CARDIOLOGY/CONCEPTS

Beyond Pulmonary Edema: Diagnostic, Risk Stratification, and

Treatment Challenges of Acute Heart Failure Management in the
Emergency Department
Sean Collins, MD, MSc
Alan B. Storrow, MD
J. Douglas Kirk, MD
Peter S. Pang, MD
Deborah B. Diercks, MD
Mihai Gheorghiade, MD

From the University of Cincinnati, Department of Emergency Medicine, Cincinnati, OH (Collins);

Vanderbilt University, Nashville, TN (Storrow); University of CaliforniaDavis, Sacramento, CA (Kirk,
Diercks); and Northwestern University, Chicago, IL (Pang, Gheorghiade).

The majority of heart failure hospitalizations in the United States originate in the emergency department
(ED). Current strategies for acute heart failure syndromes have largely been tailored after chronic heart
failure guidelines and care. Prospective ED-based acute heart failure syndrome trials are lacking, and
current guidelines for disposition are based on either little or no evidence. As a result, the majority of
ED acute heart failure syndrome patients are admitted to the hospital. Recent registry data suggest
there is a significant amount of heterogeneity in acute heart failure syndrome ED presentations, and
diagnostics and therapeutics may need to be individualized to the urgency of the presentation,
underlying pathophysiology, and acute hemodynamic characteristics. A paradigm shift is necessary in
acute heart failure syndrome guidelines and research: prospective trials need to focus on diagnostic,
therapeutic, and risk-stratification algorithms that rely on readily available ED data, focusing on
outcomes more proximate to the ED visit (5 days). Intermediate outcomes (30 days) are more
dependent on inpatient and outpatient care and patient behavior than ED management decisions.
Without these changes, the burden of acute heart failure syndrome care is unlikely to change. This
article proposes such a paradigm shift in acute heart failure syndrome care and discusses areas of
further research that are necessary to promote this change in approach. [Ann Emerg Med. 2008;51:
45-57.]
0196-0644/$-see front matter
Copyright 2008 by the American College of Emergency Physicians.
doi:10.1016/j.annemergmed.2007.07.007

INTRODUCTION
Historically emergency department (ED) patients with an
acute heart failure syndrome were thought to be most
represented by acute pulmonary edema that required emergency
intervention to prevent further deterioration. However, recent
registry data confirm that patients with acute heart failure
syndromes have a variety of acute presentations and suggest
management must be individualized to underlying
pathophysiology, acute hemodynamics, and short- and longterm risk.1-4
Although these recent data have provided insight into ED acute
heart failure syndromes, mortality and postdischarge recidivism
have remained largely unchanged during the last decade.1,3,4
Therefore, we propose a new paradigm, away from the conservative
decision to admit the heart failure patient, for acute heart failure
syndromes management, with 3 goals in mind:
Volume , . : January

1. define acute heart failure syndrome, using a hemodynamic

classification, along with underlying left-sided ventricular
function;
2. promote tailored emergency treatment of appropriate
clinical targets (whose change as a result of therapy affects
subsequent risk) according to this classification; and
3. provide real-time bedside ED risk stratification.
Although our approach is based on currently available evidence,
which is somewhat limited, we challenge the emergency medicine
and cardiology community to perform prospective clinical trials
evaluating its clinical and economic utility.

THE HEART FAILURE BURDEN AND

EMERGENCY CARE
Heart failure is a worldwide problem of epidemic
proportions5 and represents a tremendous burden to health care
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Beyond Pulmonary Edema

costs. EDs are a key component of the health care safety net,
providing 110 million patient visits yearly for people from all
levels of health, race, and socioeconomic group.6-13 Further
contributing to the burden of heart failure is the impact of the
aging population and hospital and ED crowding. The Institute
of Medicines recent report found that ED visits grew 26% from
1993 to 2003, yet during the same period, the number of EDs
decreased by 425 and the number of hospital beds decreased by
198,000.1,3 The impact of these findings in the ED is clear:
many patients are boarded in the ED, some for up to 48
hours, before an inpatient bed becomes available. As a result,
emergency physicians deliver both acute and ongoing heart
failure care. The Institute of Medicines recommendations to
improve the future of emergency care include significant
increases in federal funding for research that identifies gaps in
emergency care and the best strategy to close them. Research
into methods of safely identifying, treating, and determining
disposition of acute heart failure syndrome patients needs to be
a significant part of this effort. If alternatives to hospitalization
and methods to streamline care are not identified, the financial
burden of increased acute heart failure syndrome visits to the
ED will become unmanageable.
A coordinated process of care is extremely important for
patients with acute heart failure syndromes. This continuum
begins in the out-of-hospital environment, progresses through
hospital admission, and concludes with outpatient follow-up.
The ED is important in initial stabilization and triage to
appropriate levels of care: discharge home, observation unit stay,
and inpatient admission. Consequently, emergency physicians
play a pivotal role in the management of acute heart failure
syndromes and are in an ideal position to investigate
epidemiology, pathophysiology, acute therapy, and disposition.

ACUTE HEART FAILURE DIAGNOSIS,

TREATMENT, AND RISK STRATIFICATION
Traditional heart failure diagnostic criteria rely on
echocardiography or right-sided heart catheterization to
establish ventricular function and performance.14-17 Although
results from these procedures are reliable, they are often not
available or practical for ED patients. A cornerstone of ED
diagnostics is the availability of bedside maneuvers and tests that
deliver rapid and reliable results. These results can then be
broadly applied to the undifferentiated patient population with
signs and symptoms of acute heart failure syndromes. As such,
diagnostic strategies should keep these principles in mind as
further tests to corroborate the diagnosis of acute heart failure
syndrome are developed.
We propose a paradigm change that aims to establish a rapid,
accurate, ED diagnosis of acute heart failure syndromes, guides
therapeutic maneuvers toward specific clinical targets, and assists
with disposition decisions by accurate risk stratification. Our
suggested paradigm change includes:
1. signs and symptoms of possible acute heart failure
syndromes previously shown to accurately identify heart
failure in the general population but adapted for ED use;
46 Annals of Emergency Medicine

Collins et al
Table 1. Test characteristics of heart failure diagnostic
scoring systems.
Scoring System
Framingham
Boston*
NHANES
Gheorghiade

Sensitivity

Specificity

63%4%
35%4%
62%4%
55%4%

94%1%
99%0%
94%1%
95%1%

NHANES, National Health and Nutrition Examination Survey.

*Test characteristics for a Boston Score greater than 8.

2. initial triage based on high-risk features that require

immediate stabilization;
3. an objective measurement demonstrating increased filling
pressures and an assessment of left-sided ventricular
dysfunction;
4. further categorization and treatment disposition based on
acute ED hemodynamic presentation;
5. risk stratification and disposition.
The following 5 sections will discuss these changes in detail.
The Role of Signs, Symptoms, and Ancillary Testing in ED
Patients With Possible Acute Heart Failure Syndromes
Heart failure scoring systems. Previous research has
suggested that a combination of medical history, physical
examination, and chest radiograph findings can suggest a
diagnosis of acute heart failure syndrome. The 1971
Framingham Criteria (Table 1) are well known for providing a
useful probabilistic diagnosis of heart failure in the outpatient
setting.18,19 However, prospective validation of the criteria
suggested only intermediate overall accuracy (designed to
maximize specificity, sacrificing sensitivity)20 (Table 1), and
several of the criteria are not practical for ED use (circulation
time, vital capacity, weight loss in response to treatment, and
autopsy findings). The Boston and National Health and
Nutrition Examination Survey Criteria and the Gheorghiade
score use a similar scoring system and have been found to have
similar test characteristics when prospectively validated.20-23
Although signs, symptoms, and scoring systems can be highly
suggestive of acute heart failure syndromes, they lack sufficient
accuracy to serve as a definitive diagnostic strategy. Further,
these scoring systems have not been extensively validated in the
acute setting, making their implementation in the ED
somewhat limited.
Chest radiography. Chest radiography is a cornerstone of
the diagnostic evaluation of dyspnea. When present,
radiographic signs of congestion such as cephalization,
interstitial edema, and alveolar edema are highly specific (96%,
98%, and 99%, respectively) for acute heart failure syndromes.
However, low sensitivity (41%, 27%, and 6%, respectively)
makes chest radiography a poor screening tool for acute heart
failure syndrome.24 A recent analysis suggested that up to 18%
of ED patients with acute heart failure syndromes will have no
findings of congestion on chest radiograph.25 This finding is
most often found in end-stage heart failure patients, where
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Collins et al
radiographic congestion can be minimal despite significantly
increased wedge pressures.26 Chest radiography serves a vital
role in the evaluation of the dyspneic patient, including the
identification of other causes, but a lack of radiographic signs of
congestion does not exclude acute heart failure syndromes.
ECG. Interpretation of a 12-lead ECG is essential for every
patient who presents with acute heart failure syndromes.27 From
the ED perspective, an ECG would assist with acute treatable
conditions such as cardiac ischemia and atrial fibrillation while
aiding with other associated findings suggestive of acute heart
failure syndromes. Both the Heart Failure Society of America28
and the European Society of Cardiology recommend a 12-lead
ECG in the evaluation of patients with acute heart failure
syndromes.29 The ECG is recommended for the following
reasons:
Rhythm identification. For example, atrial fibrillation with
rapid ventricular response may be the sole cause of the heart
failure exacerbation.27
Identification of strain and hypertrophy patterns.
Identification of patients for other potential therapies. For
example, patients with interventricular conduction delay and
advanced heart failure could be evaluated for cardiac
resynchronization therapy.
Detection of ischemia or other acute coronary syndrome
patterns that would prompt consideration of a different but
related approach to management.
Other ECG patterns that would suggest other potential other
causes. For example, low limb lead voltage with a left
ventricular hypertrophy pattern would suggest sarcoidosis.30
At baseline, it is unlikely to have a completely normal ECG
result in patients with systolic heart failure. In a study of 438
patients, 96 of whom had abnormal systolic function according
to echocardiography, a normal ECG result was associated with
normal left ventricular function in 98% of cases.31 Similar to
other tests for evaluation of acute heart failure syndromes, an
ECG is a critical tool but does not definitely rule in or rule out
the presence of acute heart failure syndrome.
Natriuretic peptides. NT-proBNP and BNP have been
studied extensively and are used most often in clinical practice.
They are most helpful to clinicians when there is an
intermediate pretest likelihood of disease and the test result is
either very low or very high. Sensitivity and specificity for BNP
at values of less than 100 pg/mL (sensitivity 90%) and greater
than 400 pg/mL (specificity 95% in those younger than 70
years) are similar to NT-proBNP values of less than 300 pg/mL
(sensitivity 99%) and greater than 900 pg/mL (specificity 85%).
Intermediate natriuretic peptide values are problematic and
require further clinical correlation and investigation.32,33 Age,
sex, and to some extent renal dysfunction have an impact on
natriuretic peptide levels and need to be considered when test
results are interpreted.34-36
Other ancillary devices. Previous research suggests that an
auscultated S3 gallop is not only diagnostic for acute heart
failure syndromes but also predicts an increased risk of
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Beyond Pulmonary Edema

subsequent adverse events.37,38 However, its low amplitude and
frequency, combined with ED obstacles of ambient noise,
patient body habitus, and increased work of breathing,
significantly diminish the ability of the examining physician to
detect this on physical examination.39,40 The introduction of
bedside acoustic electrocardiography has made it possible to
objectively detect abnormal heart sounds rapidly. Preliminary
research suggests that the finding of an electrocardiographic S3
is highly specific for acute heart failure syndromes, and its use in
subjects with intermediate BNPs improves diagnostic
accuracy.39,41 The recent completion of a large-scale clinical
trial will provide more insight into the impact of this device on
ED diagnostic accuracy and medical decisionmaking.
Initial Triage Based on High-Risk Features That Require
Immediate Stabilization
Potential acute heart failure syndrome patients must undergo
2 levels of triage and concurrent treatment as diagnostic testing
occurs. The first level should focus on initial stabilization in the
subset of patients who present in extremis and must be
addressed immediately to prevent further deterioration. Those
patients with significant tachypnea, hypoxia, and mental status
changes need aggressive intervention with noninvasive
ventilation or possible endotracheal intubation to prevent
respiratory failure while definitive care is being established
(Figure 1). Noninvasive positive pressure ventilation not only
reverses underlying pathophysiologic derangements but also 2
recent meta-analyses suggest it reduces mortality and the need
for intubation. However, this modality does require patient
cooperation; those with significant mental status changes are not
candidates.42,43 Conversely, patients who present with
hypotension and evidence of end-organ hypoperfusion (altered
mental status, reduced urine output, poorly perfused
extremities) with concurrent pulmonary edema may require a
fluid challenge and aggressive inotropic therapy (Figure 2). This
subset of critically ill patients whose hemodynamic status is
unclear may benefit from right-sided heart catheterization and
most often need ICU admission for close monitoring and
continued treatment.
An Objective ED Measure of Left-Sided Ventricular
Function and Increased Filling Pressure
An objective measure of left-sided ventricular function is
important not only for diagnostic certainty of acute heart failure
syndromes but also to help determine initial therapy. Although
dividing patients into binary treatment strategies based on
ventricular function is overly simple, patients with reduced LV
function tend to be normotensive and fluid overloaded, whereas
those with preserved LV function tend to be hypertensive and
mildly hypervolemic.4 Up to 75% of ED acute heart failure
syndrome patients will have a previous diagnosis of heart
failure.1-4 Previous diagnostic testing (echocardiography, leftand right-sided heart catheterization) in these patients will often
reveal the cause of ventricular dysfunction (preserved versus
reduced systolic function).
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Beyond Pulmonary Edema

Collins et al

Figure 1. Suggested initial triage in patients with suspected acute heart failure syndromes. AHFS, Acute heart failure
syndromes; NIV, non-invasive ventilation; ETT; endotracheal intubation; BP, blood pressure; SL, sublingual; BNP, b-type
natriuretic peptide; CXR, chest xray; O2sat, oxygen saturation; LV, left ventricular.

There are several other methods to detect ventricular

dysfunction in the remainder of patients without a previous
diagnosis of left-sided ventricular dysfunction or in those
patients for whom previous results are not available. The
introduction of limited emergency bedside echocardiography to
evaluate wall motion and ejection fraction, performed by
emergency physicians, has been shown to be feasible and
correlate well with definitive testing but has not yet found
widespread acceptance.44,45 Impedance cardiography has been
evaluated as a means to noninvasively measure cardiac output
and cardiac index, as well as systemic vascular resistance.46,47
Preliminary research suggests it may have an impact on ED
physician decisionmaking and medication administration in
dyspneic ED patients,48 although large-scale ED studies on its
diagnostic accuracy have yet to be performed. Impedance
cardiography requires dedicated time to perform (approximately
10 to 15 minutes), and data acquisition can be problematic
when patients are diaphoretic or significantly tachypneic.
Direct measurement of increased filling pressure would be
ideal in ED patients with possible acute heart failure syndromes.
48 Annals of Emergency Medicine

However, not only do recent data question the efficacy of

pulmonary artery catheterization in acute heart failure syndrome
but also the required time and resources necessary make it
impractical to use in ED patients.49,50 Indirect, objective
measures of increased filling pressures must be used.
Examination findings such as jugular venous distention and
ventricular gallops can suggest increased left-sided ventricular
end diastolic pressure. However, they are limited by their poor
reliability between examiners and their low sensitivity.38,41,51
Further, jugular venous distention merely suggests increased
right-sided filling pressure and may not always be reflective of
left-sided filling pressure.
The ventricles response to the Valsalva maneuver has been
found to be predictive of increased left-sided ventricular filling
pressure and acute heart failure syndromes. In a small study of
outpatients referred for elective cardiac catheterizations, the
effect of the Valsalva maneuver on blood pressure (measured by
an automated device) was shown to correlate with left-sided
ventricular end diastolic pressure better than pulmonary
capillary wedge pressures (r0.86 and 0.81, respectively).52
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Beyond Pulmonary Edema

Figure 2. Suggested treatment algorithm for patients with hypotensive acute heart failure syndromes. NTG, nitroglycerin;
NES, nesiritide; NTP, nitroprusside.
Table 2. Hemodynamic categorization of ED patients with acute heart failure syndromes.
Acute Heart Failure
Syndromes Category

Typical Demographics

Symptom Duration

Hypertensive

Older, more frequently

women, history of
hypertension

2472 h

Normotensive

Younger, more
frequently men,
history of CAD

Days to weeks

This technology deserves prospective ED evaluation to

determine its usefulness.
We believe a definitive clinical diagnosis of acute heart failure
syndromes should involve a heightened clinical suspicion (by
signs, symptoms, and initial ED diagnostics), along with a
previously or ED-documented objective measure of both
ventricular dysfunction and increased filling pressure.
Further Categorization and Treatment Based on Acute ED
Hemodynamic Presentation
Secondary triage and categorization after initial
stabilization. Patients who proceed to the next level of triage
either do not have initial high-risk features or have high-risk
features that have been stabilized (Figure 1). Secondary triage
focuses on categorizing patients into one of 2 general categories
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Examination

Echo

Therapeutic Targets

1. Blood pressure
140/100 mm Hg
2. Acute pulmonary
edema
3. Minimal peripheral
edema
1. Normal blood
pressure
2. Leg edema, weight
gain, anasarca

Diastolic dysfunction,
preserved systolic
function

Aggressive blood pressure

control

Systolic dysfunction

Aggressive diuresis to
relieve congestion,
reduce peripheral
edema and weight gain

so that initial therapy can be tailored to the underlying

pathophysiology (Table 2). Although there is some overlap in
these diagnostic categories, they are a useful starting point to
drive therapeutics.
Hypertensive heart failure: The acute pulmonary edema
patient. Approximately 50% of acute heart failure syndromes
patients will present with a systolic blood pressure of more than
140 mm Hg.1-4 These patients tend to be older, be women,
have a history of diastolic dysfunction, and often have acute
symptoms that have been present for only 24 to 48 hours.
Because of the shorter symptom duration, they are more likely
to have acute pulmonary edema (both on examination and chest
radiograph) rather than systemic edema (weight gain, leg
edema). Symptoms are often the result of a significant increase
in afterload and fluid misdistribution rather than total body
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Collins et al

Figure 3. Suggested treatment algorithm for patients with hypertensive acute heart failure syndromes.

fluid overload. As a result, initial treatment should focus on

aggressive blood pressure control and minimize diuretic use.
Initial overaggressive use of diuretics in this subset of patients
can lead to deleterious effects 24 to 48 hours later, with
decreases in blood pressure and renal dysfunction.4
Therapeutic options for initial blood pressure control include
sublingual or topical nitroglycerin, angiotensin-converting
enzyme inhibitors (sublingual and intravenous), or intravenous
hydralazine (Figure 3). Registry data suggest that early
administration of intravenous therapy in a select group of
patients may decrease hospital lengths of stay.53 However, these
data need to be prospectively validated before they can be used
to guide therapy. Concurrent administration of a small dose of
furosemide (80 mg in a patient with normal renal function)
may also occur at this time. Response to initial therapy will then
determine the next course of action. An intravenous vasodilator
(nitroglycerin, nesiritide, nitroprusside) can be used in patients
who remain hypertensive (blood pressure 160/100 mm Hg)
and symptomatic, with a goal of continued, sustained blood
pressure reduction. Patients with an adequate response to initial
antihypertensive therapy (blood pressure 160/100 mm Hg)
can be transitioned off intravenous therapy to topical
nitroglycerin, with simultaneous oral administration of the
patients previous antihypertensive regimen.
Compared with the normotensive, volume-overloaded, acute
heart failure syndromes patient, in whom an exacerbation may
be more occult, hypertensive acute heart failure syndrome
patients may look much more acutely ill on initial presentation.
However, they also have the most to gain from appropriate
50 Annals of Emergency Medicine

early treatment. After initial blood pressure control and mild

diuresis, this group of patients often has dramatic symptom
improvement and, after initial diagnostics return, may be
retriaged to a lower care level. The downstream effects of all
therapeutic options must be considered. Care must be taken not
to mortgage the future with overaggressive diuresis in this
group of patients, who tend to not be significantly fluid
overloaded. Although patients who are aggressively diuresed
may appear to initially improve, this may be at the expense of
subsequent dehydration, renal insufficiency, increased hospital
lengths of stay, and event rates.54
Normotensive heart failure. Approximately 35% of
patients will present with mild, subacute worsening of their
symptoms during several days to weeks. These patients tend to
be younger and have systolic dysfunction and a history of
coronary artery disease. Their symptoms are primarily a result of
gradual total body fluid overload, as opposed to respiratory
distress from acute hypertension and pulmonary edema. These
patients benefit from aggressive diuresis, with a therapeutic goal
of relieving congestion and reducing total body fluid and
peripheral edema (Figure 4). Blood pressure control is often not
as problematic as it is in the hypertensive acute heart failure
syndrome patient and generally can be controlled with topical
nitroglycerin, along with resuming the patients
antihypertensive regimen. This group of patients also needs to
be retriaged after initial therapy. Those patients with an initial
blood pressure in the low normal range (90 to 120 mm Hg)
may run out of blood pressure after initial diuresis, and care
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Beyond Pulmonary Edema

Figure 4. Suggested treatment algorithm for patients with normotensive acute heart failure syndromes. APE, Acute
pulmonary edema.

must be taken to maintain a blood pressure associated with

adequate perfusion.
Risk Stratification and Disposition
A subset of patients will have obvious high-risk features on
presentation (significant tachypnea, hypoxia, mental status
changes, hypotension, hypoperfusion), and their disposition
will be determined early in their presentation. However, the
majority will proceed to risk stratification that relies in part on
response to therapy (blood pressure, pulse rate, symptoms) and
initial diagnostic test results. Unfortunately, rapid, accurate,
ED-based risk stratification is lacking; the low-risk ED acute
heart failure syndrome patient has yet to be identified. As a
result, up to one third of known heart failure patients receive
inpatient care each year, and at least 80% of ED patients
presenting for heart failure are admitted to the hospital,
regardless of risk or response to therapy.55,56 ED patients
treated, admitted, and treated in an inpatient bed for heart
failure account for the majority of expenditures.57 Up to 80% of
patients discharged from the hospital with a primary diagnosis
of heart failure come from the ED.55,58,59 According to
American College of Cardiology, American Heart Association,
and Agency for Health Care Policy and Research guidelines, it
has been suggested that up to 50% of admitted patients are low
risk and may be candidates for brief observation unit or
outpatient therapy, a potential savings of $2.5 billion.55,60
Poor ED risk stratification, particularly overestimation of
disease severity, is a fundamental cause of overuse of limited
inhospital resources for this rapidly growing patient
population.59,61 Improving the ability of the emergency
physician to decide on the most appropriate disposition for
acute heart failure syndrome patients is critical to maximizing
the allocation of resources. Current guidelines for disposition
are based on either little evidence or are provided without
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evidence.14,16,62,63 The 2005 American College of Cardiology/

American Heart Association guidelines addressed the evaluation
and management of chronic heart failure.14 In 2006, the Heart
Failure Society of America published detailed guidelines on
heart failure management and broad goals of therapy but did
not specifically address ED disposition.63 The American College
of Emergency Physicians 2007 acute heart failure syndromes
clinical policy addressed 4 critical areas of diagnosis and
management but did not give recommendations about
disposition and risk stratification.64
During the last 15 years, several studies have considered EDbased risk models for heart failure patients (Table 3).65 Selker
et al66 developed a model to predict inhospital mortality from
data available to the ED physician within the first 10 minutes of
presentation (patients age, systolic blood pressure, and findings
on ECG). The model was prospectively validated for mortality,
but its validity for morbidity and other acute sequelae is
unknown. Additionally, the ability of the model to differentiate
a low-risk patient who can be safely discharged home was not
assessed; the model was developed to identify the high-risk
patient. Chin and Goldman67 developed a risk model with a
larger number of variables (vital signs, comorbidities, ECG
findings, and laboratory data). The model was successful in
predicting morbidity and mortality, but it did not delineate the
low-risk patient.
Findings from a large cohort of patients suggest that systolic
blood pressure is an independent predictor of morbidity and
mortality in patients with heart failure and either reduced or
relatively preserved systolic function. Low systolic blood
pressure (120 mm Hg) at hospital admission identifies
patients who have a poor prognosis despite medical therapy.4
Finally, activation of vasopressin, leading to fluid retention and
hyponatremia (136 mEq/L),68 has been associated with a poor
prognosis.69 Further, patients with hyponatremia despite the use
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Collins et al

Table 3. Previous risk stratification studies in acute heart failure syndromes.

No.

Subject
Type

Diercks/2006
Burkhardt/2005
Auble/2005

499
385
33,533

E
I
I

Fonarow/2005
Felker/2004

65,275
949

First Author/Year

Study
Type

Outcome*

Significant Variables

P
R
R

LOS 24 h, 30-day events

Observation unit discharge
Inpatient complications and mortality

I
I

R
R

Inpatient mortality
60-Day mortality/readmission

4031
434
112
220
120
57
257

I
I
E
I
I
I
I

R
R
R
R
R
R
R, S

30-Day and 1-y mortality

30-Day readmission
3-mo Readmission and mortality
16-mo Mortality
Inpatient complications
Inpatient and 6-mo mortality
60-Day readmission and mortality

Chin/1996
Selker/1994
Brophy/1994

435
401
153

I
I
E

R
PA, R
P

Inpatient complications
Inpatient mortality
44-mo Mortality

Brophy/1993

153

LOS and 6-mo mortality

Esdaile/1992

191

PA, R

Inpatient mortality

Katz/1988

216

2-Day complications

55

PA, R

Inpatient and 1-y mortality

SBP, troponin I
BUN
Na, SBP, white blood cell count, pH,
creatinine
BUN, creatinine, SBP
Age, SBP, BUN, Na, Hgb, no. past
admissions, class IV symptoms
Age, SBP, RR, BUN, sodium
Sex, COPD, previous admissions
RR
SBP, creatinine, rales
O2 sat, creatinine, pulmonary edema
Sodium, sex
Marital status, comorbidity index, admission
SBP, no ST-T changes
Initial SBP, RR, sodium, ST-T changes
Age, SBP, T-wave flattening, HR
Previous HF admission, sodium, IVCD,
amount furosemide given
Left atrial size, cardiac ischemia, slow
response to diuresis
Age, chest pain, cardiac ischemia, valvular dz,
arrhythmia, new onset, poor clinical
response
4-h Diuresis, history of pulmonary edema,
T-wave abnormalities, JVD
Admit SBP, dyspnea, peak CPK

Lee/2003
Harjai/2001
Rame/2001
Cowie/2000
Butler/1998
Villacorta/1998
Chin/1997

Plotnick/1982

E, ED patients; P, prospective; LOS, length of stay; SBP, systolic blood pressure; I, inpatients; R, retrospective medical record review; BUN, blood urea nitrogen, Na,
sodium; Hgb, hemoglobin; RR, respiratory rate; COPD, chronic obstructive pulmonary disease; O2 sat, oxygen saturation; HF, heart failure; IVCD, intraventricular conduction delay; JVD, jugular venous distension; CPK, creatine phosphokinase.
*Complications include mortality.

of angiotensin-converting enzyme inhibitors have been shown

to be at the greatest risk of mortality.70
Recently, a large administrative database was used to validate
4 acute heart failure syndromes clinical prediction rules. Results
from this analysis suggest that characterization of the truly lowrisk patient remains elusive.71 The limitations of the previous
models notwithstanding, these findings form a reasonable
foundation for identifying high-risk features. Recurrently
identified variables that predict high risk of subsequent
morbidity and mortality include the following: low serum
sodium level, ischemic ECG changes, significant hypertension
or hypotension at presentation, poor diuresis in the
hypervolemic patient, and abnormal renal function. Further,
increased natriuretic peptide values have been found to suggest
an increased risk of adverse events and may add independent
information about risk beyond the treating physicians
estimation.72,73 Lack of high risk cannot be equated to presence
of low risk.
Indeed, even in patients considered to be at low physiologic
risk, poor health care behavior (access to health care, dietary and
medication compliance) can result in hospitalization and
significant morbidity, further contributing to suboptimal
disposition decisionmaking.1-4 Other studies suggest that
52 Annals of Emergency Medicine

although physiologic markers predict short- and intermediateterm event rates, health care behavior has a much higher impact
on more distant event rates.60,66,67,74-78 Several studies have
identified markers of poor health care behavior that predict late
events in acute heart failure syndrome patients. Noncompliance
(medication and diet), inadequate discharge planning and
follow-up, and previous heart failure admissions are associated
with 90-day readmission.74,76,77 Although these inpatient
studies have identified health care behavior as a risk factor for
late events, prospective ED quantification of this relationship
has yet to be performed. Further, discharge planning resources
in the ED are often limited compared with that of inpatient
units, making it even more difficult to provide adequate
transition of care to the outpatient setting. Thus, even patients
without high-risk features and with an initial adequate response
to therapy may still be difficult to discharge directly home from
the ED because of anticipated poor health care behavior. An
ED-based observation unit may serve as an alternative to
admission in non high-risk patients who would benefit from
further treatment and risk stratification while outpatient followup is arranged.
ED observation units. With the lack of validated risk
stratification tools, the observation unit provides a reasonable
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Collins et al
alternative to ED discharge. An observation unit represents an
area where ED patients can receive extended evaluation and
treatment for up to 24 hours in an attempt to further delineate
their need for hospital admission. Preliminary research suggests
the observation unit is a safe and resource-efficient alternative to
admission for acute heart failure syndrome patients.79-81 Recent
investigations suggest that ultrafiltration, a tool that may be
used in the observation unit, aids in removal of extracellular
fluid without significant alterations in vital signs.82-85
Appropriate observation unit candidates have an expectation
of hospital stays less than 48 hours, no diagnosis traditionally
requiring hospitalization, no procedures or therapies requiring
specialized hospital care, and no mortality.86 Including patients
who stay up to 48 hours (observation units are used for acute
heart failure syndrome for up to 24 hours) is justified because
ED/observation unit management is typically accelerated in
comparison to hospital management.87-90 Preliminary
retrospective research has identified criteria that characterize
acute heart failure syndrome patients suitable for safe
observation unit admission and discharge. However, prospective
validation is necessary to definitively characterize features of
patients suitable for observation unit management so caregivers
can increase observation unit use, decrease hospital admissions,
and optimize care protocols.

FUTURE DIRECTIONS
Several areas of research are still necessary to advance the
management of acute heart failure syndromes, with an overall
goal of decreasing the hospital admission rate while improving
short- and long-term event rates. To improve on the
approximately 20% ED misdiagnosis rate, practical, readily
available diagnostics that combine physician pretest probability
with an objective measurement of ventricular function and
filling pressure are necessary.25,39,91 Acute therapeutic
algorithms need to account for the underlying pathophysiology
(systolic versus diastolic dysfunction), as well as the acute
hemodynamic features, on ED presentation. Consideration of
the downstream consequences of acute therapies must also be
factored into the physicians treatment algorithm. Finally, a
change in the paradigm of the conservative decision to admit
the heart failure patient requires a novel, prospective, ED-based
approach; even with the development of new diagnostic and
prognostic tools, poor ED risk stratification and the high rate of
critical care admissions for acute heart failure syndrome patients
have not changed in decades.55,58,59 A prospectively derived,
multicenter, useful, ED risk stratification model for patients
with signs and symptoms of heart failure is sorely needed and is
the focus of an ongoing National Heart, Lung, and Blood
Institute RO1 grant being directed by emergency medicine
investigators.92 Such approaches have proven effective at safely
decreasing admissions for low-risk patients with other disease
processes such as acute coronary syndromes93-95 and
community-acquired pneumonia.96-98
Further, future studies need to alter the risk stratification
standards from prediction of adverse outcomes occurring at
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Beyond Pulmonary Edema

remote times from ED evaluation (eg, 90 days, 1 year) to
prediction of outcomes associated with the patients acute heart
failure event (5, 7, and 14 days). This is a significant and
necessary change in approach. The association between events
occurring remotely from an ED visit and the ED disposition
decision is not clear; these events depend more on inpatient and
outpatient care and patient behavior than ED disposition
decisions.67,77,78,99-103 Throughout the last 2 decades, many
studies of AHFS risk stratification have been conducted and
have identified physiologic variables (blood pressure, blood urea
nitrogen, creatinine) as predictors of early (5-day) events.68,69,75
Further, several other studies have identified markers of poor
health behavior (medication and diet compliance) that predict
late adverse events in patients with AHFS.74,76,77 The
association between events occurring remotely from an ED visit
and the ED disposition decision is not clear; these events
depend more on inpatient and outpatient care and patient
behavior than ED disposition decisions.67,76-78,99,101-103 We
speculate that prospectively categorizing patients at low risk of
intermediate term (5-day) events will facilitate more aggressive
disposition decisionmaking while focusing on health behavior
interventions that can be initiated while in the ED or
observation unit.
Improvement in comprehensive acute heart failure care
requires a unified approach by emergency physicians,
cardiologists, primary care physicians, and other caregivers.
Because the majority of heart failure admissions originate in the
ED, the emergency physician is ideally positioned to have a
profound impact on health care expenditures through costeffective disposition decisionmaking. Although a subset of
chronic heart failure patients are treated by cardiologists during
an acute exacerbation, many other acute heart failure syndrome
patients are treated by general internists (hospitalists) during an
inpatient admission.104 Differing opinions in management need
to be resolved through consensus-guided, evidence-based
algorithms that are developed after input from all specialties
involved.
Akin to trials of fibrinolytic therapy in myocardial infarction
several decades ago, early diagnosis, intervention, and guidelinedriven care are necessary to improve outcomes. To establish the
guidelines to direct care, we must come to agreement on feasible
therapeutic goals and appropriate endpoints. Diagnostic,
therapeutic, and prognostic trials need to be designed and
conducted, with input from all the stakeholders. Establishment
of an acute heart failure syndromes clinical trials network is
sorely needed. The network would facilitate input from each
specialty about appropriate study design and endpoints. Rapid
enrollment in definitive, large-scale prospective trials would be
possible. Most important, dissemination of significant results
would be possible through clinical policies from the involved
specialties societies.
To accomplish these goals, we must learn from the failures of
previous trials, in which only select subsets of acute heart failure
syndrome patients were enrolled.105,106 This select enrollment
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Beyond Pulmonary Edema

does not reflect the majority of ED patients, and, more
important, the trials were often not conducted early in the
patients presentation. Extrapolating results from inpatient trials
to ED patients has not proven useful; patients must be enrolled
and studies conducted in the ED early in the course of the acute
exacerbation. Without appropriate ED participation, we cannot
expect adoption of comprehensive diagnostic and therapeutic
strategies by emergency physicians.
Summary
Although outpatient heart failure care has improved with the
introduction of angiotensin-converting enzyme inhibitors, blockers, and cardiac resynchronization in selected patients,
acute heart failure syndromes presentations remain a diagnostic,
therapeutic, and prognostic dilemma. The misdiagnosis rate and
admission rate have remained largely unchanged for several
decades. Further, short-term morbidity, mortality, and
recidivism have also remained unacceptably high. Recent
registry data suggest that there is a variety of acute heart failure
syndromes presentations encountered in the ED, each with
dramatically different underlying pathophysiology and acute
hemodynamics. Despite this, our management strategies have
changed little, and new beneficial therapeutic agents are lacking.
An acute heart failure syndromes paradigm shift is necessary if
we are to improve overall care for this heterogeneous and
protean cohort of patients.
The authors would like to acknowledge Todd Roat and Amy
Hess for their technical assistance during article preparation and
submission.
Supervising editor: Donald M. Yealy, MD
Donald M. Yealy, MD, was the supervising editor of this
article. W. Brian Gibler, MD, did not participate in the editorial
review or decision to publish this article.
Author contributions: SC, AS, and JK conceived the article.
All authors contributed substantially to the manuscript. SC
takes responsibility for the paper as a whole.
Funding and support: By Annals policy, all authors are required
to disclose any and all commercial, financial, and other
relationships in any way related to the subject of this article,
that might create any potential conflict of interest. See the
Manuscript Submission Agreement in this issue for examples
of specific conflicts covered by this statement. SC received
research support from Biosignetics and Inovise Medical, Inc.,
and NIH/NHLBI, received previous honoraria from SCIOS,
Inovise Medical, Inc., and PDL Biopharma, and works as a
consultant for Abbott-Point-of-Care. ABS received research
support from Biosignetics, Abbott Laboratories, Inovise
Medical Inc., Inverness Medical Innovations, NIH/NHLBI, and
Biosite, Inc., and worked as a consultant for the Medicines
Company and Molecular Insights Pharmaceutical. JDK received
research support from Biosite and Inovise Medical, Inc., and
was a consultant and on the speakers bureau for Biosite.
DBD received an honorarium from SCIOS, received research

54 Annals of Emergency Medicine

Collins et al
support from Dade-Behring and Inovise. MG received research
support from NIH, Otsuk, Sigma Tau, Merck & Company, and
SCIOS; MG is a consultant for GlaxoSmithKline, PDL,
Errekappa Terapeutici, Medtronic, Debbio Pharm, and receive
honoraria from Medtronic, AstraZeneca; SCIOS,
GlaxoSmithKline, Otsuka, PDF, Abbott, and Sigma Tau.
Publication dates: Received for publication May 3, 2007.
Revisions received June 22, 2007, and June 26, 2007.
Accepted for publication July 9, 2007. Available online
September 14, 2007.
Earn CME Credit: Continuing Medical Education for this article
is available at: www.ACEP-EMedHome.com.
Reprints not available from the authors.
Address for correspondence: Sean Collins, MD, MSc,
Assistant Professor, University of Cincinnati, Department of
Emergency Medicine, 231 Albert Sabin Way, Cincinnati, OH
45267; 513-558-8079, fax 513-558-5791; E-mail
sean.collins@uc.edu.

REFERENCES
1. Adams KF Jr, Fonarow GC, Emerman CL, et al. Characteristics
and outcomes of patients hospitalized for heart failure in the
United States: rationale, design, and preliminary observations
from the first 100,000 cases in the Acute Decompensated Heart
Failure National Registry (ADHERE). Am Heart J. 2005;149:209216.
2. Fonarow G, Abraham WT, Albert NM, et al. Characteristics,
treatment and outcomes of patients hospitalized for heart failure
with preserved systolic function: a report from OPTIMIZE-HF.
J Am Coll Cardiol. 2006;47(suppl A):47A.
3. Cleland JG, Swedberg K, Follath F, et al. The EuroHeart Failure
survey programmea survey on the quality of care among
patients with heart failure in Europe. Part 1: patient
characteristics and diagnosis. Eur Heart J. 2003;24:442-463.
4. Gheorghiade M, Abraham WT, Albert NM, et al. Systolic blood
pressure at admission, clinical characteristics, and outcomes in
patients hospitalized with acute heart failure. JAMA. 2006;296:
2217-2226.
5. Tsao LCG. Heart failure: an epidemic of the 21st century. Crit
Pathways Cardiol. 2004;3:194-204.
6. Taylor TB. Threats to the health care safety net. Acad Emerg
Med. 2001;8:1080-1087.
7. Glauser J. Rationing and the role of the emergency department
as societys safety net. Acad Emerg Med. 2001;8:1101-1106.
8. Gordon JA, Billings J, Asplin BR, et al. Safety net research in
emergency medicine: proceedings of the Academic Emergency
Medicine Consensus Conference on the Unraveling Safety Net.
Acad Emerg Med. 2001;8:1024-1029.
9. Stern RS, Weissman JS, Epstein AM. The emergency department
as a pathway to admission for poor and high-cost patients.
JAMA. 1991;266:2238-2243.
10. Richardson LD, Hwang U. Access to care: a review of the
emergency medicine literature. Acad Emerg Med. 2001;8:10301036.
11. Bernstein E, Goldfrank LR, Kellerman AL, et al. A public health
approach to emergency medicine: preparing for the twenty-first
century. Acad Emerg Med. 1994;1:277-286.
12. McCaig LF, Burt CW. National Hospital Ambulatory Medical Care
Survey: 2001 emergency department summary. Adv Data. 2003;
335:1-29.

Volume , . : January

Collins et al
13. McCaig LF, Burt CW. National Hospital Ambulatory Medical Care
Survey: 2002 emergency department summary. Adv Data. 2004;
1-34.
14. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline
update for the diagnosis and management of chronic heart
failure in the adultsummary article: a report of the American
College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Writing Committee to Update the 2001
Guidelines for the Evaluation and Management of Heart Failure).
J Am Coll Cardiol. 2005;46:1116-1143.
15. Heart Failure Society of America. HFSA guidelines for the
management of patients with heart failure due to left ventricular
systolic dysfunctionpharmacological approaches. Congest
Heart Fail. 2000;6:11-39.
16. Konstam M, Dracup K, Baker D. Clinical practice guidelines No.
11: heart failure: evaluation and care of patients with leftventricular systolic dysfunction. Agency Health Care Policy and
Res. 1994;94.
17. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of
the guidelines on the diagnosis and treatment of acute heart
failure: the Task Force on Acute Heart Failure of the European
Society of Cardiology. Eur Heart J. 2005;26:384-416.
18. Ho KK, Anderson KM, Kannel WB, et al. Survival after the onset
of congestive heart failure in Framingham Heart Study subjects.
Circulation. 1993;88:107-115.
19. McKee PA, Castelli WP, McNamara PM, et al. The natural history
of congestive heart failure: the Framingham Study. N Engl
J Med. 1971;285:1441-1446.
20. Fonseca C, Oliveira AG, Mota T, et al. Evaluation of the
performance and concordance of clinical questionnaires for the
diagnosis of heart failure in primary care. Eur J Heart Fail. 2004;
6:21-22, 813-820.
21. Gheorghiade M, Beller GA. Effects of discontinuing maintenance
digoxin therapy in patients with ischemic heart disease and
congestive heart failure in sinus rhythm. Am J Cardiol. 1983;51:
1243-1250.
22. Schocken DD, Arrieta MI, Leaverton PE, et al. Prevalence and
mortality rate of congestive heart failure in the United States.
J Am Coll Cardiol. 1992;20:301-306.
23. Carlson KJ, Lee DC, Goroll AH, et al. An analysis of physicians
reasons for prescribing long-term digitalis therapy in outpatients.
J Chronic Dis. 1985;38:733-739.
24. Knudsen CW, Omland T, Clopton P, et al. Diagnostic value of
B-type natriuretic peptide and chest radiographic findings in
patients with acute dyspnea. Am J Med. 2004;116:363-368.
25. 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.
2006;47:13-18.
26. Mahdyoon H, Klein R, Eyler W, et al. Radiographic pulmonary
congestion in end-stage congestive heart failure. Am J Cardiol.
1989;63:625-627.
27. Walsh MN, Tavel ME. Evaluation and management of a patient
with congestive heart failure. Chest. 2003;124:728-731.
28. Heart Failure Society of America. Evaluation of patients for
ventricular dysfunction and heart failure. J Card Fail. 2006;12:
e16-25.
29. Nieminen MS, Bohm M, Cowie MR, et al. [Diagnosis and
treatment of acute heart failure. Guidelines of the European
Society of Cardiology]. Kardiol Pol. 2005;63:143-186;
discussion 87-89.
30. Colucci WS. Clinical Manifestations and Evaluation of the Patient
with Suspected Heart Failure. UptoDate, Inc; 2006.

Volume , . : January

Beyond Pulmonary Edema

31. Davie AP, Francis CM, Love MP, et al. Value of the
electrocardiogram in identifying heart failure due to left
ventricular systolic dysfunction. BMJ. 1996;312:222.
32. Schwam E. B-type natriuretic peptide for diagnosis of heart
failure in emergency department patients: a critical appraisal.
Acad Emerg Med. 2004;11:686-691.
33. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic
peptide and clinical judgment in emergency diagnosis of heart
failure: analysis from Breathing Not Properly (BNP) Multinational
Study. Circulation. 2002;106:416-422.
34. Maisel AS, Clopton P, Krishnaswamy P, et al. Impact of age,
race, and sex on the ability of B-type natriuretic peptide to aid in
the emergency diagnosis of heart failure: results from the
Breathing Not Properly (BNP) Multinational Study. Am Heart J.
2004;147:1078-1084.
35. Luchner A, Hengstenberg C, Lowel H, et al. Effect of
compensated renal dysfunction on approved heart failure
markers: direct comparison of brain natriuretic peptide (BNP)
and N-terminal pro-BNP. Hypertension. 2005;46:118-123.
36. Chenevier-Gobeaux C, Claessens YE, Voyer S, et al. Influence of
renal function on N-terminal pro-brain natriuretic peptide (NTproBNP) in patients admitted for dyspnoea in the emergency
department: comparison with brain natriuretic peptide (BNP).
Clin Chim Acta. 2005;361:167-175.
37. Drazner MH, Rame JE, Stevenson LW, et al. Prognostic
importance of elevated jugular venous pressure and a third
heart sound in patients with heart failure. N Engl J Med. 2001;
345:574-581.
38. Stevenson LW, Perloff JK. The limited reliability of physical signs
for estimating hemodynamics in chronic heart failure. JAMA.
1989;261:884-888.
39. Collins SP, Lindsell CJ, Peacock WF, et al. The combined utility
of an S3 heart sound and B-type natriuretic peptide levels in
emergency department patients with dyspnea. J Card Fail. 2006;
12:286-292.
40. Collins S, Lindsell CJ, Peacock WF, et al. The effect of treatment
on the presence of abnormal heart sounds in emergency
department patients with heart failure. Am J Emerg Med. 2006;
24:25-32.
41. Marcus GM, Gerber IL, McKeown BH, et al. Association between
phonocardiographic third and fourth heart sounds and objective
measures of left ventricular function. JAMA. 2005;293:22382244.
42. Collins SP, Mielniczuk LM, Whittingham HA, et al. The use of
noninvasive ventilation in emergency department patients with
acute cardiogenic pulmonary edema: a systematic review. Ann
Emerg Med. 2006;48:260-269, 9 e1-4.
43. Masip J, Roque M, Sanchez B, et al. Noninvasive ventilation in
acute cardiogenic pulmonary edema: systematic review and
meta-analysis. JAMA. 2005;294:3124-3130.
44. Moore CL, Rose GA, Tayal VS, et al. Determination of left
ventricular function by emergency physician echocardiography of
hypotensive patients. Acad Emerg Med. 2002;9:186-193.
45. Randazzo MR, Snoey ER, Levitt MA, et al. Accuracy of
emergency physician assessment of left ventricular ejection
fraction and central venous pressure using echocardiography.
Acad Emerg Med. 2003;10:973-977.
46. Garrard CL Jr, Weissler AM, Dodge HT. The relationship of
alterations in systolic time intervals to ejection fraction in
patients with cardiac disease. Circulation. 1970;42:455-462.
47. Linde M, Ohnhaus EE, Kirch W. The Heather Index in
impedance cardiography. Int J Cardiol. 1988;19:387-388.
48. Peacock WF, Summers RL, Vogel J, et al. Impact of impedance
cardiography on diagnosis and therapy of emergent dyspnea: the
ED-IMPACT trial. Acad Emerg Med. 2006;13:365-371.

Annals of Emergency Medicine 55

Beyond Pulmonary Edema

49. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of
congestive heart failure and pulmonary artery catheterization
effectiveness: the ESCAPE trial. JAMA. 2005;294:1625-1633.
50. Shah MR, Hasselblad V, Stevenson LW, et al. Impact of the
pulmonary artery catheter in critically ill patients: meta-analysis
of randomized clinical trials. JAMA. 2005;294:1664-1670.
51. Badgett RG, Lucey CR, Mulrow CD. Can the clinical examination
diagnose left-sided heart failure in adults? JAMA. 1997;277:
1712-1719.
52. Sharma GV, Woods PA, Lambrew CT, et al. Evaluation of a
noninvasive system for determining left ventricular filling
pressure. Arch Intern Med. 2002;162:2084-2088.
53. Peacock WF, Fonarow GC, Emerman CL, et al. Impact of early
initiation of intravenous therapy for acute decompensated heart
failure on outcomes in ADHERE. Cardiology. 2006;107:44-51.
54. Gheorghiade M, De Luca L, Fonarow GC, et al. Pathophysiologic
targets in the early phase of acute heart failure syndromes.
Am J Cardiol. 2005;96:11G-7G.
55. Graff L, Orledge J, Radford MJ, et al. Correlation of the Agency
for Health Care Policy and Research congestive heart failure
admission guideline with mortality: Peer Review Organization
Voluntary Hospital Association Initiative to Decrease Events
(PROVIDE) for congestive heart failure. Ann Emerg Med. 1999;
34(4 pt 1):429-437.
56. American Heart Association. Heart Disease and Stroke
Statistics2006 Update. Dallas, TX;2005.
57. National Heart, Lung and Blood Institute. Morbidity and
Mortality: 2002 Chart Book on Cardiovascular, Lung, and Blood
Diseases. Bethesda, MD: National Institutes of Health; 2002.
58. Polanczyk CA, Rohde LE, Philbin EA, et al. A new casemix
adjustment index for hospital mortality among patients with
congestive heart failure. Med Care. 1998;36:1489-1499.
59. Smith WR, Poses RM, McClish DK, et al. Prognostic judgments
and triage decisions for patients with acute congestive heart
failure. Chest. 2002;121:1610-1617.
60. Butler J, Hanumanthu S, Chomsky D, et al. Frequency of low-risk
hospital admissions for heart failure. Am J Cardiol. 1998;81:
41-44.
61. Poses RM, Smith WR, McClish DK, et al. Physicians survival
predictions for patients with acute congestive heart failure. Arch
Intern Med. 1997;157:1001-1007.
62. Hsieh M, Yealy DM. Are we ignoring the evidence? Acad Emerg
Med. 2005;12:461-462.
63. Heart Failure Society of America. HFSA 2006 comprehensive
heart failure practice guideline. J Card Fail. 2006;12:e1-2.
64. Silvers SM, Howell JM, Kosowsky JM, et al. Clinical policy:
critical issues in the evaluation and management of adult
patients presenting to the emergency department with acute
heart failure syndromes. Ann Emerg Med. 2007;49:627-669.
65. Hsieh M, Auble TE, Yealy DM. Evidence-based emergency
medicine. Predicting the future: can this patient with acute
congestive heart failure be safely discharged from the
emergency department? Ann Emerg Med. 2002;39:181-189.
66. Selker HP, Griffith JL, DAgostino RB. A time-insensitive
predictive instrument for acute hospital mortality due to
congestive heart failure: development, testing, and use for
comparing hospitals: a multicenter study. Med Care. 1994;32:
1040-1052.
67. Chin MH, Goldman L. Correlates of major complications or death
in patients admitted to the hospital with congestive heart failure.
Arch Intern Med. 1996;156:1814-1820.
68. Lee DS, Austin PC, Rouleau JL, et al. Predicting mortality among
patients hospitalized for heart failure: derivation and validation
of a clinical model. JAMA. 2003;290:2581-2587.

56 Annals of Emergency Medicine

Collins et al
69. Felker GM, Leimberger JD, Califf RM, et al. Risk stratification
after hospitalization for decompensated heart failure. J Card
Fail. 2004;10:460-466.
70. Brophy JM, Deslauriers G, Rouleau JL. Long-term prognosis of
patients presenting to the emergency room with decompensated
congestive heart failure. Can J Cardiol. 1994;10:543-547.
71. Auble TE, Hsieh M, McCausland JB, et al. Comparison of four
clinical prediction rules for estimating risk in heart failure. Ann
Emerg Med. 2007;50:127-135.
72. Harrison A, Morrison LK, Krishnaswamy P, et al. B-type
natriuretic peptide predicts future cardiac events in patients
presenting to the emergency department with dyspnea. Ann
Emerg Med. 2002;39:131-138.
73. Maisel A, Hollander JE, Guss D, et al. Primary results of the
Rapid Emergency Department Heart Failure Outpatient Trial
(REDHOT). A multicenter study of B-type natriuretic peptide
levels, emergency department decision making, and outcomes
in patients presenting with shortness of breath. J Am Coll
Cardiol. 2004;44:1328-1333.
74. Vinson JM, Rich MW, Sperry JC, et al. Early readmission of
elderly patients with congestive heart failure. J Am Geriatr Soc.
1990;38:1290-1295.
75. Fonarow GC, Adams KF Jr, Abraham WT, et al. Risk stratification for
in-hospital mortality in acutely decompensated heart failure:
classification and regression tree analysis. JAMA. 2005;293:572-580.
76. Krumholz HM, Amatruda J, Smith GL, et al. Randomized trial of
an education and support intervention to prevent readmission of
patients with heart failure. J Am Coll Cardiol. 2002;39:83-89.
77. Rich MW, Beckham V, Wittenberg C, et al. A multidisciplinary
intervention to prevent the readmission of elderly patients with
congestive heart failure. N Engl J Med. 1995;333:1190-1195.
78. Ghali JK, Kadakia S, Cooper R, et al. Precipitating factors
leading to decompensation of heart failure. Traits among urban
blacks. Arch Intern Med. 1988;148:2013-2016.
79. Peacock WFT, Remer EE, Aponte J, et al. Effective observation
unit treatment of decompensated heart failure. Congest Heart
Fail. 2002;8:68-73.
80. Storrow AB, Collins SP, Lyons MS, et al. Emergency department
observation of heart failure: preliminary analysis of safety and
cost. Congest Heart Fail. 2005;11:68-72.
81. Peacock W, Young J, Collins S, et al. Heart failure observation
units: optimizing care. Ann Emerg Med. 2006;47:22-33.
82. Sharma A, Hermann DD, Mehta RL. Clinical benefit and
approach of ultrafiltration in acute heart failure. Cardiology.
2001;96:144-154.
83. Jaski BE, Ha J, Denys BG, et al. Peripherally inserted venovenous ultrafiltration for rapid treatment of volume overloaded
patients. J Card Fail. 2003;9:227-231.
84. Marenzi G, Lauri G, Grazi M, et al. Circulatory response to fluid
overload removal by extracorporeal ultrafiltration in refractory
congestive heart failure. J Am Coll Cardiol. 2001;38:963-968.
85. Costanzo MR, Guglin ME, Saltzberg MT, et al. Ultrafiltration versus
intravenous diuretics for patients hospitalized for acute
decompensated heart failure. J Am Coll Cardiol. 2007;49:675-683.
86. Sinclair D, Green R. Emergency department observation unit:
can it be funded through reduced inpatient admission? Ann
Emerg Med. 1998;32:670-675.
87. Zwicke DL, Donohue JF, Wagner EH. Use of the emergency
department observation unit in the treatment of acute asthma.
Ann Emerg Med. 1982;11:77-83.
88. Henneman PL, Marx JA, Cantrill SC, et al. The use of an
emergency department observation unit in the management of
abdominal trauma. Ann Emerg Med. 1989;18:647-650.
89. Mace SE. Asthma therapy in the observation unit. Emerg Med
Clin North Am. 2001;19:169-185.

Volume , . : January

Collins et al
90. Hostetler B, Leikin JB, Timmons JA, et al. Patterns of use of an
emergency department-based observation unit. Am J Ther.
2002;9:499-502.
91. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type
natriuretic peptide in the diagnosis of congestive heart failure in
an urgent-care setting. J Am Coll Cardiol. 2001;37:379-385.
92. Storrow AB, Collins S, Disalvo T, et al. Improving Heart Failure Risk
Stratification in the ED: Stratify 1R01HL088459-01. NHLBI; 2007.
93. Tatum JL, Jesse RL, Kontos MC, et al. Comprehensive strategy
for the evaluation and triage of the chest pain patient. Ann
Emerg Med. 1997;29:116-125.
94. Gibler WB, Runyon JP, Levy RC, et al. A rapid diagnostic and
treatment center for patients with chest pain in the emergency
department. Ann Emerg Med. 1995;25:1-8.
95. Storrow AB, Gibler WB. Chest pain centers: diagnosis of acute
coronary syndromes. Ann Emerg Med. 2000;35:449-461.
96. Yealy DM, Auble TE, Stone RA, et al. The emergency department
community-acquired pneumonia trial: methodology of a quality
improvement intervention. Ann Emerg Med. 2004;43:770-782.
97. Marrie TJ, Lau CY, Wheeler SL, et al. A controlled trial of a critical
pathway for treatment of community-acquired pneumonia. CAPITAL
Study Investigators. Community-Acquired Pneumonia Intervention
Trial Assessing Levofloxacin. JAMA. 2000;283:749-755.
98. Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify
low-risk patients with community-acquired pneumonia. N Engl
J Med. 1997;336:243-250.

Volume , . : January

Beyond Pulmonary Edema

99. Chin MH, Goldman L. Correlates of early hospital readmission or
death in patients with congestive heart failure. Am J Cardiol.
1997;79:1640-1644.
100. Villacorta H, Rocha N, Cardoso R, et al. Hospital outcome and
short-term follow-up of elderly patients presenting to the
emergency unit with congestive heart failure. Arq Bras Cardiol.
1998;70:167-171.
101. Ashton CM, Kuykendall DH, Johnson ML, et al. The association
between the quality of inpatient care and early readmission. Ann
Intern Med. 1995;122:415-421.
102. Krumholz HM, Parent EM, Tu N, et al. Readmission after
hospitalization for congestive heart failure among Medicare
beneficiaries. Arch Intern Med. 1997;157:99-104.
103. Krumholz HM, Chen YT, Wang Y, et al. Predictors of readmission
among elderly survivors of admission with heart failure. Am
Heart J. 2000;139(1 pt 1):72-77.
104. Amin AN. The role of hospitalists in the management of acute
decompensated heart failure. Am Heart Hosp J. 2005;3:111117.
105. VMAC Investigators. Intravenous nesiritide vs nitroglycerin for
treatment of decompensated congestive heart failure: a
randomized controlled trial. JAMA. 2002;287:1531-1540.
106. Gheorghiade M, Konstam MA, Burnett JC Jr, et al.
Short-term clinical effects of tolvaptan, an oral vasopressin
antagonist, in patients hospitalized for heart failure:
the EVEREST Clinical Status Trials. JAMA. 2007;297:
1332-1343.

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