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BNP levels are < 100 pg/mL). HF can be excluded
from the differential for patients with BNP < 100
pg/mL as its negative predictive value is as high as
96%.
20
Clinicians should pay close attention to
patients with moderately elevated levels to exclude
other causes of elevated PCWP.
OU Exclusion Criteria
Severely compromised, unstable patients should
not be admitted to the OU, especially, p atients
with a high probability of unfavorable outcomes
due to acute myocardial ischemia or other critical conditions as they should be hospitalized as
inpatients. Increased blood urea nitrogen (> 43
mg/dL) and low admission systolic blood pressure (<
115 mmHg) are two of the most significant independent predictors of acute mortality in
patients with ADHF and showed a 12.9%
increased mortality rate in one study.
11,21–22
Patients with an elevated BUN (43 mg/dL), low
systolic BP (SBP <
115 mmHg), and elevated
creatinine (2.75 mg/dL) are strong predictors of
acute mortality, thus, they should not be admitted to the OU.
21–22
In addition, patients with airway instability,
cardiac arrhythmias requiring continuous intravenous (IV) intervention, and inadequate systemic
perfusion should not be admitted to the OU.
23
For
similar reasons, patients requiring vasodilator
therapy, including agents such as nitrates and
nitroprusside,
6
are generally not good OU candidates. While intravenous vasodilators have potential benefits of reversing the decompensation by
stabilizing hemodynamics, their need reflects a
severity of illness beyond OU management.
23
Appropriate OU Therapy
The main objectives of ADHF management in
OU is to determine the type of HF (e.g., systolic
or diastolic), to identify the factors that led to
acute decompensation, to reduce fluid overload,
to optimize ACE inhibitor therapy, to educate the
patient, and to arrange patient treatment after
discharge.
6
Pharmalogical Therapy
Diuretics
Diuretics are often the first line of therapy for
ADHF patients for the rapid and effective
reduction of fluid thereby relieving dyspnea.
24
One recommended regimen is presented in
Figure 23.1. Despite the substantial clinical utility
of diuretics, clinicians must understand their
potential side effects and limitations in managing
ADHF.
6
Diuretics can result in decreased renal
perfusion and neurohormonal activation by
increasing renin and norepinephrine.
25
In addition to renal dysfunction and maladaptive neurohormonal activation, a numb er of studies have
reported other adverse effects including hypotension and electrolyte imbalance.
6
Despite decades of clinical usage of loop diuretics, guidelines of dosage and mode of administration have not been firmly established. The
DOSE trial provides objective clinical outcome
with various diuretic strategies. The study prospectively compared different strategies in mode
of administration of different furosemide dosages.
Overall, there was no significant difference in the
patients’ global assessment of symptoms or in the
mean change in the creatinine level for IV bolus
and continuous infusion strategies as well as highdose or low-dose diuret ics. In fact, the high-dose
strategy was associated with greater diuresis and
more favorable outcomes in some secondary
measures, but also with transient worsening of
renal function.
26
Until the advent of new technologies, diuretics
will continue to be employed as the main therapeutic agent of ADHF, but physicians should be
aware of the adverse effects and employ diuretics
judiciously.
6
ACE Inhibitor
When used chronically, angiotensin-converting
enzyme (ACE) inhibitors have been shown to
alleviate symptoms, improve clinical status, and
reduce the risk of death and the combined risk of
death and hospitalization.
26
ACE inhibitors
antagonize the renin-angiotensin-aldosterone
system thus making them a good class of agents
for chronic HF treatment. There are many studies
showing the benefits of ACE inhibitors in chronic
HF, but few have been conducted in the acute
setting. Due to lack of large controlled studies
and the potential for adverse events such as hypotension and renal dysfunction, ACE inhibitors are
not currently considered as standard of care in the
acute management of ADHF. Nevertheless, the
limited data and anecdotal reports of successful
Heart Failure
026
20:43:41
use in the OU are encouraging and warrant further investigation to deter mine their utility in
these patients.
6
Ejection Fraction
EF is considered the “single most important
measurement in HF”
11
by noninvasively assessing
ventricular function. EF is useful in defining the
etiology and HF type and is recommended to help
determine treatment strategies.
Criteria for Hospital Admission
from the OU
Patients should be admitted to the hospital for
further management when their clinical condition
fails to improve or deteriorates. Pa tients who
exhibit sustained ventricular tachycardia, symptomatic cardiac arrhythmias, worsening renal
function, unstable vital signs, ischemic chest pain,
ECG changes, or develop elevated cardiac biomarkers of necrosis should be strongly considered for
ICU admission.
11
Even without clinical deterioration, failure to
have sufficient urinary output or a further need
for diuresis requires hospitali zation. Persistent
dyspnea or electrolyte imbalance also justifies
the need for inpatient hospitalization.
Finally, patients who require extra care in
social and medical circumstances should be considered for a long-term care plan. These patients
include those with physical disabilities, mental
challenges, financial troubles, or severe substance
abuse problems.
11
It is crucial that the utility of OU management
is not overlooked or denied because of the further
need of subsequent hospital admission after OU
management. Even when patients require hospitalization after an OU admission, they will have a
subsequently decreased overall LOS for more
than 20 hours
5
compared to similar patients dir-
ectly admitted to the hospital.
6
Criteria for Discharge
Since every HF patient presents with unique
symptoms and baseline health status, an individualized discharge evaluation should be made for
each patient. Certain basic criteria must be met
to insure an optimal outpatient course. Patients
should report subjective improvement in symptoms, have achieved an adequate response to
diuretic therapy with a total net urine output
greater than 1 liter, and have normal cardiac
biomarkers. The patients should also be ambulatory or at their baseline, exhibit stable electrolytes,
have no new presentation of clinically significant
arrhythmias, and have a normal range of vital
signs with a systolic blood pressure >
95 mmHg
and a resting pulse rate <
100 beats per minute.
11
Although improvement in clinical congestion
is a subjective assessment, objective measurements such as a reduction in jugular venous pressure, resolution of rales, edema, and orthopnea,
and change in the patient’s weight from presentation to discharge can be assessed, and suggest a
greater probability of outpatient success. This can
be also demonstrated by the patient’s ambulation
without dyspnea on exertion.
11
Discharge Instruction and Patient
Education
Every patient should be given clear discharge
instructions with adequate follow-up prior to
discharge. The optimal discharge instructions
include proper diet recommendations, medication schedules, and patient education to prevent
readmission and deteriorationoftheircardiac
condition. In order to achieve this goal, appropriate consultation from cardiology, nutritional
therapy, and social work may be required.
ADHF patients with systolic dysfunction should
be considered for beta-blockers at discharge.
Studies have demonstrated that patients who
have beta-blockers prescribed at hospital discharge are much more likely to be on this
lifesaving medication 1 year later than those
whose initiation is deferred to the outpatient
environment.
21
Finally, patient education is an important
part of OU management of ADHF to prevent
recurrent ED visits and or readmission. Patients
should be educated on general HF knowledge,
the purpose and effect of pharmacological therapies, dietary adherence, healthy lifestyle choices,
early signs and symptoms of decompensation,
advantages of smoking cessation, and medical
assistance resources. A multidisciplinary collaboration among physicians, nursing staff, and
social workers can dramatically increase the
positive outcomes from patient education thus
reducing hospital readmissions and the general
health care burden from ADHF.
Jieun Kim and W. Frank Peacock
026
20:43:41
References
1. Mensah G, Brown D. An
overview of cardiovascular
disease burden in the United
States. Health Aff 2007;26:
38–48.
2. American Heart Association,
American Stroke Association.
Heart Disease and Stroke
Statistics—2011 Update. 2011.
Available at: http://
circ.ahajournals.org/content/
123/4/e18.full.pdf. Accessed:
February 2011.
3. Graff L, Orledge J, Radford MJ,
et al. Correlation of the Agency
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Research congestive heart
failure admission guideline
with mortality: peer review
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association initiative to
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for congestive heart failure.
Ann Emerg Med. 1999;34(4 Pt
1):429–437.
4. Silva MA, Peacock WF, Diercks
DB. Optimizing treatment and
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beyond initial triage. Congest
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5. Storrow AB, Collins SP, Lyons
MS, et al. Emergency
department observation of
heart failure: preliminary
analysis of safety and cost.
Congest Heart Fail. 2005 Mar–
Apr;11(2):68–72.
6. Albert NM, WF. Patient
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heart failure management
program in an emergency
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J Internat Soc Heart and Lung
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et al. Society of Chest Pain
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the evaluation and management
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heart failure patients. Acute
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9. Amin A, Hospitalized patients
with acute decompensated
heart failure: recognition, risk
stratification, and treatment
review. Jour of Hospital
Medicine. 2008;3(6):S16–24.
10. Stevensen LW, Perloff JK. The
limited reliability of physical
signs for estimating
hemodynamics in chronic
heart failure.
JAMA. 1989;
261(6):884–888.
11. Peacock WF, Young J, Collins
S, et al. Heart failure
observation units: optimizing
care. Ann Emerg Med. 2006
Jan;47(1):22–33. Epub
2005 Aug 15.
12. Mahdyoon H, Klein R, Eyler
W, et al. Radiographic
pulmonary congestion in endstage congestive heart failure.
Am J Cardiol. 1989;63(9):
625–627.
13. Collins S, Lindsell CJ, Storrow
AB, et al. Prevalence of
negative chest radiography in
the emergency department
patient with decompensated
heart failure. Ann Emerg Med.
2005;47(1):13–18.
14. Costanzo MR, Johannes RS,
Pine M, et al. The safety of
intravenous diuretics alone
versus diuretics plus parenteral
vasoactive therapies in
hospitalized patients with
acutely decompensated heart
failure: a propensity score and
instrumental variable analysis
using the Acutely
Decompensated Heart Failure
National Registry (ADHERE)
database. Am Heart J. 2007;
154(2):267–277.
15. Januzzi JL, Camargo CA,
Anwaruddin S, et al. The NTerminal Pro-BNP
Investigation of Dyspnea in the
Emergency Department
(PRIDE) Study. Am J Cardiol.
2005;95:948–954.
16. Silver MA, Maisel A, Yanct
CW, et al. BNP Consensus
Panel 2004; a clinical approach
for the diagnostic, prognostic,
screening, treatment
monitoring, and therapeutic
roles of natriuretic peptides in
cardiovascular diseases.
Congest Heart Fail. 2004;10(5
suppl 3):1–30.
17. Di Somma S, De Berardinis B,
Bongiovanni C, et al. Use of
BNP and bioimpedance to
drive therapy in heart failure
patients. Congest Heart Fail.
2010; 16 Suppl 1:S56–61.
18. Peacock WF. Acute emergency
department management of
heart failure. Heart Fail Rev.
2003;8:335–338.
19. Hobbs RE. Using BNP to
diagnose, manage, and treat
heart failure. Cleve Clin J Med.
2003;70:333–
336.
20. Fonarow GC, Adams KF Jr,
Abraham WT, et al., for the
ADHERE Scientific Advisory
Committee, Study Group, and
Investigators. Risk
stratification for in-hospital
mortality in acutely
decompensated heart failure:
classification and regression
tree analysis. JAMA.
2005;293:572–580.
21. Elkayam U, Tasissa Gm
Binanay C, et al. Use and
impact of inotropes and
vasodilator therapy during
heart failure hospitalization
in the ESCAPE trail.
Circulation. 2004;110(17
suppl):III–515.
22. Peacock WF. Rapid
optimization: strategies for
optimal care of decompensated
congestive heart-failure
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Med. 2002;3(suppl 4):S41–S48.
23. Nieminen MS, Böhm M, Cowie
MR, et al. Executive summary
of the guidelines on the
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of the European Society of
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24. Brewster UC, Setaro JF,
Perazella MA. The reninangiotension-aldosterone
system: cardiorenal effects and
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Am Med Sci. 2003
Jul;326(1):15–24.
25. Felker GM, Lee KL, Bull DA,
et al. Diuretic strategies in
patients with acute
decompensated heart
failure. N Engl J Med
2011;364:797–805.
26. Hunt SA, Abraham W, Chin
M, et al. ACC/AHA Practice
Guideline: 2009 Focused
Update incorporated into the
ACC/AHA 2005 Guidelines for
the Diagnosis and the
Management of Heart Failure
in Adults. Circulation.
2009;119:e391–e479.
27. Peacock WF, Remer E, Aponte
J, et al. Effective observation
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Apr;8(2):68–73.
Jieun Kim and W. Frank Peacock
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Subpart IVA
Chapter
24
Clinical – Cardiac
Atrial Fibrillation
Catherine T. Puetz, MD, FACEP
Background
Atrial fibrillation (AF) is a cardiovascular disease
in which the upper chambers of the heart (the
atria) beat in a rapid disorganized manner
resulting in the presence of a fast irregular heartbeat. This arrhythmia is estimated to currently
affect more than 7 million persons in the United
States and Europe. It is the most common cardiac
arrhythmia that exists with a prevalence that
ranges from 0.1% among adults < 55 to 9% in
those > 80.
1,2
With the projection of the elderly
population increasing, the prevalence of AF is
expected to increase 2.5-fold times the current
level by the year 2050. The management and
treatment costs present a significant financial
burden on the health care system. The cost of
treatment for AF in 2005 was approximately
$6.5 billion. These costs can be attr ibuted to
increased inpatient stays and other health care
services.
3
The incidence of AF is significantly higher
in men than women, regardless of age, and
more common in whites than blacks. The presence of AF without associated comorbidities
occurs in 1 0–15 % of cases.
4
In developed countries, the most common comorbidities of AF
include hypertension and coronary artery disease (CAD), followed by valvular heart disease
(rheumatic heart disease) and thyroid disorders.
Patients with hypertension have a 1.42-fold
increase in developin g AF. Because of the relatively high incidence of hypertension in the
general population it is the most common disorder in p atients with AF.
5
Ordinarily, AF is
not associated with CAD unless it is complicated by an acute myocardial infarction (AMI)
or heart failure (HF). AF in the setting of AMI
is associated with 40% increase in mortality
compared with those patients in sinus rhythm
with AMI.
6
Pathophysiology/Electrophysiology
The primary histopathologic changes in AF are
progressive atrial fibrosis and loss of atrial muscle
mass.
7
The normal electrical conduction system
of the heart begins with an impulse fired from the
sinoatrial (SA) node that propagates to the atrioventricular (AV) node resulting in contraction of
the ventricle. In AF this synchronized cycle is
disrupted. The electrical conduction system in
patients with AF does not begin in the sinoatrial
(SA) node. Rather the irregular impulses may be
due to proarrhythmic atrial fibrotic areas, ectopic
foci within the pulmonary vein, the heart having
increased susceptibility to autonomic stimuli, circulation of antibodies against cardiac myosin
heavy chains, and very rarely atrial myocarditis.
8
As a result the normal timing of the heart’s pacemaker is thrown off causing the heart to beat
faster or quiver. The atrial rate is generally fast
(300–600 beats per minute), however, not all of
these are conducted through the AV node so the
ventricular rate is much slower (usually about
110–180 beats per minute).
9,10
The contraction
of the two upper chambers of the heart (atria)
will not be synchronized with the contractions
of bottom of the heart (ventricle) causing the
irregularly irregular heart beat of AF. The hemodynamic functions affected during AF are the loss
of synchronous atrial activity, irregular ventricular response, rapid heart rate, and impaired coronary blood flow.
The American College of Cardiology (ACC),
American Heart Association (AHA), and the
European Society of Cardiology (ESC) established
classifications of AF based on timing and duration of symptoms.
8
The classification of AF is
separated in three patterns: paroxysmal AF, persistent AF, and permanent AF. When categorizing
patients it is based on the most frequent pattern
found on presentation.
8
Paroxysmal AF is
027
20:43:53
categorized by episodes of AF that resolve spontaneously within 7 days, with most episodes
lasting < 24 hours. Paroxysmal AF is found in
younger patients and often with holter monitoring. Paroxysmal AF can progress to permanent
AF, therefore, aggressive attempts to restore and
maintain sinus rhythm are indicated. Persistent
AF is associated with recurrent episodes that last
more than 7 days.
8
Persistent AF is less likely to
spontaneously convert and will require some
form of cardioversion to restore sinus rhythm.
The persistence of AF for a long time (e.g., a year
or more) is defined as permanent AF.
8
In addition
to these classifications, the ACC/AHA/ESC guidelines define additional AF categori es in terms of
other characteristics of the patient. Lone AF is the
occurrence of AF in the absence of clinical or
echocardiographic findings of cardiovascular disease in patients < 60 years of age.
8
Nonvalvular
AF occurs in the absence of rheumatic mitral
valve disease, a prosthetic heart valve, or mitral
valve repair.
8
Secondary AF occurs in the setting
of a primary condition such as AMI, cardiac
surgery, pericarditis, alcohol intake “holiday heart
syndrome,” myocarditis, pulmonary diseases,
hyperthyroidism, or metabolic syndromes.
8
Management of AF
There are three objectives that need to be
addressed when managing patients with AF: rate
control, prevention of thromboembolism, and
rhythm restoration. It is important to remember
that 70% of patients that present acutely with AF
will convert spontaneously.
11
The choice between
rhythm control and rate control has been studied
extensively and the conclusio n was that neither
treatment was inferior to the other for the outcome measures of mortality or quality of life.
12, 13
In the emergency department (ED), the initial
therapy for hemodynamically stable AF patients
would be ventricular rate control with subsequent
consideration to some form of cardioversion
(pharmacologic versus electrical) to relieve symptoms and improve cardiac output. Rate control
occurs when AV nodal conduction is depressed.
14
The agents most commonly used are betablockers, calcium channel blockers, digoxin and
amiodarone. Beta-blockers cause prolongation of
the AV refractory period by targeting the betaadrenergic receptors. Calcium antagonists decrease
heart rate by blocking the calcium channel during
the plateau phase of the action potential during
cardiac contraction. Digoxin’s effect on the AV
node is via enhancement of vagal tone.
14
In review
of the evidence-based studies on rate control when
monotherapy was used in the treatment of AF,
both calcium antagonists and beta-blockers were
more effective than digoxin in controlling heart
rate at high levels of sympathetic drive. There was,
however, no significant difference in terms of
the effectiveness of rate control between calcium
channel blockers and beta-blockers.
14,15
Betablocker therapy is preferred in AF patients with
hypertension, AMI, and ischemic heart disease
but relatively contraindicated in asthmatics.
14
Calcium antagonists should be avoided in AF patients
with signs of HF. The effectiveness of AV nodal
blockade on restoring sinus rhythm is no better
than placebo.
14
Cardioversion is used to restore sinus rhythm.
Electrical cardioversion is the treatment of choice
in the hemodynamically unst able AF patient.
The stable AF patient can either be treated with
pharmacological cardioversion (PC) or electrical
cardioversion (EC). The restoration of sinus
rhythm by either method has a higher success
rate in the acute pres entation of AF (< 48 hour),
80–90% (EC) versus 60–80% (PC).
14
The drawbacks of using EC include the need for procedural
sedation with its associated risks. There are
advantages and disadvantages of using antiarrhythmic medication. Advantages are simplicity, convenience, and no need for procedural
sedation. Disadvantages are the drug- related
pro-arrhythmic effects and the lack of effect on
chronic AF. The most common anti-arrhythmic
medications used for PC are amiodarone, flecainide, procainamide, propafe none, sotalol, and
ibutelide.
16,17
Regardless of which treatment approach is
pursued, thromboembolic prevention is essential
in AF. Stroke is one of the major complications of
AF. The annual risk of stroke in patients with AF
is in the range of 3%–8% per year.
2
The risk of
stroke increases with age as demonstrated in
the Framingham Study. The annual risk of stroke
attributable to AF was 1.5% in parti cipants 50–59
years old and 23.5% in those aged 80–89 years
old.
2
Thromboembolic events occur as a result
of thrombus formation in the left atrium or left
atrial appendage. The uncoordinated contraction
of the atria in AF over time leads to dilation of the
right and left atrium resulting in blood stasis and
Catherine T. Puetz
027
20:43:53
clot formation. The low peak velocities present in
the left atrial appendage, as demonstrated on
pulse wave Doppler echocardiography, also promotes thrombus formation.
8
Another finding on
echocardiography is spontaneous echo contrast.
8
This is the presence of smoke-like images that are
felt to represent increased red blood cell aggregation in the setting of low flow. The presence of
this as noted on echocardiography is a predisposing factor to thrombus formation. AF also
appears to activate the clotting system as evidenced by the presence of increased thrombotic
and fibrinolytic markers in AF patients.
8
The risk
of thrombus development increases the longer AF
is present, especially when > 48 hours.
There currently are several scoring systems
available to help clinicians estimate the stroke risk
in patients with AF. One of the most popular
risk assessment tools used is the CHADS
2
score.
This scoring system assigns single points for the
following conditions: Congestive Heart Failure
(CHF), Hypertension, Age 75, and Diabetes; it
assigns two points for a prior history of stroke or
TIA. Patients with CHADS
2
score of 2 have a
high risk and merit anticoagulation therapy.
18
The CHADS2score was felt to have limitations
in assessing risk as it didn’t incorporate a number
of documented stroke risk factors.
These additional risks now addressed by the
new CHA
2DS2
-VASc Score include vascular disease (prior MI, peripheral artery disease, aortic
plaque), additional age category, and sex category
(female gender).
19
As with the previous scoring
system, the CHA
2DS2
-VASc scoring assigns one
point to each risk, with the exception of age
75 and prior CVA/TIA/thromboembolic event,
which are both given two points. The risk scores
will determine which form of anticoagulation is
recommended for AF patients . Scores 2 indicates a high risk of stroke and oral anticoagulation
is recommended. Moderate risk patients (score
1) are recommended to take oral anticoagulation therapy also and those with a score of 0 have
a very low risk and either no antithrombotic therapy or aspirin are recommended.
19
Anticoagulation is one of the most important
considerations to be made in the acute management of AF. (See Chapter 33 on anticoagulants.)
The risk of thromboembolism in either chemical
or electrical cardioversion is the same. Transesophageal echocardiography (TEE) is a good predictor of acute risk. If the presence of thrombus
is not seen in the cardiac chambers or left
atrial appendage and there is no evidence of
spontaneous echo contrast v isualized on echo,
cardioversion has a low acute risk of stroke.
8
Anticoagulation is indicated for those patients
in AF of suspected duration of > 48 hours that
will be undergoin g EC after 4–6weeksof
therapy.
8
The goal of long-term anticoagulation in AF is
to reduce risk of thromboembolism. The choice
of therapy selected should be balanced between
the risk of stroke and the risk of bleeding, whi ch
unfortunately both increase with age. Warfarin
has long been the anticoagulation treatment of
choice for AF patients with moderate to high
risk for thromboembolism. The goal of therapy
is maintaining an international normalized ratio
(INR) in the range of 2.0–3.0, except in patients
who are at significant risk for stroke (patients
with artificial valves, those with rheumatic heart
disease, and those with recurrent prior strokes)
where the goal INR should be maintained
between 2.5 and 3.5.
8
Warfarin therapy is complex because of
its narrow therapeutic window and variable pharmacodynamics and pharmacokinetics. It also
interacts with many drugs and foods and requires
frequent monitoring. These limi tations of warfarin result in undertreatment of a considerable
portion of people with AF at great risk.
Newer anticoagulation therapies have recently
become available for use. They are direct Factor
Xa inhibitors ( e.g., rivaroxaban, edoxaban,
apixaban) and direct thrombin inhibitors (e.g.,
dabigatran).
20
The results of the RE-LY trial
foundthatdabigatranatadoseof150mgwas
superior to warfarin in the reduction of stroke
and systemic embolism (per year: warfarin
1.69%, dabigatran 1.11%), but with a similar
rate of major hemorrhage (per year: warfarin
3.36%, dabigatran 3.11%).
21
These new anticoagulants have the advantage of stable pharmacodynamics and pharmacokinetics, eliminating
the need for fre quent monitoring. The major
disadvantages of their use include cost and that
there is currently no specific way to reverse the
anticoagulant effects of the drug in the event of
major bleeding with the exception of idarucizumab, which is a monoclonal antibody antidote
specifically for the reversal of dabigatran.
22
However, there is much research in this
area and it is likely that reversal agents for all
Atrial Fibrillation
027
20:43:53
of the novel or new oral anticoagulants
(NOACs) or non vitamin K oral antagonists
will be available in the near future. The specific
NOAC reversal agent, idarucizumab, is indicated
only for the reversal of the anticoagulant effects
of dabigatran for emergency surgery/urgent procedures or with life-threatening or uncontrolled
bleeding.
CHA2DS2-VASc Score
0 points- LOW RISK - ASA only
1 point- INTERMEDIATE RISK - ASA or
Coumadin or OAC after discussion of risks
and benefits with patient
2 points (!) - HIGH RISK - Coumadin or
OAC
Anticoagulation should be considered
in ALL AF patients with CHA2DS2-VASc
Score of 2 (Even if NSR is restored)
Unless other contraindications,
ANTICOAGULATION is indicated if the
patient has any of the following
1. HOCM
2. Rheumatic Mitral Stenosis
3. Thyrotoxicosis
OBS Exclusion Criteria
1. Acute CHF
2. Unstable Angina
3. Unstable Vitals/ Hypotension
4. Exacerbation of Co-morbid Disease
5. Acute Thromboembolic Event
symptoms present
CHA2DS2- VASc
1. CHF(EF < 40%) - 1pt 5. H/O CAD/PAD - 1pt
2. HTN - 1pt 6. Age 64–75 -1pt
3. Age >75 - 2pts 7. Female sex - 1pt
4. Prior CVA/TIA or
embolic event - 2pts
8. Diabetes - 1pt
Initiation of Anticoagulation Protocol
1. Follow-up must be arranged with PCP
or cardiology
2. Coumadin - 5 mg starting dose after
baseline PT/INR, repeat PT/INR in 72 hrs.
3. OAC- Pradaxa, Xarelto, or Eliquis (DO
NOT use with Mechanical Heart Valves)
Pradaxa - 150 mg BID for CrCl > 30
Xarelto - 20 mg qHS for CrCl > 50
Eliquis - 5 mg BID if < 2 of 3 of following:
1. Age 80
2. Cr < 1.5
3. Weight > 60 Kg
AF < 48 hrs and ED
eval is negative for
other etiologies or
acute illness
ED TX and Eval
1. Labs- CBC,CMP,TSH (trop/BNP if clinically
indicated)
2. Initiate Rate control (IV & PO)- Always use A and
(B or C)
A. IV Diltiazem bolus 5–10 mg, may repeat q 30
mins prn
B. Diltiazem 60 mg PO ¥ 1 dose, may give
additional 30–60 mg in 1–2 hrs
C. Metoprolol 50–100 mg ¥ 1 dose, may give an
additional 25–50 mg in 1–2 hrs
Sinus
rhythm?
Candidate for
Chemical
Cardioversion?
Transfer to OBS
Pill in Pocket Protocol
(Minimum 4hrs post
conversion monitoring)
1. IV & PO rate control
agents administered prior to
flecainide
2. Must have HR > 70 bpm
and SBP > 100 to receive
flecainide
3. Flecainide dosing
< 70 kg - 200 mg
> 70 kg - 300 mg
D/C Home
anticoagulate
if indicated
Sinus
Rhythm?
DC
cardioversion
Chemical
Cardioversion
Exclusion Criteria
1. CAD/Stents
2. EF < 50%
3. CHF
4. Severe Valvular Dz
5. BBB (QRS >120ms)
6. H/O 2nd/3rd degree
AVB
7. Long QT or Brugada
8. K < 3.0
9. Pt on antiarrythmic
10. Pregnancy
11. Hepatic/Renal
insufficiency (CrCl < 35)
12. Age > 80
DC
cardioversion
No
Yes
Yes
No
D/C Home with
outpatient F/U
Yes
No
Yes
AF < 48 hrs Protocol
Figure 24.1 Atrial Fibrillation Clinical Algorithm: Atrial Fibrillation < 48 hours duration
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Inclusion/ Exclusion Criteria
Patients appropriate for an observation unit (OU)
are those patients with symptomatic paroxysmal
AF or persistent AF that require rate control and
are hemodynamically stable. Patients that should
be excluded from OU placement are those that are
medically unstable and/or have confounding
comorbid factors as the cause of their AF (e.g.,
Exclusion Criteria
1. Acute CHF
2. Unstable Angina
3. Unstable Vitals/ Hypotension
4. Exacerbation of Co-morbid Disease
Initiation of Anticoagulation Protocol
1. Follow-up must be arranged with PCP
or cardiology
2. Coumadin - Starting dose 5 mg after
baseline PT/INR drawn, repeat PT/INR in 72
hrs
3. OAC- Pradaxa, Xarelto, or Eliquis (DO
NOT use with Mechanical Heart Valves)
Pradaxa - 150 mg BID for CrCl > 30
Xarelto - 20 mg qHS for CrCl > 50
Eliquis - 5 mg BID if < 2 of 3 of following:
1. Age 80
2. Cr < 1.5
3. Weight > 60 Kg
AF present > 48 hrs &
ED Eval is negative
for other causes or
acute illness
ED Rate control Rx (IV & PO)- Always use 1 and (2 or 3)
1. IV Diltiazem bolus 5–20 mg, may repeat q 30 mins prn
while waiting for oral medication to work (Goal is patient
comfort, not optimal rates initially)
AND
2. Diltiazem 60 mg PO ¥ 1 dose, may give additional
30–60 mg in 1–2 hrs
Or
3. Metoprolol 50–100mg ¥ 1 dose, may given additional
25–50 mg in 1–2 hrs
4. If patient is already on a rate controlling medicine, give
an additional dose of that medication in conjunction with
IV bolus
*** After both IV and oral rate control meds have
been started, consider transferring to OBS for
telemetry and further rate control indicated ***
1. If HR > 100 at rest or > 120 with
exertion increase the Toprol dose
by 25 mg or Diltiazem to next dose
level
2. If HR is not optimized within 4
hrs of 2nd dose - consider
admission
AF > 48 hours Protocol
1. If rate controlled
without ED therapy DO
NOT start any rate
control therapy
2. If ED therapy resulted
in rate control, D/C on:
Toprol XL 25–50 mg qd
or BID
or
Cardizem CD
120–180 mg qd or BID
3. Start anticoagulation
4. D/C Home with
appropriate follow up
1. D/C home on:
Toprol XL
25–50 mg qd or
BID
or
Cardizem CD
120–180 mg qd
or BID
2. Arrange for
follow up
3. Start
Anticoagulation
Rate
Controlled?
Rate Controlled
after 4-8 hrs
Yes
No
Transfer to OBS
Yes
No
CHA2DS2- VASc
CHA2DS2-VASc Score
0 points - LOW RISK - ASA only
1 point - INTERMEDIATE RISK - ASA or
Coumadin or OAC after discussion of risks
and benefits with patient
2 points (!) - HIGH RISK - Coumadin or
OAC
***Anticoagulation should be
considered in ALL AF patients with
CHA2DS2-VASc Score of 2 (Even if NSR
is restored) ***
Unless other contraindications,
ANTICOAGULATION is indicated if the
patient has any of the following
1. HOCM
2. Rheumatic Mitral Stenosis
3. Thyrotoxicosis
1. CHF(EF < 40%) - 1pt
2. HTN - 1pt
3. Age >75 - 2pts
4. Prior CVA/TIA or
embolic event - 2pts
7. Female sex - 1pt
5. H/O CAD/PAD- 1pt
6. Age 64–75 -1pt
8. Diabetes - 1pt
Figure 24.2 Atrial Fibrillation Clinical Algorithm: Atrial Fibrillation > 48 hours duration
Atrial Fibrillation
027
20:43:53
secondary causes of their AF). The observation
stay will evaluate the need for rate control,
rhythm correction (EC vs. PC), and assessing
the patient’s thromboembolic risk. (Figures 24.1
and 24.2)
Observation Interventions
AF patients in OUs should be managed on an
individual basis. The factors to be considered are
the patient’s symptoms, the known duration of
the AF, and the presence of structural heart disease. There are currently many evidence-based
studies published demonstrating a variety of ways
to treat AF in th e setting of observation.
23,24
None of these studies demonstr ated a statistically
significant difference in one treatment method
over the other. There is evidence to suggest that
the use of treatment protocols for the management of AF in observation improves patient outcomes and decreases the need for inpatient
admission.
25–24,26
(Figures 24.1 and 24.2)
Conclusion
AF is becoming a serious cardiac epidemic along
with CAD and CHF. The financial burden of this
disease process will only increase as the population continues to age. The management of AF in
OUs has been demonstrated to not only be safe
but also cost-effective due to the decreased need
for hospitalization of these patients.
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