EMERGENCY MEDICINE

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PRACTICE EMPRACTICE NET
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E

August 2002
Atrial Fibrillation In The ED: Volume 4, Number 8

Cardioversion, Rate Control, Author

Anticoagulation, And More Gary F. Pollock, MD, FACEP

Clinical Instructor of Emergency Medicine,
University of Pittsburgh Affiliated Residency in
Emergency Medicine; Assistant Education Director,
The man in bed 2 is pale and diaphoretic. The monitor shows a heart rate of 160 and a Trauma Liaison, The Mercy Hospital of Pittsburgh,
blood pressure of 70. The nurse looks at you and says, “Doctor, what should we do?” Pittsburgh, PA.
The elderly lady in the next bed is yelling, “Doctor, my chest hurts!” Her monitor tells
Peer Reviewers
all—an irregular wide complex rhythm at a rate of 130. You ponder what drug to give.
Just then, the medics break through the door with yet another patient with a fast heart Mel E. Herbert, MD, MBBS, BMedSCi, FACEP
rate. The adenosine they administered didn’t help. Assistant Professor, Medicine, UCLA School of
As the confusion and pressure mount, you hear a faint shriek of an alarm—first, Medicine; Assistant Professor, Nursing, UCLA
School of Nursing, Department of Emergency
distant; then, more insistent. You wake. Thank goodness, it was only a dream. As you
Medicine, Olive View-UCLA Medical Center,
walk into the ED for your morning shift, the charge nurse grabs your arm and says, Sylmar, CA.
“The guy in bed 2 really needs you…his heart rate is 160.”
Corey M. Slovis, MD, FACP, FACEP
Professor of Emergency Medicine and Chairman,
A TRIAL fibrillation (AF) and its close counterpart, atrial flutter (AFl),
are two of the most common arrhythmias encountered in emergency
medicine. Their wide spectrum of presentation can challenge even the savviest
Department of Emergency Medicine, Vanderbilt
University Medical Center; Medical Director, Metro
Nashville EMS, Nashville, TN.
clinician. Management concerns encompass diagnostic studies, rate control,
cardioversion, anticoagulation, and disposition. CME Objectives
The emergency physician must understand the complexity of these issues
Upon completing this article, you should be able to:
in order to manage the diverse presentations of AF. In most cases, AF and AFl 1. discuss the evaluation and management of new-
can be discussed as one entity; however, there are important differences that onset atrial fibrillation in the ED;
should be understood. This issue of Emergency Medicine Practice addresses the 2. list the common rate control agents and explain each
emergent complications of AF and AFl in an evidence-based fashion and drug’s indications and contraindications;
3. explain how and when it is appropriate to start
provides a measured approach to this often “irregular” topic.
anticoagulation in a patient with AF; and
4. discuss admission criteria and appropriate disposition
Critical Appraisal Of The Literature of patients with new-onset atrial fibrillation based on
the current literature.
Numerous studies regarding AF are pertinent to its evaluation and treatment
in the ED. There are very few studies that specifically address AF in the Date of original release: August 1, 2002.
prehospital setting, and none of them are randomized. Date of most recent review: July 11, 2002.
Of the numerous studies that evaluate rate control and conversion agents, See “Physician CME Information” on back page.

Editor-in-Chief Center School of Medicine,
Albuquerque, NM.
Stephen A. Colucciello, MD, FACEP,
W. Richard Bukata, MD, Assistant
Assistant Chair, Department of Clinical Professor, Emergency
Emergency Medicine, Carolinas Medicine, Los Angeles County/
Medical Center, Charlotte, NC; USC Medical Center, Los Angeles,
Associate Clinical Professor, CA; Medical Director, Emergency
Department of Emergency
Department, San Gabriel Valley
Medicine, University of North
Medical Center, San Gabriel, CA.
Carolina at Chapel Hill, Chapel
Francis M. Fesmire, MD, FACEP,
Hill, NC.
Director, Chest Pain—Stroke
Associate Editor Center, Erlanger Medical Center;
Assistant Professor of Medicine,
Andy Jagoda, MD, FACEP, Professor UT College of Medicine,
of Emergency Medicine; Director, Chattanooga, TN.
International Studies Program,
Valerio Gai, MD, Professor and Chair,
Mount Sinai School of Medicine,
Department of Emergency
New York, NY. Medicine, University of Turin, Italy.
Michael J. Gerardi, MD, FACEP,
Editorial Board Clinical Assistant Professor,
Medicine, University of Medicine
Judith C. Brillman, MD, Residency and Dentistry of New Jersey;
Director, Associate Professor, Director, Pediatric Emergency
Department of Emergency Medicine, Children’s Medical
Medicine, The University of Center, Atlantic Health System;
New Mexico Health Sciences Vice-Chairman, Department of
Emergency Medicine, Morristown
Memorial Hospital.
Michael A. Gibbs, MD, FACEP, Chief,
Department of Emergency
Medicine, Maine Medical Center,
Portland, ME.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine,
University of Michigan Medical
School, Ann Arbor, MI; President,
American Physicians Assurance
Society, Ltd., Bridgetown,
Barbados, West Indies; Past
President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/Emergency
Medicine, UCLA School of
Medicine; Attending Physician,
UCLA Emergency Medicine Center;
Co-Director, The Doctoring
Program, UCLA School of Medicine,
Los Angeles, CA.
Francis P. Kohrs, MD, MSPH, Associate
Professor and Chief of the Division
of Family Medicine, Mount Sinai
School of Medicine, New York, NY.
John A. Marx, MD, Chair and Chief,
Department of Emergency
Medicine, Carolinas Medical
Center, Charlotte, NC; Clinical
Professor, Department of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Michael S. Radeos, MD, MPH,
Attending Physician, Department
of Emergency Medicine,
Lincoln Medical and Mental
Health Center, Bronx, NY;
Assistant Professor in Emergency
Medicine, Weill College of
Medicine, Cornell University,
New York, NY.
Steven G. Rothrock, MD, FACEP, FAAP,
Associate Professor
of Emergency Medicine, University
of Florida; Orlando Regional
Medical Center; Medical Director of
Orange County Emergency
Medical Service, Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Professor of Emergency Medicine
and Chairman, Department of
Emergency Medicine, Vanderbilt
University Medical Center;
Medical Director, Metro Nashville
EMS, Nashville, TN.
Mark Smith, MD, Chairman,
Department of Emergency
Medicine, Washington Hospital
Center, Washington, DC.
Charles Stewart, MD, FACEP,
Colorado Springs, CO.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
Emergency Medicine, University
of Alabama at Birmingham,
Birmingham, AL.
most are small and have differing methodology, which bars
easy comparison. Outcomes vary greatly depending on
patient characteristics, drug selection, dose, and mode of
delivery. The fact that the duration of AF differs tremen-
dously between trials significantly affects outcomes.
The American College of Cardiology, American Heart
Association, and the European Society of Cardiology, in
collaboration with the North American Society of Pacing
and Electrophysiology, have published a summary report of
practice guidelines for the management of patients with AF.1
This set of guidelines is evidenced-based and well done;
however, it largely tends to focus on the management of
AF/AFl outside the ED.
The newest version of the ACLS guidelines appears to
be more evidenced-based with respect to recommenda-
tions.2 The ACLS algorithm for the management of atrial
fibrillation is complex. Patients are classed according to
heart function (something not always known in the ED),
and treatment options depend partly on the duration of the
AF. Use of the guideline may be within the standard of care
for an ED physician, but it may be somewhat too complex
for other providers who may also manage these patients.
Epidemiology
The incidence of AF increases with age and approximately
doubles with each decade of adult life. This incidence will
likely continue to increase as the population ages.3 The
prevalence of AF in the adult population has been reported
to be 1%-4%, with up to 9% of patients over the age of 80
having AF.3,4 Women appear to have a slightly lower
prevalence than men, while it is uncommon in children
except after cardiac surgery.1
AF is the most common sustained arrhythmia in
medicine and is one of the most common arrhythmias seen
in the ED. It is associated with significant morbidity,
including embolic strokes, decreased exercise tolerance, and
tachycardia-induced myopathy. Mortality rates are doubled
in patients with chronic AF compared with controls.4 The
annual risk of stroke in patients with AF averages 5%, which
is 2-7 times the rate in people without AF. According to data
from the Framingham cohort, stroke severity tends to be
greater in patients with AF than those without the disease.5
AFl is also a common arrhythmia. It is most often
associated with cardiovascular and pulmonary disease, but
it can occur in those with normal hearts. AFl is associated
with atrial fibrillation in more than half the cases, and both
of the rhythms can be present on the same ECG (fib-flutter).
Like AF, its incidence increases with age. AFl is associated
with thromboembolic events, but probably to a lesser extent
than is seen with fibrillation.6
Etiology
The common causes of atrial fibrillation are listed in Table 1.
The emergency physician should first consider immediate
and life-threatening causes, such as cardiac ischemia,
congestive heart failure (CHF), and pulmonary embolism
(PE). AF occurs in up to 20% of patients who present with
Emergency Medicine Practice
acute myocardial infarction (MI).7 Idiopathic and cardiac
causes (such as hypertensive heart disease, valvular disease,
CHF, and coronary artery disease) account for the largest
percentage of AF.4,8 Thyroid disease is another important
consideration;9 in one series, it was responsible for 6.2% of
new-onset atrial fibrillation (NOAF) cases admitted to the
hospital.8 Moderate-to-severe hypothermia (< 32°C) is
frequently associated with AF.10 Electrolyte abnormalities
(hypokalemia and hypomagnesemia), as well as drug and
medication use (especially cocaine and theophylline
toxicity) can produce AF. Medical noncompliance in patients
with known AF accounts for a large percentage of cases of
rapid AF seen in the ED.
“Holiday heart syndrome” is a colorful term applied to
arrhythmias resulting from alcohol abuse, AF being the
most common presentation of this often-seasonal disorder.
Lowenstein et al found that alcohol caused or contributed to
35% of 40 cases of NOAF at a public hospital.11 Holiday
heart syndrome is most often reported in the setting of
alcohol intoxication, but it may be caused by mild alcohol
withdrawal as well.11 The mechanism of how alcohol causes
AF is unclear. Many of these cases spontaneously convert to
normal sinus rhythm within 24 hours.11 Holiday heart
syndrome should not be ascribed to the older patient or
those with cardiac disease until other etiologies have been
ruled out.
“A good head and a good heart are always a formidable
combination.”—Nelson Mandela
Pathophysiology
AF results from chaotic depolarization of atrial tissue. The
exact cause is not entirely clear, but multiple reentry circuits
or rapidly firing atrial foci are likely involved.1 The mecha-
nism most commonly reported in AFl involves a large
reentrant circuit within the right atrium around an anatomic
obstacle. Atrial distention contributes to AF, particularly
with certain types of valvular disease. There is a saying that
“AF begets AF,”12 meaning that the longer an individual is
in AF, the more likely he or she will stay in AF. This appears
to be the result of mechanical and electrical remodeling in
the atria. Atrial remodeling in AF appears to occur quickly,
Table 1. Etiology Of Atrial Fibrillation.
Cardiac Non-cardiac
• Ischemic heart disease • Pulmonary embolism
• Valvular disease • Idiopathic
• Hypertension • Medication
• Congestive heart failure noncompliance
• Sick sinus syndrome • Thyroid disease
• Pericarditis • Holiday heart syndrome
• Infiltrative heart • Medication use
disease • Electrocution
• Cardiomyopathy • Other pulmonary disease
• Cardiac surgery • Chest trauma
• Myocarditis • Hypokalemia
• Congenital heart • Hypomagnesemia
disease • Hypothermia
2 www.empractice.net • August 2002
is progressive, and may be persistent. However, it can be
reversed with early restoration and maintenance of sinus
rhythm.13 While mechanical dysfunction of the atria can
occur with prolonged AF, restoration of sinus rhythm
will generally restore atrial function. This process can take
2-4 weeks, during which time there is an increased risk
of thromboembolism.14
In AF and AFl, the atrioventricular (AV) node plays a
crucial role in modulating the ventricular response. The AV
nodal refractory period, the amount of concealed conduc-
tion within the node, the relative degree of sympathetic
tone, and the level of circulating catecholamines all interact
to determine the ventricular rate. The untreated heart rate in
a patient with NOAF will usually be 120-160 beats per
minute (bpm). In AFl, ventricular rates are usually around
150 bpm due to 2:1 conduction of flutter waves through the
AV node. The consequences of the resultant tachycardia in
untreated AF/AFl will vary depending on the ventricular
rate, underlying heart disease, duration of AF, co-morbidi-
ties, and other patient factors.
The spectrum of physiologic effects of a rapid ventricu-
lar response (rapid AF) is broad, ranging from asymptom-
atic to severe, life-threatening symptoms such as CHF,
syncope, and angina.15 A rapid ventricular response rate
increases oxygen demand and decreases diastolic filling
time. Patients with underlying coronary artery disease may
develop ischemia during periods of rapid ventricular rate.
In addition to rate-related problems in AF, the loss of the
“atrial kick” may lead to a significant decrease in cardiac
output. This is especially prominent in those with vascular
disease and in the elderly, in whom 30% of the cardiac
output may depend on the “atrial kick.”
Stagnant blood in flow through the atria can produce
cardiac clots and subsequent embolism. Stroke is often the
first presentation of AF.8,16 Atrial flutter, despite it being a
more organized process, also carries a risk of embolic
events.17 Intra-atrial clot has been documented by
transesophageal echocardiography in up to 21% of selected
hospitalized patients with AFl.18 The risk of clot develop-
ment in AFl can be due to the flutter itself or the fact that AF
and AFl often coexist.6,17
Differential Diagnosis
When considering the differential diagnosis, the emergency
physician must consider two important questions. First, is
this atrial fibrillation, atrial flutter, or some other arrhyth-
mia? Misdiagnosing ventricular tachycardia (VT) or Wolff-
Parkinson-White (WPW) syndrome as AF/AFl can be very
dangerous. VT is a regular wide complex rhythm, whereas
AF with a bundle branch block will demonstrate gross (or
occasionally subtle) irregularity when evaluated closely.
(WPW with AF is discussed in detail under the “Special
Circumstances” section later in this article.) Physicians often
mistake multifocal atrial tachycardia for AF, as it often
appears irregular. However, the presence of discreet P
waves of varying morphology and PR intervals will make
the diagnosis.
The second question to entertain is, what is the
August 2002 • www.empractice.net
rhythm’s underlying cause? The emergency physician must
always consider the “worst first,” which, in the case of atrial
fibrillation, would include PE (and other causes of hypoxia),
coronary ischemia, and CHF. Additionally, if the AF is chronic,
high ventricular rates may be due to fever, blood loss, stress,
dehydration, or drug toxicity.
Prehospital Care
The prehospital care of a patient starts with an evaluation of
the ABCs. The airway should be assessed and stabilized,
followed by an evaluation of the patient’s respiratory and
circulatory system. A rapid pulse should prompt care
providers to place the patient on the monitor and analyze
the rhythm. An unstable patient with atrial fibrillation who is
severely compromised needs emergent synchronized cardioversion.
If the patient is stable, then a brief history and physical
examination should be performed during transport. Medics
should apply oxygen (or maintain saturations at 94%
or above), establish an IV, and institute continuous
ECG monitoring.
The evidence for the management of AF in the field is
mostly based on data from the hospital, as there are very
few prehospital studies of this condition.19-22 Current ACLS
guidelines recommend IV calcium-channel blockers or ß-
blockers as first-line therapy in stable patients with rapid
AF.2 However, a recent small, retrospective study ques-
tioned the utility of prehospital rate control of rapid AF. The
study concluded that prehospital rapid AF is an infre-
quently encountered, predominantly hemodynamically
stable cardiac arrhythmia that is readily stabilized using
symptomatic or supportive care.19 This study suggests that
the use of IV diltiazem for the treatment of rapid AF in the
field might be unnecessary.
Given the data currently available, it is hard to recom-
mend universal use of prehospital agents to control rates for
rapid AF. Most patients appear to do well with basic
monitoring, oxygen, and supportive care. Certainly, special
circumstances (e.g., long transport times, moribund
patients) may dictate more aggressive interventions.
Emergency Department Evaluation
The management of uncontrolled atrial fibrillation involves
recognition, stabilization, diagnostic testing, and disposi-
tion. Part of stabilization may involve ventricular rate
control. Diagnostic testing should avoid needless studies yet
at the same time detect significant pathology. Because AF
can lead to stroke and other forms of thromboembolism, the
emergency physician must understand the appropriate
timing and role of anticoagulation and initiate this therapy
when appropriate. There is some recent evidence to suggest
that some patients with NOAF can be converted in the ED
and discharged.23,24
“We are adhering to life with our last muscle—the heart.”
—Djuna Barnes
Initial Stabilization
Immediately assess the unstable patient to determine the
3 Emergency Medicine Practice
need for airway control or emergent cardioversion. Perform
a brief, focused history and physical examination simulta-
neously with the initial interventions. Place patients on a
cardiac monitor, apply supplemental oxygen as needed,
and establish IV access. Once the patient is stabilized, a
more detailed history and focused physical examination
are indicated.
History
Some of the most important historical questions when
evaluating a patient with AF are summarized in Table 2.
Begin with questions that will determine stability (or lack
thereof), such as chest pain, dyspnea, and syncope. Some
patients may be relatively asymptomatic.
Palpitation is the most common presenting symptom
associated with AF,8 although chest pain, dyspnea, fatigue,
and lightheadedness are common. The character of the chest
pain (such as crushing, radiating to the left shoulder, etc.)
may provide clues to ischemia. Pleuritic chest pain can be
seen with PE or pericarditis. Syncope with AF is an uncom-
mon presentation that usually indicates significant disease
such as sinus node dysfunction, valvular aortic stenosis,
hypertrophic cardiomyopathy, cerebrovascular disease, or
an accessory pathway.
Establish whether the patient has experienced AF in the
past. Is this episode new in onset, a recurrence of previous
AF, or chronic in nature? Has the patient ever required
cardioversion? Ask about medications. Does the patient
report medications for an “irregular heart,” like digoxin,
amiodarone, or warfarin (Coumadin)? Other medications
such as thyroid supplements or theophylline suggest the
need to measure drug levels. The acuity of onset may guide
therapy as well as disposition. However, Holter monitor
data suggest that the time of symptom onset may be
unknown or unreliable.15,25,26
Determine risk factors for coronary artery disease and
PE. Ask about past medical history, drug and alcohol use,
and medication use, particularly in reference to previous
cardiovascular, pulmonary, and thyroid disorders. A history
of rheumatic fever or IV drug abuse provides clues to
underlying valvular disease. Ask if the patient has a known
pre-excitation syndrome (“I have W-P-something, Doc.”).
The review of systems should address any metabolic
disturbances or neurological symptoms, such as thyrotoxi-
cosis or acute neurologic events. Ask specific “thyroid
questions” about weight loss or gain, changes in menses,
change in hair loss or texture, and nervousness or behav-
ioral changes.
Physical Examination
The vital signs are crucial in the assessment of initial patient
stability. Palpation of an irregularly irregular pulse may be
the first clue to AF, while AFl usually presents with a
regular tachycardia. Consider evaluating AF patients with
very high heart rates (>160 bpm) for thyrotoxicosis, CHF,
PE, fever, dehydration, or acute blood loss. Conversely,
those with inappropriately low untreated heart rates with
NOAF may have underlying conduction abnormalities or
perhaps take medications that mask tachycardia.
Emergency Medicine Practice
Although blood pressure measurements in AF can vary
due to the irregularity of the pulse,27 this has minimal
clinical significance in the ED. It is important to note that a
“normal” systolic blood pressure reading of 100 can be
falsely reassuring. Patients who are chronically hypertensive
may be in shock at this pressure. Mental status is a better
indication of adequate cerebral blood flow.
Look to the respiratory rate and pulse oximetry reading
for clues to airway or respiratory compromise (perhaps due
to PE, CHF, or pneumonia).
Fever may indicate sepsis, endocarditis, PE, or thyroid
storm. In patients with very rapid ventricular response,
consider obtaining a rectal temperature, especially in the
elderly. In one recent study, rectal thermometry detected a
fever in 15% of geriatric patients who were afebrile orally.28
Patient stability can usually be determined by vital
signs, pulse oximetry, and a brief mental status exam. If the
patient is stable, perform a head-to-toe examination.
Perform a good neurological examination, as patients in AF
can present with stroke as the first indication of AF.16 Subtle
findings, such as tremor, eyelid retraction, hyperhidrosis,
hyperpigmentation, vitiligo, or alopecia, suggest underlying
autoimmune or thyroid dysfunction. During examination of
the neck, pay special attention to the thyroid gland and neck
veins. Palpate the thyroid for tenderness and/or nodularity.
Patients with AF exhibit a loss of alpha waves in the jugular
venous pulse and demonstrate variable force in the pulsa-
tions of the carotid arteries. Auscultate the heart for rate,
rhythm, murmurs, and additional heart sounds. In AF, the
first heart sound usually varies in intensity. Murmurs
suggest the presence of valvular heart disease. Look and
listen for signs of heart failure, including jugular venous
distention, rales, wheezes, and pedal edema.
“Sometimes the heart sees what is invisible to the eye.”
—H. Jackson Brown, Jr.
Diagnostic Tests
Most patients with NOAF will require some testing in
the ED.29 It is important to note that some diagnostic
recommendations are arbitrary, since there are few, if any,
prospective studies evaluating their utility. It is almost
axiomatic for an ECG and a chest x-ray to be ordered on all
patients with new-onset or uncontrolled AF. Other tests
Table 2. High-Yield Historical Questions.
Have you had atrial • palpitations?
fibrillation before, and if so: • weakness?
• for how long? • lightheadedness?
• what are you treated • confusion?
with?
• are you on digoxin or Do you have a past medical
warfarin? history of:
• are you compliant? • cardiac, pulmonary, or
thyroid disease?
Do you have associated • coronary artery disease,
symptoms, such as: or risk factors for
• chest pain? pulmonary embolism?
• dyspnea? • drug and alcohol use?
• syncope? • rheumatic fever?
4 www.empractice.net • August 2002
should be based on patient presentation and risk factors for
other underlying disease.
Electrocardiogram
An ECG is the gold standard for the diagnosis of AF/AFl.
Obtain an ECG on anyone with suspected or proven AF/
AFl to establish the diagnosis, rule out other dysrhythmias,
evaluate for ischemic changes, and look for signs of
previous cardiac disease (e.g., prior MI, bundle branch
block, pre-excitation, and left ventricular hypertrophy
[LVH]). Furthermore, an evaluation of the RR, QRS, and QT
intervals is important when considering the use of certain
medications, particularly antiarrhythmics.
Several rules can help establish the correct diagnosis on
the ECG. (See Table 3.) First, the RR intervals are almost
always irregularly irregular during AF. (See Figure 1 and
Figure 2.) When the ventricular rate is very slow or very fast
during AF, the RR intervals can appear regular on a quick
visual inspection; thus, careful scrutiny of the ECG is
important. Calipers are helpful. Doubling the paper speed
on the monitor or ECG (double-speed strip) to 50 mm/sec
can also demonstrate irregularity in very fast rates. In one
study of 45 difficult, narrow complex tachycardias (heart
rate range, 150-250 bpm), the correct diagnosis improved
from 63% using the standard 25 mm/sec ECG to 71% when
the 50 mm/sec speed was used.30 Also, the absence of P
waves helps exclude other supraventricular arrhythmias,
such as multifocal atrial tachycardia, that can also appear
irregular. “Fibrillatory waves” are not always visualized in
all patients with AF; conversely, baseline noise or artifact on
the ECG can sometimes simulate these waves in patients
who are not in AF.
An irregular tachycardia with wide QRS complexes can
Table 3. ECG Diagnosis Of Atrial Fibrillation.
• Irregularly irregular RR intervals
• Absence of P waves
• Irregular fibrillatory wave forms (best seen in V1)
Figure 1. Atrial fibrillation with rapid ventricular
response in a 76-year-old man with breathlessness.
Note the irregularly irregular ventricular rhythm. Sometimes
on first look, the rhythm may appear regular, but on closer
inspection it is clearly irregular.
Used with permission from: Jenkins & Gerred,
www.ecglibrary.com.
August 2002 • www.empractice.net
be a diagnostic dilemma. True irregularity typically rules
out ventricular tachycardia and leaves a diagnosis of a
supraventricular tachycardia with aberrant conduction.
The most common causes are AF/multifocal atrial tachycar-
dia with underlying bundle branch block and/or Wolff-
Parkinson-White (WPW) syndrome. (See Figure 3 and
Figure 4 on page 6.) The absence of P waves establishes
the diagnosis of AF. In this setting, ruling out pre-excitation
syndrome (WPW) is crucial. Patients with WPW who are
given AV nodal blocking agents can suffer ventricular fibrillation
arrest.31 Suspect pre-excitation syndrome in younger
patients with AF and those with ECG findings that
suggest pre-excitation. These findings include very fast
rates (RR > 250), presence of a delta wave, and wide or
bizarre QRS complexes.
The appearance of atrial flutter on ECG is more
organized than AF. (See Figure 5 and Figure 6 on page 6.)
Many patients have a sawtooth pattern of regular atrial
activation called flutter waves, particularly visible in leads
II, III, and aVF. Untreated, the atrial rate typically ranges
from 200-300 bpm with flutter waves inverted on the ECG
in leads II, III, aVF, and upright in lead V1. The wave
activation in the right atrium can occasionally be reversed,
resulting in flutter waves that are upright in leads II, III,
aVF, and inverted in lead V1. Two-to-one AV block is
common, producing a ventricular rate of 150 bpm that can
be mistaken for another supraventricular tachycardia due to
a regular-appearing ventricular response. AFl can coexist
with AF and can be present on the same ECG.
There are some other “tricks” to picking up AFl on the
ECG that involve modified chest leads, such as the Lewis
lead and the modified chest lead 1 (MCL1). To monitor the
Lewis lead, place the right arm electrode is over the right
side of the sternum at the second intercostal space and the
left arm electrode over the fourth intercostal space (again,
on the right side of the sternum). The tracing is then
recorded on lead I.32 This lead, which is often perpendicular
Figure 2. Atrial fibrillation with pre-existing LBBB in a
60-year-old woman with hypertension.
Sometimes this can be confused with ventricular tachycardia,
but closer inspection can identify the irregularity. The
irregularly irregular rhythm suggests AF. Features of typical
left bundle branch block include wide QRS (> 120 ms), no
secondary R wave in lead V1, and no lateral Q waves.
Used with permission from: Jenkins & Gerred,
www.ecglibrary.com.
5 Emergency Medicine Practice
to atrial depolarization, may show the flutter pattern.
The use of certain maneuvers to increase the degree of
AV block and slow the QRS rate, such as the Valsalva
maneuver, carotid massage, or adenosine, can also help
determine the rhythm in cases in which it might be unclear.
However, some general caution with the use of adenosine in
wide complex rhythms may be warranted. Cases of
deterioration with its use in ventricular tachycardia and
WPW have been reported, but these cases are rare (the
pooled literature actually appears to support the overall
safety of adenosine in this setting).33 However, if the rhythm
is definitely an irregular wide complex tachycardia,
adenosine is not effective in terminating or slowing AF and
thus is not indicated.
Chest X-Ray
A chest x-ray should be obtained in cases of NOAF/AFl,
Figure 3. Wolff-Parkinson-White syndrome with atrial
fibrillation in a 47-year-old man with a long history of
palpitations and, lately, blackouts.
Note the irregularly irregular, wide complex tachycardia.
Impulses from the atria are conducted to the ventricles via
either both the AV node and accessory pathway (producing a
broad fusion complex), or just the AV node (producing a
narrow complex without a delta wave), or just the accessory
pathway (producing a very broad “pure” delta wave). People
who develop this rhythm and have very short RR intervals are
at higher risk of VF.
Used with permission from: Jenkins & Gerred,
www.ecglibrary.com.
Figure 5. Atrial flutter in a 68-year-old lady on digoxin
complaining of lethargy.
Atrial flutter often produces a characteristic “sawtooth” or
“picket-fence” waveform of an intra-atrial re-entry circuit,
usually at about 300 bpm. This lady was taking rather too
much digoxin and has a very slow ventricular response.
Used with permission from: Jenkins & Gerred,
www.ecglibrary.com.
Emergency Medicine Practice
particularly if there is hypoxia or the history and physical
examination suggest cardiac or pulmonary disease.
Evaluate the chest x-ray for the presence of a pulmonary
mass, elevated hemidiaphragm, infiltrate, or CHF. The size
and shape of the cardiac silhouette may hint at cardiomy-
opathy or valvular disease. The classic “water-bottle” heart
with clear lung fields suggests cardiac tamponade. Straight-
ening of the left cardiac border on the PA film can be caused
by the dilation of the left atrial appendage that can occur in
mitral stenosis/regurgitation. Remember, there can be an
association between a right middle lobe infiltrate and AF.
Look at the chest x-ray for the signs occasionally seen in PE
like Hampton’s hump or Westermark’s sign (although
infiltrates, atelectasis, or blunting of the costophrenic angle
are more likely presentations of this disease).
Laboratory Tests
Thyroid Studies
Although it may have an overall low yield,34 a screening
TSH should be obtained in older patients (> 55) with NOAF.
The elderly can often have very atypical presentations of
hyperthyroidism or thyrotoxicosis with very few, if any, of
Figure 4. Wolff-Parkinson-White syndrome with atrial
fibrillation in a 23-year-old man with episodes of
palpitations.
Used with permission from: Jenkins & Gerred,
www.ecglibrary.com.
Figure 6. Atrial flutter with 2:1 AV conduction in a 57-
year-old lady with palpitations.
The sawtooth waveform of atrial flutter can usually be seen in
the inferior leads II, III and aVF if one looks closely. Sometimes
the rapid atrial rate can be seen in V1. Suspect atrial flutter with
2:1 block when you see a rate of about 150 bpm.
Used with permission from: Jenkins & Gerred,
www.ecglibrary.com.
6 www.empractice.net • August 2002
the other classic signs and symptoms (like buggy eyes,
sweating, tremors, or diarrhea).35,36 Development of AF in
patients with hyperthyroidism likely accounts for some of
the increased mortality from cardiovascular and cerebrovas-
cular disease in these patients.37 Consider obtaining a TSH
in younger patients with signs of hyperthyroidism, espe-
cially those with high heart rates, or when the ventricular
rate is particularly difficult to control.
Complete Blood Count
A routine CBC is a low-yield test in most cases of NOAF;
however, the presence of anemia may be an important
finding. A hemoglobin should be performed when there are
physical signs of anemia or a history of recent blood loss. A
WBC may be elevated as a nonspecific stress reaction or can
suggest infection but has limited overall utility. A platelet
count should be obtained in patients at risk for thrombocy-
topenia when anticoagulation is being considered.
Chemistries
While they are often ordered routinely, serum chemistries
rarely affect the management of NOAF. Order them if the
patient is taking diuretics or if there are other reasons for an
electrolyte abnormality. It is important to identify hypokale-
mia when considering the use of certain antiarrhythmics, as
this combination is associated with an increased incidence
of torsades de pointes.38,39 Remember that serum magne-
sium levels do not correlate well with total body magne-
sium and are of little value. Check a BUN/Cr in patients on
diuretics and in those with a history of dehydration, renal
insufficiency, or signs of fluid overload.
Drug Levels
Obtain digoxin levels on patients taking this drug. Noncom-
pliance with digoxin often results in a rapid ventricular
response in those with chronic AF. Although many
dysrhythmias can be associated with digoxin toxicity
(paroxysmal atrial tachycardia with block, bidirectional
ventricular tachycardia, accelerated junctional rhythm), the
finding of AF with a slow ventricular response should
prompt its consideration. Digoxin toxicity (but not digoxin
use) is a relative contraindication to electrical
cardioversion/defibrillation, as case reports of asystole after
such attempts to treat tachydysrhythmias in this setting
have occurred.40
Theophylline use or toxicity can cause AF; obtaining a
level in patients on this drug is indicated.9
Coagulation Studies
Signs and symptoms of coagulation abnormalities can
usually be detected on the history and physical examina-
tion. Their presence should prompt an evaluation of the
coagulation studies and a platelet count. Obtain a protime
(PT) and international normalized ratio (INR) if the patient
is on warfarin and consider a baseline partial thromboplas-
tin time (PTT) if the patient will be placed on heparin.
Cardiac Markers
AF is a common complication of acute coronary syndrome
August 2002 • www.empractice.net
(ACS), and its development tends to be associated with
higher 30-day and six-month rates of mortality and stroke.7
Up to 20% of patients who present with acute MI will
develop AF in close proximity to the acute MI.7,41 The
incidence of MI in patients with AF on presentation to the
ED may be as high as 15% or higher.42
Despite the fact that AF is a common complication of
AMI, there are some reasonable—albeit mostly retrospective—
data to suggest that not all patients with NOAF require a
routine “rule out” set of cardiac enzymes as part of their
diagnostic evaluation. Enzymes should be reserved for
patients suspected of being at risk for having ACS.42-45 Based
on the current data, at-risk patients would include those
with ECG changes suspicious for ischemia or underlying
heart disease (prior MI, LVH, and BBB); those with signifi-
cant risk factors for CAD (patients older than 65, smokers,
or those with diabetes mellitus, hypertension, high choles-
terol, or previous CAD); and those with symptoms that
otherwise would be considered for possible angina (chest
pain, pressure, significant dyspnea, CHF, etc.).42-46 Other-
wise, patients with NOAF may not require routine “rule
out” enzymes according to the available data. Still, caution
is advised until further research is performed. (For a more
detailed discussion on this topic, see the “Disposition”
section later in this article.)
Tests For Pulmonary Embolism
Medical textbooks sometimes suggest that patients with
NOAF must be admitted to the hospital to rule out PE.
However, studies (mostly retrospective) imply that patients
with NOAF who otherwise are not suspected of having PE
are unlikely to have the disease and do not require additional
testing.45 It is advisable to exclude this diagnosis if the
patient has significant risk factors for PE or suggestive
clinical findings.
Echocardiography
Echocardiography (echo) can be a valuable tool to evaluate
cardiac abnormalities, and it may have an occasional role in
the acute management of NOAF in the ED. Consider it
(when available) in an unstable patient with AF. Echo can
demonstrate signs of right heart strain that might indicate a
diagnosis of PE.47 Echo can also help evaluate left ventricu-
lar function and the presence of valvular or pericardial
pathology. While most patients with NOAF will get an echo
at some point, this can often be done as part of the inpatient
workup, or possibly on an outpatient basis. Routine use of
echo in the ED is not recommended at this time.
There is some emerging literature to suggest that
transesophageal echo (TEE) may help guide acute conver-
sion of patients with AF of acute or unknown duration,
although this is a controversial topic.1,48-54 It is important to
note that a transthoracic echo is inadequate for the exclusion
of clot, as it cannot visualize the left atrial appendage very
well.50,52,55 If patients have AF of a short duration (<48 hours)
and no clot is present on TEE, some data support early
medical or electrical cardioversion.
Echo might also help stratify who might be successfully
converted and remain in normal sinus rhythm. Some data
7 Emergency Medicine Practice
suggest that left atrial size assessed by echo may predict the
outcome of cardioversion and subsequent maintenance of
sinus rhythm. However, not all studies support this.56,57
Treatment
Determining the stability of a patient is the first task when
considering treatment of AF/AFl, and this is not as black-
and-white as texts often imply. The ACLS guidelines
suggest that signs and symptoms of instability with AF
include “chest pain, shortness of breath, dyspnea on
exertion, [and] altered mental status.” The guidelines
recommend electrical cardioversion over medical therapy
for the unstable patient.2 In real practice, stability is not
always a dichotomous issue, but rather a continuum. Surely,
the patient who is hypotensive, diaphoretic, and who has
altered mental status is unstable, but not everyone with a
little bit of chest pain requires a jolt of electricity. The
emergency physician must always recognize the truly
unstable patient in addition to being prepared for possible
deterioration of the stable patient.
Unstable Patients
If the patient with rapid AF is unstable, then emergent direct
current cardioversion (DCC) is the treatment of choice. Fortu-
nately, this is a rare event; unfortunately, DCC in this setting
may be associated with several problems, most pressing of
which is that it might not work. An underlying illness such
as a low ejection fraction,57 thyrotoxicosis, or mitral stenosis
may make conversion impossible, difficult, and/or only
short-lived. A dilated left atria and a longer duration of AF
may decrease conversion rates.56-58 (Factors associated with
failed cardioversion are summarized in Table 4.)
Acute cardioversion is associated with a significant risk
of thromboembolism during or shortly after the procedure,
particularly if the AF has been present for more than 48
hours. (For more information regarding this topic, see the
“Anticoagulation” section later in this article.) However,
emergent DCC should not be withheld in the unstable patient due
to this risk. Even if the patient is successfully cardioverted, he
or she might not necessarily improve due to lack of me-
chanical contraction of the atrium (“atrial stunning”).
Therefore, although DCC should be attempted in the
unstable patient, failure or short-lived effects should be
anticipated, and other interventions including rate control
agents should be considered. Additionally, given the
likelihood of failure and risks of thromboembolism, rate
control might be the first line of treatment in the unstable
patient with known chronic AF.
Table 4. Factors Associated With Failed Cardioversion.
• Underlying illness—congestive heart failure, thyrotoxico-
sis, valvular disease
• Dilated left atrium
• Longer duration of atrial fibrillation
• Too low energy
• Technique
• Other patient factors
Emergency Medicine Practice
Pad Location
Successful cardioversion requires defibrillation of a critical
mass of the atria. To achieve this goal, a variety of anatomic
pad placements can be used. The apex-anterior, apex-
posterior, and the anterior-posterior are all effective.56,58
Anterior-posterior placement is possibly more useful than
the anterior-apex method,59,60 although there is controversy
regarding this subject.58 Interestingly, some patients who
do not respond to one method occasionally respond to
another method.56
Technique
Regardless of the pad placement, use a synchronized
delivery to minimize the small risk of inducing ventricular
fibrillation. For optimal energy delivery, try to shock in full
expiration (the patient’s, not yours), maintain a good
interface between the pads and the patient, and avoid the
breast tissue in women. Because firm pressure can decrease
impedance, there may be some theoretical advantage to
using the old standard manual pads as opposed to the self-
adhesive pads. However, the old paddles require the use of
gel and will not always fit on a chest littered with electrodes.
In fact, studies have shown similar efficacy with both the
paddles and adhesive pads.56
Energy Level
There are few or no data regarding the optimal starting
energy level to use in unstable patients with AF. However,
some inferences can be drawn from the literature regarding
DCC in stable patients. Although the American Heart
Association recommends starting at 100J,2 only 50% or fewer
of stable patients will convert with that energy.57,60,61 For this
reason, starting at a higher energy level seems appropriate
in an unstable patient. Data show that roughly 75% of
patients with AF will convert with 200J,60 and current trends
in the literature suggest this approach.1,59 Others recommend
using an even higher initial energy (360J), particularly if the
AF duration has been more than 48 hours. This is based on a
study by Joglar et al, who showed an initial single shock
success rate of 14% with 100J, 39% with 200J, and 95% with
360J in patients with AF for more than 48 hours.61 Interest-
ingly, the cumulative energy for successful cardioversion
was less if 360J was initially used. There was no evidence of
myocardial damage as assessed by cardiac troponin I levels
in the group receiving the high-energy shocks. Lack of
myocardial damage from DCC in AF was also seen in
another study using even higher energies.62 Thus, when
choosing an initial energy level for DCC of an unstable patient in
rapid AF, start with at least 200J, and consider 360J.
Energy levels as high as 720J have been used for
elective conversion of refractory chronic AF;63 however,
special defibrillators are required to administer those energy
levels (plus generous sedation). In addition, a method of
“double shocks” using both the apex-anterior and the
anterior-posterior methods at the same time has been
reported with some efficacy in a small number of patients.64
Pretreatment with ibutilide prior to DCC in stable patients
will increase shock success and decrease the energy
required.65 However, this might not be feasible in an
8 www.empractice.net • August 2002
unstable patient, as 1 mg of ibutilide IV is given over 10
minutes (a possibly lethal interval in an unstable patient)
prior to DCC.65
Biphasic Defibrillators
If you have a biphasic defibrillator (which requires you to
know your particular model), the manufacturer recom-
mends paddle placement for AF in the anterior-posterior
position with the anterior pad just right of the sternum and
the posterior pad over the left scapula.66 Start with 120J
synchronized, biphasic shock. Two studies suggest that a
rectilinear biphasic waveform shock in AF has better success
with less energy requirement compared to monophasic
waveform shock.66,67
Atrial Flutter
As in the case of an unstable patient with AF, DCC is also
the initial treatment of choice in the unstable patient with
AFl. Approximately 90%-100% of stable patients with AFl
respond initially to DC cardioversion;24,68 however, less in
known about success rates in unstable patients. Stable
patients with AFl often require less energy to convert than
those patients with AF,58,69 and the current ACLS guidelines
suggest starting with 50J.2 However, there are scarce data in
the current literature regarding the optimal initial energy
choice for DCC of AFl in the unstable patient. There is
reasonable evidence to suggest that in a certain percentage
of patients with AFl, starting with lower energy levels will
induce AF (an objectionable event in an already unstable
patient).58,68,69 This would suggest that 200J (or more) may be
preferable to the recommended 50J.68,69
Rate Control
Once the patient with rapid AF has been stabilized, the next
goal is ventricular rate control. It is the ventricular rate that
mostly governs symptoms. Rate control will likely improve
the patient’s overall hemodynamic status, resulting in better
ventricular filling, less myocardial oxygen demand, and
improved cardiac output. Many options for rate control are
available, and emergency physicians must understand the
indications, contraindications, and nuances of each of these
interventions. Sometimes patients with chronic AF will present
acutely with a rapid ventricular response due to a physiologic
stress, such as fever, dehydration, pain, or anemia. Treatment in
such cases would be acetaminophen, fluids, opioid analgesics, and
blood transfusion, respectively—not cardioactive drugs.
The most common choices for rate control agents can
be found in Table 5. Calcium-channel blockers, ß-blockers,
and digoxin are not conversion agents and are not intended
for such purposes. While 25%-60% of patients with NOAF
may spontaneously convert while on these agents, patients
who receive no intervention or placebo demonstrate similar
conversion rates.70-73 Amiodarone possesses antiarrhythmic
properties in addition to its rate control effects. When
choosing a rate control agent, strongly consider whether or not the
patient could have an accessory pathway; the use of an AV nodal
blocking agent would be contraindicated in that situation. (See
the “Special Circumstances” section later in this article.)
Cardioversion
DCC is the quickest way to obtain rate control, even in a
stable patient. However, it requires procedural sedation,
with all of its accompanying risks. Acute DCC is also
associated with some potential complications, particularly
embolic events and cardiac arrhythmias, which should be
minimized prior to “elective” cardioversion of a stable
patient (see below). However, in an unstable patient, DCC
may save a life. It has been shown to be safe and efficacious
in the hands of emergency physicians when managing

Table 5. Rate Control Agents.

Modality Administration
Electrical cardioversion Start with 200J synchronized, monophasic shock or 120J synchronized, biphasic shock*
Calcium-channel blockers
• Diltiazem 0.25 mg/kg IV over two minutes followed by a second bolus of 0.35 mg/kg IV over two minutes
if there is inadequate response at 15 minutes
or 5 mg increments slow IV up to 50 mg followed by drip 5-15 mg/h
• Verapamil 2.5-5.0 mg over 2-3 minutes followed by 5-10 mg in 15-30 minutes if necessary ± drip 5 mg/h
or up to 0.005 mg/kg/min
ß-blockers
• Metoprolol 5 mg IV every 5 minutes up to 15 mg
• Propranolol 1 mg IV every 2 minutes to max of 5-8 mg
• Atenolol 5 mg IV over 5 minutes; repeat after 10 minutes if inadequate response
• Esmolol 0.5 mg/kg IV bolus over 1 minute, followed by a 0.05-0.2 mg/kg/min IV infusion. Repeat cycle and
increase drip if no effect.
Cardiac glycoside
• Digoxin Load 0.5 mg IV and repeat 0.25 mg every 4-6 hours for three doses
Others
• Amiodarone 150 mg IV over 10 minutes followed by infusion of 1 g over six hours. May repeat bolus if needed.
• Magnesium 2 g bolus over 10-15 minutes followed by 1 g/h infusion
• Clonidine 0.1 mg PO
* With atrial flutter, consider lower starting energy (100J), monophasic to start

August 2002 • www.empractice.net 9 Emergency Medicine Practice

stable23 as well as unstable patients with AF.
Calcium-Channel Blockers
Calcium-channel blockers (CCBs) are the first-line treatment for
rate control in rapid AF.74 They are efficacious, act quickly, and
are relatively safe. The two most commonly cited agents
used in the ED are diltiazem and verapamil; much contro-
versy exists in the literature as to which agent is better.75-79
They both act on the sinoatrial and AV nodes but do not
prolong the refractoriness of accessory pathways. Both
agents reduce systemic vascular resistance, and the most
frequent complication is hypotension.80 The risk of hypoten-
sion can be minimized by the use of IV calcium as a pretreatment
prior to giving these drugs, or as a rescue agent if hypotension
occurs.81-83 CCBs are effective in controlling ventricular
response during exercise in chronic AF.84
Pretreatment With Calcium
If a patient develops hypotension in the setting of receiving
a CCB, it can often be reversed or attenuated with IV
calcium. Life-threatening tetany has also been reported after
IV diltiazem that responded to IV calcium chloride.85
Emergency physicians treating AF/AFl patients with CCBs
should have quick access to IV calcium.
Alternatively, calcium as a pretreatment should be
considered in patients with marginal blood pressure prior to
receiving a CCB.81-83 Calcium has been shown to be effica-
cious in preventing the negative inotropic effects of the
CCBs but does not affect the drugs’ chronotropic effects.
Side effects of calcium pretreatment are rare and mild,
including flushing and a feeling of “generalized heat”
lasting 2-3 minutes.81 While the optimal dose for pretreat-
ment is not known, it seems reasonable to use 1-3 cc of
calcium chloride or 5-10 cc of calcium gluconate.
Verapamil vs. Diltiazem
Comparison trials of CCBs (mainly verapamil and
diltiazem) with placebo in rapid AF show that the CCBs are
more than 90% successful in reducing heart rate.80,84,86-89 This
holds true for patients with AFl as well.80,87 CCBs quickly
control ventricular response—often in less than five
minutes—when given intravenously.87,90 CCBs are more
effective for acute rate control than digoxin.90-92 In a compari-
son study, Schreck et al showed a statistically significant
reduction in heart rate for diltiazem-treated patients at five
minutes vs. 180 minutes in digoxin-treated patients.90 The
combination of IV diltiazem with IV digoxin may result in
more efficacious ventricular rate control with fewer
fluctuations than that of IV diltiazem alone;93 however, some
feel the addition of digoxin is unnecessary. In critical care
patients, diltiazem slows the heart rate more profoundly
than IV amiodarone, although it produces significantly
more hypotension.94
So which agent should we use—diltiazem or
verapamil? Advocates of diltiazem state that it has less risk
of hypotension and that patients can be maintained on a
drip after the initial bolus. Verapamil users state that neither
agent has been shown to be definitively better and that
verapamil is cheaper. There is some truth to both sides of
Emergency Medicine Practice
this debate. Most of the debate regarding which agent
produces less hypotension stems from animal data and
studies on diseased human heart tissue performed by Bohm
et al.75,77 They suggested that verapamil caused greater
reduction in contractility than diltiazem, but these findings
have been challenged.76,80,84,88,90
The only “head-to-head” human trial did not settle the
debate.78 This randomized, double-blind, crossover trial
compared the effects of IV diltiazem and verapamil in 17
adults with AF or AFl and a baseline heart rate of 120 bpm
or higher. No pretreatment with calcium was used in the
trial. Both agents showed similar efficacy for heart rate
control at two minutes; however, three of the 17 patients
initially entered into the study developed symptomatic
hypotension after verapamil, which prompted withdrawal
from the study. Hypotension was considered life-threaten-
ing in one patient who was found to have an ejection
fraction of 20%. This study has led many to declare that
clearly diltiazem is better than verapamil because of the
hypotension. However, the trial was small, and the dosing
protocol of the study still leaves this question open to
debate. In the patient who has a borderline blood pressure,
it may be prudent to use diltiazem. However, the choice of
drug may be less important than how much and how
quickly it is given. Titrate CCBs over several minutes.
Another reason that diltiazem is commonly quoted as
being better than verapamil is that diltiazem can be
followed by a drip. A diltiazem bolus followed by a drip did
show better efficacy compared with a diltiazem bolus
followed by placebo over 24 hours, which is not surprising
given the half-life of the drug. However, a verapamil drip
has been described and is effective.95 (However, since not
many people are familiar with it, you might get some blank
stares if you order one.) Some evidence suggests that
patients may be quickly switched to oral forms of the CCBs
to maintain adequate rate control, possibly avoiding the
issue of a drip altogether.96 While verapamil is cheaper than
diltiazem by about $10, this difference is unlikely to start a
run on the bank.
Contraindications/Cautions
Kuhn and Schriger published a retrospective review of
patients who received verapamil despite a contraindication,
and they reported a higher incidence of adverse outcomes
and drug failures in that group compared with those who
did not have a contraindication.97 CCBs are contraindicated
in patients with an accessory pathway, because these
patients may develop a rapid ventricular response and
induction of ventricular fibrillation secondary to reflex
sympathetic stimulation of the accessory pathway.31,33
Hypotension is the most common significant side effect of
CCBs.81-83 (See Table 6 on page 11.)
Special mention of the use of CCBs in patients with
signs of CHF is worthwhile. CCB use in patients with CHF
is controversial according to some authors, but the literature
suggests overall safety and efficacy.84,98-100 Rapid AF with
CHF is not necessarily a contraindication to CCB use; in fact,
it may be part of the appropriate treatment, particularly in
relatively stable patients, and perhaps in unstable patients in
10 www.empractice.net • August 2002
whom cardioversion fails. (Remember that the moribund,
severely dyspneic patient with acute CHF and rapid AF
should be considered unstable and likely have attempts at
cardioversion prior to medical therapy.)
In the setting of rapid AF with signs of CHF, the use of
CCBs may improve cardiac function by slowing ventricular
rate, decreasing oxygen demand and increasing diastolic
filling time. Several small studies in patients with Class 3 or
4 heart failure have established CCB relative safety in this
setting.84,99,100 In a study by Goldenberg et al of 37 patients
with rapid AF and moderate-to-severe CHF, 97% responded
well to one or two doses of diltiazem followed by a drip.
Hypotension was the most common adverse event (11%),
but in all cases, patients responded with nonpharmacologic
treatment. No patient was reported to have an exacerbation
of the CHF due to the diltiazem bolus or the drip.84
Heywood et al showed similar results with eight out of nine
patients with clinical signs of CHF and rapid AF responding
to diltiazem without clinical and objective signs of worsen-
ing.100 However, in the trial by Phillips et al, the three
patients who received verapamil and became hypotensive
had moderate-to-severe LV dysfunction, leading the authors
to recommend that IV verapamil be administered with
caution to control the ventricular response in patients with
AF or AFl and concomitant LV dysfunction.78
Dosing
The recommended manufacturer dosing for diltiazem is
0.25 mg/kg IV over two minutes followed by a second
bolus of 0.35 mg/kg IV over two minutes if there is inad-
equate response at 15 minutes.79,80 Due to the occurrence of
hypotension, some authors have recommended starting at
even lower doses, perhaps 0.15 mg/kg IV,79 although
published data with this dose are limited. Others have
recommended giving 5 mg increments IV slowly up to a
maximum of 50 mg. The initial dose(s) can be followed by a
drip of 5-15 mg/h for maintenance therapy.80 Verapamil
dosing should be 2.5-5.0 mg over 2-3 minutes followed by 5-
10 mg in 15-30 minutes if necessary. As discussed previ-
ously, it can be followed by a drip as well, typically starting
at 5 mg/h or up to 0.005 mg/kg/min.79 With either drug,
start with lower dosages, particularly in patients with
underlying CHF or borderline blood pressure, and perhaps
the elderly.
ß-Blockers
A number of different ß-blockers are available (see Table 5
on page 9) that are highly effective in controlling the rapid
ventricular rate associated with NOAF. ß-blockers work by
decreasing the conduction through the AV node. They act
Table 6. Contraindications To The Use Of Calcium-
Channel Blockers.
Second- or third- degree heart block or sick sinus syndrome
Severe hypotension
Cardiogenic shock
AF/AFl with a known or presumed accessory bypass tract
Concurrent use or in close proximity to IV ß-blockers
Ventricular tachycardia
August 2002 • www.empractice.net
rapidly after IV administration, and adequate rate control
can often be established within two minutes of drug
administration.101-103 There is likely some benefit to using
these agents as the first line in clinical scenarios associated
with high adrenergic tone, such as thyrotoxicosis, acute
hypertensive crisis, and MI. Particularly in MI patients,
ß-blockers decrease both short-term and long-term morbid-
ity and mortality.
Contraindications to ß-blockers are very similar to
CCBs, with the same risks in accessory pathways, VT, and
high-degree blocks. In addition, ß-blockers are also contrain-
dicated in patients with active bronchospasm or severe
asthma, although the ß1-selective agents may have fewer
problems associated with their use. ß-blockers do have
negative inotropic effects and thus must be used with
caution in patients with LV dysfunction. The most fre-
quently reported significant side effect is hypotension.101-103
Esmolol, a ß1-selective agent, has a rapid onset and an
ultra-short half-life (7-9 minutes), which has some benefits
in patients with rapid AF. Plattia et al found IV esmolol to
have similar efficacy to verapamil for rate control in AF.101
Hypotension was reported in both groups, but the authors
preferred esmolol because of its short half-life and noted
that the infusion could be stopped if the patient suffered
side effects. Treatment with esmolol is somewhat cumber-
some, however, as it requires repeated bolus dosing and
multiple infusion steps. It is also expensive compared with
other agents. Alternatives to esmolol include IV propranolol
(a nonselective ß-blocker) and metoprolol (a ß1-selective
agent). Both of these agents have the disadvantage of longer
half-lives, but the advantages of much lower cost and ease
of administration. Propranolol is a non-cardioselective ß-
blocker and must be used cautiously in patients with a
history of bronchospasm.
Digoxin
Digoxin has been used to treat AF for more than two
centuries. Until recent years, digoxin was almost mandatory
in a patient with NOAF. It has fallen out of favor due to its
lack of efficacy compared to other agents, its hazardous
side-effect profile, and the arrival of newer agents. It is now
considered second (or third) line for rate control.104 Al-
though digoxin has some direct influence on the atria and
AV node, it affects the autonomic nervous system as well. In
AF, the drug exerts its main electrophysiologic effect
indirectly, by modulating vagal tone. In the resting patient
on digoxin, vagal influences on the AV node and atrium are
enhanced, and, as a result, the ventricular rate is slowed.
As digoxin’s predominant rate control effects are due to
increased vagal tone, it loses its effectiveness as a rate
control agent when a patient is active or if there is increased
autonomic sympathetic stimulation. This loss of vagal
stimulation in the setting of increased sympathetic tone
would also make digoxin a poor choice in patients with
rapid AF associated with fever, thyrotoxicosis, hypoxia, or
acute blood loss. Some authors suggest that the physician
should ask the question, “If this patient were in sinus
rhythm, would he or she have a sinus tachycardia?”104 If the
answer is yes, then digoxin alone is unlikely to control the
11 Emergency Medicine Practice
ventricular rate, and other agents should be considered.
Digoxin does have some modest positive inotropic effects
likely due to effects on calcium, and it might still have a role
in the management of AF patients with CHF or low cardiac
output. One study showed digoxin’s use with esmolol may
have helped prevent hypotension, perhaps due to its
positive inotropic effects.102 Another study showed some
possible benefit using a combination of diltiazem and
digoxin over digoxin alone in 52 patients with rapid AF.93
Some of the other limitations of digoxin in rapid AF are
its slow onset time and some potential toxicity, particularly
with long-term use. It takes 30-180 minutes to slow the
ventricular rate significantly,70,71,105 compared with CCBs and
ß-blockers, which often work within minutes.90,101 Digoxin
blocks the AV node but not accessory pathways and thus is
contraindicated in patients with WPW. It does not convert
AF, and there is no evidence that it has primary antiarrhyth-
mic actions. This has been shown consistently in three
randomized clinical trials in which digoxin, in the absence
of heart failure, was no better at conversion than pla-
cebo.70,71,105 Furthermore, based on animal data, digoxin may
increase the chance of a recurrence of AF after restoration of
sinus rhythm by attenuating the recovery from electrical
remodeling of the atria.106 A small upside of digoxin is that it
costs about as much as water (unless you buy the ultra-
pure, spring water in designer bottles). In summary, digoxin
is a drug that will likely continue to fall in and out of favor.
However, except maybe in rare circumstances (e.g., CHF), it
is a drug that has been replaced with better, safer, and more
efficacious agents.
Amiodarone
Although amiodarone has been used to control AF, it
is not approved in North America for any supraventricular
arrhythmia. Despite this, IV amiodarone has been evaluated
in the treatment of AF for its rate control properties and
antiarrhythmic effects. Amiodarone is classified as a Class
III antiarrhythmic agent but also does have effects similar
to Class I, II, and IV agents. Most studies with amiodarone
show that it slows ventricular rate in rapid AF typically
with significant rate control effects within 20 minutes of a
bolus administration.72,94,107,108 Conversion rates are highly
variable (4%-100%) depending on study characteristics.
Amiodarone is slower in onset and less effective than
diltiazem for rate control but may have less associated
hypotension in critically ill patients.94 Several dosing
regimens of amiodarone have been used, and no large
trial comparing the efficacy and safety of the different
dosages in rapid AF has been performed. If you choose
to use amiodarone for rapid AF, give an initial loading
bolus followed by an infusion.94
Despite causing a prolongation of the QT, amiodarone
appears to have a relatively low frequency of pro-arrhyth-
mic effects,109 and the incidence of torsades de pointes is less
than 1% according to two evidence-based reviews.107,110
Amiodarone in the acute setting can result in hypotension,
which is usually transient and well-tolerated. Hypotension
generally responds to IV fluids and stopping the drug.72,110-112
Occasional, seemingly rare episodes of LV failure have been
Emergency Medicine Practice
reported,108,113 as have exacerbations of bradyarrhythmias.114
However, amiodarone appears to have few or no negative
inotropic effects and appears relatively safe in patients with
CHF and LV dysfunction.107 Superficial thrombophlebitis
can occur when the drug is administered through a periph-
eral vein.108,111,113 Because it works on accessory pathways as
well as on AV nodal conduction, amiodarone may be useful
in WPW and other pre-excitation syndromes. However, case
reports of VF have been reported with its IV administration
in WPW patients,115 and the drug’s peculiar combination of
different electrophysiologic actions might cause differing
effects when given intravenously vs. orally. Disadvantages
include cost, variable effectiveness, and side effects that can
be significant if given long term. The drug is generally well-
tolerated in the short term.
The current literature does not support the routine use
of amiodarone in AF in the ED for treatment of most cases of
AF/AFl. An emergency physician might consider its use in
the patient with an irregular wide complex tachycardia.
Magnesium
Magnesium, which some advocates declare a “wonder
drug,” is useful in the management of ventricular
dysrhythmias, and it has been studied in atrial arrhythmias
as well. Magnesium likely exerts its effects in AF by
decreasing conduction within the AV node. Several small
studies have suggested its effectiveness as a rate control
agent in rapid AF;116-119 however, its use is most often
recommended as adjunctive therapy, commonly with
digoxin. Both Brodsky et al120 and Hays et al116 have reported
synergistic effects of digoxin with magnesium. Usually
magnesium is given as a bolus of 2 g over 10-20 minutes,
sometimes followed by an infusion (studies use different
regimens). Rate control is relatively rapid, reported to be
within five minutes.116 It is well-tolerated, with mild
flushing, warmth, and tingling accounting for the majority
of side effects, which are likely related to the rate of the
infusion.116 Occasionally, with rapid infusion or large doses
(8-10 g), respiratory muscle fatigue, hypotension, and
cardiac pauses can be seen.120 The drug can accumulate
rapidly in patients with renal failure and should generally
be avoided in these patients. In addition to its good safety
profile, magnesium has the benefits of being very inexpen-
sive, readily available, and easily administered.
Studies with magnesium show that it controls rate
when given alone116 and can convert 50%-60% of patients
with recent-onset atrial tachyarrhythmias.117,119,120 A study
comparing magnesium with amiodarone in critical care
patients with atrial tachyarrhythmias (most of which were
AF) found that magnesium controlled ventricular rate just
as well as amiodarone.118 In addition, at 24 hours, the
magnesium group had significantly more patients convert
to sinus rhythm compared with the amiodarone group.
Similarly, in a study of 46 patients who presented with a
prolonged episode of paroxysmal AF, more patients (57%)
converted with magnesium at six hours compared to
diltiazem (22%).119 Although largely unproven, magnesium
therapy might be particularly useful in alcoholics, who
typically suffer from total body magnesium depletion.121 In
12 www.empractice.net • August 2002
summary, magnesium is efficacious as a rate control agent
in rapid AF, and it might have some antiarrhythmic effects
compared to standard agents.
Anticoagulation
Traditionally, in the ED, the patient with NOAF has been
stabilized, rate controlled, and admitted for further treat-
ment, workup, and testing. Recently, this dogma has been
challenged in the literature and in practice. Some suggest
that certain patients with NOAF can be converted (either
chemically or electrically) in the ED and sent home. This
practice is somewhat controversial.43-45 Whether patients
with AF/AFl are admitted, converted acutely, or dis-
charged, thromboembolism is a concern. Some data do
suggest who is at most risk and how anticoagulation
might prevent stroke or other complications. However,
anticoagulation is not without its own risks. Roughly
4%-18% of patients with conventional anticoagulation
therapy for seven weeks surrounding conversion will
have a minor bleeding episode, while 1.5%-2.0% will have
a major event.48,54
AF, and to a lesser extent AFl, are associated with an
increased long-term risk of stroke6,16,17 as well as an in-
creased risk of thromboembolism in the post-conversion
period.14 The dysfunctional atria in AF/AFl cause stagnation
of blood flow, which can lead to clot formation and subse-
quent embolization prior to or after conversion.14,122 Conver-
sion of AF to sinus rhythm results in further transient
mechanical dysfunction of the left atrium and left atrial
appendage, known as “stunning.”122 Recovery of the
mechanical dysfunction may take up to several weeks,
which could explain why patients with a negative TEE prior
to cardioversion can develop post-conversion thromboem-
bolic events. The overall risk of thromboembolism in all
patients with AF after conversion appears to be as high as
5%-7% without anticoagulation.1,48,123 The overall risk
appears to drop to 0%-1.6% if conversion is preceded by 2-4
weeks of anticoagulation or shorter-term anticoagulation
and a negative screening TEE.48,54,123 (Circumstances
associated with a high risk of thromboembolic events are
summarized in Table 7.)
The point at which a patient with NOAF develops a
significant risk of clot formation and subsequent emboliza-
tion is controversial. Traditionally, it has been felt that the
risk of clot formation is very low in the first 48-72 hours of
the onset of AF, and acute conversion without prior
Table 7. Risk Factors For Thromboembolism With
Conversion Of Atrial Fibrillation.
Advanced age
Rheumatic mitral valve disease
History of diabetes
Previous stroke or transient ischemic attack
History of hypertension
Left ventricular dysfunction
Prolonged atrial fibirllation
Hypercoagulability
Presence of clot on TEE
August 2002 • www.empractice.net
anticoagulation was presumed safe. One study confirmed
that the occurrence of embolic events in patients without
prior anticoagulation was very low, with either spontaneous
or active conversion within the first 48 hours.123 The rate of
embolic events in this study (0.8%, with a confidence
interval up to as high as 2.4%) was very similar to the
reported incidence of embolism after “standard therapy” of
anticoagulation for 3-4 weeks followed by conversion.
Within the past few years, the safety of acute conver-
sion of AF with an onset time of less than 48 hours has been
questioned. Patients can be wrong or uncertain regarding
the duration of symptoms.15,25,26 The use of TEE has revealed
that up to 13% of patients with onset time of AF of less than
72 hours have a clot present in the atrium, which appears to
place them at a higher risk of embolization.124 For this and
other reasons (such as atrial stunning), some authorities
recommend that most NOAF patients should be anticoagu-
lated (unless contraindicated) prior to conversion regardless
of the onset time, and the anticoagulation should continue
after conversion for a period of 3-4 weeks.48,125
Role Of Transesophageal Echocardiography
TEE may help determine the duration of anticoagulation
necessary before cardioversion. A large, multicenter,
randomized, prospective clinical trial has compared
conventional therapy to the use of TEE with brief prior
anticoagulation for the conversion of patients with onset of
AF of more than 48 hours.54 The study showed similar
embolic rates and risk of hemorrhage in conventionally
treated patients (anticoagulation for three weeks prior to
conversion) and in patients converted after brief anticoagu-
lation and a negative TEE. Patients in the TEE group were
treated with IV unfractionated heparin (target-activated
PTT, 1.5-2.5 times the control value), and cardioversion was
performed within 24 hours. However, this technology is
readily available in few EDs.
Recommendations
So what should emergency physicians do regarding
anticoagulation for those patients with AF they see in the
ED? The answer is not completely straightforward. (See also
the Clinical Pathway, “Anticoagulation With Atrial Fibrilla-
tion,” on page 17.)
AF Duration Of 48 Hours Or More
In patients whose duration time in AF is unknown or
clearly 48 hours or more, the literature supports anticoagu-
lation prior to conversion. This is true even if a TEE will
be used in the decision analysis. Whether anticoagulation
needs to begin in the ED prior to hospital admission
remains unknown.
AF Duration Of Less Than 48 Hours
With patients whose onset time is known to be less than
48 hours, the role of anticoagulation is less clear.
Options include:
1. Perform blind cardioversion (no echo) in low-risk
patients; avoid in high-risk patients (see Table 7).
2. Perform a TEE:
13 Emergency Medicine Practice
 • if negative, cardiovert the patient without
anticoagulation.
• if positive, anticoagulate for three weeks with
follow-up TEE.53,55
3. Anticoagulate all patients regardless of risk.
A discussion of these options with the patient’s primary
care physician and/or a cardiologist may be helpful. If
a patient with NOAF is already on anticoagulants (war-
farin), cardioversion in those with an adequate INR
might be reasonable.
Anticoagulation does not always require an admission.
In the past, if the decision to start anticoagulation was made,
then heparin was started in the ED and the patient was
admitted. However, a dose of heparin followed by immedi-
ate cardioversion is not warranted in those with AF of
greater than 48 hours’ duration except perhaps in unstable
patients.1 (Anticoagulation should not delay cardioversion
for the moribund patient, but it should be started afterward
if not contraindicated.)
The introduction of low-molecular-weight heparin
(LMWH) creates the opportunity for outpatient anticoagula-
tion of AF/AFl. Two small studies have evaluated LMWH
in patients with AF and found it to be efficacious at preven-
tion of embolization in patients with chronic AF.126,127 A TEE-
guided conversion trial with the use of LMWH is currently
ongoing (ACUTE II), and a cost-analysis model suggests
this approach could be cost-effective.51
“I believe every human has a finite number of heartbeats.
I don’t intend to waste mine running around doing exercises.”
—Neil Armstrong
Disposition
Traditionally, patients with NOAF were admitted to the
hospital for further treatment, evaluation, anticoagulation,
and possible conversion. Admission has also been recom-
mended for ruling out serious causes of AF that might cause
morbidity and mortality, namely MI and PE. Recently, this
routine admission of all patients with NOAF has been
challenged in the literature. However, support for discharg-
ing low-risk patients is largely retrospective and must be
interpreted with caution.
New-Onset Atrial Fibrillation
And Myocardial Infarction
Several studies have evaluated the usefulness of admitting
or obtaining enzymes in all patients with NOAF to “rule
out” MI.42-46 In a small retrospective study, Friedman et al
showed that all of the MIs (n=5) in the setting of NOAF
could have been predicted on arrival to the ED from a set of
high-risk criteria. These criteria included left ventricular
hypertrophy, ECG evidence of old MI, cardiac-sounding
chest pain, and cardiac symptoms of less than four hours.44
Friedman et al then prospectively examined a group of
patients admitted with NOAF (without obvious evidence of
MI on arrival) to identify risk factors associated with in-
hospital complications.42 Of note, 15% of the patients
Emergency Medicine Practice
admitted developed enzymatic evidence of non-Q-wave MI.
Risk factors for complications (including MI) were signs of
CHF on arrival and lack of conversion to normal sinus
rhythm within six hours. Zimetbaum et al published a
prospective cohort study in which they reported on 109
patients who underwent a standard “rule-out MI” proto-
col.46 They found ECG changes to be the most important
discriminator as to which patients were likely to develop
MI. Chest pain was a very sensitive, but nonspecific, marker
of MI. However, this study shows that those patients with
NOAF and chest pain (how many don’t have some chest
pain?) require admission to evaluate for ischemia. After
pooling the data from these studies and another retrospec-
tive study by Mulcahy et al,43 it does appear that some very
select patients with NOAF are at low risk for MI and may
not require admission. (See Table 8.) It is important to note
that these criteria have not been prospectively evaluated.
Admission Criteria
Mulcahy et al published a study that specifically looked at
NOAF patients and tried to address the question of when
admission is medically justified.43 They looked retrospec-
tively at 216 patients admitted to the hospital with NOAF.
They believed that only 143/216 (66%) of the admissions
were medically justified based on complications they had or
developed in the hospital. Of the 143 patients who were
ultimately classified as medically justified admissions, 140
(98%) could have been predicted from criteria fulfilled while
in the ED. They suggested that patients with NOAF as the
sole reason for admission (33% in this study) “can be
managed as outpatients if they are hemodynamically stable
and the ventricular rate can be controlled in the ED.”
However, the authors rightfully point out that their study
was retrospective and should be validated in a prospective
trial. It is interesting to note, however, that two of the three
patients who would not have met the author’s admission
criteria, but were still admitted, died. In addition, patients
categorized as not medically justified still spent several days
in the hospital.128
Discharge Criteria
So who are the truly low-risk patients who might go home
safely? Suggested criteria at this time would include:
• younger patients (<60);
• patients without significant comorbid disease;
Continued on page 19
Table 8. Predictors For Myocardial Infarction
In New-Onset Atrial Fibrillation. *
ECG changes
Other ECG findings—left ventricular hypertrophy, bundle
branch block, old MI
Chest pain
Signs of congestive heart failure
Hypotension
Suspicion for MI
Age over 65
*Important to note—these have not been validated in a large,
prospective fashion.
14 www.empractice.net • August 2002
 Clinical Pathway: Managing Unstable Patients
With Atrial Fibrillation
Assess patient stability

Unstable Stable

➤
Anticipate instability
Electrical cardioversion (Class I)

➤
• Monophasic 200J-360J (Class I)
• Biphasic 120J (Class II)
• If atrial flutter, may consider lower energy Go to “Clinical Pathway: Rate Control For Stable Patients
• Anticipate failure With New-Onset Atrial Fibrillation With Rapid Ventricular
Response” on page 16
➤

Success?

Yes No
➤

• Reassess stability • Increase energy level incrementally (Class I)

• Further stabilize*
• Begin workup
➤

• Anticipate
decompensation Success?
• Admit
(Class I) Yes No
➤

➤
• Reassess stability Suspicion for accessory pathway?
• Further stabilize*
• Begin workup Yes No
➤

➤
• Anticipate
decompensation
• Admit • Procainamide (Class II) • Ibutilide 1 mg over 10
(Class I) or minutes followed by
• Ibutilide 1 mg IV over 10 cardioversion (Class II-III)
minutes (Class II-III) • Rate control agents
or • Diltiazem (Class II)
• Amiodarone (Class II-III) • Magnesium (Class II-III)
or • Amiodarone (Class II-
• Further electrical III)
cardioversion • Procainamide (Class II)
• alternate paddle • Further cardioversion
placement (Class II) (Class II)
• alternate paddle
placement

* Consider post-conversion or concomitant anticoagulation when possible and not contraindicated—especially if onset unknown
or greater than 48 hours

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright ©2002 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.

August 2002 • www.empractice.net 15 Emergency Medicine Practice

 Clinical Pathway: Rate Control For Stable Patients
With New-Onset Atrial Fibrillation With Rapid Ventricular Response
Anticipate instability

➤
Suspicion for accessory pathway?

Yes No
➤

➤
Indication for anticoagulation? Suspicion for MI/thyrotoxicosis?

Yes No Yes No
➤

➤
Contraindication to Contraindication
Anticoagulate (Class I) ➤ sedation? to ß-blocker?

Yes No Yes No
➤

➤
• Procainamide (Class II) • Electrical cardioversion Significant? Use ß-blocker for rate
• Amiodarone (Class III) (Class I-II) control (Class I-II)
Yes No
or
➤

➤
• Procainamide (Class II)
Congestive heart
or Avoid ß-blocker Esmolol
failure or
• Amiodarone (Class III) (Class I) (Class II)
borderline blood
pressure?

Yes No
➤

➤
Contraindication to calcium-channel blockers? Contraindication to calcium-channel blockers?

Yes No Yes No
➤

Consider:
• Esmolol (Class II-III)
• Cardioversion (Class II)
• Consider anticoagula-
tion and sedation
Pretreat with calcium—
5 cc calcium gluconate
slow IV (Class I-II)
➤
➤
Consider: Consider pretreatment
• Esmolol (Class II-III) with calcium (Class II)
• Cardioversion (Class II)
• Consider anticoagu-
➤
lation and sedation

issues issues • Verapamil (Class I-II) 2.5

• Magnesium (Class II-III) Diltiazem (Class II-III) • Magnesium (Class mg IV q10-15min until
• Digoxin (in addition to • 5 mg slow IV q5min II-III) rate <120, conversion,
another agent) (Class II) until rate < 120, • Digoxin (in addition hypotension, max 20 mg
• Amiodarone (Class II-III) conversion, or 50 to another agent) or
mg max (Class II) • Diltiazem (Class I-II) 0.25
• Consider drip after • Amiodarone (Class mg/kg IV over 2 min
bolus (Class I-II) II-III) (followed by bolus of 0.35
mg/kg IV over 2 min if
inadequate response at
15 minutes) until rate
The evidence for recommendations is graded using the following scale. For complete definitions, see back page.
<120, conversion,
Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful.
Good evidence provides support. Class III: May be acceptable, possibly useful. Fair-to-good evidence provides hypotension, max 50 mg
support. Indeterminate: Continuing area of research.
➤

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and Consider adjunct treatment
may be changed depending upon a patient’s individual needs. Failure to comply with this pathway • Magnesium (Class II)
does not represent a breach of the standard of care. • Digoxin (Class II)
Copyright ©2002 EB Practice, LLC. 1-800-249-5770. No part of this publication • Avoid ß-blockers (Class
may be reproduced in any format without written consent of EB Practice, LLC. I-II)

Emergency Medicine Practice 16 www.empractice.net • August 2002

 Clinical Pathway: Anticoagulation With Atrial Fibrillation
Therapeutic on anticoagulant?

Yes No
➤

➤
Onset time of AF?
Consider for cardioversion
(Class II)
< 48 Unknown or

➤
hours > 48 hours

Risk for thromboembolism?

• Advancing age Ongoing or active bleeding?
• Previous cerebrovascular
accident/transient Yes No

➤
ischemic attack
• Mitral valve disease
• LV dysfunction • Control bleeding • Anticoagulate (Class II)
• History of hypertension, • Reassess risk for • Observe for spontane-
diabetes mellitus anticoagulation ous cardioversion
• Hypercoagulable • Do not convert actively (Class II)
unless unstable or
(Class II-III) • Arrange inpatient or
High Low outpatient conversion
➤

depending on stability
Significant risk of • Consider blind (Class II-III)
bleeding or cardioversion (Class II)
anticoagulation or
contraindicated? • Observe for spontaneous
cardioversion (Class II)

Yes No
➤

• Consider blind cardioversion (Class II) • Strongly consider anticoagulation prior to cardioversion
or (Class II-III)
• TEE (Class II)

(+) clot (-) clot

➤

• Admit and observe Consider cardioversion

(Class indeterminate) (Class II-III)
• Reassess risk of
anticoagulation (Class
indeterminate)

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright ©2002 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.

August 2002 • www.empractice.net 17 Emergency Medicine Practice

 Clinical Pathway: ED Cardioversion Of Stable Patients
With Atrial Fibrillation*
• Consider need for anticoagulation (see “Clinical Pathway: Anticoagulation With Atrial Fibrillation“ on page 17)
• Anticipate instability

➤
Contraindication for sedation?

Yes No
➤

➤
Contraindication to medical cardioversion?
• Sedation and analgesia (Class I) followed by:
• hypokalemia
• Direct current cardioversion
• suspected magnesium deficiency
200J monophasic (Class I-II)
• prolonged QT
120J biphasic (Class II)
• history of torsades de pointes
May consider lower starting energy in AFI, very recent onset
AF, and those without suspected structural heart disease
Yes No
➤

Arrange DCC when
sedation possible (Class II)
➤
• Ibutilide (Class II)
Success?
• Procainamide (Class II)
• Amiodarone (Class II-III)
• Propafenone/flecainide Yes ➤ No

➤
(Class II) (Only available
PO in the U.S. Slower in
onset.) • Reassess patient (Class • Increase energy level
indeterminate) (Class I-II) to max 360J
• Arrange further monophasic
workup, disposition
(Class II)

➤
Success?

Yes No
➤

➤
• Reassess patient (Class Consider:
indeterminate) • Change pad place-
• Arrange further ment (Class II)
workup, disposition • Biphasic defibrillator
(Class II) (Class II)
• Medical
cardioversion**

* Only done in the ED after careful consideration of risks and benefits. Remember, 50% of patients with NOAF will convert
spontaneously within 24 hours.
** Success rate after failed electrical cardioversion not expected to be high

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright ©2002 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.

Emergency Medicine Practice 18 www.empractice.net • August 2002

Continued from page 14
• patients in whom there is no clinical suspicion of PE
or MI;
• patients in whom the AF converts in ED or the rate is
controlled; and
• patients for whom follow-up is ensured.
Cost-Effective Strategies For New-Onset Atrial Fibrillation/Atrial Flutter
1. Avoid “shotgun testing.”
Not every patient who comes to the ED with NOAF requires a
CBC, chemistries, toxicology screen, alcohol level, thyroid
function panel, d dimer, V/Q scan, coagulation studies, and a
bedside echo. Testing should be focused, based on patient
stability and findings of the history and physical examination.
An alcohol level and drug testing in the right clinical scenario
and a TSH in the elderly may be of some value.
Caveat: Most of the findings suggesting that certain “low-
risk” patients with NOAF do not require cardiac enzymes or
evaluation for PE come from retrospective data; further
study is required. Do not assume that because a patient has
been drinking alcohol that the NOAF is only due to holiday
heart syndrome. Unstable patients may benefit from having
a bedside echo (after cardioversion) to rule out right heart
strain (suggestive of a PE) or acute valvular dysfunction.
2. Do the simple stuff.
When trying to diagnose a complex arrhythmia, consider
simple, easily available tests. Use calipers to determine
whether the arrhythmia is regular or irregular. In the case of a
rapid ventricular response of unknown etiology, press the
speed button on the ECG to obtain a “double-speed” tracing
that may demonstrate irregularity in the R-R interval. When
atrial flutter is a possibility, move the chest leads to obtain a
Lewis lead or modified chest lead that could emphasize the
flutter waves.
Caveat: Sometimes these interventions still leave you in
doubt. When the nature of the arrhythmia is uncertain,
assume the worst and call for help.
3. Consider (very carefully) ED conversion and discharge
with close follow-up in some patients.
Not all patients with NOAF require admission, particularly
those with a very low suspicion of coronary artery disease, PE,
or significant heart disease. If a patient spontaneously
converts and does not appear to have another indication for
admission, it may be safe to send that patient home with
close follow-up. This is especially true in young patients with
an obvious case of holiday heart syndrome. Patients who are
already anticoagulated for another reason may be candidates
for early conversion in the ED with possible discharge.
Caveat: Most of the evidence for discharge of patients with
AF is derived from retrospective data. Some authors
consider this practice risky. Also, given that up to 40%-70%
of patients with NOAF will spontaneously convert within
the first 24 hours, careful observation for conversion will
avoid the unnecessary use of electricity or antiarrhythmic
drugs in a majority of patients.
August 2002 • www.empractice.net
The elderly and those with chest pain should usually be
admitted. In some cases, patients may benefit from a brief
workup (including cardiac enzymes and echocardiography)
for risk stratification in an observational-type unit.129 In this
unit, patients might be rate controlled, started on anticoagu-
lation (possibly LMWH), and discharged to see if spontane-
4. Do not admit all NOAF patients to the CCU.
At some hospitals, all NOAF patients are admitted to the CCU
to “rule out MI.” This practice is not cost-effective, as the vast
majority of patients with NOAF do not have acute coronary
syndrome. The overall incidence of MI with NOAF appears to
be 5%-15%. Most patients who do not otherwise appear at
risk for acute coronary syndrome (hemodynamically stable,
no ECG changes, no ongoing chest pain or significant
symptoms, no prior MI or CHF, age < 65, no other cardiac risk
factors) can be admitted to a telemetry bed (and may not
require cardiac enzymes at all).
Caveat: The evidence for this practice comes largely from
retrospective data and must not take the place of good
clinical judgment.
5. Avoid using the latest and greatest (and most expensive)
drug on the market when what we have works as well
or better.
Newer (read “expensive”) drugs for the treatment of AF are
heavily promoted. However, just because an agent is newer or
more expensive does not necessarily mean it is better.
Magnesium, an inexpensive agent with few side effects, is as
effective as amiodarone for rate control and conversion of
AF—and you’ll never see it advertised in the latest journal.
When new drugs are trialed, their use is often limited to a
very select group of patients. Only when used in the general
population do all of the complications come to light.
6. When considering elective conversion of stable AF in the
ED, consider it again—and then if you still want to do it,
consider electrical cardioversion over medical therapy.
Electrical cardioversion of NOAF in the stable patient
has a reported success rate of 90%-100% vs. chemical
therapy (which has a reported success of roughly 50%).
Electrical cardioversion is effective and safe in the ED. While
the use of electrical cardioversion is not without risks,
antiarrhythmics are associated with significant
proarrhythmic potential, and patients often require a
prolonged period of observation.
Caveat: Some consider elective conversion of AF to be
outside the routine practice of emergency medicine. In
addition, procedural sedation (necessary for conversion of
the stable patient) carries a potential risk of aspiration and
airway compromise. Patients should be NPO for several
hours prior to the procedure, something that’s not always
practical in the ED. Before considering elective conversion
in the ED, a conversation with the patient’s primary care
physician and/or cardiologist is prudent. Discuss
anticoagulation during this conversation. ▲
19 Emergency Medicine Practice
ous conversion occurs. Upon follow-up, an outpatient TEE
could guide further therapy and intervention.
Early follow-up is mandatory for all NOAF patients
being discharged. Patients must be given good discharge
instructions regarding the importance of follow-up and
signs or symptoms that should prompt a return to the ED.
Cutting-Edge/Controversy
“Elective” Conversion In The ED
“Elective” conversion of certain stable patients with AF/AFl
in the ED is gaining some momentum in the literature. It
remains controversial, however. “Pro-ED converters” point
out that the literature supports early conversion to prevent
atrial remodeling and increase the likelihood of maintaining
normal sinus rhythm.12,13 They point out the (relative) safety
of early conversion if the arrhythmia has been present for
less than 48 hours. Furthermore, early conversion can
reduce the need for anticoagulation and the associated risks
of bleeding. Many of these patients may be discharged to
outpatient testing and evaluation, which decreases costs.
Opponents argue that a stable patient should never be
converted electively in the ED. They emphasize the risk of
thromboembolism and argue that patients should be
admitted for heparinization prior to cardioversion. They
also argue that the majority of patients with NOAF require
Ten Pitfalls To Avoid
1. “The patient was intoxicated, so this was clearly holiday
heart syndrome. When his atrial fibrillation spontaneously
converted, I sent him home with family to sober up.”
Unfortunately, the patient you thought was “just drunk” was 68
years old, a diabetic, and a longtime smoker who told the
nurse (but not you) that he had “crushing chest pain.” If you
had pulled his old ECG, you would have noted some
disturbing new changes. Although he converted shortly after
arrival, the signs and symptoms of ischemia associated with
significant cardiac risk factors mandated admission.
2. “The ibutilide worked great. The patient felt much better
and wanted to go home immediately.”
While ibutilide works to convert AF/AFl approximately
40%-50% of the time, it has significant risks—most notably
torsades de pointes and other ventricular tachyarrhythmias.
The pharmacokinetics of the drug require a four-hour
period of monitoring after use.
3.“This was a case of routine atrial fibrillation in a young
female. Yes, she felt slightly short of breath, but her heart rate
was 160. I controlled her rate and even admitted her to the
hospital. Her physician said he would start anticoagulation
therapy in the morning if she did not convert.”
Had you only asked about the long plane ride she had just
been on, and the fact that she was recently diagnosed with
ovarian cancer, you might have more strongly considered
the diagnosis of pulmonary embolism. Deal with the atrial
fibrillation, but also consider the differential diagnosis,
Emergency Medicine Practice
hospitalization to facilitate a complete diagnostic evaluation.
In addition, conversion in the ED can greatly increase the
length of stay in the ED, as the use of some of the chemical
agents requires prolonged observation even after successful
conversion (e.g., ibutilide). Because a large percentage of
patients (40%-71%) with NOAF spontaneously convert in
the first 24 hours,70-73,105 some have questioned whether
patients should be exposed to the risk of conversion agents
or electricity without a trial of observation.72 Finally, some
ask whether patients with AF should be converted at
all,130,131 as the benefit of conversion and maintenance of
sinus rhythm is not always greater than rate control alone132
(certainly a minority opinion). The Atrial Fibrillation
Follow-up Investigation of Rhythm Management (AFFIRM)
study is a large, ongoing, prospective trial that addresses
this issue.133
Both electrical and chemical interventions are reason-
able options for elective cardioversion in the ED.23,24 With
either method of conversion, determine the possible need
for anticoagulation. Before proceeding, explain the risks and
benefits and obtain informed consent.
Electricity
Despite all of the newer drugs for chemical cardioversion,
the traditional gold standard is DCC. DCC is relatively safe
and has a 90%-100% acute success rate in various settings,
especially those causes associated with significant
morbidity and mortality.
4. “I gave the patient the commonly quoted starting dose
of diltiazem, a 20 mg bolus. It is unfortunate that she got
profoundly hypotensive, seized, and arrested, but I did
nothing wrong.”
Had you considered that the patient to whom you gave the
diltiazem weighed no more than 80 pounds soaking wet, you
might have started with a lower dose and titrated it slowly. You
can always give more drug, but it’s hard to take it back. Also,
you might have given calcium pretreatment or at least had it
at the bedside prior to pushing the diltiazem when the
patient’s starting blood pressure was 100/60 mmHg. Always
have the nurses give these medications slowly over a few
minutes (and never “push” them) to minimize hypotension.
5. “When the diltiazem didn’t give a good response, I
decided to try another drug. I believe her complete heart
block was from the acute coronary syndrome she was
having, not what I did.”
A classic blunder—giving an IV ß-blocker soon before or after
an IV calcium-channel blocker. It is safe to give one of these
two classes of drugs IV—cautiously—if the patient is on an
oral version of the other class, but not both intravenously.
6. “I thought the patient might be having acute coronary
syndrome and therefore used a ß-blocker for its beneficial
effects. The patient just seemed to decompensate around
Continued on page 21
20 www.empractice.net • August 2002
including the ED.23,24 (The sustained conversion rates,
particularly in certain groups of patients, are much lower.)
The downsides of the procedure include the need for
sedation and the attendant possibility of respiratory failure.
The emergency physician must also be prepared to intubate
and manage induced arrhythmias, although most of these
are transient and resolve spontaneously.
To perform DCC, take the usual precautions with
sedation. Place the patient on a monitor, oxygen, pulse
oximeter, and obtain good IV access. Have airway and
cardiac resuscitation equipment readily available. Adminis-
ter adequate sedation whenever possible, as it is considered
a travesty to cardiovert someone who is completely awake
(the exception being the moribund patient, in whom
sedation may be a luxury neither the physician nor the
patient can afford). Once a state of relaxation is obtained,
cardiovert with paddles in the anterior-posterior position
starting with 200J for AF and 100J for AFl using a standard
monophasic defibrillator. If using a biphasic defibrillator,
begin with 120J for AF and 70J for AFl. If maximal energy
levels do not convert the patient, change the paddle
positions to the anterior-lateral position and reattempt.
One study and one abstract have been published that
address electrical cardioversion of patients in the ED. The
study, published in Annals of Emergency Medicine by Michael
et al,23 was a retrospective study of 289 conversions of AF in
Ten Pitfalls To Avoid (continued)
that same time—an unfortunate coincidence.”
While there are some advantages to the use of a ß-blocker
in NOAF in the setting of acute coronary syndrome or
thyrotoxicosis, remember the drug’s contraindications. Had
you noticed the significant wheezing on examination and
stopped to think that the patient was frequently on home
nebulizers for asthma, you might have given a calcium-
channel blocker instead (or at least given a short-acting
ß-blocker such as esmolol).
7. “It was clearly irregular. I’m positive it was atrial
fibrillation, and that’s why I gave diltiazem. I was quite
surprised when the heart rate actually got worse.”
Had you looked more carefully at the ECG, you might have
noticed the delta wave and prolonged QRS duration that
suggested a reentrant pathway. Consider an accessory
pathway in AF with any of the following: a wide complex
irregular rhythm (especially if the complexes vary within the
ECG), a very fast rhythm (RR > 250), a history of an accessory
pathway (don’t miss this one), and a younger patient with
NOAF. Giving AV nodal blocking agents is contraindicated
when an accessory pathway is present. Theses drugs block the
AV node, thus making the conduction down the accessory
pathway worse, with a resultant increase in ventricular rate. A
safer choice might be procainamide, amiodarone, or
cardioversion, depending on the situation.
8. “Sure her AF was one week old, but I did a TEE that
showed no left atrial clot, and therefore I cardioverted the
August 2002 • www.empractice.net
the ED. Eighty of the patients, most of whom had failed
chemical conversion in the same visit, had electrical
cardioversion, with an 89% success rate. Emergency
physicians performed 93% of these electrical cardioversions.
There were no reported complications, and most of the
patients were discharged. The authors reported this practice
to be “safe and effective” but admitted that this needs to be
validated in a prospective trial. Also, it should be noted that
the follow-up in this study was not ideal. An abstract also
reports on the electrical cardioversion of patients in the ED.24
This study, which appears to be retrospective, reported 315
out of 350 successful electrical cardioversions by emergency
physicians, with an overall 2.5% rate of complications, most
of which were reported as minor. As of this printing, a
MEDLINE search has not revealed this study published in
its entirety, which limits further interpretation of the results.
Drugs
Several classes of antiarrhythmic drugs have potential for
use in the ED for conversion of AF. (See Table 9 on page 22.)
As of this time, ibutilide is the only IV medication with FDA
approval for acute termination of AF and AFl. However,
many other drugs have been studied for this indication,
including a few agents that are not available intravenously
in the United States (dofetilide, sotalol, flecainide, and
propafenone). Comparison between the different antiar-
patient and sent her home. She was just one of the
unfortunate people who had a thromboembolic event.”
Although there is some suggestion in the literature that the
method you used might be reasonable, the data suggest that
anticoagulation would be required even with a negative TEE in
this situation. If someone has been in AF for more than 48
hours, TEE may not show a clot, but there may still be as high
as a 2% incidence of thromboembolism after conversion.
Patients with AF for greater than 48 hours (and sometimes
even less) likely benefit from anticoagulation therapy at least
after the procedure, and possibly before.
9. “She didn’t look bug-eyed to me.”
In the elderly, thyrotoxicosis can present very atypically,
without the common findings that usually occur in younger
patients. A TSH is a reasonable screening test in the elderly
with NOAF.
10. “I gave diltiazem because the patient was not
anticoagulated, and I did not want to cardiovert her
and cause a stroke.”
The patient was diaphoretic, with decreased mental status,
and had a blood pressure of 60/palp and an irregular
heart rate of 160. That defines unstable. Electrical
cardioversion is the initial treatment of choice. While it
does carry a risk of thromboembolism, the risk of death
from sustained shock is greater. After the unstable patient
cardioverted, start heparin as soon as possible if there is
no significant contraindication. ▲
21 Emergency Medicine Practice
rhythmic agents is difficult, because the published studies
vary greatly in quality and applicability to patients in the
ED. Overall success rates average around 50% depending
on the drug used, patient characteristics, study design, and
mode of delivery. Most trials are small, and thus conclusions
regarding safety and efficacy are questionable. Placebo arms
are not always available in these trials, thus limiting easy
comparison of agents. Remember that at least 40%-71% of
patients with AF convert spontaneously within the first 24
hours,70-73,105 whereas patients with chronic AF are unlikely
to convert spontaneously. Therefore, the duration of AF in
study patients (which can vary greatly from trial to trial)
would significantly affect the overall reported success of the
conversion agent. Furthermore, some studies only include
patients who have already failed a previous attempt at
conversion, and thus the reported success may appear
very low.
The realistic chemical options (if there are any) for
conversion in the typical ED setting at this time appear to be
ibutilide, amiodarone, procainamide, and possibly the Class
IC agents (flecainide and propafenone), although the latter
are only available PO in the United States. Although the oral
forms have been used and studied for the conversion of AF,
the ED use of these agents is not widespread. Some argue
that the initiation of the oral forms of these drugs warrants
prolonged observation for proarrhythmic effects. Elective
chemical conversion by the ED physician is best performed
in consultation with the patient’s primary care physician or
cardiologist, as these drugs can have serious side effects.
Ibutilide is worth mentioning, as its use in the ED
setting has been suggested due to its short half-life. The
major risk of the drug is the ability to induce torsades de
pointes in up to 8% of patients, which can occur up to
several hours after the drug is given.39,134-136 Thus, careful
monitoring for four hours after administration—even with
successful conversion—must be mandatory. Amiodarone has

Table 9. Elective Conversion Agents.

Dosing Contraindications/Cautions Comments

Electrical Start with 200J monophasic, 120J
cardioversion biphasic synchronized (if unstable,
maximal initial doses are likely indicated)
Class IA
• Procainamide 100 mg IV q 5-10 minutes to maximum
of 1000 mg or as a 20 mg/kg IV infusion
to a maximum of 20 mg/kg
• Quinidine 200-300 mg sulfate PO, followed in 1-2
hours by 400 mg
Class IC
• Flecainide 2 mg/kg IV over 10 minutes*
or 300 mg PO times 1
• Propafenone 2 mg/kg IV over 10 minutes*
or 600 mg PO times 1
Class III
• Ibutilide 0.01 mg/kg IV over 10 minutes (max,
1 mg). Repeat times 1 if no response
10 minutes after first dose completed
• Dofetilide 0.5 mg PO bid. Not available IV
• Amiodarone 150 mg IV over 10 minutes followed by
infusion of 1 g over 6 hours. May repeat
bolus if needed. Or, 30 mg/kg PO times 1
• Sotalol 1.5 mg/kg IV over 30 minutes*
*Not currently available in the United States
Sedation required
Stop drug if conversion, prolonged
QT/QRS, torsades de pointes,
hypotension
High proarrhythmic effects and
negative inotropic effects in those
with structural heart disease
Hypokalemia, hypomagnesemia,
LV dysfunction, prolonged QT.
Induction of torsades de pointes
as high as 8%
Similar to ibutilide
Hypotension may occur with IV use
Significant reactive airway disease
Consider lower starting doses in
NOAF, AFl, and in patients unlikely
to have structural heart disease
Rate control agent should precede
its use given a risk of increased
conduction through the AV node
Not used much currently
Highest reported success rate
among various drugs
Conversion rate better for AFl than
AF; expensive ($200 per 1 mg); very
short half life, but use warrants
observation for at least four hours
for torsades de pointes
ED use unlikely as FDA has
restricted access in United States.
Use of drug likely warrants 72-hour
period of observation
May be used for rate control,
conversion, and maintenance;
low proarrhythmic effects
Effective for rate control and
conversion; however, generally
poor conversion efficacy. Blocks
accessory pathways

Emergency Medicine Practice 22 www.empractice.net • August 2002

the advantage of having rate control effects as well as some
success at the conversion of AF/AFl. Of note, however, are
its poor success rate compared to other drugs and its slow
onset, which limit its utility. Despite the lack of FDA
approval for acute conversion in AF, procainamide has been
used extensively and can be given easily IV, which makes it
a reasonable option in the ED. Because it can increase
conduction through the AV node, an AV nodal blocking agent
should be used prior to its use as it could induce an increased
ventricular response if given alone.
So which drug is best? That’s a hard question to
answer, as the reported success of each drug often varies
largely from study to study, making it difficult to place the
drug’s usefulness in context. The bottom line is that there is
not likely a single drug of choice at this time for the acute
conversion of AF.
Special Circumstances
Accessory Pathways
The management of pre-excitation syndromes like Wolff-
Parkinson-White syndrome is particularly challenging
in patients with AF.137 The short refractory period of
these accessory pathways can result in extremely fast
ventricular rates.
So when should one consider WPW in a patient with
AF? Certainly a history of WPW will give it away, but there
are other findings that should raise suspicion. (See Figure 3
and Figure 4 on page 6.) AF with bizarre wide complexes of
different morphologies, a very rapid ventricular rate (RR
interval > 250), and younger patients should all be consid-
ered for an underlying accessory pathway. Look for the
presence of a delta wave, which is a slurred, slow-rising
onset of the QRS complex.138
Do not use AV nodal blocking agents in anyone you suspect
as having an accessory pathway (unless you pretreat with
procainamide).31,138 These drugs can actually increase the
ventricular response in patients with WPW and result in
ventricular fibrillation.31 In patients with accessory path-
ways and rapid AF, ß-blockers, CCBs, and digoxin are all
contraindicated as sole treatment agents.
Synchronized electrical cardioversion is the treatment
of choice in unstable patients with accessory pathways,
and some authors recommend it as first-line treatment
even in stable patients. For reasons discussed earlier in
this article, starting at 200J-360J synchronized monophasic
shock is appropriate.
For stable patients, procainamide followed by an AV
nodal blocking agent is also reasonable. Procainamide slows
conduction through accessory pathways but can increase
conduction through the AV node and thus should be
followed by an AV nodal blocking agent. Procainamide can
be loaded in 50-100 mg boluses IV every 5-10 minutes or by
an infusion at up to 30 mg/min. No more than 17 mg/kg
total should be given, and it should be stopped if the QRS
widens greater than 50%, hypotension occurs, or the patient
converts to sinus rhythm. Amiodarone might have a role in
the treatment of accessory pathways, but a few case reports
have reported ventricular rate acceleration with IV adminis-
August 2002 • www.empractice.net
tration of the drug in WPW.115 In Europe, propafenone and
sotalol are used, but these drugs are not available in IV form
in the United States.138
Summary
Atrial fibrillation and its close counterpart, atrial flutter, are
commonly encountered in the ED, and their incidence will
only continue to rise. It is imperative for emergency
physicians to keep abreast of the latest literature regarding
the management of these patients. Cardiovert the truly
unstable patient, but anticipate possible failure or short-
lived effects. For stable patients, be familiar with the
appropriate use of rate-control medications. Ventricular rate
control remains the most commonly required ED interven-
tion in patients with NOAF. Anywhere from 40%-70% of
patients with NOAF will spontaneously convert without
electricity or toxic drugs.
The role of anticoagulation regarding patients with
NOAF of less than 48 hours is hotly debated. Although
there are no large, prospective trials, some data suggest that
patients can be risk stratified to determine the need for
anticoagulation and admission. Some literature suggests
that stable patients with AF of short duration may be safely
converted in the ED; however, this practice can hardly be
considered routine. Admission and discharge decisions are
best made on an individual basis and should incorporate
factors such as age, likelihood of a serious underlying
etiology, comorbidities, clinical stability, and access to early
follow-up. Although many questions regarding the manage-
ment of AF in the ED remain unanswered, “the beat goes
on”—even if it is irregular. ▲
References
Evidence-based medicine requires a critical appraisal of the
literature based upon study methodology and number of
subjects. Not all references are equally robust. The findings
of a large, prospective, randomized, and blinded trial
should carry more weight than a case report.
To help the reader judge the strength of each reference,
pertinent information about the study, such as the type of
study and the number of patients in the study, will be
included in bold type following the reference, where
available. In addition, the most informative references cited
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proarrhythmic effects: a review with special reference to torsades de
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(Prospective; 23 patients)
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Physician CME Questions
17. When dealing with atrial fibrillation with a rapid
ventricular response and a wide complex QRS with a
delta wave, which of the following drugs is the safest
to use?
a. Digoxin
b. Procainamide
c. Esmolol
d. Diltiazem
e. Verapamil
26 www.empractice.net • August 2002
18. When using calcium as pretreatment to calcium-
channel blockers, which of the following is true?
a. Calcium will block the chronotropic effects
of the calcium-channel blocker, but not its
inotropic effects.
b. Side effects may include a feeling of warmth
or flushing.
c. Calcium gluconate has more calcium per amp
than calcium chloride.
d. It should not be used unless the patient is
in extremis.
e. It should never be given to anyone with
osteoporosis.
19. Diltiazem has clearly been shown to be more effica-
cious and has a higher safety profile than verapamil
in any patient with a rapid ventricular response.
a. True
b. False
20. When considering cardioversion of an unstable
patient with atrial fibrillation, which of the
following is true?
a. It should never be done due to the risk of
thromboembolism.
b. Intubation should precede cardioversion.
c. Cardioversion should be performed synchronized.
d. 50J would be expected to work more than 80%
of the time.
e. Atrial flutter generally requires more energy to
convert than atrial fibrillation.
21. Every patient with NOAF should have cardiac
enzymes and be admitted to the hospital to rule
out MI.
a. True
b. False
22. When considering the risk of thromboembolism after
cardioversion of atrial fibrillation, which of the
following is true?
a. The risk of thromboembolism is zero if the patient
has been properly anticoagulated.
b. Patients with hypercoagulability are probably
more at risk.
c. The risk of thromboembolism after the patient
has received three months of anticoagulation
is 5%-10%.
d. It is clearly without risk if the patient has had
atrial fibrillation for less than 72 hours.
e. A transesophageal echocardiogram is not likely to
be as helpful as a transthoracic echocardiogram.
23. Which of the following is true regarding NOAF?
a. It is uncommon in the ED.
b. Thyrotoxicosis is an extremely common cause.
c. There is no risk of thromboembolism if conversion
is less than 48 hours.
d. It often presents in children.
e. Assuming no other disease process or medication
use, the ventricular rate typically seen is around
150 bpm.
August 2002 • www.empractice.net
24. Digoxin:
a. is faster than verapamil for rate control in atrial
fibrillation with a rapid ventricular response.
b. is better than placebo for conversion of
atrial fibrillation.
c. is expensive.
d. works not only through direct effects on the AV
node, but also has some indirect effects through
vagal stimulation.
e. can be given safely in WPW.
25. Which of the following is true regarding atrial
fibrillation with a rapid ventricular response?
a. The coronary arteries will have less time to fill.
b. Cardiac output will likely be decreased, especially
in the elderly.
c. There is a loss of the “atrial kick.”
d. All of the above.
26. Amiodarone:
a. has a high incidence of torsades de pointes.
b. can be used for rate control and conversion.
c. is inexpensive.
d. has zero incidence of hypotension when
given rapidly.
27. ß-blockers:
a. should not be given to diabetics with atrial
fibrillation.
b. are less effective than digoxin for acute rate
control when given IV.
c. are less likely to cause bronchospasm than
calcium-channel blockers.
d. may be useful in patients with atrial fibrillation
suspected of having acute coronary syndrome.
e. should be given intravenously along with
calcium-channel blockers to have maximal effects.
28. Which of the following has/have been shown to be
effective in rate control of atrial fibrillation?
a. Magnesium
b. Verapamil
c. Diltiazem
d. Esmolol
e. All of the above
29. Atrial flutter:
a. rarely, if ever, occurs in association with AF.
b. has zero risk of thromboembolism when
converted.
c. can mimic other supraventricular tachycardias.
d. is typically much more difficult to convert than AF.
30. Giving an IV calcium-channel blocker:
a. is absolutely contraindicated with signs of
congestive heart failure.
b. can be done safely immediately after a few
doses of IV propranolol are given.
c. will not work if the patient recently
received calcium.
d. is a first-line rate control agent in NOAF at
this time.
e. should always be given with magnesium.
27 Emergency Medicine Practice
31. Which of the following is true? Physician CME Information
a. All patients with NOAF should have a d dimer This CME enduring material is sponsored by Mount Sinai School of Medicine and
as a part of the workup to rule out PE. has been planned and implemented in accordance with the Essentials and
b. Magnesium has no effect on ventricular rate in Standards of the Accreditation Council for Continuing Medical Education. Credit
may be obtained by reading each issue and completing the printed post-tests
AF with a rapid ventricular response. administered in December and June or online single-issue post-tests
c. Calcium must be given prior to administration of administered at www.empractice.net.
a calcium-channel blocker to anyone with NOAF. Target Audience: This enduring material is designed for emergency medicine
physicians.
d. Approximately 40%-50% of patients with
Needs Assessment: The need for this educational activity was determined by a
NOAF will convert within the first day survey of medical staff, including the editorial board of this publication; review
regardless of treatment. of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and
evaluation of prior activities for emergency physicians.
32. Ibutilide:
Date of Original Release: This issue of Emergency Medicine Practice was published
a. is inexpensive. August 1, 2002. This activity is eligible for CME credit through August 1,
b. has no significant side effects. 2005. The latest review of this material was July 11, 2002.
c. is not FDA approved for use in atrial fibrillation. Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that
d. may cause torsades de pointes in up to 8%
is outside Food and Drug Administration approved labeling. Information
of patients. presented as part of this activity is intended solely as continuing medical
e. if successful at conversion, will usually enable education and is not intended to promote off-label use of any pharmaceutical
product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice
immediate discharge due to the drug’s short
discusses several antiarrhythmic agents used for elective conversion in the ED.
half-life. While several trials report their use, ibutilide is the only IV agent with FDA
approval for this purpose. (See text.)
Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and
Guidelines, all faculty for this CME activity were asked to complete a full
disclosure statement. The information received is as follows: Dr. Slovis is on the
Class Of Evidence Definitions speaker bureau and receives consultation fees and honoraria from Genentech,
Merck, Cor-Key, and Wyeth. Dr. Pollock and Dr. Herbert report no significant
Each action in the clinical pathways section of Emergency Medicine Practice
financial interest or other relationship with the manufacturer(s) of any
receives an alpha-numerical score based on the following definitions.
commercial product(s) discussed in this educational presentation.
Class I • Case series, animal studies, Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation
• Always acceptable, safe consensus panels Council for Continuing Medical Education to sponsor continuing medical
• Definitely useful • Occasionally positive results education for physicians.
• Proven in both efficacy and
Indeterminate Credit Designation: Mount Sinai School of Medicine designates this educational
effectiveness
• Continuing area of research activity for up to 4 hours of Category 1 credit toward the AMA Physician’s
Level of Evidence: • No recommendations until Recognition Award. Each physician should claim only those hours of credit
• One or more large prospective further research actually spent in the educational activity. Emergency Medicine Practice is approved
studies are present (with by the American College of Emergency Physicians for 48 hours of ACEP Category
rare exceptions) Level of Evidence:
1 credit (per annual subscription). Emergency Medicine Practice has been reviewed
• High-quality meta-analyses • Evidence not available
and is acceptable for up to 48 Prescribed credit hours by the American Academy
• Study results consistently • Higher studies in progress
of Family Physicians. Emergency Medicine Practice has been approved for 48
positive and compelling • Results inconsistent,
Category 2B credit hours by the American Osteopathic Association.
contradictory
Class II • Results not compelling Earning Credit: Two Convenient Methods
• Safe, acceptable • Print Subscription Semester Program: Physicians with current and valid
• Probably useful licenses in the United States who read all CME articles during each
Significantly modified from: The
Emergency Medicine Practice six-month testing period, complete the post-
Level of Evidence: Emergency Cardiovascular Care
test and the CME Evaluation Form distributed with the December and June
• Generally higher levels Committees of the American Heart
issues, and return it according to the published instructions are eligible for
of evidence Association and representatives
up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition
• Non-randomized or retrospec- from the resuscitation councils of
Award (PRA) for each issue. You must complete both the post-test and CME
tive studies: historic, cohort, or ILCOR: How to Develop Evidence-
Evaluation Form to receive credit. Results will be kept confidential. CME
case-control studies Based Guidelines for Emergency
certificates will be delivered to each participant scoring higher than 70%.
• Less robust RCTs Cardiac Care: Quality of Evidence
• Results consistently positive and Classes of Recommendations; • Online Single-Issue Program: Physicians with current and valid licenses in
also: Anonymous. Guidelines for the United States who read this Emergency Medicine Practice CME article
Class III cardiopulmonary resuscitation and and complete the online post-test and CME Evaluation Form at
• May be acceptable emergency cardiac care. Emergency www.empractice.net are eligible for up to 4 hours of Category 1 credit
• Possibly useful Cardiac Care Committee and toward the AMA Physician’s Recognition Award (PRA). You must complete
• Considered optional or Subcommittees, American Heart both the post-test and CME Evaluation Form to receive credit. Results will
alternative treatments Association. Part IX. Ensuring be kept confidential. CME certificates may be printed directly from the Web
Level of Evidence: effectiveness of community-wide site to each participant scoring higher than 70%.
• Generally lower or intermediate emergency cardiac care. JAMA
1992;268(16):2289-2295. Emergency Medicine Practice is not affiliated with any
levels of evidence
pharmaceutical firm or medical device manufacturer.

Publisher: Robert Williford. Executive Editor: Heidi Frost.

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Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions expressed are not necessarily
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Emergency Medicine Practice 28 www.empractice.net • August 2002