Heart Center
• Atrial Fibrillation Symptoms
• Heart Rhythm Disorders Overview
• Atrial Fibrillation Causes
• Atrial Fibrillation Treatment
• Atrial Fibrillation Overview
• Stroke Center
• Stroke Overview
• Supraventricular Tachycardia Overview

• Atrial Fibrillation Worsens Advanced Systolic Heart Failure
• Atrial Fibrillation Increases Risk of Death in Diabetics
• Post-Pacemaker Atrial Fibrillation Has Minimal Impact on Quality of Life

• Hypertension, Stroke and the Impact of Atrial Fibrillation
• Management of Atrial Fibrillation in Patients With Heart Failure: From Drug Therapy to Ablation
• Atrial Fibrillation Studies Shed Light on Promising New Antiarrhythmics, Strategies, and Statin Therapy for Management and Prevention

• Atrial Fibrillation Resource Center