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86
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Atrial fi brillation
Kristin Cochran
1
& Shamai Grossman
2
1
Instructor in Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center,
Boston, Massachusetts, USA
2
Director, Cardiac Emergency Center and Clinical Decision Unit, Beth Israel Deaconess
Medical Center, Assistant Professor of Medicine, Harvard Medical School, Boston,
Massachusetts, USA
6
Section I: Case presentation
A 78-year-old woman is brought in by her son after
he visited her at home, and found her to be lethargic
and complaining of “not feeling well.” Her son stated
that she looked like she was having trouble breathing,
so he convinced her to let him take her to the emer-
gency department (ED), but she refused to let him
call an ambulance. The son cannot recall her medica-
tions, but states that she had a history of high blood
pressure, high cholesterol, depression, “some kind of
heart problem,” and that he thought she was taking
a “water pill.” The patient on ED arrival was lethar-
gic but arousable. She was oriented to place being the
hospital, but didn’t know the correct year. She needed
to be constantly re-aroused to answer questions. She
denied chest pain, but did complain of shortness of
breath and cough. She did not recall fevers at home.
Upon examination, she appeared somewhat lethargic
and tachypneic. The initial vital signs were: tempera-
ture 38.6˚C (101.4˚F), heart rate 146 beats/min with an
irregular pulse, blood pressure 92/48 mmHg, respira-
tory rate 26 breaths/min, O
2
saturation 91% on room
air. There was no jugular venous distention. The mucus
membranes appeared somewhat dry. The chest exami-
nation revealed rhonchi at the right base. The heart
sounds were irregularly irregular without a murmur.
The abdomen was soft and nontender, and the rectal
examination revealed hemoccult negative stool. The
skin was warm and dry and the patient appeared to be
perfusing well. There was 1⫹ pitting edema in the lower
extremities. The patient was given 100% O
2
via a non-
rebreather mask, and the oxygen saturation improved
to 97%. An electrocardiogram (EKG) was performed,
revealing atrial fi brillation at a rate of 142 beats/min
without any clear ST changes. The blood pressure was
then observed to be 83/40 mmHg with a heart rate of
148 beats/min and persistent atrial fi brillation.
Section II: Case discussion
Dr Peter Rosen: We have a patient who presents, as do
many of our elderly patients, looking ill in a nonspecifi c
way, and with nonspecifi c complaints. We have a fairly
common ED scenario in that the patient appears some-
what confused, and the history-giver, her son, doesn’t
really know very much about her, so that we’re basi-
cally performing geriatric veterinary medicine. Other
than the history of hypertension, and that she may be
on a diuretic, what in this particular clinical presenta-
tion would move you to consider a cardiac emergency?
Dr Amal Mattu: My fi rst impression when I see her
is that this is not necessarily a cardiac emergency. She
has a fever of 38.6°C (101.4°F), she’s short of breath,
a bit tachypneic, and hypoxic, so the fi rst thing I think
of is that she probably has pneumonia. Next, I might
consider a pulmonary embolus, which can also cause
ATRIAL FIBRILLATION
87
is value in placing a central line and measuring the
central venous pressure (CVP) in a patient who does
not respond to fl uid, and who remains hypotensive.
A CVP line would be very useful in this patient if she
doesn’t respond to two liters of fl uid, and that’s what
should be the next step.
PR: How do you distinguish acute from chronic atrial
fi brillation, when history is unavailable?
AM: Besides history and maybe a prior medication
list, little else would defi nitely tell me if somebody has
acute or chronic atrial fi brillation. In reading the EKG,
a subtle clue is to look at the baseline atrial rhythm.
Patients with new-onset atrial fi brillation often have
a more coarse atrial rhythm; at times, it can look as
if there is concurrent fl utter co-existing with atrial
fi brillation. If a person has atrial fi brillation of longer
duration, the size of the atrial waves become smaller
and smaller, and it becomes more of a fi ne atrial fi bril-
lation rather than a coarse atrial fi brillation, but that’s
not always reliable.
PR: Is there any utility in looking for atrial enlarge-
ment on EKG to help determine chronicity or acuity
of atrial fi brillation?
SG: If you fi nd atrial enlargement, it would make
chronic atrial fi brillation more conceivable, but fi nd-
ing it on the EKG is not enough to say this patient has
chronic atrial fi brillation as many people have atrial
enlargement without atrial fi brillation. Although I
might look for atrial enlargement on the EKG, it is
more useful to put an ultrasound probe on the patient
to look for enlargement of the atrium; however, left
atrial enlargement, even by ultrasound, remains a
nonspecifi c marker for atrial fi brillation.
PR: Let’s say you had a better history and knew that
this was new-onset atrial fi brillation (AF); would you
be inclined to immediately convert this person to a
sinus rhythm?
AM: If the reminder of the presentation was unchanged,
I would not attempt immediate cardioversion. When
someone has new-onset AF, there are two questions
that you ask yourself. Question number one: Did the
new-onset AF cause the symptoms that the patient is
having? Question number two: Is there some underly-
ing condition that has caused the atrial fi brillation? In
this case, I think the latter is correct. The patient has
underlying sepsis and pneumonia, and that condition
low-grade fevers. However, she’s very tachycardic at
146 beats/min and the blood pressure is borderline
at 92/48 mmHg, making septic shock more likely.
Instead of dwelling on the diagnosis here, I would
obtain IV access, begin fl uid resuscitation, place her
on a monitor, obtain an EKG and a quick chest X-ray
study, though not because I thought this was a cardiac
emergency. Even when I see the EKG, it seems like
her primary problem is not a cardiac problem, but an
infectious one, with a secondary cardiac problem.
Dr Shamai Grossman: I fi nd that sometimes we become
obsessed with one element of the patient’s presentation,
such as physical fi ndings, history, or EKG, and we miss
looking at the patient as a whole. This is a great exam-
ple of a patient who looks like sepsis, but who also has
a cardiac emergency and the cardiac emergency is the
lesser evil. The priority here is to address the greatest
life threat fi rst. Here, this means treating what is likely
an acute infectious process or sepsis infl ammatory syn-
drome, and to succeed one needs to jump on the band-
wagon early and begin therapy aggressively.
PR: One of the few physical fi ndings that help you in
making a cardiac diagnosis is the irregular irregular-
ity of the pulse. Clearly, patients who have underlying
atrial fi brillation can suffer from diseases that are not
directly related to the heart, such as pulmonary embo-
lism (PE), stroke, and even pump failure, all of which
should be considered in this patient. This presentation
must also make you consider metabolic disease, even
though sepsis is higher on our list; a patient who is hav-
ing complications of diabetes or adrenal insuffi ciency
can also look like this. The initial approach to all
of these problems is fl uid resuscitation, antibiotics,
and an attempt to fi nd the source of the sepsis, looking
at the urine as well as the chest, even though it sounds
more like pneumonia. We fi nd many patients in whom
we end up concentrating on the dysrhythmia, when
what we should be concentrating on is the tachycar-
dia itself as a form of volume depletion. Do you see
any utility in placing a central line in this patient?
AM: I would only use a central line if we need to admin-
ister vasopressors. As long as you can get good periph-
eral access with large bore IVs, you can rehydrate this
patient and effectively administer antibiotics.
SG: There is growing evidence that goal-oriented
treatment for sepsis signifi cantly reduces mortality
in sepsis. As part of this treatment regimen, there
CHAPTER 6
88
SG: Echocardiography should be limited to a patient
whose CVP measurements do not respond to your
initial volume-repletion or antibiotic therapy, and
remain hypotensive and tachycardic.
PR: Here we have a patient who clearly looks and acts
ill, has a source of fever, and even though she initially
responds somewhat to therapy, she continues to look
ill. Would you agree that it’s well worth taking away the
work of ventilation from this patient by intubating her?
AM: I think intubation in sick septic patients is useful
not only by decreasing the work of breathing, but, as
in our patient, to also help maximize the oxygenation.
However, we must remember that when we intubate
patients, we increase intrathoracic pressure, and if
this patient is already hypotensive and hypovolemic,
increasing intrathoracic pressure is going to decrease
preload and decrease cardiac output and blood pres-
sure even more. So when this type of patient gets
intubated, we need to do everything possible to get
fl uids in as quickly as possible, otherwise that patient
is going to drop the blood pressure further right after
intubation.
PR: Although I wouldn’t worry about the patient’s atrial
fi brillation until we felt that we had strongly and effec-
tively managed the sepsis, atrial fi brillation always wor-
ries me with its potential for cerebral embolization. Is
this a patient who you feel ought to be anticoagulated?
AM: I would anticoagulate a patient if there was uncer-
tainty regarding how long the atrial fi brillation had
been going on. Given the uncertainty in this patient’s
history, and I don’t think that you are going to get
more useful information here, I would start heparin.
SG: There is no rush to anticoagulate here since the
AF may terminate itself over the course of the next
few hours, while treatment for sepsis gets underway
in earnest.
PR: It looks like the patient was thought to have sep-
sis. Aggressive management of the sepsis was under-
taken, and the atrial fi brillation was thought to be less
important in the management of this patient. Should
this patient have any other cardiac evaluations, or are
you content to just leave your money on sepsis?
AM: I would check the rest of the electrolytes and
renal function, but the only additional test that I
would do is to check thyroid function studies.
caused atrial fi brillation. When AF is caused by some-
thing else, initially you have to focus more on treat-
ing the underlying condition. The patient’s infection
needs to be treated aggressively; the patient needs
fl uid resuscitation, and if you under-resuscitate and
just give medications to treat the AF, then you might
allow the blood pressure to bottom out even more,
and thus make a sick patient even sicker.
SG: I might add that if you try to treat the AF with-
out trying to treat the underlying disease, most likely
the atrial fi brillation will recur. Unless you change the
circumstances that enabled the AF to start in the fi rst
place, you are not likely to successfully convert the
patient to a sinus rhythm.
PR: We used to treat chronic AF patients with digoxin,
which in turn would prompt a series of questions: is
the patient adequately digitalized, or over-digitalized,
is digoxin the cause of the tachycardia, or is digoxin
playing its proper role? In order to see if the patient’s
tachycardia was capable of changing with medication
management, we would give a dose of atropine, and
if the heart rate speeded up, then the patient needed
more digoxin; but, if the heart rate didn’t speed up,
then the patient was maximally digitized. In later
years, we could do digoxin levels to help ensure that
the patient was adequately dosed. If you found that
one of our patient’s medications was digitalis, what
would make you concerned about toxicity?
AM: Usually with digoxin toxicity, you can have under-
lying atrial fi brillation or paroxysmal atrial tachycardia,
with varying degrees of atrioventricular (AV) block.
However, when a patient is digoxin toxic, the ventricular
response is usually much slower than 100, let alone 146,
so in this case I would not suspect digoxin toxicity.
SG: Beyond that, if the patient is maintaining this
rhythm even if they are digoxin toxic, and even if you
run a digoxin level and it’s high, running a tachycar-
dia in this case is not necessarily a bad thing. As an
aside, this is why digoxin levels are often not useful.
Many patients can be clinically therapeutic at seem-
ingly toxic levels, while others can be clinically digi-
talized at very low levels.
PR: Is there utility in obtaining an early echocardio-
gram on this patient, potentially looking for a PE?
Even though she has infi ltrates, couldn’t she have had
a PE as the precipitating cause?
ATRIAL FIBRILLATION
89
Case resolution
By the following morning, the patient had spontane-
ously converted to sinus rhythm, was off all pressors
and oxygen support, and was able to transfer out of
intensive care. She was discharged from the hospital
2 days later, and was doing well in sinus rhythm on
her 6-month follow up.
Section III: Concepts
Background
The mechanism of atrial fi brillation is that of multiple
disorganized re-entrant circuits within the atria. The
atrial rate is often so fast (350–600) that P waves are
not seen on an EKG, and since the atrial discharge
rate may be in the 300s, many of these impulses will
encounter refractory myocardium at the AV node.
Only a portion of atrial impulses will reach the ven-
tricles, causing an irregular and sometimes rapid
ventricular rate (Figure 6-1). This affects hemody-
namics predominantly in two ways: (1) rapid ven-
tricular rates decrease the time of diastolic fi lling, and
(2) the loss of an organized atrial impulse eliminates
PR: I think that’s a very good idea, as we forget
that atrial fi brillation may be the presentation of
hyperthyroidism in the elderly, and that cardiac
manifestations often outweigh the peripheral mani-
festations that we see in younger patients with thy-
rotoxicosis. Nevertheless, this is not somebody who
needs immediate management of a thyroid condi-
tion, unless this were thyroid storm.
AM: If we truly were considering thyroid storm, then
I would start steroids, and maybe give earlier consid-
eration to the use of a beta-blocker, but the rest of her
treatment with propylthiouracil (PTU) and iodine, I
would coordinate with the admitting team. I would
still focus on fl uid resuscitation.
SG: I’m very reluctant to give beta-blockers to patients
in shock, and would be very judicious in their use in
this population.
PR: In summary, we have a patient whose care could
easily be blinded by the dysrhythmia, but the correct
approach is the one that was taken here; go after the
sepsis and worry less about the dysrhythmia until after
your sepsis has been addressed, and by then hopefully
your patient will have responded.
Discharge
Score 1-2 =
clinician
judgment
aspirin vs.
warfarin
ATRIAL FIBRILLATION
> 48 hours or unknown
Rate control
CHADS2
Score 0 =
Aspirin
Score 3 or greater
= warfarin
Stable
Elective DC
Cardioversion
< 48 hours
Observe x 6 hrs
Afib
Sinus x 2 hr
Discharge
ADMIT
Dysrhythmia is primary
cause of instability
Anticoagulate and
DC cardiovert
Unstable
Treat the primary
cause of instability
Other primary cause
of instability
Figure 6.1 Atrial fi brilation.
CHAPTER 6
90
blood pressure ⬍90 mmHg, heart failure, or reduced
consciousness.
5,6,7
If the patient is found to be unstable, then time is of
the essence. Obtaining a few other key clues from his-
tory and physical examination will help direct you to
the safest course of action, as not all unstable patients
with atrial fi brillation are unstable because of the atrial
fi brillation. Advanced cardiac life support guidelines
recommend immediate DC cardioversion for all unsta-
ble patients with rapid atrial fi brillation; however, con-
sidering that the tachycardia may have been triggered
by the body’s effort to compensate for hypotension
caused by another primary source (such as hypov-
olemia or sepsis), attempts to slow the rate in these
cases have potential to worsen the patient’s condition.
In these specifi c situations, the safest course of action
may be to direct therapy to the primary source of insta-
bility rather than at the atrial fi brillation (for instance,
by providing volume or pressor support that may, in
itself, reduce the ventricular response rate). A focused
physical examination at this juncture should look for
other sources of instability such as infection, other sep-
sis, gastrointestinal hemorrhage, hypovolemia, or signs
of chronic heart disease like diffuse volume overload.
Similarly, a focused history at this time, if obtainable,
in addition to assessing for symptoms of instability like
chest pain, should investigate symptoms suspicious for
infection, gastrointestinal bleeding, hypovolemia, cor-
onary artery disease, thyroid disease, alcohol use, and
drug use, as well as the duration of the current symp-
toms. A history of symptoms for fewer than 48 hours
may contribute to management decisions, given that
anticoagulation has typically been recommended prior
to cardioversion of patients with symptoms for longer
than 48 hours. However, the risk of thromboembolic
events in patients with atrial fi brillation for less than
48 hours has been shown to be less than 1%, and
thus, in this instance, anticoagulation is generally
not needed.
8
It is also important to know if this is
the fi rst episode of atrial fi brillation, or a recurrence
of paroxysmal atrial fi brillation. If it is not new-onset
atrial fi brillation, then it is also valuable to know the
patient’s history related to atrial fi brillation including
home medications (including any anticoagulants), any
history of cardioversion, and subsequent recurrence.
Lastly, if the patient is unstable, and you anticipate
having to initiate treatment rapidly, anticoagulation
may be indicated, and it is important to know if the
patient has any contra-indications to anticoagulation.
the contribution of the atria to ventricular fi lling. Also,
because of the loss of the organized atrial contraction,
there is a stasis of blood in the atria that leads to a sig-
nifi cant risk of thrombus formation and subsequent
embolization of that thrombus. In part due to this
mechanism, atrial fi brillation is a signifi cant cause of
morbidity and mortality in the US. The cardiovascular
event risk for patients older than 60 with lone atrial
fi brillation has been quoted as high as 5% per year.
1
Atrial fi brillation increases the risk of stroke fi vefold
and, even when adjusted for other cardiovascular con-
ditions, atrial fi brillation is associated with as high as
a 1.5 to 1.9-fold increase in mortality.
2,3
Furthermore,
atrial fi brillation is estimated to be present in approxi-
mately 2.3 million Americans, and has been projected
to affect 5.6 million by the year 2050.
4
Initial atrial fi brillation workup
The fi rst consideration when encountering a patient
with atrial fi brillation, much like any other patient in
the ED, is the question: Is the patient stable or unsta-
ble? Does the patient appear to be in distress? What
are the vital signs? Is the patient tachycardic, hypoten-
sive or hypoxic? Is the patient showing signs of hypo-
perfusion such as altered mental status, chest pain, or
mottling? Does the patient show signs of pulmonary
edema? Does the patient have other signs of heart fail-
ure such as jugular venous distention or pedal edema?
As these assessments are being made, the patient should
be placed on oxygen and monitoring. Laboratory tests
should be drawn, and access should be obtained, pref-
erably with the placement of two large bore IVs if the
patient is unstable. An EKG should be obtained and
interpreted fully, particularly for rhythm, rate, and
signs of ischemia. Other clues from the EKG that may
aid in management include signs of electrolyte abnor-
malities, atrial enlargement, left ventricular hypertro-
phy, and right heart strain. Look for delta waves or
wide complex rhythms that may be due to an under-
lying Wolfe-Parkinson-White syndrome (WPW); this
would change management decisions regarding phar-
macologic rate control, as AV nodal blocking agents
are contra-indicated in wide complex WPW tachy-
cardias. The UK National Institute for Health and
Clinical Excellence and the joint American-European
Atrial Fibrillation guidelines, as well as the European
Resuscitation Council guidelines, defi ne instability as
ventricular rates ⬎150, persistent chest pain, systolic
ATRIAL FIBRILLATION
91
infl ammatory change underlies the development of
atrial fi brillation.
15
This theory also explains why
low-level chronic infl ammatory states like diabetes
and coronary artery disease are risk factors for the
development of atrial fi brillation, as well as why
acute infl ammatory states (like postoperative recov-
ery, ischemia or infection) can precipitate or exacer-
bate atrial fi brillation.
A particularly complicating fact is that in the case
of congestive heart failure or hypotension, atrial fi bril-
lation can be either the cause or the effect, and the
correct sequence as to which came fi rst can be hard to
distinguish, especially in the acute care setting.
Testing
The testing indicated varies greatly with the clinical
situation. The diagnosis of atrial fi brillation itself
can be made simply by reviewing an EKG; however,
diagnosing the etiology of the atrial fi brillation, or the
acute episode of rapid ventricular response, is more
of a challenge given the myriad of etiologies listed
previously. In the patient presenting with a new-
onset asymptomatic atrial fi brillation without obvi-
ous cause, an acceptable workup in the ED would
include complete blood count, electrolytes, TSH, and
chest X-ray study. Patients who are being maintained
on anticoagulants should have a coagulation panel
checked. For the remainder of patients, the workup is
directed by a pertinent history and other complaints.
For instance, in the diabetic patient with abdominal
pain, mesenteric ischemia should be ruled out. For the
cancer patient with sudden onset pleuritic chest pain,
pulmonary embolism should be investigated. The
patient who has signifi cant chest pain and ST-segment
changes on EKG should be ruled out for myocardial
infarction (MI).
The patient with chest pain and ST changes on
EKG can be a challenge, because depending on the
rate of the atrial fi brillation, there may be chest
symptoms and EKG changes that are simply related
to rate. Zimetbaum, et al.
16
examined the incidence
and predictors of myocardial infarction among 255
patients with atrial fi brillation in the ED. They fi nd
the incidence of acute MI in new-onset atrial fi brilla-
tion patients to be approximately 11%, agreeing with
a prior study that cites the incidence at 11% for new
onset AF.
17
The incidence of MI in all comers to the
Etiologies of atrial fi brillation
The etiologies of atrial fi brillation are varied and
numerous, including everything from infectious to
ischemic, endocrine, toxicologic, postsurgical, and
obstructive causes. In fact, anything that can pre-
cipitate sinus tachycardia can also precipitate atrial
fi brillation; examples include infection, congestive
heart failure, hypovolemia, anemia, pulmonary
embolism, alcohol intake, hyperthyroidism, elec-
trolyte abnormalities, valvular disease, and even
electrocution. The Framingham study demonstrates
diabetes, hypertension, congestive heart failure,
valvular disease, and myocardial infarction to be
signifi cant risk factors in the development of atrial
fi brillation.
3
In addition to all of the previously
mentioned etiologies, atrial fi brillation can also be
idiopathic.
Binge alcoholics frequently present with atrial dys-
rhythmias, the most common of which is an atrial
fi brillation that usually converts to normal sinus
rhythm within 24 hours. This syndrome, called
a “ holiday heart,” should be considered in all ED
patients presenting with new-onset atrial fi brillation
without structural heart disease. Possible mechanisms
include increased secretion of epinephrine and norepi-
nephrine, increased sympathetic output, and a rise in
the level of plasma-free fatty acids and acetaldehyde
metabolites of alcohol. Calcium channel blockade is
very effective if rate control is needed. If the patient
is failing, has chest pain, or doesn’t convert within
24 hours, then this may not be “holiday heart,” and
general protocols for atrial fi brillation management
should be followed.
9,10,11
Atrial fi brillation may be a consequence of infl am-
matory states that cause atrial structural remodel-
ing. Correlation has been found between elevated
C-reactive protein (CRP) levels and the atrial fi brilla-
tion burden, meaning that those patients with atrial
fi brillation have higher levels of CRP than controls,
and that those patients with persistent atrial fi bril-
lation have higher CRP levels than those with par-
oxysmal episodes.
12,13
Patients with atrial fi brillation
and underlying idiopathic dilatated cardiomyopathy
have higher serum levels of CRP than those with-
out.
14
In addition, myocardial tissue samples from
patients with atrial fi brillation demonstrate increased
levels of oxidative damage as compared to controls
without atrial fi brillation, supporting the theory that
CHAPTER 6
92
depending on the clinical situation. Critical decision
points are whether the patient is stable or not, and
whether the patient has been in atrial fi brillation for
longer than 48 hours.
Determination of instability has been outlined
above. Current clinical guidelines dictate direct current
cardioversion for patients determined to be unstable.
6
Given these guidelines, it is unethical to randomize
acutely unstable patients to other treatments, and, as
such, there are no prospective clinical trials investigat-
ing other therapies (e.g., fl uids or pressors) directed
toward treating underlying causes of unstable atrial
fi brillation, such as sepsis or hypovolemia. DC car-
dioversion is recommended over chemical cardiover-
sion in this setting because of the delayed effect of
chemical cardioversion. Furthermore, even for the
stable patient who has been in atrial fi brillation for
under 48 hours, DC cardioversion is often preferred
to chemical cardioversion, not only because of the
immediate effect of electrical cardioversion, but also
because of the higher success rate and lower incidence
of prodysrhythmic complications with DC cardiover-
sion.
18
Current ACC/AHA guidelines also recommend
administration of heparin prior to emergent cardio-
version; however, this should not signifi cantly delay
cardioversion.
19
Once the patient in AF has been determined to be
stable, the choice becomes rate control or rhythm
control. If the patient has been in atrial fi brillation
for less than 48 hours, the risk of atrial thrombus
is less than 1%; therefore, attempts may be made
at elective cardioversion to sinus rhythm in the ED
without necessitating anticoagulation for three weeks
prior to cardioversion.
8
However, atrial thrombi are
reported to be present on transesophageal echocar-
diogaphy (TEE) in 15% of patients whose symptoms
were reported to be less than 48 hours in duration.
20
In addition, atrial fi brillation very frequently has
“silent” or asymptomatic episodes, so a patient’s
description of duration of symptoms may inaccu-
rately predict actual duration of the dysrythmia.
21
Therefore, current ACC/AHA guidelines do rec-
ommend starting anticoagulation with heparin or
lovenox at presentation even for patients with atrial
fi brillation of less than 48 hours duration, as there
may still be thrombus formation even after sinus
rhythm is restored.
6,22–24
Current guidelines suggest
that anticoagulation be used postcardioversion for
all patients who have other stroke risk factors (based
ED with AF is 2.3% in the Zimetbaum study; how-
ever, this does not exclude patients who had preexist-
ing atrial fi brillation. The sensitivity and specifi city of
chest pain for acute MI in atrial fi brillation are 100%
and 65%, respectively, with a positive predictive value
of 14%. The most sensitive and specifi c predictor of
MI is the presence of major ST-segment deviation—
defi ned as ⬎2 mm of ST-segment depression or any
ST-segment elevation—on the presenting EKG. This
factor has a positive predictive value of 86% and a
negative predictive value of 100%. This study does
not note the average heart rate on the presenting EKG
for these patients.
There is controversy about whether to measure
levels of cardiac enzymes in patients with atrial
fi brillation, and specifi cally with rapid atrial fi bril-
lation. Troponins may be elevated as the result of
demand ischemia, the mechanism for which is two-
fold. Tachycardia causes an increase in the myocar-
dial oxygen demand, while also decreasing the time
for diastolic subendocardial perfusion. The clinical
signifi cance of this subendocardial demand ischemia
is largely dependent on the degree of ischemia. This
can also be further modifi ed by the patient’s under-
lying coronary artery disease, diastolic dysfunction,
and length of time in tachycardia. As such, the next
challenging decision for the emergency physician
is what to do about the elevated troponin when it
results. In some scenarios, it may be hard to dif-
ferentiate ischemia as the cause or the effect of
the rapid ventricular response. Some would argue
that if cardiac ischemia is unlikely to be the cause
of the atrial fi brillation, and if clinically signifi cant
demand ischemia is unlikely, measuring cardiac
enzymes may provide more questions than useful
answers. Appropriate rate or rhythm control should
be undertaken as needed, and measurement of car-
diac enzymes may be undertaken depending on the
clinical scenario. Decisions regarding how to treat
elevated enzymes may necessitate cardiology consul-
tation, and hospital admission for further observa-
tion or testing.
Acute management
Atrial fi brillation with rapid ventricular response is a
common occurrence in the ED, and can be appropri-
ately treated with rate control, rhythm control, directed
therapy for the underlying cause, or anticoagulation,
ATRIAL FIBRILLATION
93
who have a signifi cant contra-indication to antico-
agulation, TEE should be performed to assess the
presence of thrombus before any attempt at elective
cardioversion is made.
There are several options for rate control of atrial
fi brillation in the ED, including calcium channel
blockers (e.g., diltiazem, verapamil), beta-blockers
(e.g., esmolol, metoprolol), magnesium, and amio-
darone (Table 6-2). The use of digoxin acutely in the
ED is limited due to its delayed effect on rate control.
The use of IV amiodarone for acute rate control has a
high incidence of side effects including hypotension.
26
Magnesium has been shown to be safe and effective
for rate control, and has been demonstrated to be as
effective as amiodarone and diltiazem for this purpose
regardless of underlying magnesium depletion.
27
The
two most popular options are calcium channel block-
ade and beta-blockade. Diltiazem has been shown to
be superior to both digoxin and amiodarone for acute
rate control in atrial fi brillation.
28
In addition, another
study demonstrates that diltiazem and metopolol are
both safe and effective for ventricular rate control;
however, the effect with diltiazem is greater and is
seen earlier than that of metoprolol.
29
Depending on
the clinical situation, one class may be more benefi cial
on CHADS2, see Table 6-1) or if the patient has had
more than one episode of paroxysmal atrial fi bril-
lation.
6
The AFFIRM trial in 2002 demonstrates
that rate control is at least equivalent to rhythm
control in the management of atrial fi brillation.
25
Considering this, and the frequency with which
the length of the dysrythmia is unknown, many ED
patients, including all who have stable symptoms of
greater than 48 hours duration, are treated with rate
control and some form of anticoagulation. Patients
may electively be cardioverted as outpatients after
an adequate period of anticoagulation. For patients
Table 6-1. The CHADS2 score.
A decision tool guiding long-term anticoagulation in
patients with atrial fi brillation based on stroke risk.
C Congestive heart failure 1
H Hypertension 1
A
Age ⬎75
1
D Diabetes 1
S Prior stroke 2
Score 0: aspirin therapy only
Score 1–2: physician judgment
Score 3 or greater: coumadin
Table 6-2. Rate control medications for atrial fi brillation with rapid ventricular response.
Drug
Patient
Population Loading Dose
Maintenance
Dose Onset
Approximate
Half-life Side Effects
Diltiazem Stable patients 0.25mg/kg IV
over 2 min
5–15 mg/hr 2–7 min Moderate
(hours)
Hypotension,
decreased AV
nodal conduction
Metoprolol Ischemia,
thyrotoxicosis
2.5–5mg IV
bolus over 2 min.
Up to 3 doses
n/a 5 min Moderate
(hours)
Hypotension,
decreased AV
nodal conduction,
bronchospasm
Esmolol Ischemia,
thyrotoxicosis
0.5mg/kg
over 1 min
0.05–0.2
mg/kg/min
5 min Short
(minutes)
Hypotension,
decreased AV
nodal conduction,
bronchospasm
Magnesium Mg-depleted
(alcoholics)
1g over
20 min
Variable 5 min Short
(minutes)
Hypotension
Amiodarone Wide complex
tachycardia
150mg IV
bolus over
10 min
1mg/min for 6 hr,
then 0.5mg/min
for 18hr
20 min Long (days) Hypotension
Digoxin Refractory to fi rst
line therapy
0.25mg IV Q2hrs
up to 1.5mg
n/a 2 hours Long (days) Digoxin toxicity,
heart block
CHAPTER 6
94
have been in atrial fi brillation for less than 48 hours
will spontaneously revert back to a sinus rhythm.
33
Current guidelines recommend administering heparin
or lovenox upon presentation for these patients.
6
One
study evaluated a protocol for observation of these
patients in the ED, with electrical cardioversion at
6 hours if not already spontaneously converted. Eighty-
fi ve percent of patients are able to be discharged from
the observation unit after converting to a sinus thythm,
and remaining in a sinus rhythm for 2 hours. Thirty-
two percent convert spontaneously with only rate con-
trolling medications.
34
The utility of ED observation
protocols for this clinical scenario greatly depends on
the volume and resources of each individual ED.
Section IV: Decision making
Decide if the patient is stable or unstable.•
Treat the underlying cause of instability fi rst.•
If the rapid ventricular rate is the cause, emergently
cardiovert and anticoagulate.
If there is a more likely physiologic cause of
instability, initial treatment should be directed
here.
In the stable ED patient with atrial fi brillation, •
attempt rate control or DC cardioversion if within
48 hours of onset.
Admission may not be necessary unless there are •
underlying signs of ischemia or concurrent acute
medical issues.
Most patients should have anticoagulation •
postcardioversion.
References
Kopecky SL, Gersh BJ, McGoon MD, et al. Lone atrial 1
fi brillation in elderly persons: a marker for cardiovascu-
lar risk. Arch Intern Med. 1999;159:1118–1122.
Wolf PA, Abbott RD, Kannel WB. Atrial fi brillation as 2
an independent risk factor for stroke: the Framingham
Study. Stroke. 1991;8:983–988.
Benjamin EJ, Wolf PA, D’Agostino RB, et al. Impact of 3
atrial fi brillation on the risk of death: the Framingham
Heart Study. Circulation. 1998;98:946–952.
Go AS, Hylek EM, Phillips KA, et al. Prevalence of 4
diagnosed atrial fi brillation in adults: national implica-
tions for rhythm management and stroke prevention: the
than the other. For instance, in the case of myocar-
dial ischemia or postcardiac surgery patients, beta-
blockade may have additional benefi t. In the case of
the patient with systolic dysfunction, calcium channel
blockade may be more likely to precipitate hypoten-
sion. There are some studies, however, that report that
pretreatment with IV calcium may blunt the hypoten-
sive effect of calcium channel blockers while preserv-
ing the rate controlling effects.
30
In the patient with
underlying reactive airway disease, calcium channel
blockade may be chosen over beta-blockade to pre-
vent the precipitation of bronchospasm.
In addition to controlling rate or rhythm, atten-
tion needs to be paid to decreasing the incidence of
secondary embolic events with anticoagulation. The
CHADS2 scoring system (Table 6-1) has been vali-
dated as a tool to determine which patients in atrial
fi brillation need chronic anticoagulation.
31,32
Patients
get one point each for congestive heart failure, hyper-
tension, age greater than 75 years, and diabetes, and
two points for having a prior stroke. By this scoring
system, patients with a score of 0 may be managed
with aspirin therapy only. Scores of 1–2 are left up
to the physician’s clinical judgment (though current
guidelines favor warfarin therapy), and a score of 3 or
greater indicates chronic warfarin therapy.
6
Disposition
Emergency department patients with new-onset atrial
fi brillation who have other signifi cant comorbidities
(particularly cardiac disease), instability, or concur-
rent ischemia should be admitted to the hospital for
further management. Furthermore, patients for whom
anticoagulation is indicated benefi t from inpatient
admission for initiation of anticoagulation and rate
controlling therapy. Patients who have signifi cant
contraindications to anticoagulation may need to be
admitted to the hospital for TEE to assess for throm-
bus formation, and to weigh the risks and benefi ts of
cardioversion versus chronic rate control.
Patients who have been in stable atrial fi brillation
for less than 48 hours and who convert back to a sinus
rhythm in the ED may be observed for a short period
and discharged with close follow up. Another choice
in managing patients with stable atrial fi brillation for
less than 48 hours is to simply observe the patient
for a period, as approximately 50% of patients who