YAJEM-57274; No of Pages 9

American Journal of Emergency Medicine xxx (2018) xxx–xxx

Contents lists available at ScienceDirect

American Journal of Emergency Medicine

journal homepage: www.elsevier.com/locate/ajem

Emergency medicine considerations in atrial fibrillation

Brit Long, MD a,⁎, Jennifer Robertson, MD, MS b, Alex Koyfman, MD c,
Kurian Maliel, MD FACC d, Justin R. Warix, DO, FAAEM e
a
San Antonio Military Medical Center, Department of Emergency Medicine, 3841 Roger Brooke Dr, Fort Sam, Houston, TX 78234, United States
b
Emory University, Dept of EM, 531 Asbury Circle, Annex Bldg, Suite N340, Atlanta, GA 30322, United States
c
The University of Texas Southwestern Medical Center, Department of Emergency Medicine, 5323 Harry Hines Boulevard, Dallas, TX 75390, United States
d
Wright Patterson Military Medical Center, Department of Cardiology, 4881 Sugar Maple Dr, Dayton, OH 45433, United States
e
Central Peninsula Hospital, 250 Hospital Pl, Soldotna, AK 99669, United States

a r t i c l e i n f o a b s t r a c t

Article history: Background: Atrial fibrillation (AF) is an abnormal heart rhythm which may lead to stroke, heart failure, and
Received 2 November 2017 death. Emergency physicians play a role in diagnosing AF, managing symptoms, and lessening complications
Received in revised form 22 January 2018 from this dysrhythmia.
Accepted 23 January 2018 Objective: This review evaluates recent literature and addresses ED considerations in the management of AF.
Available online xxxx
Discussion: Emergency physicians should first assess patient clinical stability and evaluate and treat reversible
causes. Immediate cardioversion is indicated in the hemodynamically unstable patient. The American Heart As-
Keywords:
Dysrhythmia
sociation/American College of Cardiology, the European Society of Cardiology, and the Canadian Cardiovascular
Atrial fibrillation Society provide recommendations for management of AF. If hemodynamically stable, rate or rhythm control
Tachycardia are options for management of AF. Physicians may opt for rate control with medications, with beta blockers
Tachydysrhythmia and calcium channel blockers the predominant medications utilized in the ED. Patients with intact left ventricular
Cardiology function should be rate controlled to b110 beats per minute. Rhythm control is an option for patients who possess
longer life expectancy and those with AF onset b48 h before presentation, anticoagulated for 3–4 weeks, or with
transesophageal echocardiography demonstrating no intracardiac thrombus. Direct oral anticoagulants are a safe
and reliable option for anticoagulation. Clinical judgment regarding disposition is recommended, but literature
supports discharging stable patients who do not have certain comorbidities.
Conclusion: Proper diagnosis and treatment of AF is essential to reduce complications. Treatment and overall
management of AF include rate or rhythm control, cardioversion, anticoagulation, and admission versus dis-
charge. This review discusses ED considerations regarding AF management.
Published by Elsevier Inc.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
2. Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.1. Stable patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.2. Echocardiography in the ED . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.3. Rate versus rhythm control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.4. Rhythm control options. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.5. Rate control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.6. Considerations in anticoagulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.7. Unstable patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
3.8. Disposition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
4. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
Conflicts of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0

⁎ Corresponding author at: 3841 Roger Brooke Dr., San Antonio, TX 78234, United States.
E-mail address: brit.long@yahoo.com (B. Long).

https://doi.org/10.1016/j.ajem.2018.01.066
0735-6757/Published by Elsevier Inc.

Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
2 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx

1. Introduction including ED evaluation, rate and rhythm control, anticoagulation, and

Atrial fibrillation (AF) is one of the most common dysrhythmias, af-
fecting up to 1–2% of the population and 9% in those over age 80 [1-5].
Not only is AF the most common dysrhythmia overall, but it is also the
most common dysrhythmia diagnosed in the ED. A study in 2013
demonstrates over a 29% increase in ED AF visits, with the dysrhythmia
accounting for up to 0.5% of all ED visits [6]. When associated with other
concomitant pathologies such as CHF, AF patients who present to the ED
tend to be older and have higher mortality [6]. As the population
continues to age, the dysrhythmia will likely increase in prevalence.
The dysrhythmia is strongly associated with stroke and heart failure
[1-6]. Men, Caucasians, and the elderly demonstrate greater risk for AF,
although women more commonly present with stroke from AF [7-15].
The risk of stroke approaches 5% annually with no anticoagulation,
which decreases to b1% with appropriate management [10,16]. Mortal-
ity in patients with AF is close to double that of patients with normal
sinus rhythm [8-15]. Hypertension, diabetes mellitus, obesity, ethanol
use, coronary artery disease (CAD), valvular heart disease, thyroid dis-
ease, autonomic or electrolyte disturbances, and prior cardiac surgery
contribute to AF [7-13,15-22], and up to 70% of patients with AF have
associated heart disease [16-22]. A recent retrospective review of 564
ED patients with recent onset AF found hypertension to be the most
common comorbidity, followed by ischemic heart disease [23]. Other
contributing factors include channelopathies, stimulant use, pulmonary
disease, enhanced vagal tone, extreme exercise, smoking, and chronic
kidney disease (CKD) [7,8,11,21–27].
In a normal heart, impulses originate from the sinus node, followed
by regular atrial and ventricular activation and contraction [8,28]. AF re-
sults from depolarization of multiple microreentry circuits, which reach
the AV node at 300–600 atrial impulses per minute. The AV node refrac-
tory period is responsible for the irregularly irregular ventricular re-
sponse [8-10]. On electrocardiogram (ECG), p waves will be absent
and the R-R intervals irregular. These irregular atrial beats cause ineffec-
tive atrial contraction, leading to thrombus formation predominantly in
the left atrial appendage [8-10,16,22,23]. The irregular beats also can
lead to rapid ventricular activity, which if not well controlled, decrease
myocardial blood flow, decrease cardiac output, and cause long term
damage to the myocardium [8-11,28]. The QRS complex is narrow in
those without bundle branch block (BBB), though QRS width N120 ms
is found in those with ventricular BBB. Some patients with complete
heart block and AF may present with regular rhythm and no discernable
p waves. Patients with WPW syndrome and AF may demonstrate an
ECG resembling ventricular tachycardia, though AF with preexcitation
demonstrates an irregularly irregular rhythm [8-13,16].
Atrial fibrillation is comprised of several categories [8-13,16]. Parox-
ysmal AF consists of episodes that terminate spontaneously or with in-
tervention within 7 days of onset, while persistent AF is present for
longer than 7 days [8-13,15,16]. Recurrent AF is defined by more than
two episodes. Longstanding persistent AF is continuous AF for greater
than one year. Permanent AF is defined as the presence of continuous
AF, with joint decision between patient and clinician to stop further at-
tempts to maintain sinus rhythm. If permanent AF is eventually treated
with rhythm control, it is redefined as longstanding persistent AF [8-
13,15,16]. Prolonged AF makes restoration of normal sinus rhythm dif-
ficult [8-11].
2. Methods
This is a narrative review of AF emergency evaluation and manage-
ment. The objective is to evaluate recent literature and address current
considerations in the management of AF in the ED. The literature search
was limited to inclusion of recent studies from the prior 20 years. Rather
than discussing AF in its entirety, the authors have investigated specific
components of the condition relevant to emergency physicians
patient disposition.
3. Discussion
When evaluating and managing the patient with AF with rapid ven-
tricular response (RVR), the physician should consider if the patient is
unstable and whether this is due to primary AF versus another cause.
Hypotension and tachycardia may not be due to AF solely, but rather
sepsis, myocardial infarction, gastrointestinal hemorrhage, alcohol
withdrawal, pulmonary embolism, and other causes [29,30]. This is
termed complex AF [29,30]. Inflammation and oxidative stress, seen in
sepsis, may play a role in the development of AF, as they may directly
change the electrical activity of the cardiac myocyte [7,8,25]. Up to
25% of hospitalized patients with sepsis develop AF [7]. If the etiology
of tachycardia and hypotension is due to another primary etiology, the
patient will likely not improve with interventions targeting specifically
AF alone. Attempts to control the heart rate or rhythm in these patients
are usually less successful and may be harmful. Rather, the etiology
must be properly evaluated and treated [29,30]. Scheuermeyer et al.
evaluated 416 patients with AF or atrial flutter in a retrospective de-
scriptive cohort study [29]. Of these patients evaluated, 105 underwent
rate control and 30 rhythm control, and 55 adverse events occurred in
this group of 135 patients (40.7%), while the 281 patients not managed
with rhythm or rate control demonstrated 20 adverse events (7.1%)
[29]. Patients with complex AF demonstrated a 5.7-fold increase in ad-
verse events and 11.7-fold increase in major adverse events with rate
or rhythm control, and patients with sepsis or heart failure with AF
demonstrated the highest number of adverse events, though others in-
cluded acute coronary syndrome (ACS), acute renal failure, obstructive
lung disease, gastrointestinal bleeding, and stroke [29,30]. These pa-
tients may need the relative tachycardia to compensate. If no underlying
cause of AF is suspected on evaluation, management should focus on
symptom improvement and reduction in potential complications [7-
12,30]. If another condition is suspected on focused history and exami-
nation and the patient has AF with RVR, the underlying etiology should
be managed (Fig. 1), as treatments focusing on AF alone may result in
patient harm.
3.1. Stable patients
Most patients with AF with RVR who present to the ED possess a
well-perfusing blood pressure [8,11,13,30]. Focused history and physi-
cal examination are warranted, with the physician inquiring on onset,
frequency, duration of symptoms, associated symptoms, prior episodes,
medications (anticoagulants, antiarrhythmics, rate control agents), past
medical history (heart disease), and instigating factors. Evaluation in-
cluding electrolyte panel, complete blood cell count, chest x-ray, and
ECG is advised. Thyroid panel may assist if the patient demonstrates
other symptoms associated with thyroid abnormality. Additional test-
ing including brain natriuretic peptide (BNP) or troponin is not recom-
mended on a routine basis, but rather, depends on the clinical situation.
Pregnancy testing in reproductive aged-women is recommended, and
evaluation for pulmonary embolism should be based on the clinical sit-
uation [30].
Evaluation for ACS can be challenging, as a significant number of pa-
tients with AF have coexisting coronary artery disease (CAD) [30-34].
Chest pain is present in 20% of patients presenting with AF with RVR,
which is not usually due to a primary ischemic event [31,32]. Patients
without significant ST-segment changes are at low risk for acute myo-
cardial infarction [31,32]. One prospective cohort study suggested
chest pain and ST segment depression b2 mm (mm) are common find-
ings in AF, but they have limited ability to diagnose or predict ACS [32].
ST segment elevation or depression ≥2 mm was found to be a reliable
predictor of concomitant ischemia [32]. Similarly, a 2007 retrospective

Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx
Fig. 1. AF management pathway.
study of ED patients with chest pain and AF demonstrated the presence
of AF did not change the risk of ACS in patients with chest pain [33].
Clinical judgment is required when assessing risk of ACS with AF. Pa-
tient assessment and ECG before and after rate or rhythm control should
be strongly considered in the evaluation of ACS [30-34]. Patients with
significant ST changes after treatment require consideration for ACS.
3.2. Echocardiography in the ED
Transesophageal echocardiography (TEE) allows assessment for in-
tracardiac thrombus before cardioversion and cardiac function. TEE
should be conducted if symptom duration is N48 h or unknown before
cardioversion to evaluate for thrombus [8-13]. However, if required
for situations such as hemodynamic instability, cardioversion can be
performed emergently without TEE. In younger, healthy patients with
known time of onset b48 h, transthoracic echocardiography (TTE) is
low yield and likely not beneficial in the ED, though older patients
with greater likelihood of cardiac abnormality may benefit from echo-
cardiography. The American and European guidelines recommend TTE
for patients with AF as part of the initial evaluation to assess for struc-
tural heart disease, cardiac function (right and left heart), and atrial
size, which can occur as outpatient [8-13].
3.3. Rate versus rhythm control
Symptom improvement may occur via rate or rhythm control, al-
though controversy surrounding rate versus rhythm control still exists.
Rhythm control for AF of ≤48 h duration is viable, with stroke risk ap-
proaching b1% if the patient is cardioverted within 48 h [35]. Patients
who present after 48 h require rate control before rhythm control is
considered due to increased risk of stroke [8-13,16]. Patients with no in-
tracardiac thrombus on TEE or those on anticoagulation for 3–4 weeks
may also undergo rhythm control. Patients can spontaneously convert
to sinus rhythm on their own. Several studies conducted in the last sev-
eral years sought to determine if rate control or rhythm control is the
better option for overall survival and quality of life [36-45]. In 2002,
the Atrial Fibrillation Follow-up Investigation of Rhythm Management
Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
3
(AFFIRM) trial, a randomized multicenter comparison study, was con-
ducted, though the study population included patients from clinical
sites other than the ED. [39,40] Two treatment strategies were com-
pared, including pharmacologic or non-pharmacologic rhythm methods
and rate control medications including diltiazem, verapamil, and beta
blockers [39,40]. There were no significant differences between the
rate and rhythm control groups for overall mortality. More of the
rhythm control patients were hospitalized and sustained more adverse
drug effects than the rate control patients, but there were no differences
in stroke when controlled for anticoagulation [39,40]. A similar 2002
study showed rate control to be non-inferior to rhythm control in
terms of death, heart failure, thromboembolic complications, require-
ment of a pacemaker, and severe adverse drug effects [41]. A 2008
study of patients with AF and heart failure suggested rhythm control
does not contribute to improved survival as compared to rate control
with anticoagulation [42].
A meta-analysis released in 2013 found no difference between rate
versus rhythm control in mortality, stroke, embolism, worsening heart
failure, myocardial infarction, and bleeding [44]. Patients younger than
65 years in subgroup analysis demonstrate rhythm control to be supe-
rior in prevention of all-cause mortality (relative risk 3.03; 95% confi-
dence interval 1.59–5.75) [44]. The Okcun 2004 study was a single
center RCT evaluating AF N48 h, finding rhythm control to be associated
with fewer deaths (15% versus 43%), with no difference in embolic
events [45]. The J-RHYTHM study in 2009 was a multicenter RCT con-
ducted in patients over 18 years with AF b48 h, finding rhythm versus
rate control was associated with lower events (defined by total mortal-
ity, symptomatic cerebral infarction, systemic embolism, hospitalization
for heart failure, major bleeding, or physical/psychological disability re-
quiring treatment strategy alteration), 15% versus 22%, respectively
[46]. The American Heart Association/American College of Cardiology
(AHA/ACC), the Canadian Cardiovascular Society (CCS), and the Euro-
pean Society of Cardiology (ESC) suggest that ultimately patients should
be cardioverted in the long run, which can improve quality of life and
decrease symptoms [8-13,16].
In patients b65 years of age with known onset of b48 h, rhythm con-
trol can be safe and useful. Spontaneous cardioversion may occur,
4 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx
especially in younger patients. Rate control is advised in patients with
valvular disease or chronic AF, though patients with CHF may undergo
rhythm control [8-13,16].
3.4. Rhythm control options
Guidelines suggest rhythm control may be beneficial for younger pa-
tients with greater life expectancy [8-16]. Older patients likely warrant
rate control before rhythm control is considered, though initial rhythm
control is a valid option in specific circumstances including known onset
of AF b48 h, TEE with no intracardiac thrombus, or on anticoagulation at
therapeutic levels for 3–4 weeks [39-41]. Rate control is the first option
for several situations before rhythm control is considered (Table 1).
Rhythm control includes cardioversion, whether by pharmacologic or
electrical means. ED studies demonstrate electrical cardioversion to be
90% effective and pharmacologic cardioversion to be 60% effective [8-
11,36-38,47]. Some patients with new onset AF may covert to sinus
rhythm within a few hours, negating the need for medical or electrical
cardioversion.
Airakinsen et al. evaluated adult patients age N 18 with acute onset
AF (b48 h) treated with cardioversion in the ED. [48] The primary
study outcome was thromboembolic event within 30 days after cardio-
version. A total of 7660 cardioversions were performed, but the analysis
for embolic complications included 2481 patients with no peri-proce-
dural or post-procedural anticoagulation. At 30 days, the authors
noted 38 thromboembolic events: 31 strokes, 4 TIAs, 2 pulmonary em-
boli, and 1 combined stroke and a systemic embolism. Median time to a
thromboembolic event was 2 days. Further analysis revealed heart fail-
ure, diabetes, and age N60 years were associated with thromboembolic
events [48]. The authors conclude that while overall embolic events are
low (1.5% of patients), risk is elevated in patients with older age, female
gender, heart failure, and diabetes. While some patients may clearly
present with AF in less than a 48 h period, they require risk stratification
[48].
Canadian physicians have repeatedly demonstrated cardioversion to
be efficacious and safe. The “Ottawa Aggressive Protocol” consists of
acute rhythm control and discharge home for hemodynamically stable
patients with recent onset (b48 h) rapid AF or atrial flutter [37]. Stiell
et al. evaluated this protocol in 660 patient visits, with a mean patient
age 64.5 years. Using intravenous (IV) procainamide or electric cardio-
version, 96.8% of patients were discharged home, and 93.3% remained
in normal sinus rhythm. If procainamide is used, 1 g (g) IV over 60
min is provided. In patients cardioverted with procainamide, 44% dem-
onstrate return to normal sinus rhythm with 500 mg. If systolic blood
pressure decreases below 100 mm Hg, the infusion is discontinued.
One hour after cardioversion, the patient can be considered for dis-
charge. No anticoagulation was provided upon discharge for most pa-
tients [37]. There were few adverse effects, including hypotension in
6.7%, bradycardia in 0.3%, and a 7 day relapse rate of 8.6%, with no
strokes and no deaths. However, no long-term follow-up for patients
occurred, and this is not a common strategy in the U.S. [37,38].
Ibutilide, vernakalant, and flecainide were evaluated in a prospective
observational study in patients with AF onset b48 h and average age
66.8 years [49]. All patients were anticoagulated with low molecular
weight heparin, and 72.5% of patients converted with one medication
Table 1
Rhythm control/cardioversion contraindications [8-13].
Contraindications to ED cardioversion (electrical or medication)
– Unknown duration of AF
– AF duration ≥48 h
– Patient is high risk for stroke: mechanical heart valve, rheumatic heart disease, or
recent stroke or transient ischemic attack
– Patient is high risk for ventricular dysrhythmia: electrolyte abnormality such as
severe hypomagnesemia or hypokalemia, digoxin toxicity
Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
[49]. Ibutilide is a Vaughan-Williams Class III antidysrhythmic, often
given in doses of 1 mg IV over 10 min, which may be repeated in an-
other dose of 1 mg IV. It may result in QTc prolongation and ventricular
tachycardia in 3% of patients, and ejection fraction (EF) must be N30%.
Before administering ibutilide, serum potassium and magnesium
should be assessed and repleted if needed. Prolonged QTc is a contrain-
dication to ibutilide. Magnesium can improve the ability to cardiovert to
sinus rhythm by 60% [50], and it can also improve the efficacy of
ibutilide in cardioversion [51].
The AHA provides a Class I Recommendation with Level of Evidence
A for flecainide, dofetilide, propafenone, and ibutilide for pharmacologic
cardioversion [7], while amiodarone receives a Class IIa Recommenda-
tion, Level of Evidence A [8]. These guidelines fail to mention procain-
amide, which is also absent in the Canadian guidelines [8,12,13,16].
The European guidelines recommend flecainide, propafenone, ibutilide,
vernakalant, or amiodarone [9-11]. With the efficacy demonstrated in
the Ottawa studies and availability of procainamide in the ED, this re-
view recommends procainamide for pharmacologic cardioversion.
3.5. Rate control
Rate control is recommended for stable patients with AF duration
N48 h [8-13,30]. For rate control, beta blockers and nondihydropyridine
calcium-channel blockers are the most commonly used agents in the
ED. Others include digoxin and amiodarone. Digoxin has been used in
the ED for AF, though it does not adequately control heart rate in the
ED setting unless the patient is sedentary [30,52]. Digoxin may be
used for patients in whom beta blocker or calcium channel blocker ther-
apy is not effective, as well as in patients with decompensated heart fail-
ure [8-13,52,53]. Amiodarone suppresses AV nodal conduction through
its sympatholytic and calcium antagonistic properties, and it may be
used for rate control in patients with reduced EF. Amiodarone requires
up to 6–7 h to achieve rate control [8-13]. Agents including beta
blockers, calcium-channel blockers, digoxin, and amiodarone should
not be used in patients with pre-excitation and AF, in which the medi-
cations have the potential to decrease the refractoriness of bypass tracts
and accelerate the ventricular rate [54,55]. This review will discuss beta
blockers and nondihydropyridine calcium-channel blockers, which
demonstrate greater rate control efficacy in the ED. Beta blockers, pre-
dominantly metoprolol, or nondihydropyridine calcium channel
blockers, primarily diltiazem, can be used (Table 2).
Heart rate target varies in the literature, with early guidelines
recommending strict heart rate b80 beats per minute (bpm). The
most recent European and U.S. guidelines recommend rate control
b110 bpm, with Canadian guidelines recommending b100 bpm [8-
13,16]. These guidelines are based on the Rate Control Efficacy in Per-
manent Atrial Fibrillation: a Comparison between Lenient versus Strict
Rate Control II (RACE II) trial [56]. This trial found lenient rate control
to be noninferior in preventing cardiovascular death, CHF hospitaliza-
tion, stroke, embolism, bleeding, or life-threatening dysrhythmia over
3 years. The lenient control group met criteria for heart rate control in
98% of cases with 75 hospital visits, compared to the strict control
group meeting heart rate target in 78% of cases with 684 hospital visits
(close to nine times as many visits) [56].
Several studies have compared medication class efficacy (calcium
channel blocker versus beta blocker) in rate control. A randomized,
open-label study in 1989 compared esmolol and verapamil in 45 pa-
tients, finding a decline in heart rate from 139 bpm to 100 bpm with
esmolol and 142 bpm to 97 bpm with verapamil [57]. Close to 50% of pa-
tients with esmolol converted to sinus rhythm, while 12% of the verap-
amil group converted [57]. A 2005 study compared 20 patients
receiving metoprolol (0.15 mg/kg, maximum 10 mg) to 20 patients re-
ceiving diltiazem (0.35 mg/kg, maximum 25 mg) [58]. Success was de-
fined by decrease in heart rate b100, decrease in ventricular rate by 20%,
or conversion to sinus rhythm. The diltiazem group demonstrated
greater success at 2 min, (50% versus 15%) [58]. One of the best designed
 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx 5

Table 2
Rate control agentsa.

Medication Form Standard dose Note

Beta blocker
Metoprolol IV 5 mg slow push, repeat up to 15 mg HR effect typically seen 5 min after dose
PO 12.5–100 mg 2×/day 37.5 mg, 50 mg are options
Carvedilol PO 3.125 mg 2×/day, titrated to max dose 25 mg 2×/day Used in heart failure
Bisoprolol PO 2.5–5 mg once/day Often used in reactive airways
Esmolol IV 500 mcg/kg bolus, then 50–300 mcg/kg/min

Calcium-channel blocker
Diltiazem IV 0.25 mg/kg slow push, may give a second 0.35 mg/kg dose 15 min from first dose Maximal HR control 2–7 min after dose, infusion 5–15 mg/h after 2nd dose
PO 120–240 mg 1–2×/day (extended)
30–90 mg 4×/day (immediate)
Verapamil IV 0.075–0.15 mg/kg; may give additional 10 mg Greater chance of hypotension
PO 40–80 mg up to 3×/day

Digitalis glycoside
Digoxin IV 0.25 mg, up to maximum 1.5 mg over 1 day Little effect on HR, requires hours for effect
PO 0.125–0.25 mg

Others
Amiodarone IV 150–300 mg May be used in critically ill patients or those with reduced EF for rate
PO 100–200 mg every day control, though several hours are needed for effect
Magnesium IV 2 g over 15 min Adverse effects including flushing and hypotension
a
Abbreviations: g – grams; HR – heart rate; IV – intravenous; kg – kilogram; PO – per os; mcg – microgram; mg – milligram; EF – ejection fraction.

studies evaluating this question was published in 2015, which evalu-
ated 52 patients in a prospective, randomized, double blind trial, with
primary outcome defined by heart rate b100 bpm [59]. Dosing included
diltiazem 0.25 mg/kg (maximum 30 mg) and metoprolol 0.15 mg/kg
(maximum 10 mg), with a second dose provided after 15 min if heart
rate control was not obtained. The primary outcome was reached in
95.8% of patients in the diltiazem group and 46.4% of patients in the
metoprolol group within 30 min. However, this was a convenience sam-
ple, and the maximum dose of metoprolol was 10 mg (5 mg three times
can be provided) [59]. A 2012 prospective study found rate control was
successful for 71% of patients receiving calcium channel blockers and
79% for those receiving beta blockers, though authors did not report sta-
tistical analysis [60].
Metoprolol and diltiazem are both effective, but the highest quality
study to date suggests diltiazem performs better in controlling heart
rate. A systematic review released in 2015 evaluating diltiazem versus
metoprolol demonstrated that diltiazem possesses approximately an
80% greater likelihood for controlling heart rate [61]. If the patient is
not on a rate controlling agent, diltiazem may offer better ability to de-
crease ventricular rate. Several patient factors must be considered [62-
66]. Treatment with beta-blockers may improve survival in patients
with heart failure with reduced EF but not heart failure with preserved
EF [62-66]. However, the use of beta blockers acutely in patients with
decompensated heart failure and AF may result in cardiogenic shock
[62-66]. Calcium channel blockers such as diltiazem are associated
with decreased long-term outcomes in heart failure patients with re-
duced EF, though use for short-term rate control may be efficacious. In
ischemic heart disease, beta blockers are associated with reduction in
ventricular dysrhythmia and sudden cardiac death, though these bene-
fits attenuate over time in the post-MI setting [62-66]. Beta blockers are
recommended in thyrotoxicosis. In hypertension, calcium channel
blockers are one of the first-line medications [67,68].
Magnesium has been evaluated for rate control in several studies
[69-74]. Chiladakis et al. evaluated diltiazem 25 mg over 15 min
followed by diltiazem infusion compared to magnesium 2.5 g IV over
15 min, then 7.5 g over 6 h [69]. This study found similar efficacy in re-
ducing rate at 1 h [69]. Davey et al. compared digoxin and magnesium
2.5 g IV over 20 min and 2.5 g over 2 h [70]. Magnesium was more likely
to achieve heart rate b100 bpm (65% versus 24%, RR 1.89; 95% CI 1.38–
2.59) [70]. Joshi et al. evaluated verapamil 5 mg versus magnesium 2 g
and found verapamil more likely to achieve heart rate b100 bpm
(55.6% versus 19.5%) [73]. In a prospective, randomized trial, Gullestad
found verapamil 5 mg IV was more likely than magnesium 1.2 g over
5 min to achieve heart rate b100 bpm (48% versus 28%) [72]. Two
meta-analyses concluded magnesium to be safe and effective compared
to placebo and digoxin, though the majority of the rate control data
comes from placebo-controlled trials [50,73]. The meta-analysis by
Onlan found magnesium approximately doubled the chance of rate con-
trol [50]. Another ED trial compared normal saline to magnesium 2.5 g
over 15 min, with no change in heart rate. Adverse effects include flush-
ing and mild hypotension, and magnesium does not appear effective in
patients with chronic AF [50,73].
3.6. Considerations in anticoagulation
Thromboembolic risk is an important consideration due to increased
stroke risk. Stroke rates may approach 2.75% in males and 2.55% in fe-
males with anticoagulation, though this increases in patients over age
65 [8-13,16]. Annual stroke risk may reach 5% in older patients with
no anticoagulation and close to 10% if the patient has experienced
prior stroke [8-13,16]. Unfortunately, many patients who meet criteria
for oral anticoagulation (OAC) do not receive appropriate therapy
[30,75]. Several scores are available for assessment of stroke risk, includ-
ing CHADS2 (Congestive Heart Failure, Hypertension, Age N75 years, Di-
abetes Mellitus and Prior Stroke or transient ischemic attack (TIA)) and
CHA2DS2-VASc (CHADS2 plus vascular disease, age 65–74 years and fe-
male gender) [1-13,16,75-77]. In patients with CHADS2 N 2 who war-
rant anticoagulation, 38% receive only aspirin, and 40% of those with
CHA2DS2-VASc ≥ 2 receive only aspirin (Table 3) [75]. The ED is a vital
component to initiating proper therapy including anticoagulation, as
patients discharged from the ED with anticoagulation are more likely
to be receiving it later at 1 year when prescribed in the ED. [30,75].
The AHA/ACC, CCS, and ESC guidelines recommend using a risk score
such as CHADS2 or CHA2DS2-VASc to determine if a patient is eligible for
oral anticoagulation (Table 3) [8-13,16,76,77]. These societies recom-
mend patients with AF should be risk stratified using a prediction
model [8-13,16].
The AHA/ACC proposes the use of CHA2DS2-VASc as the risk score of
choice in determining anticoagulation needs [8]. The AHA/ACC recom-
mends that any patient with prior stroke, TIA, or CHA2DS2-VASc score
≥2 should be anticoagulated with warfarin, dabigatran, rivaroxaban, or
apixaban [8]. If a patient has non-valvular AF and CHADs2-Vasc score
0, no oral anticoagulant therapy is recommended. Warfarin is the rec-
ommended anticoagulant in patients with AF and mechanical heart

Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
6 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx

Table 3 inhibitors (dabigatran) and Factor Xa inhibitors (apixaban, edoxaban,

CHA2DS2-VASc score [76,77]. rivaroxaban) [78-81]. Apixaban, rivaroxaban, and dabigatran are ap-
Criteria Scoring proved by the FDA for use in nonvalvular AF (Table 4) [78-81].
Age b65 0
DOAC therapy offers several advantages over warfarin, such as no re-
65–74 1 quirement for routine anticoagulation monitoring (unless the patient
≥75 2 has renal disease, in which the patient needs repeat renal function mon-
Sex Female 1 itoring) and less interaction with diet and medications [78-81]. Assess-
Male 0
ment of the patient's renal function is recommended before these
CHF history Yes 1
No 0 agents are used [78-81]. When compared to warfarin in patients with
Hypertension Yes 1 AF, DOACs are associated with decreased stroke risk overall and lower
No 0 mortality [82-87]. DOACs are also associated with decreased major
Stroke/TIA/thromboembolism history Yes 1 bleeding and intracranial hemorrhage (RR 0.49, 95% CI 0.38–0.64) as
No 0
Vascular disease history Yes 1
compared to warfarin, though GI bleeding may be increased with
No 0 DOACs (RR 1.25, 95% CI 1.01–1.55) [80]. The Randomized Evaluation
Diabetes history Yes 1 of Long-Term Anticoagulation (RE-LY) trial [82], Rivaroxaban Once
No 0 daily oral direct factor Xa inhibition Compared with vitamin K antago-
AHA/ACC score interpretation 0 points – Low risk, no anticoagulation
nism for prevention of stroke and Embolism Trial in AF (ROCKET-AF)
1 point – Low-moderate risk, consider
antiplatelet or anticoagulation medication trial [83], and Apixaban for Reduction in Stroke and Other Thromboem-
N2 points – Moderate-high risk, offer bolic Events in Atrial Fibrillation (ARISTOTLE) trial [84] demonstrate the
anticoagulation efficacy and safety of rivaroxaban, apixaban, and dabigatran when com-
pared to warfarin (Table 5). However, warfarin is recommended in pa-
tients with mechanical heart valves and mitral stenosis [78-87]. Patients
with renal impairment typically require dose adjustment [78-80,86,87].
valve [8]. If patients have a CHA2DS2-VASc score 1, the AHA/ACC leaves The use of anticoagulation should be considered when treating pa-
the choice to the patient and the clinician and recommends tients with AF in the ED, whether the patient is stable or unstable or if
anticoagulation, aspirin, or no anticoagulation [8]. rate or rhythm control is utilized. Patients who are high risk for stroke,
The ESC endorses the use of the CHA2DS2-VASc score [9-11]. The ESC based on the recommendations above, should be considered candidates
denotes low risk as a CHA2DS2-VASc score 0 for males and 1 for females. for anticoagulation, even in emergent situations [8-13,16].
These patients do not require anticoagulation per the ESC. Unlike the All three guidelines recommend use of the HAS-BLED score (Table 6)
AHA/ACC, the ESC recommends anticoagulation for any patient with a to identify those at increased risk of bleeding who may have factors that
CHA2DS2-VASc score of ≥1 for men and ≥2 for women [9-11]. If can be modified to decrease this risk [8-13,16]. This score was devel-
anticoagulation is prescribed, the ESC recommends a vitamin K antago- oped from the Euro Heart Survey from 3978 patients to assess one-
nist, a direct thrombin inhibitor, or an oral factor Xa inhibitor [9-11]. The year bleeding risk in AF. Patients with ≤1 point experience a 3.4% chance
ESC does not recommend one specific anticoagulant, and clinicians of bleeding in validation, with 5.8% chance with score N3 points [88-90].
should consider patient variables, cost, and drug compliance tolerability
in determining the medication used [9-11]. 3.7. Unstable patients
The Canadian Guidelines recommend using the CHADS2 score to es-
timate initial stroke risk but still consider age ≥65 as an initial risk com- Hemodynamic stability of the patient with AF and RVR is not a di-
ponent that is not included in the CHADS2 score. Anyone age ≥65 with chotomous state, but a continuum. Per the AHA, hemodynamic instabil-
AF should receive OAC therapy [12,13,16]. If a patient is b65 and has ity is defined by systolic blood pressure b 90 mm Hg, altered mental
any CHADS2 risk factors, OAC is recommended. If a patient is b65 and status, cardiac ischemia, or severely decompensated heart failure (for
has no CHADS2 risk factor, then the CHA2DS2-VASc score is used as a example pulmonary edema) due to the underlying rhythm [8]. The
complement to determine OAC need. If patients are b age 65 with no clearly unstable patient requires immediate resuscitation [8-13,16].
CHADS2 risk factors but have vascular disease, aspirin is recommended. Anticoagulation is recommended if dysrhythmia onset is unknown or
The Canadian guidelines do not consider female gender or vascular dis- N48 h. If due to AF primarily, electrical cardioversion is advised, no mat-
ease alone as sufficient reasons for OAC [12,13,16]. ter the duration of atrial fibrillation [ 8-13,16,30]. Most patients hemo-
The most common anticoagulation regimen previously included dynamically unstable due to AF demonstrate heart rate N 140–150
warfarin, a vitamin K antagonist, for anticoagulation. However, warfarin bpm. Physicians should evaluate for other conditions resulting in AF
requires repeat laboratory assessments and has significant interactions with RVR, which may be compensatory for an underlying condition
with food and other medications. Direct oral anticoagulants (DOACs), (Fig. 1) [29,30]. If electrical cardioversion is chosen, 100–200 J biphasic
also known as novel oral anticoagulants, include direct thrombin should be provided, though authors recommend 200 J as initial starting

Table 4
DOAC therapy [78-81].

Medication Rivaroxaban (Xarelto®) Apixaban (Eliquis®) Edoxaban (Savaysa®) Dabigatran (Pradaxa®)

Mechanism Factor Xa inhibitor Factor IIa inhibitor

Dose 20 mg once/day with evening meal⁎ 5 mg twice/day⁎⁎ 60 mg once/day⁎ 150 mg twice/day⁎
Renal elimination 66% 25% 35% 80%

Notes – Caution warranted in those on medications affecting cytochrome P450 3A4 or p-glycoprotein.
– DOAC therapy should be avoided in patients with severe renal or liver disease, those who cannot comply with consistent dosing, recent bleeding, and platelets b70,000/mm3.
– Cost may be prohibitive for long-term therapy.
– Patients with cancer should be provided low molecular weight heparin over DOAC.
⁎ Rivaroxaban, edoxaban, and dabigatran dosing depends on patient creatinine clearance (CrCl). Patients with CrCl 15–50 ml/min should receive rivaroxaban 15 mg/day or edoxaban
30 mg/day. Patients with CrCl 15–30 ml/min should 75 mg twice/day.
⁎⁎ Apixaban dose 2.5 mg if age ≥ 80 years, body weight ≤ 60 kg, or serum creatinine ≥1.5 mg/dL.

Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx
Table 5
Prominent studies evaluating DOAC therapy in AF [78-87].
Study Medication compared Age – DOAC vs. Warfarin
to Warfarin (mean in years)
RE-LY Dabigatran 71.5 vs. 71.6
ROCKET-AF Rivaroxaban 73 vs. 73
ARISTOTLE Apixaban 70 vs. 70
ENGAGE AF-TIMI Edoxaban 72 vs. 72
dose [30]. Anterior-posterior pad placement may demonstrate greater
efficacy than anterior-lateral placement [91]. For sedation, authors uti-
lize etomidate 0.1 mg/kg IV with fentanyl IV. Ketamine may be used
as well. Anticoagulation should be provided if warranted in the hemo-
dynamically unstable patient, but this should not delay cardioversion.
Anticoagulation is warranted if the onset of AF is unknown or perma-
nent AF [ 8-13,16,30].
Chronic AF may not respond to electrical cardioversion, requiring
other therapies. Hypotension warrants careful attention. Definitive
therapy of hypotension requires correction of the underlying condition
[8-13,16,30]. Small IV boluses (250–500 ml) of fluid can be used.
Physicians should be wary of causing pulmonary edema. To improve
perfusion and blood pressure, vasopressors may be needed. Norepi-
nephrine, starting at 5 mcg/min IV and titrating to improved clinical sta-
tus or improved blood pressure is warranted. Phenylephrine can be
used, but only in patients without significant heart failure, as it is contra-
indicated in patients with significant systolic dysfunction. If electrical
cardioversion is ineffective and AF is the predominant cause of hemody-
namic instability, heart rate control is vital. Diltiazem, metoprolol, and
amiodarone are options. Diltiazem can be given as 0.25 mg/kg IV (or
25 mg) over 10–15 min. Otherwise, small doses of 2.5 mg per minute
can be given. Once heart rate improves, a diltiazem drip of 5–15 mg/h
or 30–60 mg by mouth is needed. Extended release diltiazem may be
used, with maximum dosing 360 mg per day. Calcium may have benefi-
cial properties in pretreatment before a calcium channel blocker [92-
96]. While calcium may reduce hypotension with verapamil [92,95], lit-
erature suggests calcium may not demonstrate the same effects with
diltiazem [96].
Other medications include amiodarone, which can be given as 150
mg IV over 10 min, then 1 mg/min IV infusion for the first 6 h. In this
setting, amiodarone is used for rate control, not cardioversion, which
can take up to 6 h [8-13,16]. This medication is given a grade IIA recom-
mendation, level B evidence, recommendation by the AHA/ACC for rate
control in critically ill patients. Magnesium may be given as 2– g IV over
10–15 min, which may increase the chance of spontaneous reversion to
normal sinus rhythm. Digoxin may be utilized in unstable patients at
doses of 0.25 mg IV [8-13,16].
Table 6
Risk of hemorrhage [88-90].
HAS-BLED score for major bleeding risk (each factor scores 1 point)
– Hypertension (uncontrolled, N160 mm Hg systolic)
– Abnormal renal or liver function (Renal disease (dialysis, transplant history,
Cr N 2.26 mg/dL or N200 μmol/L); Liver disease defined by cirrhosis or bilirubin
N2× normal or AST/ALT/AP N3× normal)
– Stroke history
– Bleeding event or predisposition to bleeding
– Labile INR (unstable/high INRs, time in therapeutic range b 60%)
– Elderly (age ≥ 65 years)
– Drugs or alcohol (drugs defined by anticoagulants, alcohol use defined by ≥8
drinks/week)
Score b 1 warrants consideration of anticoagulation, as patient has low bleeding risk
Score 2 warrants consideration of anticoagulation, but patient has moderate
bleeding risk
Score N 3 is high risk for bleeding, and factors associated with higher bleeding risk
should be addressed
Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
7
Patients Stroke or systolic embolic Major bleeding RR
event RR (95% CI) (95% CI)
18,113 0.66 (0.53–0.82) 0.94 (0.82–1.07)
14,264 0.88 (0.75–1.03) 1.03 (0.90–1.18)
18,201 0.80 (0.67–0.95) 0.71 (0.61–0.90)
21,105 0.88 (0.75–1.02) 0.80 (0.71–0.90)
3.8. Disposition
Significant variation in patient disposition is present when manag-
ing patients with AF [97-100]. A 2015 study by Barrett et al. showed
69% of U.S. patients with a primary diagnosis of AF resulted in hospital-
ization, while only 37% were hospitalized in Canada [98]. Physicians in
Canada are more likely to cardiovert and discharge stable patients
home [30,31,36-38]. Studies have shown that discharge from the ED is
safe for most patients [30,31,37]. The introduction of anticoagulation
with DOACs allows safe, early discharge in patients requiring
anticoagulation as well. It has been suggested the patients should be ad-
mitted if they have another ED diagnosis such as pneumonia, CAD, heart
failure, or failure to achieve rate or rhythm control [30,31,100]. Other-
wise, patients are likely safe to be discharged with close outpatient fol-
low-up [100]. If anticoagulation is needed, DOACs are reliable and safe
[78-87].
In 2011, Barrett et al. developed a clinical decision model that risk
stratifies patients with symptomatic AF [97]. The authors' aim was to
estimate a patient's risk of experiencing an adverse event 30 days
after ED visit. Primary adverse outcomes included an ED return visit
within 30 days, unscheduled hospitalization, cardiovascular complica-
tion, or death. Researchers found older age, a smoking history, inade-
quate ED rate control, shortness of breath, and beta blocker treatment
were associated with an increased risk of 30-day adverse events [97].
Of the total 832 patients studied, 216 (25.9%) experienced at least 1 of
the 30-day adverse events. The authors combined these risk factors
into a clinical prediction model called the Risk Estimator Decision Aid
for Atrial Fibrillation (RED-AF). RED-AF assigns points according to
age, sex, preexisting disease such as heart failure and hypertension,
physical examination findings, and amount of rate control [97].
In a subsequent prospective cohort study, Barrett et al. validated the
RED-AF score as an aid to clinical decision making [98]. The primary out-
come was ≥1 AF-related adverse outcome such as ED revisits, re-hospi-
talization, cardiovascular complications, and death within 30 days. Of
the included patients, 24% had ≥1 adverse event within a 30-day period,
and a RED-AF score of 87 was determined to be the optimum score with
a sensitivity of 96% and specificity of 19% [98]. The RED-AF score also
had a positive predictive value of 27% and a negative predictive value
of 19%. Overall the authors conclude the RED-AF score is “moderately
better” than chance for determining adverse event, and clinicians
should not completely rely on the score. Future studies are necessary
to determine whether the score may aid in clinician assessment of risk
and disposition decisions [98]. Clinicians should continue to utilize cur-
rent society recommendations, consider discharge in otherwise stable
patients without comorbid conditions, and continue to use their own
judgment when determining the proper disposition of stable patients
with rapid AF. If secondary causes of AF are ruled out; follow-up can
be arranged; and chest pain, ST changes, CHF, and uncontrolled rate
are not present, the patient may be appropriate for discharge [8-
13,16,30,99,100].
4. Conclusions
AF is a common dysrhythmia that may lead to stroke, heart failure,
and death. Recent literature has evaluated several components of ED
8 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx
care, including evaluation, rate versus rhythm management, cardiover-
sion, anticoagulation, and disposition. The emergency physician should
first assess hemodynamic status and evaluate for secondary causes of AF
with RVR. Cardioversion is warranted in the patient with hemodynamic
instability due to AF. Several studies suggest that cardioversion in the ED
may be useful in stable patients under age 65 years with known AF
onset b48 h and limited comorbidities, as well as those with negative
TEE for intracardiac thrombus or on anticoagulation for 3–4 weeks. Pa-
tients with new onset AF may spontaneously revert to sinus rhythm
without medical or electrical cardioversion. Other patients warrant
rate control, with medication choice based on patient and situational
factors. Anticoagulation is an important consideration, with use of scor-
ing systems to calculate risk of bleeding and thromboembolism. Clinical
judgment regarding disposition is recommended, but some literature
supports discharging stable patients in specific circumstances.
Conflicts of interest
None.
Acknowledgements
This manuscript did not utilize any grants, and it has not been pre-
sented in abstract form. This clinical review has not been published, it
is not under consideration for publication elsewhere, its publication is
approved by all authors and tacitly or explicitly by the responsible au-
thorities where the work was carried out, and that, if accepted, it will
not be published elsewhere in the same form, in English or in any other
language, including electronically without the written consent of the
copyright-holder. This review does not reflect the views or opinions of
the U.S. government, Department of Defense or its Components, U.S.
Army, U.S. Air Force, or SAUSHEC EM Residency Program.
References
[1] McCartney DE, Lomas O, Cahill TJ. Atrial fibrillation. InnovAiT 2015;8(8):485–92.
[2] Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for
stroke: the Framingham study. Stroke 1991;2:983–8.
[3] Hobbs FR, Taylor CJ, Geersing GJ, et al. European primary care cardiovascular soci-
ety (EPCCS) consensus guidance on stroke prevention in atrial fibrillation (SPAF) in
primary care. Eur J Prev Cardiol 2016 Mar;23(5):460–73.
[4] Albers GW, Amarenco P, Easton JD, et al. Antithrombotic and thrombolytic therapy
for ischemic stroke. The seventh ACCP conference on antithrombotic and thrombo-
lytic therapy. Chest 2004;126 483S–S128.
[5] Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics-2014 up-
date: a report from the American Heart Association. Circulation 2014;129(3):e28.
[6] Atzema CL, Austin PC, Miller E, et al. A population-based description of atrial fibril-
lation in the emergency department, 2002 to 2010. Ann Emerg Med 2013;62:
570–7.
[7] Al-Zaiti SS. Inflammation-induced atrial fibrillation: pathophysiological perspec-
tives and clinical implications. Heart Lung 2015;44(1):59–62.
[8] January C, Wann S, Joseph S, et al. AHA/ACC/HRS guidelines for the management of
patients with atrial fibrillation: executive summary. J Am Coll Cardiol 2014;2014.
[9] Camm AJ, Kirchhof P, Lip GY, et al. Guidelines for the management of atrial fibrilla-
tion. Eur Heart J 2010 Oct;31(19):2369–429.
[10] Camm AJ, Lip GY, De Caterina R, et al. 2012 Focused update of the ESC guidelines for
the management of atrial fibrillation. Eur Heart J 2012;33(21):2719–47.
[11] Kirchhof P, Benussi S, Kotecha D, et al. 2016 guidelines for the management of atrial
fibrillation developed in collaboration with EACTS. Eur Heart J 2016;37:2893–962.
[12] Cairns JA, Connolly S, McMurtry S, et al. Canadian cardiovascular society atrial fi-
brillation guidelines 2010: prevention of stroke and systemic thromboembolism
in atrial fibrillation and flutter. Can J Cardiol 2011;27(1):74–90.
[13] Macle L, Cairns J, Leblanc K, et al. 2016 Focused update of the Canadian cardiovas-
cular society guidelines for the management of atrial fibrillation. Can J Cardiol
2016;32(10):1170–85.
[14] Dewland TA, Olgin JE, Vittinghoff E, et al. Incident atrial fibrillation among Asians,
Hispanics, blacks and whites. Circulation 2013 Dec 3;128(23):2470–7.
[15] Shenasa M, Shenasa H, Soleimanieh M. Update on atrial fibrillation. The Egyptian
Heart Journal 2014;66(3):193–216.
[16] Verma A, Cairns JA, Mitchell LB, et al. 2014 Focused update of the Canadian cardio-
vascular society guidelines for the management of atrial fibrillation. Can J Cardiol
2014;30(10):1114–30.
[17] Lloyd-Jones DM, Wang TJ, Leip EP, et al. Lifetime risk for development of atrial fi-
brillation. Circulation 2004;111(9):1042–6.
Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
[18] Mcdonald AJ, Pelletier AJ, Ellinor PT, et al. Increasing US emergency department
visit rate and subsequent hospital admissions for atrial fibrillation from 1993 to
2004. Ann Emerg Med 2008;51(1):58–65.
[19] Shenasa M, Soleimanieh M, Shenasa F. Individualized therapy in patients with
atrial fibrillation: new look at atrial fibrillation. Europace 2012;14(Suppl. 5):
v121–4.
[20] Kozlowski D, Budrejko S, Lip GY, et al. Lone atrial fibrillation: what do we know?
Heart 2010;96(7):498–503.
[21] Samokhvalov AV, Irving HM, Rhem J. Alcohol consumption as a risk factor for atrial
fibrillation: a systematic review and meta-analysis. Eur J Cardiovasc Prev Rehabil
2010;17(6):706–12.
[22] Auer J, Scheibner P, Mische T, et al. Subclinical hyperthyroidism as a risk factor for
atrial fibrillation. Am Heart J 2001;142(5):838–42.
[23] Hamilton A, Clark D, Gray A, et al. The epidemiology and management of recent-
onset atrial fibrillation and flutter presenting to the emergency department. Eur J
Emerg Med 2015;22(3):155–61.
[24] Chen PS, Chen LS, Fishbein MC, et al. Role of the autonomic nervous system in atrial
fibrillation pathophysiology and therapy. Circ Res 2014;114(9):1500–15.
[25] Kuipers S, Klouwenberg PMK, Cremer OL. Incidence, risk factors and outcomes of
new onset atrial fibrillation in patients with sepsis: a systematic review. Crit Care
2014;18:688.
[26] Sriram CS, Naccarelli GV, Luck JC. An atypical case of vagally mediated atrial fibril-
lation in an elderly woman: electrocardiographic caveats to diagnosis. J
Electrocardiol 2014;47(5):734–7.
[27] Thyagarajan B, Alagusundaramoorthy SS, Agrawal A. Atrial fibrillation due to over
the counter stimulant drugs in a young adult. JCDR 2015;9(8):OD05.
[28] Wakili R, Voigt N, Kaab S, et al. Recent advances in the molecular pathophysiology
of atrial fibrillation. J Clin Invest 2011;121(8):2955.
[29] Scheuermeyer FX, Pourvali R, Rowe BH, et al. Emergency department patients with
atrial fibrillation or flutter and an acute underlying medical illness may not benefit
from attempts to control rate or rhythm. Ann Emerg Med 2015;65:511–22.
[30] Atzema CL, Barrett TW. Managing atrial fibrillation. Ann Emerg Med 2015;65:
532–9.
[31] Stiell IG, Clement CM, Brison RJ, et al. Variation in management of recent-onset
atrial fibrillation and flutter among academic hospital emergency departments.
Ann Emerg Med 2011;57:13–21.
[32] Zimetbaum PJ, Josephson ME, McDonald MJ, et al. Incidence and predictors of myo-
cardial infarction among patients with atrial fibrillation. J Am Coll Cardiol 2000;36:
1223–7.
[33] Brown AM, Sease KL, Robey JL, et al. The risk for acute coronary syndrome associ-
ated with atrial fibrillation among ED patients with chest pain syndromes. Am J
Emerg Med 2007;25:523–8.
[34] Soliman EZ, Safford MM, Muntner P, et al. Atrial fibrillation and the risk of myocar-
dial infarction. JAMA Intern Med 2014;174(1):107–14.
[35] Weigner MJ, Caulfield TA, Danias PG, et al. Risk for clinical thromboembolism asso-
ciated with conversion to sinus rhythm in patients with atrial fibrillation lasting
less than 48 hours. Ann Intern Med 1997;126:615–20.
[36] Stiell IG, Clement CM, Symington C, et al. Emergency department use of intrave-
nous procainamide for patients with acute atrial fibrillation or flutter. Acad
Emerg Med 2007;14:1158–64.
[37] Stiell IG, Clement CM, Perry JJ, et al. Association of the Ottawa aggressive protocol
with rapid discharge of emergency department patients with recent-onset atrial fi-
brillation or flutter. CJEM 2010;12(3):181–91.
[38] Stiell IG, Healey JS, Cairns JA. Safety of urgent cardioversion for patients with re-
cent-onset atrial fibrillation and flutter. Can J Cardiol 2015;31(23):9e241.
[39] Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm
control in patients with atrial fibrillation. N Engl J Med 2002;347(23):1825–33.
[40] AFFIRM investigators. Clinical factors that influence response to treatment strate-
gies in atrial fibrillation: the atrial fibrillation follow-up investigation of rhythm
management (AFFIRM) study. Am Heart J 2005;149(4):645–9.
[41] Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and
rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J
Med 2002;347(23):1834–40.
[42] Roy D, Talajic M, Nattel S, et al. Rhythm control versus rate control for atrial fibril-
lation and heart failure. N Engl J Med 2008;358(25):2667–77.
[43] de Denus S, Sanoski CA, Carlsson J, et al. Rate vs rhythm control in patients with
atrial fibrillation: a meta-analysis. Arch Intern Med 2005;165(3):258–62.
[44] Chatterjee S, Sardar P, Lichstein E, et al. Pharmacologic rate versus rhythm-control
strategies in atrial fibrillation: an updated comprehensive review and meta-analy-
sis. Pacing Clin Electrophysiol 2013;36:122–33.
[45] Okcun B, Yigit Z, Arat A. Comparison of rate and rhythm control in patients with
atrial fibrillation and nonischemic heart failure. Japan Heart J 2004;45:591–601.
[46] Ogawa S, Yamashita T, Yamazaki T, et al. Optimal treatment strategy for patients
with paroxysmal atrial fibrillation: J-RHYTHM study. Circ J 2009;73:242–8.
[47] Michael JA, Stiell IG, Agarwal S, et al. Cardioversion of paroxysmal atrial fibrillation
in the emergency department. Ann Emerg Med 1999;33:379–87.
[48] Airaksinen KE, Gronberg T, Nuotio I, et al. Thromboembolic complications after car-
dioversion of acute atrial fibrillation: the FinCV (FinnishCardioVersion) study. J Am
Coll Cardiol 2013;62(13):1187–92.
[49] Kriz R, Freynhofer MK, Weiss TW, et al. Safety and efficacy of pharmacological car-
dioversion of recent-onset atrial fibrillation: a single-center experience. Am J
Emerg Med 2016 Aug;34(8):1486–90.
[50] Onalan O, Crystal E, Daoulah A, et al. Meta-analysis of magnesium therapy for the
acute management of rapid atrial fibrillation. Am J Cardiol 2007;99(12):1726–32.
 B. Long et al. / American Journal of Emergency Medicine xxx (2018) xxx–xxx
[51] Kalus JS, Spencer AP, Tsikouris JP, et al. Impact of prophylactic i.v. magnesium on
the efficacy of ibutilide for conversion of atrial fibrillation or flutter. Am J Health
Syst Pharm 2003 Nov 15;60(22):2308–12.
[52] David D, Segni ED, Klein HO, et al. Inefficacy of digitalis in the control of heart rate
in patients with chronic atrial fibrillation: beneficial effect of an added beta adren-
ergic blocking agent. Am J Cardiol 1979;44:1378–82.
[53] National Library of Medicine. Dailymed. Lanoxin—digoxin. Available at https://
dailymed.nlm.nih.gov/dailymed/archives/fdaDrugInfo.cfm?. archiveid.13577.
Accessed May 25, 2017.
[54] Gulamhusein S, Ko P, Carruthers SG, et al. Acceleration of the ventricular response
during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil.
Circulation 1982;65:348–54.
[55] Khand AU, Rankin AC, Martin W, et al. Carvedilol alone or in combination with di-
goxin for the management of atrial fibrillation in patients with heart failure? J Am
Coll Cardiol 2003;42:1944–51.
[56] Van Gelder IC, Groenveld HF, Crijins HJ, et al. Lenient versus strict rate control in
patients with atrial fibrillation. N Engl J Med 2010;362:1363–73.
[57] Platia EV, Michelson EL, Porterfield JK, Das G. Esmolol versus verapamil in the acute
treatment of atrial fibrillation or atrial flutter. Am J Cardiol 1989;63(13):925–9.
[58] Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison of the effectiveness of in-
travenous diltiazem and metoprolol in the management of rapid ventricular rate in
atrial fibrillation. Emerg Med J 2005;22(6):411–4 Erratum in: Emerg Med J
2005;22(10):758.
[59] Fromm C, Suau SJ, Cohen V, et al. Diltiazem vs. metoprolol in the management of
atrial fibrillation or flutter with rapid ventricular rate in the emergency depart-
ment. J Emerg Med 2015 Apr 22;49(2):175–82.
[60] Vinson DR, Hoehn T, Graber DJ, Williams TM. Managing emergency department
patients with recent-onset atrial fibrillation. J Emerg Med 2012;42(2):139–48.
[61] Martindale JL, deSouza IS, Silverberg M, et al. β-blockers versus calcium channel
blockers for acute rate control of atrial fibrillation with rapid ventricular response:
a systematic review. Eur J Emerg Med 2015 Jun;22(3):150–4.
[62] Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised
Intervention Trial in Congestive Heart Failure (MERIT-HF), Lancet 1999 Jun 12;353
(9169):2001–7.
[63] Effect of verapamil on mortality and major events after acute myocardial infarction
(the Danish Verapamil Infarction Trial II–DAVIT II), Am J Cardiol 1990 Oct 1;66
(10):779–85.
[64] The Multicenter Diltiazem Postinfarction Trial Research Group. The effect of diltia-
zem on mortality and reinfarction after myocardial infarction. N Engl J Med 1988
Aug 18;319(7):385–92.
[65] Yancy CW, Jessup M, Bozkurt B, et al. American College of Cardiology Foundation;
American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA
guideline for the management of heart failure: a report of the American College
of Cardiology Foundation/American Heart Association Task Force on Practice
Guidelines. J Am Coll Cardiol 2013 Oct 15;62(16):e147-39.
[66] Turi ZG, Braunwald E. The use of beta-blockers after myocardial infarction. JAMA
1983 May 13;249(18):2512–6.
[67] James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the manage-
ment of high blood pressure in adults: report from the panel members appointed
to the Eighth Joint National Committee (JNC 8). JAMA J Am Med Assoc 2014 Feb
5;311(5):507–20.
[68] Leenen FHH, Nwachuku CE, Black HR, et al. Clinical events in high-risk hyperten-
sive patients randomly assigned to calcium channel blocker versus angiotensin-
converting enzyme inhibitor in the antihypertensive and lipid-lowering treatment
to prevent heart attack trial. Hypertension 2006 Sep;48(3):374–84.
[69] Chiladakis J, Stathopoulos C, Davlouros P, Manolis A. Intravenous magnesium sul-
fate versus diltiazem in paroxysmal atrial fibrillation. Int J Cardiol 2001;79(2–3):
287–91.
[70] Davey M, Teubner D. A randomized controlled trial of magnesium sulfate, in addi-
tion to usual care, for rate control in atrial fibrillation. Ann Emerg Med 2005;45(4):
347–53.
[71] Joshi P, Deshmukh P, Salkar R. Efficacy of intravenous magnesium sulphate in sup-
raventricular tachyarrhythmias. J Assoc Physicians India 1995;43(8):529–31.
[72] Gullestad L, Birkeland K, Mølstad P, Høyer M, Vanberg P, Kjekshus J. The effect of
magnesium versus verapamil on supraventricular arrhythmias. Clin Cardiol 1993;
16(5):429–34.
[73] Ho K, Sheridan D, Paterson T. Use of intravenous magnesium to treat acute onset
atrial fibrillation: a meta-analysis. Heart 2007;93(11):1433–40.
[74] Chu K, Evans R, Emerson G, Greenslade J, Brown A. Magnesium sulfate versus pla-
cebo for paroxysmal atrial fibrillation: a randomized clinical trial. Acad Emerg Med
2009;16(4):295–300.
Please cite this article as: Long B, et al, Emergency medicine considerations in atrial fibrillation, American Journal of Emergency Medicine (2018),
https://doi.org/10.1016/j.ajem.2018.01.066
9
[75] Hsu JC, Maddox TM, Kennedy K, et al. Aspirin instead of oral anticoagulant pre-
scription in atrial fibrillation patients at risk for stroke. J Am Coll Cardiol 2016 Jun
28;67(25):2913–23. https://doi.org/10.1016/j.jacc.2016.03.581.
[76] Gage BF, Waterman AD, Shannon W, et al. Validation of clinical classification
schemes for predicting stroke: results from the national registry of atrial fibrilla-
tion. JAMA 2001;285(22):2864–70.
[77] Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical risk stratification for predicting
stroke and thromboembolism in atrial fibrillation using a novel risk factor-based
approach: the euro heart survey on atrial fibrillation. Chest J 2010;137(2):263–72.
[78] Pollack C. New oral anticoagulants in the ED setting: a review. Am J Emerg Med
2012;30:2046–54.
[79] Raja AS, Geyer B. Emergency department management of patients on novel oral an-
ticoagulant agents. Emerg Med Pract 2013;15(10):1–18.
[80] Ruff CT, et al. Comparison of the efficacy and safety of new oral anticoagulants with
warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials.
Lancet 2014;383(9921):955–62.
[81] Baglin T. The role of the laboratory in treatment with new oral anticoagulants. J
Thromb Haemost 2013;11(Suppl. 1):122–8.
[82] Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treat-
ment of acute venous thromboembolism. N Engl J Med 2009;361(24):2342–52.
[83] Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular
atrial fibrillation. N Engl J Med 2011;365(10):883–91.
[84] Granger CB, Alexander JH, JJ McMurray, et al. Apixaban versus warfarin in patients
with atrial fibrillation. N Engl J Med 2011;365(11):981–2.
[85] Guigliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with
atrial fibrillation. N Engl J Med 2013;369(22):2093–104.
[86] Miller CS, Grandi SM, Shimony A, et al. Meta-analysis of efficacy and safety of new
oral anticoagulants (dabigatran, rivaroxaban, apixaban) versus warfarin in patients
with atrial fibrillation. Am J Cardiol 2012 Aug 1;110(3):453–60.
[87] Villines TC, Peacock WF. Safety of direct oral anticoagulants: insights from
postmarketing studies. Am J Med 2016 Nov;129(11S):S41–6.
[88] Lip GH, Frison L, Halperin JL, Lane DA. Comparative Validation of a novel risk score
for predicting bleeding risk in anticoagulated patients with atrial fibrillation: the
HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history
or predisposition, labile INR, elderly, drugs/alcohol concomitantly) score. J Am
Coll Cardiol 2011;57(2):173–80.
[89] Apostolakis S, Lane DA, Guo Y, et al. Performance of the HEMORR(2)HAGES, ATRIA,
and HAS-BLED bleeding risk-prediction scores in patients with atrial fibrillation un-
dergoing anticoagulation: the AMADEUS (evaluating the use of SR34006 compared
to warfarin or acenocoumarol in patients with atrial fibrillation) study. J Am Coll
Cardiol 2012 Aug 28;60(9):861–7.
[90] Roldán V, Marín F, Fernández H, et al. Predictive value of the has-bled and atria
bleeding scores for the risk of serious bleeding in a “Real-World” population with
atrial fibrillation receiving anticoagulant therapy. Chest 2013;143(1):179–84.
[91] Kirchhof P, Eckardt L, Loh P. Anterior-posterior versus anterior-lateral electrode po-
sitions for external cardioversion of atrial fibrillation: a randomised trial. Lancet
(London, England) 2002;360(9342):1275–9.
[92] Allen R. Preventing hypotension effect of calcium channel blockers. Am Fam Physi-
cian 2003;67(5):940.
[93] Lipman J, Jardine I, Roos C, et al. Intravenous calcium chloride as an antidote to ve-
rapamil-induced hypotension. Intensive Care Med 1982;8(1):55–7.
[94] Midtbo K, Hals O. Can blood pressure reduction induced by slow calcium channel
blockade (verapamil) be reversed by calcium infusion? Pharmacol Toxicol 1987;
60(5):330–2.
[95] Weiss AT, Lewis BS, Halon DA, et al. The use of calcium with verapamil in the man-
agement of supraventricular tachyarrhythmias. Int J Cardiol 1983;4(3):275–84.
[96] Kolkebeck T, Abbrescia K, Pfaff J, et al. Calcium chloride before IV diltiazem in the
management of atrial fibrillation. J Emerg Med 2004;26(4):395–400.
[97] Barrett TW, Martin AR, Storrow AB, et al. A clinical prediction model to estimate
risk for 30-day adverse events in emergency department patients with symptom-
atic atrial fibrillation. Ann Emerg Med 2011;57(1):1–12.
[98] Barrett TW, Jenkins CA, Self WH. Validation of the Risk Estimator Decision Aid for
Atrial Fibrillation (RED-AF) for predicting 30-day adverse events in emergency de-
partment patients with atrial fibrillation. Ann Emerg Med 2015;65(1):13–21.
[99] Barrett TW, Self WH, Jenkins CA, et al. Predictors of regional variations in hospital-
izations following emergency department visits for atrial fibrillation. Am J Cardiol
2013;112(9):1410–6.
[100] Atzema CL, Austin PC, Chong AS, et al. Factors associated with 90 day death after
emergency department discharge for atrial fibrillation. Ann Emerg Med 2013;61
(5):539–48.